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Was Rome's fall due to heavy metal poisoning making Romans dumber?Ice cores that preserve traces of atmospheric pollutants through history have revealed that industrial activity by Romans – particularly the use and production of lead – meant the air the Romans breathed was heavily contaminated. The levels were high enough to cause neurological problems, including a drop in cognitive function across the population. Joe McConnell and his team at the Desert Research Institute published their findings in the journal PNAS.Bats are surfing storms to make migration easierMigrating bats in Europe have to fly up to 2000km while pregnant, but they've figured out how to get a lift from the weather. The bats have been observed waiting for storm fronts, and then surfing the strong winds in front of the storm to save energy during their migration. Dina Dechmann from the Max Planck Institute of Animal Behaviour, and colleagues, were able to tag bats with tiny specialized sensors to track their nocturnal movements during migration. Their paper was published in the journal Science.Squirrels have developed a taste for vole fleshSquirrels in California have been taking advantage of a boom in the population of tiny rodents called voles – by hunting and eating them. This widespread carnivorous behaviour was captured for the first time on videos and photos by a team led by behavioural ecologist Jennifer Smith, as a part of a long-term study of the squirrels. The researchers found dozens of instances of the squirrels killing the voles, which they say changes our fundamental understanding of ground squirrels. Their paper was published in the Journal of Ethology.EEG tattoos could outperform standard electrodes EEG is a valuable technology that allows researchers to monitor the electrical activity of the brain, but standard EEG electrodes are cumbersome and are hampered by the difficulty of attaching them. A new temporary EEG tattoo, made by printing conductive ink on the scalp, could be a step ahead. Luize Vasconcelos, a postdoctoral fellow at the University of Texas at Austin helped create this ink. The research is published in the Cell Press journal Cell Biomaterials.To monitor cat brain waves, researchers made them cute hatsAude Castel, a veterinary neurologist from the Université de Montréal, and her team were  studying chronic pain in cats — and ways to alleviate it — when she realized that she could crochet hats for the cats and add EEG electrodes to them in order to study their brains. Their research was published in the Journal of Neuroscience Methods. When North America went to the dogs (or vice-versa)Researchers examining canid bones from Alaska dating to the last ice age have been intrigued by the complex picture it shows of dog domestication at the time. Their findings were published in the journal Science Advances. Signs of the animals' diet are preserved in the bones, and shows that humans were clearly feeding their dogs, a clear sign of domestication. François Lanoë from the University of Arizona led the work.

JCO PO authors Dr. Philippe Bedard (Staff Medical Oncologist at Princess Margaret Cancer Centre and Professor of Medicine at University of Toronto) and Dr. Alberto Hernando Calvo (Medical Oncologist at Vall d´Hebron University Hospital) share insights into their JCO PO article, “Combined Transcriptome and Circulating Tumor DNA Longitudinal Biomarker Analysis Associates With Clinical Outcomes in Advanced Solid Tumors Treated With Pembrolizumab,” one of the top downloaded articles of 2024. Host Dr. Rafeh Naqash and Drs. Bedard and Hernando Calvo discuss how combined transcriptome and ctDNA longitudinal analysis associates with pembrolizumab outcomes. TRANSCRIPT Dr. Rafeh Naqash: Hello and welcome to JCO Precision Oncology Conversations where we bring you engaging conversations with authors of clinically relevant and highly significant JCO PO articles. I'm your host, Dr. Rafeh Naqash, podcast editor for JCO Precision Oncology and Assistant Professor at the OU Health Stephenson Cancer Center at the University of Oklahoma.  Today we are excited to be joined by Dr. Philippe Bedard, Staff Medical Oncologist at the Princess Margaret Cancer Center and Professor of Medicine at the University of Toronto, as well as by Dr. Alberto Hernando-Calvo, Medical Oncologist at the Vall d'Hebron University Hospital, both authors of the JCO Precision Oncology article titled, “Combined Transcriptome and Circulating Tumor DNA Longitudinal Biomarker Analysis Associates With Clinical Outcomes in Advanced Solid Tumors Treated With Pembrolizumab.”  Thank you for joining us today. Phil and Alberto. Dr. Alberto Hernando-Calvo: Thank you. Dr. Philippe Bedard: Great to be with you. Thanks for having us.  Dr. Rafeh Naqash: One of the reasons we do this podcast, as some of the listeners who listen to this podcast regularly may know, is to bring in novel approaches and try to understand how the field is moving towards a space where we are understanding biomarkers better. So your manuscript that was published in JCO Precision Oncology fulfills many of those criteria. And interestingly enough, I was at a conference at the Society for Immunotherapy of Cancer last month earlier in November and a lot of excitement at SITC was revolving around novel transcriptomic biomarkers, proteomic biomarkers or imaging based biomarkers. So could you tell us a little bit about why you started looking at biomarkers? This is an extremely competitive field. Why did you think that looking at the transcriptome is somewhat different from or more interesting from tumor mutational burden PDL-1 than other biomarkers that we currently use? And that question is for you Alberto to start off.  Dr. Alberto Hernando-Calvo: So I think gene expression profiles may have a predictive performance as compared to already existing biomarkers and this was one of the points that we describe in our manuscript. The gene expression signature that we developed back in 2019 at Vall d'Hebron Institute of Oncology was initially developed based on over 45 different tumor types and tested in over 1000 patients treated with antiPD-1 and anti PDL-1. And back then and in this manuscript, we proved that for instance the gene expression signature VIGex that we developed has a potential complementary role to other predictive biomarkers. In this case, we observe this predictive power with ctDNA dynamics and we then see a correlation with other existing biomarkers such as tumor mutational burden. So I don't think we need to use one or the other, but rather they may have additive predictive power. So we need to better individualize predictive biomarkers based on tumor types and select the best combination possible to improve the performance.  Dr. Rafeh Naqash: I completely agree that one size does not fit all, especially in the landscape of immunotherapy. From your perspective, when you developed the original signature, how did you choose what genes to look at? I looked at the manuscript, on the methodology side, some of the signatures are pro-inflammatory STING interferon gamma based, so how did you try to identify that these are the 7 to 10 or whatever number of signatures on the transcriptome side? And then why did you try to combine it with ctDNA based changes?  Dr. Alberto Hernando-Calvo: Back in our initial manuscript, published in Med from Cell Press, we developed the VIGex gene expression signature, as I mentioned, with taking into consideration over 1000 tumor samples from FFPE that we can consider real world samples because they are from real patients coming from the clinic notes as part of real investigational protocol doing or performing biopsies on patients. We did observe after doing a VIGex research and doing different tests, we eventually collected these 12 different genes. Because there is a combination of both genes involved in the interferon gamma pathway, we have genes associated with Tregs as well as T cell memory cells. So it's not only looking at genes that are associated with T cell activation or CD8+ T cell infiltration, but also looking at genes that may be overactivated, overexpressed, an immunosuppressive tumor microenvironment. So it was both selecting genes, the minimum number of genes to do it more scalable and having the minimum dataset of genes and including in the signature genes that are already at targets for immune sequent inhibitors or are being tested in immunotherapy combinations.  Dr. Rafeh Naqash: Thank you. And Phil, for the sake of our listeners, could you elaborate upon this aspect of using ctDNA? So this was tumor-informed ctDNA from what I understood in the manuscript. You guys basically try to use it to understand changes in the ctDNA with treatment and then try to combine it with the transcriptome signature. How did the idea come up initially and how did you plan on combining this with an RNA-based signature? Because I have seen manuscripts and other data where people are either using one or the other, but not necessarily both together. So how did you guys come up with that idea? Dr. Philippe Bedard: Well, we thought that this was a great opportunity to look at the combination of the transcriptome as well as the ctDNA dynamics because we had run an investigator-initiated phase 2 clinical trial called INSPIRE at our institution at Princess Margaret from 2016 to 2018, where patients across five different tumor groups received single agent pembrolizumab. And we really did a deep dive on these patients where there were tumor biopsies before and while on treatment. We did exome sequencing, we did RNA sequencing to capture the transcriptome. And in a prior analysis, we had partnered with Natera to look at their Signatera assay, which is a bespoke ctDNA assay, to look at ctDNA dynamics using this test and the association with response outcomes as well as survival outcomes. So we thought that this was a really unique data set to try and address the question of whether or not there was complementarity in terms of looking at the transcriptome and transcriptome signatures of IO benefit together with the ctDNA dynamics. Dr. Rafeh Naqash: From a patient treatment standpoint, it sounded like you mostly tried to include individuals who were treated with pembrolizumab. Did this not include individuals who were treated with chemoimmunotherapy or chemotherapy with pembrolizumab? Just pembrolizumab alone? And if that's the case, some of the tumor types there included, from what I remember, ovarian cancer and some other unusual cancers that don't necessarily have approvals for single agent pembrolizumab, but perhaps in the TMB-high setting. So can you elaborate on the patient selection there for the study?  Dr. Philippe Bedard: Yeah, that's a great question. So at the time that the study was designed in 2015, this was really the early days of immune checkpoint inhibitor therapy, so we didn't have the approvals that we have now in specific tumor types for immunotherapy and chemotherapy combinations. So when the study was designed as an investigator initiated clinical trial, the idea was really to capture patients across different tumor types - so head and neck squamous cell carcinoma, malignant melanoma, ovarian cancer, triple negative breast cancer, and a kind of mixed histology solid tumor cohort, where we knew that there were some patients who were going to be immunotherapy responsive, where there was already approvals or evidence of single agent activity, and others where the responses were more anecdotal, to try and understand in a phase 2 clinical trial with kind of a deep dive, which patients benefited from treatment and which didn't. Dr. Rafeh Naqash: Interesting approach. Going to the results, Alberto, could you help us understand some of the important findings from these data? Because there's different sections of how you tried to look at the response rates, the survival, looking at the immune deconvolution, if you could explain that. Dr. Alberto Hernando-Calvo: So the first thing that we tried was to further confirm the external validation of this immune gene expression signature, VIGex in the INSPIRE asset. So what we observed at VIGex-Hot, the category defined by VIGex-Hot tumor microenvironment, was associated with better progression free survival. After including that in a multivariable analysis adjusted by other biomarkers such as TMB, PDL-1 or tumor type, this was also confirmed for overall survival. So then the next step was to really try to hypothesize if the addition of ctDNA dynamics, taking into consideration the ctDNA quantification at baseline as compared to cycle three, if those dynamics could further improve the predictive performance of VIGex categories taken in the baseline samples. What we did observe was that, for instance, VIGex-Hot tumors in baseline tumor samples that were having a ctDNA decrease, as I mentioned before on cycle three assessment as compared to baseline, were having both better progression free survival and better prognosis overall. Another important finding was the evaluation of response rate across tumor types considering both biomarkers. I would say the most important finding is that when we were considering a cold tumor microenvironment in baseline samples before pembrolizumab initiation plus an increase in ctDNA values, what we observed is that those patients were having a 0% response rate. So this may help as a future strategy either for intensification of immunotherapy regimens in a more individualized way or for an early stop to immunotherapy and try to avoid financial toxicities as well as toxicities for our patients. Dr. Rafeh Naqash: From the data that you showed, it seems that there was a strong correlation, as you sort of mentioned, between individuals that had ctDNA clearance and baseline immune pro-inflammatory signatures. So do you really need the transcriptome signature or could the ctDNA just serve as an easy quick surrogate? Because from a cost standpoint, doing whole transcriptome sequencing or more RNA sequencing or tissue standpoint, where tissue is often limited, can become a big issue. So do you think that validation of this may perhaps more revolve around using ctDNA as an easier metric or surrogate? Or am I overestimating the utility of ctDNA? Dr. Philippe Bedard: I think it's a really good question. In our data set which was relatively small, there were 10 patients who had ctDNA clearance, meaning ctDNA that was positive at baseline was not detected. And so 9 out of those 10 patients, as you alluded to, were VIGex-Hot. So the question is a good one, could you do the same with just ctDNA clearance alone, particularly in identifying these patients who really do well, who have long term disease control on immunotherapy? I think it's a tough question to answer because the field is also changing in terms of sensitivity of detection of ctDNA tests. So we know now that there are newer generations of tests which can detect even at logs down in terms of allele variants in the circulation. So I think we need more data to address the question. I think it is important as to what is the best test, what is the endpoint that we should be using from a drug development point of view in terms of really trying to push and understand which treatment regimens are the most effective and have early readouts in terms of activity. Because we all recognize in the clinic that radiographic response doesn't tell the whole story, especially early radiographic assessments using RECIST or other criteria that we apply in clinical trials. Dr. Rafeh Naqash: From a clinical trial standpoint, we often talk about validation of these studies. You may have heard of other tests where, for example, the NCI iMatch, which is incorporating transcriptome sequencing based approach to stratify patients as an integral biomarker for treatment stratification. Is that something that you guys are thinking of using, this approach where individuals who are signature highly inflamed perhaps get lesser therapies or there's a de-intensification of some sort similar to what people are trying to do with ctDNA-based approaches? Dr. Philippe Bedard: I think that's a great question. I think it makes a lot of sense. And certainly, with the new wave antibody drug conjugates in terms of identifying patients who have expression of targets for antibody drug conjugates, that's very attractive as an approach because we don't necessarily have IHC markers for all of the different targets of antibody drug conjugates. We don't necessarily have IHC markers to completely understand different contributions to the tumor microenvironment and whether or not tumors are inflamed. But it's also a challenging approach too because RNA-seq currently is not a routine clinical test. Sometimes there are issues, particularly in patients who have stored specimens that are formalin-fixed and paraffin-embedded in terms of the quality of the RNA for RNA sequencing. And it's not always feasible to get pre-treatment biopsies and turn them around in an approach. So I think it is an attractive approach for clinical trials, but it's a hypothesis that needs to be tested. It's not something that is ready for clinical prime time today in 2024. Dr. Rafeh Naqash: One of the other interesting observations that I came across in your manuscript was that tumor mutational burden, interestingly, did not correlate with signature high tumors. What is the explanation for that? Because generally you would expect a TMB high to perhaps also have an immune gene high signature. Could it have something to do with the tumor types because there was a heterogeneous mixture of tumor type? Or I'm not sure. What else could you possibly think of that you didn't see those correlations or just sample size limitations? Dr. Alberto Hernando-Calvo: Yes. So our findings are consistent with prior data suggesting for instance T cell inflamed gene expression profile was also not correlated with tumor mutational burden and both biomarkers in a prior publication. So to have additive predictive performance for identifying patients most likely to benefit from anti PD-1 regimen, so we somehow were expecting this observation, the fact that both biomarkers are not very correlated. Dr. Rafeh Naqash: So given the proof of concept findings from your study, Phil, what is the next interesting step that you guys are thinking of to expand this? Would you think that a nivolumab-ipilimumab treated cohort would have similar findings? Or is this a treatment specific single agent immunotherapy specific correlation that you found versus something else that you may find in a nivo-ipi cohort or a doublet immune checkpoint cohort?  Dr. Philippe Bedard: The findings are really hypothesis generating. They require additional validation. And you're quite right, there may be nuances in terms of specific tumor types, combinations with other immunotherapy or combinations with chemotherapy or other agents. So I think it would be great if there are other data sets that are collecting this type of information that have ctDNA dynamics and also have transcriptome and potentially exome or genome analysis to look at these types of questions because the field is moving quickly and we really need more data sets in order to understand some of the nuances and greater numbers to validate the signals that we see. Dr. Rafeh Naqash: And one thing, as you said, the field is definitely moving very quickly. I was meeting with a company an hour back and they have an imaging-based approach using fresh tissue to look at pharmacodynamic biomarkers. And I used to work in the NCI with a group that was very interested and they developed an immuno-oncology pharmacodynamic panel that has been used and published in a few clinical trials where they did phosphorylation status. So the final theme that comes out of most of these research based studies that are being done is that one size does not fit all. But the question that comes to my mind is how many things do you necessarily need to combine to get to a predictive biomarker that is useful, that is patient centric, and that perhaps is able to identify the right therapy for the right patient. What is your take on that, Phil?  Dr. Philippe Bedard: Yeah, that's a great question too. The challenge is it depends on the context in terms of what degree of positive predictive value do you need as well as the negative predictive value to drive clinical decisions. So I think in certain situations where you don't have other approved treatment options and with a therapy that is potentially low toxicity and low financial toxicity, then I think the bar is very high in terms of being able to really confidently identify that patients aren't going to benefit. I think the nuance and the challenge becomes when you move into earlier lines of therapy, or when you talk about combinations of agents, or trying to understand within the context of other available options, particularly with treatments that have significant side effect profiles as well as financial risks, then it becomes a much more nuanced question and you really need comparative studies to understand how it fits versus the existing treatment paradigm. So I'm not really answering your question with a specific number because I think it's hard to give you a number. Some of that we also need input from patients in terms of what kind of level of validation do you need and what kind of level of discrimination do you need in order to drive decisions that are meaningful for them. Dr. Rafeh Naqash: Definitely early days, as you pointed out. More and more work in this field will hopefully lead us in the direction that we all want to go in.  Now, going to a different aspect of this podcast, which is trying to understand the trajectories for both of you, Phil and Alberto. And as you mentioned, this project seemed to have started in 2015. So I'm guessing there's a history there between Princess Margaret and Vall d'Hebron. Could you highlight that a little bit? And then perhaps, Alberto, after that you could tell us a little bit about your career when you worked at Princess Margaret as a fellow and then now back at Vall d'Hebron. Phil, you as well. Dr. Philippe Bedard: So absolutely. We have a long history of collaborating with Vall d'Hebron in Barcelona. It's really a great cancer institution with a lot of like minded individuals. We have a formal partnership and we have a lot of informal links in terms of scientists and clinicians who we work with and who we collaborate with on early phase clinical trials, as well as through different investigator networks and other translational projects. So this was really how this collaboration came about and we were fortunate to have Alberto, who came to work with us for two years and brought this great idea of looking at this signature they had developed at Vall d'Hebron in their phase one group and applying it to a data set that we had through the INSPIRE clinical trial.  Dr. Rafeh Naqash: Sounds like a very successful academia-academic collaboration, which is very nice to see. So, Alberto, could you tell us a little bit about your career trajectory and how you ended up at Princess Margaret and then back at Vall d'Hebron and what you do currently? Dr. Alberto Hernando-Calvo: Yes. So I did my oncology residency at Vall d'Hebron in Barcelona, Spain. Then I decided to further specialize in early drug development as well as head and neck cancer oncology. So I decided to pursue a clinical research fellowship under the supervision of Phil Bedard, among others. And so we decided to further validate the signature that we had developed both in the cancer genomic lab at Vall d'Hebron Institute of Oncology and the phase one unit at Vall d'Hebron, and apply the signature that have been originally tested in patients receiving anti PD-1 or anti PDL-1 combinations in early phase clinical trials. In the phase 2 clinical trial of INSPIRE, where we also had ctDNA dynamics and allowed us to test both biomarkers and see that additive predictive power when we were using both. That was one of my research topics under the mentorship of Dr. Bedard and my fellowship at Princess Margaret. And this was one of the manuscripts describing all the findings of this collaboration between Vall d'Hebron and Princess Margaret Cancer Center. Dr. Rafeh Naqash: And then, Phil, if you could highlight some of the things that you've done over the course of your career and perhaps some advice for early career junior investigators and trainees.  Dr. Philippe Bedard: I finished my oncology, medical oncology training at the University of Toronto in 2008. And then I did a breast cancer fellowship in Brussels at Breast International Group. At the time, I was really intrigued because it was really kind of the early days of microarray and RNA signatures in terms of expressing signatures were being used as part of a clinical trial that BIG was running called the MINDACT Study. And so when I finished my fellowship, I came back to Princess Margaret, started on staff. I've been here now for 15 years. I was fortunate to work with the phase 1 group and kind of my career has sort of morphed in terms of early drug development as well as genomics. I've been involved with the American Association for Cancer Research project GENIE, where I'm the current chair. This is really an international data sharing project with panel based sequencing, which both Princess Margaret and Vall d'Hebron have contributed to. And I've been fortunate to work with a number of really talented early career investigators like Alberto, who spend time with us in our drug development program and launched transitional research projects that leverage some existing data sets at their own institutions and also bring together with different research groups at our institution to lead to publications like this one. Dr. Rafeh Naqash: Thank you so much. This was very exciting. Phil and Albert, thanks for joining us today and thank you for allowing us to discuss your interesting manuscript and hopefully we'll see more of this biomarker work from you guys in the near future, perhaps published in JCO Precision Oncology.   And thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review and be sure to subscribe so you never miss an episode. You can find all ASCO shows at asco.org/podcasts.     The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions.  Guests on this podcast express their own opinions, experience and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.

Superimposed on an impressive body of work on the blood-brain-barrier and immune system, Prof Akassoglou and her collaborators just published an elegant study in Nature that centered on the direct binding os the SARS-CoV-2 spike protein to fibrin with marked downstream pro-inflammatory effects. The findings and potential treatments have implications beyond Covid, Long Covid to other neurologic diseases.Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with links to audio and to relevant papers, graphicsEric Topol (00:07):Well, hello this is Eric Topol with Ground Truths, and with me today is Katerina Akassoglou. She is at the Gladstone Institute and she is a remarkable neuroimmunologist who has been doing extraordinary work for three decades to unravel the interactions between the brain, blood vessels and the role of inflammation. So Katerina, there's a lot to discuss, so welcome.Katerina Akassoglou (00:40):Thank you. Thank you so much. It's a great pleasure to join.By Way of BackgroundEric Topol (00:43):It's really interesting going back in your career. First of all, we're thankful that you immigrated here from Greece, and you have become one of the leading scientists in this discipline of important discipline of neuroimmunology, which is not just about Covid that we're going to talk about, but Alzheimer's and neurodegenerative diseases. This is a really big hot area and you're definitely one of the leaders. And what I was impressed is that all these years that you've been working on the integrity of the blood-brain barrier, the importance of fibrinogen and fibrin, and then comes along the Covid story. So maybe what we can do is start with that, which is you've made your mark in understanding this whole interaction between what can get into the brain, through the blood-brain barrier and incite inflammation. So this has been something that you've really taken to the extreme knowledge base. So maybe we can start with your work there before we get into the important seminal Nature paper that you recently published.Katerina Akassoglou (01:57):Yes, of course. So since very early on, I was still a graduate student when we made the first discovery and at the time was like mid-90s, so it was really ahead of its time. That dysregulation of cytokine expression in the brain of mice was sufficient to induce the whole cascade of events, triggering neurodegeneration, demyelination in pathological alterations, very reminiscent of multiple sclerosis pathology. And it was really hard to publish that study at the time because it was not yet accepted that this regulation of the immune system modeling the brain can be linked to neurodegeneration. So that was 1995 when we made that discovery, and I became really interested, what are the pathogenic triggers that actually polarized the immune cells in the brain? So with this, of course, this transgenic animal was expressing TNF, it was an artificially made animal that we made, but naturally what were the triggers that would polarize the innate immune cells? So I looked really early on in this mice and what I found was that the very first event was leaks of blood-brain barrier. It was opening of the blood-brain barrier in this mouse before inflammation, before demyelination, before neuronal loss. And this is really what shaped the question that, is it possible that these blood leaks that happened very early in the pathology, could this be the instigators of pathogenic inflammation in the brain?Eric Topol (03:34):Yeah. So in a way, you got at this question because of the chicken-and-egg and what happens first, and you got to the temporal saying, which happened first as you said, the leak before you could see evidence of inflammation and being able to study this of course in the experimental model, which you couldn't really do in people. And what I love about the description of your career, which has been quite extraordinary contributions is connecting the dots between the blood, the inflammatory response and the brain. Perhaps no one has done that like you have. And before we get into the recent paper, a lot of people are not aware that a year ago, a group in the UK known as PHOSP-COVID, they published a really important paper in Nature Medicine of over 1,800 people who were hospitalized with Covid and they found that fibrinogen was the best marker for cognitive deficits at 6 and 12 months (Figure below)(04:40):So that's just one of many papers, but it's a particularly well done study that already before you got into this work that recently published had emphasized fibrinogen. And by the way, again, having spent a lot of years in clots in the arteries, for me, we have to just get it down to fibrinogen plus thrombin gets you to fibrin. Okay, so fibrin is a major player here when fibrinogen is cleaved. So here we have the basis that you established, which is the fibrinogen leakage into the brain, activating inflammation, activating microglia, which like the macrophages of the brain and inciting the whole process. And before we close, I want to not just talk about Covid, but Alzheimer's too. But now let's get into the study that you did, [Fibrin drives thromboinflammation and neuropathology in COVID-19] which is striking, I mean really striking. And can you kind of take us through, because you not only demonstrated the importance of fibrin in inciting neuroinflammation in this model, but also how you could reverse it or prevent it. So this, and you looked at it in many different ways, this was a systematic approach. Maybe you can take us through how you were able to make such compelling evidence.The Multimodal EvidenceKaterina Akassoglou (06:09):Yes, thank you. First of all, thank you for bringing up the human relevance because this was also our inspiration for the work that we did in the Covid study. So as you mentioned in Covid patients, fibrinogen unbiased mass spec analysis was identified as the predictive biomarker for cognitive impairment in Long Covid patients. And this was in addition to also neuropathology data about the abundance of fibrin deposition in the brain. And these were studies that were done by NIH that have found deposition of fibrin in the brain and the reports for the abnormal and puzzling coagulation in Covid that is not setting other infections and also in many cases not always relating with the severity of symptoms. So even mild cases of Covid also had increased coagulation. I was really intrigued by this human, all this evidence in human data, and I thought that maybe the way that we're thinking about this, that it's systemic inflammation that drives the clotting.(07:24):Maybe there's another aspect to this. Maybe there is a direct effect of the virus with the coagulation cascade, and in this way maybe this can be an instigator of inflammation. So this was the original idea to be able to reconcile this data from the clinic about why do we have this prevalence of coagulopathy in Covid. And of course, the second question is, could this also be a driver of the disease? And of course, we're in a unique position because we have been studying this pathway now for over 20 years to have all the toolbox, the genetic toolbox, the pharmacologic toolbox to be able to actually really address these questions with genetic loss of function studies, with a blood innate immunity multiomics pipeline that we have set up in the lab. And of course, with preclinical pharmacology in our ABSL3 facility. So we had the infrastructure in place and the source in place to actually really dissect this question with both genetic tools as well as also technology platforms.Eric Topol (08:29):And you had in vivo imaging, you're the director of in vivo imaging for Gladstone and UCSF. So you do have the tools to do this.Katerina Akassoglou (08:38):Yes. The imaging that you mentioned is really important because this is, we employed that very early in our studies over now 15 years ago. And the reason was sometimes from snapshots of histopathology, you cannot really understand the sequence of events. So by being able to image these processes, both neuronal activity, microglia activation, infiltration of peripheral cells in the brain, this is how we could see the steps that what happens early on and to be able to answer these chicken-and-egg questions that you mentioned. So these were very, they're very important experiments, especially at the beginning because they were hypothesis driving and we were able to ask the right questions to drive our research program.Eric Topol (09:26):Now was the binding of the spike protein to one key site in fibrinogen, was that known before? [See outstanding Figure below from Trends in Immunology]Katerina Akassoglou (09:36):No, this was not known. So there was evidence that there are abnormal clots in Covid, but it was not known whether the spike protein would directly bind to protein to the coagulation cascade. So one of the key discoveries in our study was to use peptide array mapping and be able to identify not only the binding, but exactly the domains on fibrin that spike binds too. And what we found was two key domains, one the inflammatory domain and the other the plasmin binding site, which is important for fibrin degradation. So this suggested a potential dual deleterious role for this interaction, both by maybe affecting inflammation, but also delaying fibrinolysis, which is the degradation of this toxic protein from the brain. And indeed, we found that this interaction was responsible for all these two aspects, including decreased degradation, more inflammation, but also at the same time increased, increased coagulation. So it was a really pathogenic interaction.Eric Topol (10:47):Yeah, actually it's pretty striking. You have these two sites, the plasmin cleavage site of fibrinogen, which as you say, we knew there was a problem with clots. We knew that, but we didn't know exactly the spike protein how exactly it was implicated, particularly with fibrinogen. And then this other site, the CD11b-C18, now that's fancy for surface receptors of macrophages. And basically, this is critical because it's this microglia activation in the brain, and I know you saw it in the lungs as well through this other site that spike protein activated. So you had a twofer here of things that you discovered that the SARS-CoV-2 spike protein was capable of doing. This was a really big revelation. And then you also looked at mice that were genetically manipulated. So maybe you can, because before we get to your antibody monoclonal, the ways that you proved this were, I mean, one thing after another is really systematic. So maybe you can teach us about that.Thanks for reading Ground Truths! This post is public so feel free to share it.Establishing CausalityKaterina Akassoglou (12:08):Yeah, sure. So the first was about chemistry experiment. So this of course, we had to get to the next step to see is there any causality for this pathway. So we employed genetic loss of function studies and we had knockout mice, either fibrinogen knockout mice, this mice have all blood proteins except fibrinogen, and they have a delay in coagulation so they don't clot properly. But we also had a mutant mouse, which is a fibrinogen NK mouse. And this was a mutation only within this inflammatory domain that you mentioned, inflammatory domain that binds to C11b-C18. Other names for this is of course complement receptor 3, Mac-1 (αMβ2). It's the same, many names for this receptor, that as you mentioned, is expressed not only in microglial in the brain, but also peripheral immune cells including macrophages as well as also neutrophils which are CD11b expressing.(13:12):So we now have genetic models to be able to look at both complete depletion of fibrinogen, but also a very specific mutation and very selective mutation that only blocks the inflammatory properties without affecting the properties of fibrin in hemostasis. And these mice were made many years ago by a very close collaborator, Jay Degen at the University of Cincinnati. So what we found is that when we block either the inflammatory domain or we completely deplete fibrinogen, there was this profound protection after infection in internasal infection with the virus in lung inflammation. And this was both suppression of oxidative stress and this pathogenic inflammation in the lung, but also decreasing fibrosis, which has been associated with also Long Covid. And the surprise came from the transcriptomic data. So when we did transcriptomic analysis in this mice in the lungs, we found perhaps the expected decrease in the immune signatures in macrophages. This was in line with our previous work in, as you mentioned, Alzheimer's models, multiple sclerosis models. But what also was really surprising is there was that genes that are associated with activation of NK cells were upregulated. And of course this was the first time we had infected these mice, previously we had not done an infection before. So I think that maybe because of this region we had not seen before in our data this immunomodulatory role of fibrin that not only surprises the macrophage response, but also increases these NK cells that are important for viral clearance.Eric Topol (15:00):So again, the finding another important unique finding is the natural killer (NK) cells and effect there from the activation of this, as you said, the inflammation site or the CD11b-C18 that we've been talking about. So now another layer of this, a dimension of your Nature paper was that you tested an antibody that you already had developed so-called 5B8. A monoclonal that specifically binds to the domain of the one we're talking about this inflammation domain of fibrinogen. So can you tell us about what that showed?Katerina Akassoglou (15:45):Yes, so we tested this antibody in different models of Covid, which were both models with neuroinvasion and models without neuroinvasion. So we used both transgenic mice for hACE2, the human ACE2 infected with Delta, but we also use mouse adapted viruses like Beta that is just in the wild type mice with no transgenic being involved that these are without neuroinvasion. And we wanted to see if the antibody had any potential protective effects. And what we found is that the antibody protected from inflammation in the lung. So the data looked so similar with a genetic mutation of this pathway, protection from inflammation, decreased fibrosis, increased viral clearance, so decreased spike and viral proteins in the lungs. But we also found a protection in the brain. So the brains of this mice, including both the models we used with neuroinvasion and without, they both have had microglia activation in the brain. And we also found neuronal loss in the Delta infected mice and the antibody protected from both neuroinflammation but also improved neuronal survival in the mice. Showing that there can be this despite regardless of which model we used, there was this protective effect suggesting that by blocking fibrin, either the periphery or in the brain, this could be protected for these models.Eric Topol (17:28):Yeah, so I mean this is fascinating because until now, until this report of yours and your colleagues at Gladstone, there was knowledge that there would be neuroinflammation from Covid, both in patients from various biomarkers and imaging as well as in experimental model. But what this did was take it to the fibrin story, and I guess that's one of the questions you nailed that how important fibrin is, but that doesn't necessarily rule out other triggers of neuroinflammation, right?Katerina Akassoglou (18:04):Oh, absolutely not. So I think that this is one of the mechanisms that can be very important, especially in some patients. But we know that there are additional of course mechanisms of neuroinflammation including auto-antibody responses, as well as also endotheliopathy that are persistent endotheliopathy, this can be interacting also with each other. So I think that it's important for future research that we understand how do these mechanisms feed into each other? Are there a positive feedback loops between autoimmune mechanisms and coagulopathy and endothelial dysfunction with inflammation? But I think most importantly, I think that if we're thinking of this in the context of patients, can we identify patients with mechanism that might be more prevalent in specific cases of Long Covid and tailor our potential future clinical trials towards the needs of Long Covid patients?Towards TreatmentEric Topol (19:06):Absolutely. I did interview some months back on Grounds Truths, Michelle Monje at Stanford, who I'm sure and interact with, and she's also works not so much on the fibrin side, but on neuroinflammation and the likeness between this condition in people and chemo brain because of the inflammation that's seen there. So we've talked about the multiple triggers that could contribute to brain inflammation, which I think most people would say in Long Covid this is one of the most, besides obviously the lack of energy, the profound fatigue and disability, but the cognitive function hit, not just brain fog is often profound. And we've just seen some reports about that, and particularly in hospitalized patients, how bad that can be. So that gets us to a potential treatment. Now, one of the things that's out there dangling, there's many things that people have talked about in terms of why can't we have a treatment for Long Covid?(20:13):And now of course this fibrin pathway, if you will, lends itself to many possibilities, whether it's anticoagulants or fibrinolytics like a tPA or things like nattokinase, which is a Japanese food enzyme that you could get at the nutrition centers or whatever. What are your thoughts? Because we don't have any good studies. There are all these little, tiny studies and they don't provide much conclusion, and you have an antibody that could potentially be effective. As I understand it, you set up a company some years ago, Therini Bio and used to be called MedaRed. You're the first woman scientist at Gladstone to develop a spin out company, which is another point of congratulations on that. But could the antibody be tested in patients or what do you think about these other possibilities?Katerina Akassoglou (21:15):Yes, yes. These are great questions. So first of all, the different approaches that you mentioned have very different mechanism of action. So degrading fibrin, the degradation products of fibrin also can have deleterious effects. The dimer, for example, can be very pro-inflammatory. So at the same time, blocking coagulation can also have a diverse effects because this can lead to excessive hemorrhage. So the approach that we took was to selectively block the inflammatory properties of fibrin without affecting beneficial effects of the molecule in normal hemostasis. So the challenge when I made the antibody was to be able to dissect these two functions of fibrin. It's our most important clotting factor, but at the same time, a molecule with profound pro-inflammatory capacity. So the observation that these two domains, the clotting domain and inflammatory domain were not overlapping, was really the foundation of this invention was that we could maybe create this antibody to be able to target them in a selective way.Other Neurologic Conditions (22:31):So the antibody I developed is neutralizing blood toxicity by blocking the inflammatory domain of fibrin without adverse coagulation effects. And it's now completing phase one trials. So it has already completed the single ascending dose at 40 milligram per kilogram. It's interim data were announced already for this trial, with no safety signals. So if the antibody completes this year, the phase one trials, then it should be possible to be tested in different patient populations. You mentioned before chemo brain, and I think it's important that we think that blood-brain barrier disruption occurs among many neurological conditions, and it's an early event associated with early disease onset and worse prognosis in multiple sclerosis, Alzheimer's disease, traumatic injuries. So I think that it's by developing a strategy, therapeutic strategy to neutralize blood toxicity, this can have applications in a wide range of neurological conditions with vascular dysfunction.Eric Topol (23:54):Yeah, no. In your Nature Immunology 2020 piece [Figure below], you started with the 1883 identification of multiple sclerosis (MS) lesions were “engorged with blood”, the first link between blood leaks and brain inflammation. So this has enormous potential. And what I like about this Katerina is that you've dissected the clot component versus the inflammatory trigger of the fibrinogen and fibrin story. And this is so vital because if you keep throwing these things that just going to work on the clot and not deal with the pro-inflammatory consequences, then you're going to get the wrong impression that clots are not that important. And by the way, you did mention, and I want to come back to that too, endothelial inflammation, which is another feature of Long Covid is another kind of interactive part of this because when the lining of the blood vessel is inflamed, it will attract microthrombi and also be a participant in this whole affair. What do you think about Alzheimer's and the prospects of being able to interfere with Alzheimer's? We have 20 years in someone before this process takes hold and meets clinical manifestations. Would an antibody like this ever be useful along the way?Katerina Akassoglou (25:29):Yeah, so well, our antibody was tested first in Alzheimer's, this models when it was originally published, and we performed reversal trials in Alzheimer's models. So we dosed mice when they have established amyloid plaques, microglia activation, neuronal loss, and we could reverse this effect so it could increase cholinergic neurons in mice, reduce inflammation in a very selective way, only the neurotoxic part of inflammation and for genetic depletion of this pathway with akin mice in Alzheimer's disease. Also, improves from cognitive impairment, and we now have a new paper in Cell Press that is showing this effects also with really nice and unbiased machine learning models for behavioral segmentation [Figure below].So I think that there is the data both from genetic studies and the antibody show projection in Alzheimer's disease. And of course, as you might have read the recent Lancet report from the Lancet committee on dementia that identified the vascular risk factors as the key contributors, especially post sporadic cases of Alzheimer's disease that is over 90% of Alzheimer's disease that is not genetically linked.(26:58):So I think that there is a real need in Alzheimer's disease to be able to block this vascular induced pathology. And an antibody like the fibrin neutralizing therapy could be positioned to be protective from the vascular induced immune-mediated neurodegeneration in this disease as well. I mean, ultimately, I think that we need to be thinking the terms of efficacy. So we want to have a drug that is efficacious, but we also want it to be selective. And the selectivity is really important because the immune system has so many protective functions. So if we block phagocytosis, we end up with more debris, decrease of neurorepair, anti-myelination. So by blocking a ligand here and not blocking, not eliminating a cell type or blocking a global pathway in this cell, but biologic a single ligand, I think we have been able to achieve this balance between efficacy, but also safety because we only block this neurotoxic populations and not the entire innate immune response that also has been beneficial for metastatic functions in the brain.Blocking NeuroinflammationEric Topol (28:19):So you're bringing up another critical concept about targeting the inflammation, this kind of goldilocks story of how much you interfere with the immune response and how much you are able to reduce the adverse pro-inflammatory effects. So that gets me to what if we don't know in any given patient how much fibrin is having a role in their Long Covid. Although we know it has to be a prominent feature because we saw it in, not just a hospitalized patient series that I mentioned we reviewed, but other papers as well. But what about if you just try to take on inflammation like through a GLP-1 drug or cGAS–STING or any of these really strong anti-inflammatory pathways. Do you see a difference in a generalized approach versus a specific approach that is really fibrin centered?Katerina Akassoglou (29:22):Yeah, so we have a focus actually on both because we wanted to dissect the downstream intracellular pathways of fibrin, and it's interesting that we can find specific inflammatory mediators that potentially can also be targeted as well, to be able to preserve that specificity, which I think is really important because if we don't preserve the specificity, we'll end up with a lot of adverse effects by eliminating major immune responses. But the point that you raised I think is really important because it's not enough to have an efficacious and selective drug if you don't know the patient population that will benefit from this drug. So I think that in addition to the drug discovery studies, it's important to develop also biomarker programs with both fluid biomarkers, but also imaging biomarkers to be able to identify the patient populations that will benefit from such treatment.(30:25):So if for example, a patient population has a fibrin deposition, blocking only downstream might not be enough, and it might be really important to neutralize this fibrin toxicity in the brain of patients. And with our target engagement studies, we show that at least in animal models, the antibody can be there. So I'm very encouraged by also programs that are going on now in the scientific community to develop noninvasive ligands to be able to image fibrin in the brain that are already tested in different patient populations like multiple sclerosis. Because I think we're going to learn so much from the biology as we start interrogating and asking these questions now in different patient populations.Eric Topol (31:14):I think that's a vital point you're making because the success of a clinical trial here in a clinical syndrome that is mosaic with lots of different types of pathways. If you can nail down the patients that would have the most to stand to benefit from a particular intervention, that the chance of you not missing the benefit that is matching the marker, what image marker or other markers is so vital. Well, we've talked, I think, about some fascinating discoveries that you and your colleagues have made. I mean, it's really extraordinary, and obviously we need this in Long Covid. But you know what, Katerina, it's almost made me think that you were warming up to this for three decades, that somehow or other you were working on all this stuff and then came Covid. Is that how you see it, that somehow or other you didn't know that all the work you were doing was going to wind up in this space?Katerina Akassoglou (32:18):Oh, I never thought I would work in a virology project. This collaboration started over Zoom with Warner Greene. We were both sheltering in place. It was the beginning of the pandemic, and the first reports were coming out about this puzzling coagulopathy. And our labs were hardly operational at the time, as you know, we had to close down our labs for a while. And however, this was a very big problem, and we thought that this is our role as scientists. If we feel that we can contribute and we have the tools to contribute, we felt that it's important that we pivot some part of our research, and even we wouldn't be doing this before, but it was important to pivot a part of our research and collaborate. And I think studies like this, this study would have been impossible without a team of collaborators. As you know, there were over 50 scientists involved at Gladstone, UCSF, UCLA, UCSD, Stanford University. Without collaboration, this study wouldn't be possible. So I'm really grateful to everyone who came together to solve this problem because I think that's what scientists should be doing. We should be solving problems as they arise.Eric Topol (33:41):Well, and also, I think a lot of people don't realize that, for example, when the Covid vaccines came along, people think, oh, well, it all got done in 10 months since the sequence of the virus, when in fact it took 30 years at least between all the factors that went into having an mRNA and sequencing virus and nanoparticles. And in many ways, your arc of this work is like that because it took three decades to have all the tools and the basic understanding, the antibody that you had developed for different reasons and this fascinating unraveling of what's going on in the model and undoubtedly in some patients at least as well. So before we wrap up, have I missed anything about this just remarkable work you've done?Katerina Akassoglou (34:33):Oh, thank you. I just want to thank you for this discussion and thank you for emphasizing the different areas and the different decisions that this pathway can have implications both for our understanding, our basic understanding of the blood brain immune interface, as well as also potential translation. And I think that the curiosity sometimes of how things work, I never thought it would work on Covid, like you mentioned at the beginning, but I think that basic science and curiosity driven science can sometimes lead to discoveries with translational implications that hopefully might benefit patients one day.Eric Topol (35:21):Yeah, well, undoubtedly it will. We're indebted to you, Katerina and all the folks that you have teamed up with, connecting the dots at the neurovascular interface. Phenomenal work and will follow the subsequent with great interest and it will likely not just a story about Long Covid, but other areas as well, so thank you.*********************************Thanks for listening, reading or watching!The Ground Truths newsletters and podcasts are all free, open-access, without ads.Please share this post/podcast with your friends and network if you found it informative!Voluntary paid subscriptions all go to support Scripps Research. Many thanks for that—they greatly help fund our summer internship programs.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff for audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in. Get full access to Ground Truths at erictopol.substack.com/subscribe

The second part of this installment of Unearthed! gets into the listener-favorite subject of shipwrecks, plus animals, art, edibles and potables, and the catch-all potpourri category. Research: 19 News Investigative Team. “Exhumation of Cleveland Torso Killer's unidentified victims now underway.” https://www.cleveland19.com/2024/08/09/exhumation-cleveland-torso-killers-unidentified-victims-now-underway/ Abdallah, Hanna. “Hydraulic lift technology may have helped build Egypt's iconic Pyramid of Djoser.” EurekAlert. 8/5/2024. https://www.eurekalert.org/news-releases/1051645 Addley, Esther. “Dorset ‘Stonehenge' under Thomas Hardy's home given protected status.” The Guardian. 9/24/2024. https://www.theguardian.com/uk-news/2024/sep/24/dorset-stonehenge-discovered-under-thomas-hardy-home-dorchester Adhi Agus Oktaviana et al, Narrative cave art in Indonesia by 51,200 years ago, Nature (2024). 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Volume 170, 2024, 106040, ISSN 0305-4403, https://doi.org/10.1016/j.jas.2024.106040. Gouevia, Flavia. “Donegal farmer uncovers 22kg slab of ancient bog butter.” The Irish News. 9/13/2024. https://www.irishnews.com/news/ireland/donegal-farmer-uncovers-22kg-slab-of-ancient-bog-butter-YUJKZVXG6NH43G3SBZ3DAUDCHI/ Hawkins, Grant. “Texas A&M's Quest To Save An Alamo Cannon.” Texas A&M Today. 7/31/2024. https://today.tamu.edu/2024/07/31/texas-ams-quest-to-save-an-alamo-cannon/ Howe, Craig and Lukas Rieppel. “Why museums should repatriate fossils.” Nature. 6/18/2024. https://www.nature.com/articles/d41586-024-02027-y Ian G. Barber et al, American sweet potato and Asia-Pacific crop experimentation during early colonisation of temperate-climate Aotearoa/New Zealand, Antiquity (2024). DOI: 10.15184/aqy.2024.143 Imai, Kunihiko. “Researchers identify mystery artifact from ancient capital.” The Ashai Shimbun. 9/5/2024. https://www.asahi.com/ajw/articles/15415562 Kael, Sascha. “The plague may have caused the downfall of the Stone Age farmers.” EurekAlert. 7/10/2024. https://www.eurekalert.org/news-releases/1050694 Kokkinidis, Tasos. “Second Ancient Shipwreck Discovered at Antikythera, Greece.” Greek Reporter. 7/1/2024. https://greekreporter.com/2024/07/01/second-ancient-shipwreck-discovered-antikythera-greece/ Kovac, Adam. “17th-Century Mummified Brains Test Positive for Cocaine.” 8/27/2024. https://gizmodo.com/17th-century-mummified-brains-test-positive-for-cocaine-2000491460 Kuta, Sarah. “Divers Can Now Explore Historic Shipwrecks in Lake Michigan More Easily.” Smithsonian. 8/23/2024. https://www.smithsonianmag.com/smart-news/divers-can-now-explore-historic-shipwrecks-in-lake-michigan-more-easily-180984959/ Kuta, Sarah. “Divers Find Crates of Unopened Champagne in 19th-Century Shipwreck.” Smithsonian. 7/31/2024. https://www.smithsonianmag.com/smart-news/divers-find-shipwreck-loaded-with-champagne-near-sweden-180984784/ Kuta, Sarah. “DNA Reveals Identity of Officer on the Lost Franklin Expedition—and His Remains Show Signs of Cannibalism.” Smithsonian. 9/26/2024. https://www.smithsonianmag.com/smart-news/dna-reveals-identity-of-officer-on-the-lost-franklin-expedition-and-his-remains-show-signs-of-cannibalism-180985154/ Kuta, Sarah. “Shipwreck Found in Lake Michigan 130 Years After Sinking With Captain's ‘Intelligent and Faithful' Dog Onboard.” Smithsonian. 7/25/2024. https://www.smithsonianmag.com/smart-news/shipwreck-found-in-lake-michigan-130-years-after-sinking-with-captains-intelligent-and-faithful-dog-onboard-180984766/ Larson, Christina. “Stonehenge's 'altar stone' originally came from Scotland and not Wales, new research shows.” Phys.org. 8/17/2024. https://phys.org/news/2024-08-stonehenge-altar-stone-scotland-wales.html Lawson-Tancred, Jo. “A Marble God Is Found in an Ancient Roman Sewer.” Artnet. 7/9/2024. https://news.artnet.com/art-world/marble-hermes-ancient-roman-sewer-2509628 Lawson-Tancred, Jo. “Legal Battle Intensifies Over Tunnel That May ‘Irreversibly Harm' Stonehenge.” Artnet. 7/24/2024. https://news.artnet.com/art-world/legal-battle-stonehenge-tunnel-2515809 Martin B. Sweatman, Representations of calendars and time at Göbekli Tepe and Karahan Tepe support an astronomical interpretation of their symbolism, Time and Mind (2024). DOI: 10.1080/1751696X.2024.2373876 Merrington, Andrew. “Archaeological scanners offer 2,000-year window into the world of Roman medicine.” Phys.org. 7/16/2024. https://phys.org/news/2024-07-archaeological-scanners-year-window-world.html#google_vignette Metcalfe, Tom. “3 shipwrecks from 'forgotten battle' of World War II discovered off remote Alaskan island.” LiveScience. 8/18/2024. https://www.livescience.com/archaeology/3-shipwrecks-from-forgotten-battle-of-world-war-ii-discovered-off-remote-alaskan-island Moreno-Mayar, J.V., Sousa da Mota, B., Higham, T. et al. Ancient Rapanui genomes reveal resilience and pre-European contact with the Americas. Nature 633, 389–397 (2024). https://doi.org/10.1038/s41586-024-07881-4 National Museum of Ireland. “Appeal for information about Bronze Age axeheads found in Westmeath.” https://www.museum.ie/en-IE/News/Appeal-for-information-about-Bronze-Age-Axeheads-F Nichols, Kaila. “A history buff bought a piece of a tent from Goodwill for $1,700. It really did belong to George Washington.” CNN. 7/21/2024. https://www.cnn.com/2024/07/21/us/george-washington-tent-fragment-goodwill/index.html Ogliore, Talia. “Archaeologists report earliest evidence for plant farming in east Africa.” EurekAlert. 7/9/2024. https://www.eurekalert.org/news-releases/1050678 Orie, Amarachi. “New Titanic photos show major decay to legendary wreck.” CNN. 9/2/2024. https://www.cnn.com/2024/09/02/science/titanic-photos-show-major-decay-intl-scli/index.html Owsley DW, Bruwelheide KS, Harney É, et al. Historical and archaeogenomic identification of high-status Englishmen at Jamestown, Virginia. Antiquity. 2024;98(400):1040-1054. doi:10.15184/aqy.2024.75 org . “New finds in treasure-laden shipwreck off Colombia.” 8/9/2024. https://phys.org/news/2024-08-treasure-laden-shipwreck-colombia.html#google_vignette Pirchner, Deborah. “Pompeii skeleton discovery shows another natural disaster may have made Vesuvius eruption even more deadly.” EurekAlert. 7/18/2024. https://www.eurekalert.org/news-releases/1050523 Qiblawi, Adnan. “A Metal Tube in a Polish Museum Turns Out to Be a 150-Year-Old Time Capsule.” Artnet. 7/5/2024. https://news.artnet.com/art-world/polish-museum-time-capsule-2508303 Cooley et al, Rainforest response to glacial terminations before and after human arrival in Lutruwita (Tasmania), Quaternary Science Reviews (2024). DOI: 10.1016/j.quascirev.2024.108572 Schrader, Adam. “Historian Identifies Lost Henry VIII Portrait in Background of Social Media Photo.” Artnet. 7/26/2024. https://news.artnet.com/art-world/historian-identifies-henry-viii-portrait-social-media-photo-2517144 Seaton, Jamie. “Did Prehistoric Children Make Figurines Out of Clay?” Smithsonian. 7/2/2024. https://www.smithsonianmag.com/science-nature/did-prehistoric-children-make-figurines-out-of-clay-180984534/ Solly, Melian. “Archaeologists Say They've Solved the Mystery of a Lead Coffin Discovered Beneath Notre-Dame.” Smithsonian. 9/18/2024. https://www.smithsonianmag.com/smart-news/archaeologists-say-theyve-solved-the-mystery-of-a-lead-coffin-discovered-beneath-notre-dame-180985103/ Stockholm University. "Study reveals isolation, endogamy and pathogens in early medieval Spanish community." ScienceDaily. ScienceDaily, 28 August 2024. www.sciencedaily.com/releases/2024/08/240828154921.htm. Strickland, Ashley. “Archaeologists unearth tiny 3,500-year-old clay tablet following an earthquake.” CNN. 8/16/2024. https://www.cnn.com/2024/08/16/science/ancient-cuneiform-tablet-turkey-earthquake/index.html Svennevig, Birgitte. “Chemical analyses find hidden elements from renaissance astronomer Tycho Brahe's alchemy laboratory.” EurekAlert. 7/24/2024. https://www.eurekalert.org/news-releases/1052085 The History Blog. “Animal figurine found in early Viking settlement in Iceland.” 8/27/2024. http://www.thehistoryblog.com/archives/70960 The History Blog. “Bronze Age axe found off Norwegian coast.” 7/14/2024. http://www.thehistoryblog.com/archives/70697 The History Blog. “Tomb of military leader in Augustus' wars in Spain found in Pompeii.” 7/17/2024. http://www.thehistoryblog.com/archives/70715 The History Blog. “Wolf teeth found in ancient Venetii cremation burial.” 9/25/2024. http://www.thehistoryblog.com/archives/71171 Thomas AE, Hill ME, Stricker L, et al. The Dogs of Tsenacomoco: Ancient DNA Reveals the Presence of Local Dogs at Jamestown Colony in the Early Seventeenth Century. American Antiquity. 2024;89(3):341-359. doi:10.1017/aaq.2024.25 Thorsberg, Christian. “Sticks Discovered in Australian Cave Shed New Light on an Aboriginal Ritual Passed Down for 12,000 Years.” Smithsonian. 7/9/2024. https://www.smithsonianmag.com/smart-news/sticks-discovered-in-australian-cave-shed-new-light-on-an-aboriginal-ritual-passed-down-for-12000-years-180984642/ Whiddington, Richard. “Van Gogh's ‘Irises' Appear Blue Today, But Were Once More Violet, New Research Finds.” Artnet. 7/24/2024. https://news.artnet.com/art-world/van-gogh-irises-getty-2515593 Whiddington, Richard. “Was Venice's Famed Winged Lion Statue Actually Made in China?.” Artnet. 9/17/2024. https://news.artnet.com/art-world/bronze-venice-lion-from-china-2537486 Wizevich, Eli. “Newly Deciphered, 4,000-Year-Old Cuneiform Tablets Used Lunar Eclipses to Predict Major Events.” Smithsonian. 8/9/2024. https://www.smithsonianmag.com/smart-news/newly-deciphered-4000-year-old-cuneiform-tablets-used-lunar-eclipses-to-predict-major-events-180984871/ Woolston, Chris. “New study challenges drought theory for Cahokia exodus.” Phys.org. 7/3/2024. https://phys.org/news/2024-07-drought-theory-cahokia-exodus.html Potter, Lisa. “Genetics reveal ancient trade routes and path to domestication of the Four Corners potato Genetic analysis shows that ancient.” EurekAlert. 7/24/2024. https://www.eurekalert.org/news-releases/1052517 Cell Press. "World's oldest cheese reveals origins of kefir." ScienceDaily. ScienceDaily, 25 September 2024. www.sciencedaily.com/releases/2024/09/240925122859.htm See omnystudio.com/listener for privacy information.

Part one of this edition of Unearthed! is mostly updates - about two-thirds of the episode. The rest is weapons, medicine, and books and letters.  Research: 19 News Investigative Team. “Exhumation of Cleveland Torso Killer's unidentified victims now underway.” https://www.cleveland19.com/2024/08/09/exhumation-cleveland-torso-killers-unidentified-victims-now-underway/ Abdallah, Hanna. “Hydraulic lift technology may have helped build Egypt's iconic Pyramid of Djoser.” EurekAlert. 8/5/2024. https://www.eurekalert.org/news-releases/1051645 Addley, Esther. “Dorset ‘Stonehenge' under Thomas Hardy's home given protected status.” The Guardian. 9/24/2024. https://www.theguardian.com/uk-news/2024/sep/24/dorset-stonehenge-discovered-under-thomas-hardy-home-dorchester Adhi Agus Oktaviana et al, Narrative cave art in Indonesia by 51,200 years ago, Nature (2024). DOI: 10.1038/s41586-024-07541-7 Agence France-Presse. “‘Virtually intact' wreck off Scotland believed to be Royal Navy warship torpedoed in first world war.” The Guardian. 8/17/2024. https://www.theguardian.com/uk-news/article/2024/aug/17/virtually-intact-wreck-off-scotland-believed-to-be-royal-navy-warship-torpedoed-in-wwi Anderson, Sonja. “A Statue of a 12-Year-Old Hiroshima Victim Has Been Stolen.” Smithsonian. 7/16/2024. https://www.smithsonianmag.com/smart-news/statue-of-a-child-killed-by-the-bombing-of-hiroshima-has-been-stolen-180984710/ Anderson, Sonja. “An 11-Year-Old Boy Rescued a Mysterious Artwork From the Dump. It Turned Out to Be a 500-Year-Old Renaissance Print.” Smithsonian. 9/17/2024 https://www.smithsonianmag.com/smart-news/this-11-year-old-boy-rescued-a-mysterious-artwork-from-the-dump-it-turned-out-to-be-a-500-year-old-renaissance-print-180985074/ Anderson, Sonja. “Archaeologists Uncover Ancient Warship's Bronze Battering Ram, Sunk During an Epic Battle Between Rome and Carthage.” Smithsonian. 8/28/2024. https://www.smithsonianmag.com/smart-news/archaeologists-uncover-ancient-warships-bronze-battering-ram-sunk-during-epic-battle-between-rome-and-carthage-180984983/ ANderson, Sonja. “Someone Anonymously Mailed Two Bronze Age Axes to a Museum in Ireland.” Smithsonian. 7/15/2024. https://www.smithsonianmag.com/smart-news/two-anonymously-sent-bronze-age-axes-arrive-at-an-irish-museum-in-a-pancake-box-180984704/ Anderson, Sonja. “These Signed Salvador Dalí Prints Were Forgotten in a Garage for Half a Century.” Smithsonian. 8/29/2024. https://www.smithsonianmag.com/smart-news/these-signed-salvador-dali-prints-were-forgotten-in-a-garage-for-half-a-century-180984994/ Anderson, Sonja. “What Is the Secret Ingredient Behind Rembrandt's Golden Glow?.” Smithsonian. 8/1/2024. https://www.smithsonianmag.com/smart-news/what-secret-ingredient-behind-rembrandt-golden-glow-180984816/ “Jamestown DNA helps solve a 400-year-old mystery and unexpectedly reveals a family secret.” Phys.org. 8/13/2024. https://phys.org/news/2024-08-jamestown-dna-year-mystery-unexpectedly.html#google_vignette Ariane E. Thomas et al, The Dogs of Tsenacomoco: Ancient DNA Reveals the Presence of Local Dogs at Jamestown Colony in the Early Seventeenth Century, American Antiquity (2024). DOI: 10.1017/aaq.2024.25 Artnet “Previously Unknown Mozart Composition Turns Up in a German Library.” 9/20/2024. https://news.artnet.com/art-world/unheard-mozart-composition-manuscript-found-leipzig-2540432 ArtNet News. “Conservation of a Rubens Masterpiece Turns Up Hidden Alterations.” Artnet. 6/20/2024. https://news.artnet.com/art-world/rubens-judgement-of-paris-conservation-national-gallery-2501839 Artnet News. “Gardner Museum Is Renovating the Room That Witnessed a Notorious Heist.” 9/18/2024. https://news.artnet.com/art-world/gardner-museum-renovate-dutch-room-2538856 Benzine, Vittoria. “Turkish Archaeologists Uncover Millefiori Glass Panels for the First Time.” Artnet. 9/12/2024. https://news.artnet.com/art-world/millefiori-glass-panels-turkey-2535407 Binswanger, Julia. “A Thief Replaced This Iconic Churchill Portrait With a Fake. Two Years Later, the Original Has Been Recovered.” Smithsonian. 9/16/2024. https://www.smithsonianmag.com/smart-news/a-thief-replaced-this-iconic-churchill-portrait-with-a-fake-two-years-later-the-original-has-been-recovered-180985075/ Binswanger, Julia. “A Viking-Era Vessel Found in Scotland a Decade Ago Turns Out to Be From Asia.” Smithsonian. 9/4/2024. https://www.smithsonianmag.com/smart-news/a-viking-era-vessel-found-in-scotland-a-decade-ago-turns-out-to-be-from-asia-180985021/ Binswanger, Julia. “Hidden Self-Portrait by Norman Cornish Discovered Behind Another Painting .” Smithsonian. 7/24/2024. https://www.smithsonianmag.com/smart-news/a-hidden-norman-cornish-self-portrait-is-discovered-on-the-back-of-a-painting-180984741/ Binswanger, Julia. “Students Stumble Upon a Message in a Bottle Written by a French Archaeologist 200 Years Ago.” Smithsonian. 9/25/2024. https://www.smithsonianmag.com/smart-news/students-discover-french-archaeologists-200-year-old-message-in-a-bottle-just-in-time-on-an-eroding-coast-180985129/ Brinkhof, Tim. “Amateur Sleuths Are Convinced They Have Found Copernicus's Famous Compass.” Artnet. 8/7/2024. https://news.artnet.com/art-world/copernicus-compass-poland-2521967 Brinkhof, Tim. “The U.K. Bars Export of Alan Turing's Wartime Notebooks.” Artnet. 8/19/2024. https://news.artnet.com/art-world/turing-notebooks-uk-export-bar-2525678 Brown, DeNeen L. “Navy exonerates Black sailors charged in Port Chicago disaster 80 years ago.” Washington Post. 7/17/2024. https://www.washingtonpost.com/history/2024/07/17/port-chicago-disaster-navy-exonerates-black-sailors/ Bryant, Chris. “Second World War codebreaker Alan Turing's ‘Delilah' project papers at risk of leaving the UK.” Gov.UK. https://www.gov.uk/government/news/second-world-war-codebreaker-alan-turings-delilah-project-papers-at-risk-of-leaving-the-uk Byram, Scott et al. “Clovis points and foreshafts under braced weapon compression: Modeling Pleistocene megafauna encounters with a lithic pike.” PLOS One. 8/21/2024. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0307996#sec013 Cascone, Sarah. “Long-Lost Artemisia Gentileschi Masterpiece Goes on View After Centuries of Obscurity.” Artnet. 9/9/2024. https://news.artnet.com/art-world/kimbell-art-museum-artemisia-gentileschi-2533554 Cascone, Sarah. “Mythical French ‘Excalibur' Sword Goes Missing.” Artnet. 7/10/2024. https://news.artnet.com/art-world/durandal-sword-in-the-stone-gone-missing-2510560 Casey, Michael. “Discovery of musket balls brings alive one of the first battles in the American Revolution.” Associated Press. 7/17/2024. https://apnews.com/article/revolutionary-war-musket-balls-national-park-service-33dc4a91c00626ad0d27696458f09900 David, B., Mullett, R., Wright, N. et al. Archaeological evidence of an ethnographically documented Australian Aboriginal ritual dated to the last ice age. Nat Hum Behav 8, 1481–1492 (2024). https://doi.org/10.1038/s41562-024-01912-w Davis, Lisa Fagan. “Multispectral Imaging and the Voynich Manuscript.” Manuscript Road Trip. 9/8/2024. https://manuscriptroadtrip.wordpress.com/2024/09/08/multispectral-imaging-and-the-voynich-manuscript/ Deliso, Meredith. “Witness gets emotional recounting doomed Titan dive during Coast Guard hearing on submersible implosion.” ABC News. 9/19/2024. https://abcnews.go.com/US/oceangate-titan-coast-guard-hearing-mission-specialist/story?id=113843817 Feldman, Ella. “Painting Attributed to Rembrandt Found Tucked Away Inside an Attic in Maine.” 9/6/2024. https://www.smithsonianmag.com/smart-news/painting-attributed-to-rembrandt-found-tucked-away-inside-an-attic-in-maine-180985036/ Fox, Jeremy C. “A French ship that sank after a collision in fog in 1856 off the Mass. coast has been found.” Boston Globe. 9/7/2024.. https://www.bostonglobe.com/2024/09/07/metro/ship-sank-1856-found-massachusetts/?event=event12 com News Staff. “Bullet found with remains during excavation at Oaklawn Cemetery, marks 3rd confirmed gunshot victim.” 8/2/2024. https://www.fox23.com/news/bullet-found-with-remains-during-excavation-at-oaklawn-cemetery-marks-3rd-confirmed-gunshot-victim/article_bf2eb2c8-5122-11ef-b13a-7f883d394aae.html Giordano, Gaia et al. “Forensic toxicology backdates the use of coca plant (Erythroxylum spp.) in Europe to the early 1600s.” Journal of Archaeological Science. Volume 170, 2024, 106040, ISSN 0305-4403, https://doi.org/10.1016/j.jas.2024.106040. Gouevia, Flavia. “Donegal farmer uncovers 22kg slab of ancient bog butter.” The Irish News. 9/13/2024. https://www.irishnews.com/news/ireland/donegal-farmer-uncovers-22kg-slab-of-ancient-bog-butter-YUJKZVXG6NH43G3SBZ3DAUDCHI/ Hawkins, Grant. “Texas A&M's Quest To Save An Alamo Cannon.” Texas A&M Today. 7/31/2024. https://today.tamu.edu/2024/07/31/texas-ams-quest-to-save-an-alamo-cannon/ Howe, Craig and Lukas Rieppel. “Why museums should repatriate fossils.” Nature. 6/18/2024. https://www.nature.com/articles/d41586-024-02027-y Ian G. Barber et al, American sweet potato and Asia-Pacific crop experimentation during early colonisation of temperate-climate Aotearoa/New Zealand, Antiquity (2024). DOI: 10.15184/aqy.2024.143 Imai, Kunihiko. “Researchers identify mystery artifact from ancient capital.” The Ashai Shimbun. 9/5/2024. https://www.asahi.com/ajw/articles/15415562 Kael, Sascha. “The plague may have caused the downfall of the Stone Age farmers.” EurekAlert. 7/10/2024. https://www.eurekalert.org/news-releases/1050694 Kokkinidis, Tasos. “Second Ancient Shipwreck Discovered at Antikythera, Greece.” Greek Reporter. 7/1/2024. https://greekreporter.com/2024/07/01/second-ancient-shipwreck-discovered-antikythera-greece/ Kovac, Adam. “17th-Century Mummified Brains Test Positive for Cocaine.” 8/27/2024. https://gizmodo.com/17th-century-mummified-brains-test-positive-for-cocaine-2000491460 Kuta, Sarah. “Divers Can Now Explore Historic Shipwrecks in Lake Michigan More Easily.” Smithsonian. 8/23/2024. https://www.smithsonianmag.com/smart-news/divers-can-now-explore-historic-shipwrecks-in-lake-michigan-more-easily-180984959/ Kuta, Sarah. “Divers Find Crates of Unopened Champagne in 19th-Century Shipwreck.” Smithsonian. 7/31/2024. https://www.smithsonianmag.com/smart-news/divers-find-shipwreck-loaded-with-champagne-near-sweden-180984784/ Kuta, Sarah. “DNA Reveals Identity of Officer on the Lost Franklin Expedition—and His Remains Show Signs of Cannibalism.” Smithsonian. 9/26/2024. https://www.smithsonianmag.com/smart-news/dna-reveals-identity-of-officer-on-the-lost-franklin-expedition-and-his-remains-show-signs-of-cannibalism-180985154/ Kuta, Sarah. “Shipwreck Found in Lake Michigan 130 Years After Sinking With Captain's ‘Intelligent and Faithful' Dog Onboard.” Smithsonian. 7/25/2024. https://www.smithsonianmag.com/smart-news/shipwreck-found-in-lake-michigan-130-years-after-sinking-with-captains-intelligent-and-faithful-dog-onboard-180984766/ Larson, Christina. “Stonehenge's 'altar stone' originally came from Scotland and not Wales, new research shows.” Phys.org. 8/17/2024. https://phys.org/news/2024-08-stonehenge-altar-stone-scotland-wales.html Lawson-Tancred, Jo. “A Marble God Is Found in an Ancient Roman Sewer.” Artnet. 7/9/2024. https://news.artnet.com/art-world/marble-hermes-ancient-roman-sewer-2509628 Lawson-Tancred, Jo. “Legal Battle Intensifies Over Tunnel That May ‘Irreversibly Harm' Stonehenge.” Artnet. 7/24/2024. https://news.artnet.com/art-world/legal-battle-stonehenge-tunnel-2515809 Martin B. Sweatman, Representations of calendars and time at Göbekli Tepe and Karahan Tepe support an astronomical interpretation of their symbolism, Time and Mind (2024). DOI: 10.1080/1751696X.2024.2373876 Merrington, Andrew. “Archaeological scanners offer 2,000-year window into the world of Roman medicine.” Phys.org. 7/16/2024. https://phys.org/news/2024-07-archaeological-scanners-year-window-world.html#google_vignette Metcalfe, Tom. “3 shipwrecks from 'forgotten battle' of World War II discovered off remote Alaskan island.” LiveScience. 8/18/2024. https://www.livescience.com/archaeology/3-shipwrecks-from-forgotten-battle-of-world-war-ii-discovered-off-remote-alaskan-island Moreno-Mayar, J.V., Sousa da Mota, B., Higham, T. et al. Ancient Rapanui genomes reveal resilience and pre-European contact with the Americas. Nature 633, 389–397 (2024). https://doi.org/10.1038/s41586-024-07881-4 National Museum of Ireland. “Appeal for information about Bronze Age axeheads found in Westmeath.” https://www.museum.ie/en-IE/News/Appeal-for-information-about-Bronze-Age-Axeheads-F Nichols, Kaila. “A history buff bought a piece of a tent from Goodwill for $1,700. It really did belong to George Washington.” CNN. 7/21/2024. https://www.cnn.com/2024/07/21/us/george-washington-tent-fragment-goodwill/index.html Ogliore, Talia. “Archaeologists report earliest evidence for plant farming in east Africa.” EurekAlert. 7/9/2024. https://www.eurekalert.org/news-releases/1050678 Orie, Amarachi. “New Titanic photos show major decay to legendary wreck.” CNN. 9/2/2024. https://www.cnn.com/2024/09/02/science/titanic-photos-show-major-decay-intl-scli/index.html Owsley DW, Bruwelheide KS, Harney É, et al. Historical and archaeogenomic identification of high-status Englishmen at Jamestown, Virginia. Antiquity. 2024;98(400):1040-1054. doi:10.15184/aqy.2024.75 org . “New finds in treasure-laden shipwreck off Colombia.” 8/9/2024. https://phys.org/news/2024-08-treasure-laden-shipwreck-colombia.html#google_vignette Pirchner, Deborah. “Pompeii skeleton discovery shows another natural disaster may have made Vesuvius eruption even more deadly.” EurekAlert. 7/18/2024. https://www.eurekalert.org/news-releases/1050523 Qiblawi, Adnan. “A Metal Tube in a Polish Museum Turns Out to Be a 150-Year-Old Time Capsule.” Artnet. 7/5/2024. https://news.artnet.com/art-world/polish-museum-time-capsule-2508303 Cooley et al, Rainforest response to glacial terminations before and after human arrival in Lutruwita (Tasmania), Quaternary Science Reviews (2024). DOI: 10.1016/j.quascirev.2024.108572 Schrader, Adam. “Historian Identifies Lost Henry VIII Portrait in Background of Social Media Photo.” Artnet. 7/26/2024. https://news.artnet.com/art-world/historian-identifies-henry-viii-portrait-social-media-photo-2517144 Seaton, Jamie. “Did Prehistoric Children Make Figurines Out of Clay?” Smithsonian. 7/2/2024. https://www.smithsonianmag.com/science-nature/did-prehistoric-children-make-figurines-out-of-clay-180984534/ Solly, Melian. “Archaeologists Say They've Solved the Mystery of a Lead Coffin Discovered Beneath Notre-Dame.” Smithsonian. 9/18/2024. https://www.smithsonianmag.com/smart-news/archaeologists-say-theyve-solved-the-mystery-of-a-lead-coffin-discovered-beneath-notre-dame-180985103/ Stockholm University. "Study reveals isolation, endogamy and pathogens in early medieval Spanish community." ScienceDaily. ScienceDaily, 28 August 2024. www.sciencedaily.com/releases/2024/08/240828154921.htm. Strickland, Ashley. “Archaeologists unearth tiny 3,500-year-old clay tablet following an earthquake.” CNN. 8/16/2024. https://www.cnn.com/2024/08/16/science/ancient-cuneiform-tablet-turkey-earthquake/index.html Svennevig, Birgitte. “Chemical analyses find hidden elements from renaissance astronomer Tycho Brahe's alchemy laboratory.” EurekAlert. 7/24/2024. https://www.eurekalert.org/news-releases/1052085 The History Blog. “Animal figurine found in early Viking settlement in Iceland.” 8/27/2024. http://www.thehistoryblog.com/archives/70960 The History Blog. “Bronze Age axe found off Norwegian coast.” 7/14/2024. http://www.thehistoryblog.com/archives/70697 The History Blog. “Tomb of military leader in Augustus' wars in Spain found in Pompeii.” 7/17/2024. http://www.thehistoryblog.com/archives/70715 The History Blog. “Wolf teeth found in ancient Venetii cremation burial.” 9/25/2024. http://www.thehistoryblog.com/archives/71171 Thomas AE, Hill ME, Stricker L, et al. The Dogs of Tsenacomoco: Ancient DNA Reveals the Presence of Local Dogs at Jamestown Colony in the Early Seventeenth Century. American Antiquity. 2024;89(3):341-359. doi:10.1017/aaq.2024.25 Thorsberg, Christian. “Sticks Discovered in Australian Cave Shed New Light on an Aboriginal Ritual Passed Down for 12,000 Years.” Smithsonian. 7/9/2024. https://www.smithsonianmag.com/smart-news/sticks-discovered-in-australian-cave-shed-new-light-on-an-aboriginal-ritual-passed-down-for-12000-years-180984642/ Whiddington, Richard. “Van Gogh's ‘Irises' Appear Blue Today, But Were Once More Violet, New Research Finds.” Artnet. 7/24/2024. https://news.artnet.com/art-world/van-gogh-irises-getty-2515593 Whiddington, Richard. “Was Venice's Famed Winged Lion Statue Actually Made in China?.” Artnet. 9/17/2024. https://news.artnet.com/art-world/bronze-venice-lion-from-china-2537486 Wizevich, Eli. “Newly Deciphered, 4,000-Year-Old Cuneiform Tablets Used Lunar Eclipses to Predict Major Events.” Smithsonian. 8/9/2024. https://www.smithsonianmag.com/smart-news/newly-deciphered-4000-year-old-cuneiform-tablets-used-lunar-eclipses-to-predict-major-events-180984871/ Woolston, Chris. “New study challenges drought theory for Cahokia exodus.” Phys.org. 7/3/2024. https://phys.org/news/2024-07-drought-theory-cahokia-exodus.html Potter, Lisa. “Genetics reveal ancient trade routes and path to domestication of the Four Corners potato Genetic analysis shows that ancient.” EurekAlert. 7/24/2024. https://www.eurekalert.org/news-releases/1052517 Cell Press. "World's oldest cheese reveals origins of kefir." ScienceDaily. ScienceDaily, 25 September 2024. www.sciencedaily.com/releases/2024/09/240925122859.htm See omnystudio.com/listener for privacy information.

Job for a Cowboy, Kollapse, Cell Press, Weston Super Maim, The Sawtooth Grin, Earthtone9, Exist and God Mother. PLUS we get a voice note from Cancer Christ and we discuss the kind of jobs that might be suitable for a half-cow half-boy hybrid. Thanks.

"I heard elders talk about 'the shakes,' but I now know that language reflects deep historical inequities that have denied us access to healthcare, knowledge, and research that could help us alleviate burdens and strengthen our health—enough with the shakes!" —Senegal Alfred Mabry, in CellParkinson's disease is the second most common neurodegenerative disorder in the United States. According to a 2022 study, some 90,000 people a year in the US are diagnosed with Parkinson's. It's a progressive disease that worsens over time, producing unintended or uncontrollable movements, such as tremors, stiffness, and difficulty with balance and coordination.Researchers are working to better understand the causes of the disease, how it connects to other health conditions, and how to slow or prevent its effects. Senegal Alfred Mabry is a third year PhD student in neuroscience at Cornell University, and was recently named a recipient of this year's Rising Black Scientist Award by Cell Press. His research involves interoception—a sense that allows the body to monitor its own processes—and the autonomic nervous system. He joins Ira to talk about his research into Parkinson's disease, and the importance of scientific research being connected to communities.Transcripts for each segment will be available after the show airs on sciencefriday.com.  Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.

On this episode of Metal on Metal, we sat down PQ. PQ is the vocalist of the Montreal sludge band Cell Press In this interview, we discuss their new album Cages. We also discuss Stompin' Tom Connors, Kool Keith, Disco Naps, and the possibility of an Animal Ethics reunion. Links mentioned in this episode: *https://www.youtube.com/watch?v=gVn_sDY-onY https://cellpress.bandcamp.com/album/cages This podcast is hosted by ZenCast.fm

In 2023, SEE YOU NEXT TUESDAY released Distractions their first new album in over a decade via Good Fight Music. One year later, they've made a quick return with a remixed edition of that return album titled Relapses. Guitarist Drew Slavik explains it all in this lengthy discussion on the band, the new record, and their future.Music by:Cell PressSee You Next TuesdayDissimulatorIntro music by:Hot ZonePatreon: https://www.patreon.com/GettingitoutpodcastEmail: dan@gettingitout.netWebsite: http://gettingitout.net/Instagram: @getting_it_out_podcastFacebook: www.facebook.com/gettingitoutpodcastX: @GettingItOutPod Get bonus content on PatreonSupport this show http://supporter.acast.com/getting-it-out. Hosted on Acast. See acast.com/privacy for more information.

Azizi Seixas, Ph.D., is Inaugural Chair of the Department of Informatics and Health Data Science at the University of Miami Miller School of Medicine. He is also Founding Director of The Media and Innovation Lab (The MIL), Associate Director of the Center for Translational Sleep and Circadian Sciences (TSCS) and Director of Population Health Informatics in the Institute for Data Science and Computing. He was recently awarded one of Miami's Most Influential and Powerful Black Business Leaders, an Education Champion Awardee by Amazon Web Services for his innovative work using cloud computing technology and his advocacy for improving education and has been recognized by Cell Press as one of the top 100 most inspiring Black scientists in America. His work has been widely supported by National Institutes of Health (NIH), National Science Foundation (NSF) and several industry and foundation partners.Dr. Seixas has over 175 high impact peer-reviewed publications, book chapters and conference presentations and his work appears in several media-outlets such as CBS, CNN, NBC, Associated Press, The Guardian, Huffington Post, and is the sleep expert for NBC Health News.

Pastor Josh jumps back into the "Joy From a Jail Cell" series in the book of Philippians and encourages us to PRESS ON because we have a bright future that God wants to bring us into.

Plants Scream Like Us When Under Stress? Geez Who Knew? Now that I know I'll try and be more sensitive, but truthfully, thank God I can't hear them or I'd be drinking a lot more lol. Pal Jill Brooke Editor In Chief of Flower Power Daily got my attention with a piece she posted on the subject by Rebecca Ann Hughs titled 'Plants "Scream" When Under Stress - Just Like Us' Jill joined me to talk about the latest research on this phenomenon right on time for plant season. It's true. Although they might not be audible to human ears, plants do make noises. "Researchers in Israel found that plants make a high-frequency clicking sound when placed under stress. Their findings were published this week in the peer-reviewed journal Cell Press." Those researchers spent 6 years listening to plants like tomatoes, grapevines, tobacco and wheat. The plants made noises when they were cut or when they were thirsty and appranelty the sound is like a pop of popcorn or bubble wrap.  Also just because we can't hear plants, it doesn't mean that they are silent to other forms of life. Insects like moths, or mammals such as mice bats, can hear plants. Who Knew?  Whats interesting about these findings is that scientists now want to apply this knowledge to agriculture and farming to better care for crops. Think 'sensors' that tell growers when plants need watering. According to the study, “more precise irrigation can save up to 50% of the water expenditure and increase the yield.”  Wow it does pay to listen! Enjoy this friendly screaming plant update podcast with Jill Brooke Editor In Chief of Flower Power Daily from out fun live conversation on The Debbie Nigro Show.     

Have questions about publishing in academic journals? Sheila Chari, Ph.D., editor in chief of Cell Stem Cell, explains the process from pre-submission through publication. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 38722]

Have questions about publishing in academic journals? Sheila Chari, Ph.D., editor in chief of Cell Stem Cell, explains the process from pre-submission through publication. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 38722]

Have questions about publishing in academic journals? Sheila Chari, Ph.D., editor in chief of Cell Stem Cell, explains the process from pre-submission through publication. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 38722]

Have questions about publishing in academic journals? Sheila Chari, Ph.D., editor in chief of Cell Stem Cell, explains the process from pre-submission through publication. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 38722]

Have questions about publishing in academic journals? Sheila Chari, Ph.D., editor in chief of Cell Stem Cell, explains the process from pre-submission through publication. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 38722]

Have questions about publishing in academic journals? Sheila Chari, Ph.D., editor in chief of Cell Stem Cell, explains the process from pre-submission through publication. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 38722]

Have questions about publishing in academic journals? Sheila Chari, Ph.D., editor in chief of Cell Stem Cell, explains the process from pre-submission through publication. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 38722]

Join Af as he learns about the incredible advances in DNA manipulation with Kevin Davies, the author of Editing Humanity: The CRISPR Revolution and the New Era of Genome Editing. Kevin has 30+ years in science publishing as an editor of leading academic journals (with Nature Genetics, Nature and Cell Press); in trade publishing (Bio-IT World), and as a publisher (C&EN). In 2018, he spearheaded the launch of The CRISPR Journal, published by Mary Ann Liebert Inc. His books include "The $1,000 Genome"​ (Free Press, 2010), "Cracking the Genome" (Free Press, 2001), and "Breakthrough: The Race for the Breast Cancer Gene." Kevin is the founding editor of Nature Genetics, the first offshoot from Nature. He holds an undergraduate degree in Biochemistry from Oxford University and a PhD in molecular genetics from the University of London.

In Part 2 of our conversation with Dr. Azizi Seixas, we discuss the relationship between medical academia and the opportunities afforded by big tech. In his work in the Media and Innovation Lab (MIL) at the University of Miami Miller School of Medicine, he teaches new generations of healthcare innovators to stay curious about the solutions to the biggest problems facing healthcare today.  In his pursuit of a vibrant and equitable future, Dr. Seixas looks for solutions in unexpected places. Open to all possibilities and ideas, he believes that true innovation stems from a purpose-driven life. He uses medicine and technology as tools to create a better world.    Dr. Seixas (Say-shas) is an Associate Professor of Psychiatry and Behavioral Science and the Director of the Media and Innovation Lab at the University of Miami Miller School of Medicine. He is also the Associate Director for the Center for Translational Sleep and Circadian Sciences (TSCS) and an Assistant Professor in the Departments of Population Health and Psychiatry at NYU Langone.  Innovation means keeping an open mind Dr. Seixas teaches students to be innovative leaders of the future. What does that mean? According to Dr. Seixas, it means keeping an open mind - and being a student forever.  Dr. Seixas encourages us to think of ourselves as expert students with more to learn, humble and always receptive to new ideas. This philosophy is useful in innovation by keeping us on a path of exploration, leading us to exciting solutions we may not have seen otherwise.  The innovative future of healthcare When it comes to new solutions to today's problems, Dr. Azizi Seixas doesn't shy away from challenging questions. When asked about the relationship between healthcare and big tech companies, his answer was surprising - he's all for it.  Rather than approaching the issue with concern, Dr. Seixas is curious about how we could create massive, positive change using funding from big tech. He also sees opportunities for us to build a system of checks and balances, preventing issues before they arise. He envisions a world where healthcare is accessible from the comfort of our own homes, where we don't have to take time off work to get the care we need and we don't need to sit in a waiting room to talk with physicians.  Enjoy Part 2 of this exciting forward-thinking conversation about the future of healthcare with Dr. Azizi Seixas! Quotes “When you grow up in a poor working-class family, you become an innovator. You have to find solutions!”  “In order to stay sharp, you have to force yourself to be a student.” “To innovate and do bold things, you have to flow forward and chase your goal. When you're constantly chasing your vision, you'll always end up being ahead of the curve.” “My mother always told me, ‘Never take no for an answer'. As a scientist, I think you need to think like this. You need to be flexible - cognitively and emotionally flexible. It allows me to see things optimistically.” “This is where big tech comes in - they have the infrastructure to scale, and scale quickly. Science gives itself some time to ensure that the results they have are not flukes, and that they are vetted over a period of time. But when it comes to invention and innovation, sometimes we need to do things quickly! We need to accelerate it. Through partnerships where we can quickly implement and iterate on solutions, that's where medicine needs to go.” “If you're pitching an idea, it must have a research question and a problem that you're solving. If you're very clear on that, you're good.” “If you're doing the business of serving people, you should never compromise your values for others.” Links mentioned in this episode: Visit Dr. Seixas' website: https://draziziseixas.com/  Hire Dr. Seixas to speak, giving your audience an inspiring vision of the future of health: https://draziziseixas.com/speaking/  Check out the Media and Innovation Lab (MIL) at the University of Miami School of Medicine: https://med.miami.edu/programs/mil  See Dr. Seixas featured in the official 2020 Cell Press “100 inspiring Black scientists in America”: https://crosstalk.cell.com/blog/100-inspiring-black-scientists-in-america  Check out Dr. Seixas' research timeline as Assistant Professor in the Departments of Population Health and Psychiatry at NYU Langone: https://med.nyu.edu/faculty/azizi-a-seixas

Dr. Azizi Seixas has an impressive bio, but the most extraordinary thing about him is his passion and his purpose.   Dr. Seixas (Say-shas) is an innovator, scientist, thought leader, and technologist. He was voted top 100 most inspiring Black Scientists in America by Cell Press. Currently, he acts as Associate Professor of Psychiatry and Behavioral Science and the Director of the Media and Innovation Lab at the University of Miami Miller School of Medicine. He is also the Associate Director for the Center for Translational Sleep and Circadian Sciences (TSCS) and an Assistant Professor in the Departments of Population Health and Psychiatry at NYU Langone. He studies artificial intelligence and technology with the intention of revolutionizing healthcare systems. Growing up in inner-city Jamaica, Dr. Seixas got his driven attitude from his hard-working single mother who earned a college, then Master's degree while working full-time. His passion came from his force-of-nature grandmother, who taught him to question the status quo. “The two things in life that level off human beings are death and education,” she told young Azizi. Motivated to create a more equitable future for all people, he decided to pursue medicine. Where does your passion come from? When it comes to the tension between faith and science, Dr. Seixas insists this is a false dichotomy. Steadfast in his faith and belief in people, he uses his pursuit of excellence in health and technology as a tool to help underserved communities get the healthcare they need.  Despite the common belief that faith and business are in competition with one another, Dr. Seixas encourages us to use one to serve the other. How can you use your entrepreneurial skills, innate talents and spiritual purpose to drive your mission forward? Innovation is more than just technology. When we think about innovation, we usually think about technology-What apps are trending, new ways to communicate or share files, and creative ways to work online. But Dr. Seixas reminds us that innovation is about so much more than that! Innovative thinking is fresh and creative, making complex things simpler and more accessible. Dr. Seixas spends his career teaching young innovators to think about the communities they're serving and how to most efficiently show up for them.  What systems can be developed to make healthcare available in their area? What difficulties are they facing that you can create solutions for? And what products or technologies can be produced to serve those needs? Dr. Seixas will inspire you to take an innovative look at your own business, ultimately helping you provide more value to your clients. Quotes “I have this burning desire to improve the lives of the have-nots, and to ensure that they can have better health outcomes and live a happy life.” “We're trying to reimagine academic medicine and health. We're doing this by reimagining healthcare by considering education, ensuring research leads us to comprehensive causes of disease, making delivery systems work for people, and creating next-level solutions.” “Find what you're here to do. Be passionate about it and work unceasingly so that it's not about you, it's for the betterment of others. It so happens that science and medicine are the vehicles through which I can do that.” “I believe that everyone is super talented, everyone is special and unique. There just aren't enough people breathing happiness, joy and love into these individuals.” “In order for you to have a purpose-driven life, it must be steeped in excellence so that people can reap the benefits of your work.” “It's a false tension, where science and faith are inadmissible. They go hand in hand. My purpose is driven by what I'm here to do.” “We imagine a world where instead of going to your physician once or twice a year, we want to shift home as being the primary place where health is done. We want to create infrastructure to provide personalized treatments. We want more prevention, better prevention, and lower costs.” “Instead of thinking about underserved communities last or not at all, we can roll out programs and studies to look immediately at people across different socioeconomic strata.”   “When we think about innovation, we think tech. But innovation can be many things! Innovation can mean an innovative practice to increase access to care, making complex things simple. That's what we're doing.” Links mentioned in this episode: Visit Dr. Seixas' website: https://draziziseixas.com/  Hire Dr. Seixas to speak, giving your audience an inspiring vision of the future of health: https://draziziseixas.com/speaking/  See Dr. Seixas featured in the official 2020 Cell Press “100 inspiring Black scientists in America”: https://crosstalk.cell.com/blog/100-inspiring-black-scientists-in-america  Check out Dr. Seixas' research timeline as Assistant Professor in the Departments of Population Health and Psychiatry at NYU Langone: https://med.nyu.edu/faculty/azizi-a-seixas

#crispr #geneticediting #editinghumanity #biotech CRISPR- EDITING HUMANITY'S FUTURE & RE-IMAGINING HEALTHCARE Kevin Davies is a renowned British science journalist and the executive editor of The CRISPR Journal Plus Nature Genetics. He has authored various books such as Breakthrough: The Race to Find the Breast Cancer Gene in the early 1990s Cracking the Genome, which details the dramatic story of one of the greatest scientific feats ever accomplished: the mapping of the human genome The $1,000 Genome, DNA: The Story of the Genetic Revolution And his most recent release, Editing Humanity: The CRISPR Revolution and the New Era of Genome Editing, for which he won a Guggenheim Fellowship for science writing in 2017. Kevin studied at Oxford University and moved to the US in 1987 after earning his Ph.D. in genetics. He is the founding editor of the Nature Genetics journal and Bio-IT World magazine, former editor-in-chief of Cell Press, and the first publisher of C&EN, the weekly magazine of the American Chemical Society. https://www.linkedin.com/in/kevin-davies-52b912 https://twitter.com/kevinadavies Watch our highest viewed videos: 1-India;s 1st Quantum Computer- https://youtu.be/ldKFbHb8nvQDR R VIJAYARAGHAVAN - PROF & PRINCIPAL INVESTIGATOR AT TIFR 2-Breakthrough in Age Reversal- -https://youtu.be/214jry8z3d4DR HAROLD KATCHER - CTO NUGENICS RESEARCH 3-Head of Artificial Intelligence-JIO - https://youtu.be/q2yR14rkmZQShailesh Kumar 4-STARTUP FROM INDIA AIMING FOR LEVEL 5 AUTONOMY - SANJEEV SHARMA CEO SWAAYATT ROBOTS -https://youtu.be/Wg7SqmIsSew 5-TRANSHUMANISM & THE FUTURE OF MANKIND - NATASHA VITA-MORE: HUMANITY PLUS -https://youtu.be/OUIJawwR4PY 6-MAN BEHIND GOOGLE QUANTUM SUPREMACY - JOHN MARTINIS -https://youtu.be/Y6ZaeNlVRsE 7-1000 KM RANGE ELECTRIC VEHICLES WITH ALUMINUM AIR FUEL BATTERIES - AKSHAY SINGHAL -https://youtu.be/cUp68Zt6yTI 8-Garima Bharadwaj Chief Strategist IoT & AI at Enlite Research -https://youtu.be/efu3zIhRxEY 9-BANKING 4.0 - BRETT KING FUTURIST, BESTSELLING AUTHOR & FOUNDER MOVEN -https://youtu.be/2bxHAai0UG0 10-E-VTOL & HYPERLOOP- FUTURE OF INDIA"S MOBILITY- SATYANARAYANA CHAKRAVARTHY -https://youtu.be/ZiK0EAelFYY 11-NON-INVASIVE BRAIN COMPUTER INTERFACE - KRISHNAN THYAGARAJAN -https://youtu.be/fFsGkyW3xc4 12-SATELLITES THE NEW MULTI-BILLION DOLLAR SPACE RACE - MAHESH MURTHY -https://youtu.be/UarOYOLUMGk Connect & Follow us at: https://in.linkedin.com/in/eddieavil https://in.linkedin.com/company/change-transform-india https://www.facebook.com/changetransformindia/ https://twitter.com/intothechange https://www.instagram.com/changetransformindia/ Listen to the Audio Podcast at: https://anchor.fm/transform-impossible https://podcasts.apple.com/us/podcast/change-i-m-possibleid1497201007?uo=4 https://open.spotify.com/show/56IZXdzH7M0OZUIZDb5mUZ https://www.breaker.audio/change-i-m-possible https://www.google.com/podcasts?feed=aHR0cHM6Ly9hbmNob3IuZm0vcy8xMjg4YzRmMC9wb2RjYXN0L3Jzcw Kindly Subscribe to CHANGE- I M POSSIBLE - youtube channel www.youtube.com/ctipodcast

Today, you'll learn about the real science behind the five second rule and why you may wanna reconsider eating that candy off the ground, why researchers are looking to our furry friends to build better early warning systems for natural disasters, and why the first animal to ever fly had a real issue keeping its lunch down.Drop a french fry? Maybe just leave it there. 5-second rule: Science debunks food myth that stretches back to Gengis Khan by Sarah Wellshttps://www.inverse.com/science/five-second-rule-myth-debunkThe Science Behind The Five-Second Rule by Paul Dawson and Brian Sheldonhttps://www.sciencefriday.com/articles/the-science-behind-the-five-second-rule/Still Good? 5-Second Rule a Myth, Study Finds by Rachael Rettnerhttps://www.livescience.com/56158-5-second-rule-myth.htmlDouble Dipping? 5-Second Rule? Scientists Separate Food Fact From Fiction In New Book by Robin Younghttps://www.wbur.org/hereandnow/2018/11/16/double-dipping-5-second-rule-food-safetyWhat are your pets trying to tell you? Maybe there's an earthquake incoming. The animals that detect disasters by Norman Millerhttps://www.bbc.com/future/article/20220211-the-animals-that-predict-disastersCan Birds Tip Us Off to Natural Disasters? by Jason Gregghttps://www.smithsonianmag.com/science-nature/can-birds-tip-us-natural-disasters-180978571/Can animals sense when an earthquake is about to happen? by Anne Quainhttps://phys.org/news/2021-09-animals-earthquake.htmlBirds sensed severe storms and fled before tornado outbreak adapted from Cell Press publishing, article authored by Henry M Streby et alhttps://www.sciencedaily.com/releases/2014/12/141218131413.htmCell Press published articlehttps://www.cell.com/current-biology/fulltext/S0960-9822(14)01428-6Earthquake Warning Systems by Wikipediahttps://en.wikipedia.org/wiki/Earthquake_warning_systemNature of Pre-Earthquake Phenomena and their Effects on Living Organisms by Friedemann Freund and Viktor Stolchttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4494396/Predicting the unpredictable; evidence of pre-seismic anticipatory behaviour in the common toad by Rachel Granthttps://www.researchgate.net/publication/227651706_Predicting_the_unpredictable_evidence_of_pre-seismic_anticipatory_behaviour_in_the_common_toadClues to how birds migrate using Earth's magnetic field by Helen Briggshttps://www.bbc.com/news/science-environment-57582451What do the first flying dinosaurs have in common with owls? Pellets. Fossils reveal that pterosaurs puked pellets by Carolyn Gramlinghttps://www.sciencenews.org/article/pterosaur-fossils-puke-pellet-regurgitation-foodYou may have missed… by Imma Perfettohttps://cosmosmagazine.com/health/you-may-have-missed-30/Like Owls, Some Prehistoric Flying Reptiles May Have Regurgitated Pellets by Margaret Osbornehttps://www.smithsonianmag.com/smart-news/like-owls-some-pterosaurs-may-have-regurgitated-pellets-180979551/What Is a Pterosaur? by American Museum of Natural Historyhttps://www.amnh.org/exhibitions/pterosaurs-flight-in-the-age-of-dinosaurs/what-is-a-pterosaurFollow Curiosity Daily on your favorite podcast app to get smarter with Calli and Nate — for free! Still curious? Get exclusive science shows, nature documentaries, and more real-life entertainment on discovery+! Go to https://discoveryplus.com/curiosity to start your 7-day free trial. discovery+ is currently only available for US subscribers.Midroll Ad Stamp: 9:34Episode 14Title: Burn Them Cals, Magic of Mushrooms, Flying at Mach 16Description: Today, you'll learn about some new, emerging data that is giving us surprising insight into human metabolism, how magic mushrooms are on the forefront of mental health treatment and new jet technology that could get us anywhere in the world in under two hours.True or False: your metabolism slows as you age. The answer isn't what you think! “Burn, baby, burn: the new science of metabolism” by David Coxhttps://www.theguardian.com/science/2021/oct/30/burn-baby-burn-the-new-science-of-metabolism“Surprising findings about metabolism and age” by Fatima Cody Stanford, MD, MPH, MPA, FAAP, FACP, FTOS and Chika Anekwe, MD, MPHhttps://www.health.harvard.edu/blog/surprising-findings-about-metabolism-and-age-202110082613“Middle-age spread isn't down to metabolism, but we know how to beat it” by Sara Novakhttps://www.newscientist.com/article/mg25333774-900-middle-age-spread-isnt-down-to-metabolism-but-we-know-how-to-beat-it/“3 lifestyle changes that can boost your metabolism and prevent weight gain” by Brianna Steinhilberhttps://www.today.com/health/diet-fitness/boost-metabolism-prevent-weight-gain-rcna19394Mushrooms are more magical than fueling your next trip - they could help treat depression. “Psilocybin treatment for major depression effective for up to a year for most patients, study shows” by Marisol Martinezhttps://hub.jhu.edu/2022/02/16/psilocybin-relieves-depression-for-up-to-a-year/“Efficacy and safety of psilocybin-assisted treatment for major depressive disorder: Prospective 12-month follow-up” by Natalie Gukasyan, Alan K Davis, Frederick S Barrett, Mary P Cosimano, Nathan D Sepeda, Matthew W Johnson, and Roland R Griffithshttps://journals.sagepub.com/doi/10.1177/02698811211073759“Psychoactive ingredient in 'magic' mushrooms may treat depression for much longer than traditional antidepressants when combined with therapy, study backed by Tim Ferriss finds” by Dr. Catherine Schuster-Brucehttps://www.businessinsider.com/magic-mushroom-depression-mental-health-treatment-psilocybin-therapy-tim-ferriss-2022-2“Can psychedelics meet their potential for treating mental health disorders?” by Laura Sandershttps://www.sciencenews.org/article/psychedelic-drugs-treatment-mental-health-disorders-depression“Decriminalizing 'magic mushrooms'? Rhode Island lawmakers are considering it. Here's why:” by Patrick Andersonhttps://www.providencejournal.com/story/news/politics/2022/03/08/rhode-island-considering-decriminalizing-magic-psilocybin-mushrooms/9412817002/Getting anywhere in the world in 2 hours may not be the stuff of science fiction for much longer! "The Experimental Engine That Could Get Us Anywhere in the World in 2 Hours" by Caroline Delberthttps://www.popularmechanics.com/science/a34840801/sodramjet-engine-hypersonic-flight-test/“Chinese team test jet engine ‘able to reach anywhere on Earth within 2 hours'” by Stephen Chenhttps://www.scmp.com/news/china/science/article/3111985/chinese-team-test-jet-engine-able-reach-anywhere-earth-within-2“China Tests Hypersonic Jet Engine That Can Go 16 Times the Speed of Sound” by  Fabienne Langhttps://interestingengineering.com/china-tests-hypersonic-jet-engine-that-can-go-16-times-the-speed-of-sound“Scientists Test Hypersonic Jet Engine Prototype That Could Travel Anywhere On Earth In 2 Hours” by Jack Dunhillhttps://www.iflscience.com/technology/scientists-test-hypersonic-jet-engine-prototype-that-could-travel-anywhere-on-earth-in-2-hours/“How Does a Jet Engine Work” by NASAhttps://www.grc.nasa.gov/WWW/K-12/UEET/StudentSite/engines.html“Aircraft Propeller Basics” by Southern Wingshttps://www.southernwings.co.nz/aircraft-propeller-basics/“Keeping the SR-71 Blackbird (the World's First Stealth Plane) Secret Was Near Impossible” by Robert Beckhusenhttps://nationalinterest.org/blog/the-buzz/keeping-the-sr-71-blackbird-the-worlds-first-stealth-plane-17936“SR-71 Blackbird: Stories, Tales, and Legends” by Richard H. Grahamhttps://books.google.com/books?id=ZHkAJAq-2HQC&lpg=PA223&ots=9AS2-nsLCs&dq=limits%20on%20General%20staff%20on%20one%20flight&pg=PA223#v=snippet&q=record&f=falseFollow Curiosity Daily on your favorite podcast app to get smarter with Calli and Nate — for free! Still curious? Get exclusive science shows, nature documentaries, and more real-life entertainment on discovery+! Go to https://discoveryplus.com/curiosity to start your 7-day free trial. discovery+ is currently only available for US subscribers.

Can selection act on ecosystems, societies, or planets such that some persist and others disappear? Must such systems reproduce to evolve? On this episode of Big Biology, we talk to Tim Lenton, Director of the Global Systems Institute (@GSI_Exeter) and a Professor of Climate Change and Earth System Science at the University of Exeter. In his 2021 Trends in Ecology & Evolution paper “Survival of the Systems,” Tim outlined his idea that large, complex systems--such as grasslands, coral reefs, and even human economies--are subject to a kind of natural selection based on their ability to persist. Tim argues that systems better able to extract and recycle resources will spread across landscapes and outcompete other such systems. This episode is produced in collaboration with Trends in Ecology & Evolution (@Trends_Ecol_Evo). TREE, published by Cell Press, is a monthly review journal that contains polished, concise and readable Reviews and Opinions in all areas of ecology and evolutionary science. It aims to keep scientists informed of new developments and ideas across the full range of ecology and evolutionary biology--from the pure to the applied, and from the molecular to the global. Visit: http://www.cell.com/trends/ecology-evolution.

When we try to help people, who are we really serving? When we support our loved ones through Recovery, there is a fine line between helping and gaining a sense of doing something right or accomplish the goal of being a better person. So, are we helping to make ourselves feel better? Is this something we learned in childhood? Why are we REALLY helping? Digging into the concept of helping others can be both introspective and revealing. No doubt, it is a journey worth traveling with a Licensed Therapist. 0:45 - Evoke Therapy, Finding you Intensives Therapy Programs1:40 - Trauma Bond as defined by Psychology Today2:00 - Advice, and when to give it (so many little gems in this article)2:45 - Al Anon Meeting Finder, Families Anonymous Meeting Finder (you'll see the one I host in Ponte Vedra, FL), Nar-Anon Meeting Finder3:35 - Find a Therapist5:15 - Psychology Today article, 'The Neuroscience of Giving' by  Eva Ritvo M.D.6:50 - LifeSpan Podcast7:15 - Cell Press article, "Empathic Care and Distress: Predictive Brain Markers and Dissociable Brain Systems"8:25 - A "fixer", or what is termed as the "White Knight Syndrome".9:25 -  Families Anonymous, "Helping"Thank you for listening and please visit www.siblinghoodofrecovery.com for free resources, links to organizations, groups and individuals who can offer help in the Journey of Recovery towards healing from substance use disorders. If you like this Podcast, please leave a rating on wherever you're listening. It will help to get the word out. If there is one message I can leave you with, the best you can offer your loved one battling addiction is love and a healthier you. Walk gently, my friend.

In Episode #191 I sit down with Stanford University Professor's Dr Christopher Gardner and Dr Justin Sonnenburg to talk about fermented foods, fibre, gut health and immunity. This conversation was organised following the results of their latest randomised controlled trial 'Gut-microbiota-targeted diets modulate human immune status' which was published in Cell Press in 2021. In this conversation we cover: Dr Sonnenburg's background and journey into studying the microbiome Defining the terms ‘microbiome' and ‘microbiota The development of technology in learning more about the microbiome What defines a healthy microbiome and dysbiosis Studying the microbiomes of traditional populations such as the Hadza tribe The benefits of microbiome diversity Lack of microbiome diversity Intestinal permeability How Justin and Christopher came to working together The mission behind their study of fibre and fermented foods The methodology of the study The definition of fermented foods Microbes being added to packaged fermented foods What the study found in terms of fermented food Conducting studies with humans vs animals What can the study tell us about the effectiveness of probiotics Sodium in fermented foods What the study found in terms of fibre intake Accuracy of stool/microbiome testing Key takeaways from the study and plenty more Justin Sonnenburg, PhD bio: Dr Sonnenburg is an associate professor in the Department of Microbiology and Immunology at the Stanford University School of Medicine, where he studies the gut microbiota in health and disease and co-directs the Center for Human Microbiome Studies. He and his wife Erica, are the authors of the book The Good Gut: Taking Control of Your Weight, Your Mood, and Your Long-Term Health. Their laboratory at Stanford develops and employs diverse technologies to understand basic principles that govern interactions within the intestinal microbiota and between the microbiota and the host. An ongoing objective of the research program is to devise and implement innovative strategies to prevent and treat disease in humans via the gut microbiota. Current pursuits include genetic engineering commensal bacteria to enable therapeutic delivery within the gut, as well as understanding the health impact of microbiome change that has occurred during industrialization. Justin conducted his Ph.D. in Biomedical Sciences at the University of California, San Diego in the laboratory of Ajit Varki. His postdoctoral work was conducted at Washington University in Saint Louis, Missouri in the laboratory of Jeffrey Gordon. He has received an NIH Director's New Innovator Award and Pioneer Award. He serves on several scientific advisory boards and is a co-founder of Novome Biotechnologies. Christopher Gardner, PhD bio: Dr Gardner is the Rehnborg Farquhar professor of medicine at Stanford, the director of Stanford Prevention Research Center's (SPRC) Nutrition Studies Group, and the director of the SPRC postdoctoral research fellow training program. His primary research focus for the past decade has been randomized controlled nutrition intervention trials (soy, garlic, antioxidants, ginkgo, omega-3 fats, vegetarian diets, weight loss diets), testing the effects of these on chronic disease risk factors that have included blood cholesterol, weight, inflammatory markers, and the microbiome. His research interests have recently shifted to two new areas. The first is to approach helping individuals make healthful improvements in diet through motivators beyond health, linking to ongoing social

In Episode #191 I sit down with Stanford University Professor's Dr Christopher Gardner and Dr Justin Sonnenburg to talk about fermented foods, fibre, gut health and immunity. This conversation was organised following the results of their latest randomised controlled trial 'Gut-microbiota-targeted diets modulate human immune status' which was published in Cell Press in 2021.In this conversation we cover:Dr Sonnenburg's background and journey into studying the microbiomeDefining the terms ‘microbiome' and ‘microbiotaThe development of technology in learning more about the microbiomeWhat defines a healthy microbiome and dysbiosisStudying the microbiomes of traditional populations such as the Hadza tribeThe benefits of microbiome diversityLack of microbiome diversityIntestinal permeabilityHow Justin and Christopher came to working togetherThe mission behind their study of fibre and fermented foodsThe methodology of the studyThe definition of fermented foodsMicrobes being added to packaged fermented foodsWhat the study found in terms of fermented foodConducting studies with humans vs animalsWhat can the study tell us about the effectiveness of probioticsSodium in fermented foodsWhat the study found in terms of fibre intakeAccuracy of stool/microbiome testingKey takeaways from the studyand plenty moreJustin Sonnenburg, PhD bio:Dr Sonnenburg is an associate professor in the Department of Microbiology and Immunology at the Stanford University School of Medicine, where he studies the gut microbiota in health and disease and co-directs the Center for Human Microbiome Studies. He and his wife Erica, are the authors of the book The Good Gut: Taking Control of Your Weight, Your Mood, and Your Long-Term Health. Their laboratory at Stanford develops and employs diverse technologies to understand basic principles that govern interactions within the intestinal microbiota and between the microbiota and the host. An ongoing objective of the research program is to devise and implement innovative strategies to prevent and treat disease in humans via the gut microbiota. Current pursuits include genetic engineering commensal bacteria to enable therapeutic delivery within the gut, as well as understanding the health impact of microbiome change that has occurred during industrialization. Justin conducted his Ph.D. in Biomedical Sciences at the University of California, San Diego in the laboratory of Ajit Varki. His postdoctoral work was conducted at Washington University in Saint Louis, Missouri in the laboratory of Jeffrey Gordon. He has received an NIH Director's New Innovator Award and Pioneer Award. He serves on several scientific advisory boards and is a co-founder of Novome Biotechnologies.Christopher Gardner, PhD bio:Dr Gardner is the Rehnborg Farquhar professor of medicine at Stanford, the director of Stanford Prevention Research Center's (SPRC) Nutrition Studies Group, and the director of the SPRC postdoctoral research fellow training program. His primary research focus for the past decade has been randomized controlled nutrition intervention trials (soy, garlic, antioxidants, ginkgo, omega-3 fats, vegetarian diets, weight loss diets), testing the effects of these on chronic disease risk factors that have included blood cholesterol, weight, inflammatory markers, and the microbiome. His research interests have recently shifted to two new areas. The first is to approach helping individuals make healthful improvements in diet through motivators beyond health, linking to ongoing social movements around animal rights and welfare, climate change, and social justice, and their relationships to food. The second is to focus less on trying to improve individual behaviors around food, and more on a food systems approach that addresses the quality of food provided by universities, worksites, hospitals, schools, etc., using a community-based participatory research approach and taking advantage of the many complementary disciplines represented on the Stanford campus, such as medicine, business, education, law, and earth sciences.Resources:The new study on fermented foods, fibre and the immune systemDr Gardner on TwitterThe Sonnenburg lab on TwitterSonnenburg Lab websiteThe Good Gut by Drs Justin & Erica SonnenburgPrevious episodes with Dr Christopher Gardner on plant-based meat and low versus high carb diets and weight loss.Want to support the show?If you are enjoying the Plant Proof podcast a great way to support the show is by leaving a review on the Apple podcast app. It only takes a few minutes and helps more people find the episodes.Simon Hill, Nutritionist, Sports PhysiotherapistCreator of Plantproof.com and host of the Plant Proof PodcastAuthor of The Proof is in the PlantsConnect with me on Instagram and TwitterDownload my two week meal plan

Kevin Davies is a renowned British science journalist and the executive editor of The CRISPR Journal, based in New York. His literary career began with Breakthrough: The Race to Find the Breast Cancer Gene in the early 1990s, followed by Cracking the Genome, which details the dramatic story of one of the greatest scientific feats ever accomplished: the mapping of the human genome. His other titles include the $1,000 Genome, DNA: The Story of the Genetic Revolution, and his most recent release, Editing Humanity: The CRISPR Revolution and the New Era of Genome Editing, for which he won a Guggenheim Fellowship for science writing in 2017. Kevin studied at Oxford University and moved to the US in 1987 after earning his Ph.D. in genetics. He is the founding editor of the Nature Genetics journal and Bio-IT World magazine, former editor-in-chief of Cell Press, and the first publisher of C&EN, the weekly magazine of the American Chemical Society. In today's episode, Kevin elaborates on his career trajectory and explains why he believes that hanging up his lab coat was the best decision he ever made. We also touch on the common themes that run through his books, some of the challenges scientific publishers and editors face, and the importance of promoting the work of women scientists. We also cover vectors, CRISPR babies, the cost of gene therapy, and so much more! Make sure not to miss this fascinating discussion with the remarkable Kevin Davies. “How we turn this stunning 21st-century medicine into therapies that are affordable is going to be a Nobel Prize-winning discovery if anybody can crack that one.” — @KevinADavies Key Points From This Episode: Kevin's career trajectory and his so-called “desperate” shift to science journalism. How Kevin believes the field of genetics has evolved since he was a geneticist in the 1980s. Learn about the impetus behind the Nature Genetics journal and The CRISPR Journal. What motivated Kevin to write Breakthrough, including a meeting with Mary-Claire King. Three elements in all of his books: genetics, medical or societal impact, and personal drama. Hanging up his lab coat to join Nature and the access to authors that it afforded him. Kevin reflects on the demographic representation and “race to the finish line” issues in scientific publishing and the burden editors face. The lens through which Nobel Prizes are considered and how it can shift perspectives. The importance of promoting women in science, who have traditionally been overlooked. How Kevin's book, Editing Humanity, coincided with Doudna and Charpentier making history as the first two women to share a Nobel Prize. Stanley Qi's role in the CRISPR story, which Kevin calls an “unsung contribution.” Speculation and trepidation surrounding vectors: Kevin shares some new thinking. Germline genome editing, CRISPR babies, He Jiankui, and controversy in Hong Kong. Learn more about the exponential cost of gene therapies and gene editing drugs.

This Podcast is for educational purposes only not intended to treat cure diagnose or prevent sickness illness disease or mental health issues if you are making any lifestyle changes to your health and wellness routine for yourself and family consult with your medical doctor first. #Holistictalk #Autismspectrumdisorder #alternativemedicine #healing #holistichealth #holistichealth #alternativehealing #wellness #selfcare Reference: American Psychiatric Association (2013). "Autism Spectrum Disorder. 299.00 (F84.0)". Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Arlington, VA: American Psychiatric Publishing. pp. 50–59. Cell Press. (2016, June 9). Autism is not just a disorder of the brain, mouse study suggests. Zhao, G., Walsh, K., Long, J., Gui, W., & Denisova, K. (2018). Reduced structural complexity of the right cerebellar cortex in male children with autism spectrum disorder. PloS one, 13(7), e0196964. --- Send in a voice message: https://anchor.fm/rdlc/message

This week Harry is joined by Kevin Davies, author of the 2020 book Editing Humanity: The CRISPR Revolution and the New Era of Genome Editing. CRISPR—an acronym for Clustered Regularly Interspaced Short Palindromic Repeats—consists of DNA sequences that evolved to help bacteria recognize and defend against viral invaders, as a kind of primitive immune system. Thanks to its ability to precisely detect and cut other DNA sequences, CRISPR has spread to labs across the world in the nine years since Jennifer Doudna and Emmanuel Charpentier published a groundbreaking 2012 Science paper describing how the process works. The Nobel Prize committee recognized the two scientists for the achievement in 2020, one day after Davies' book came out. The book explains how CRISPR was discovered, how it was turned into an easily programmable tool for cutting and pasting stretches of DNA, how most of the early pioneers in the field have now formed competing biotech companies, and how the technology is being used to help patients today—and in at least one famous case, misused. Today's interview covers all of that ground and more.Davies is a PhD geneticist who has spent most of his career in life sciences publishing. After his postdoc with Harvey Lodish at the Whitehead Institute, Davies worked as an assistant editor at Nature, the founding editor of Nature Genetics (Nature's first spinoff journal), editor-in-chief at Cell Press, founding editor-in-chief of the Boston-based publication Bio-IT World, and publisher of Chemical & Engineering News. In 2018 he helped to launch The CRISPR Journal, where he is the executive editor. Davies' previous books include Breakthrough (1995) about the race to understand the BRCA1 breast cancer gene, Cracking the Genome (2001) about the Human Genome Project, The $1,000 Genome (2010) about next-generation sequencing companies, and DNA (2017), an updated version of James Watson's 2004 book, co-authored with Watson and Andrew Berry.Please rate and review MoneyBall Medicine on Apple Podcasts! Here's how to do that from an iPhone, iPad, or iPod touch:1. Open the Podcasts app on your iPhone, iPad, or Mac. 2. Navigate to the page of the MoneyBall Medicine podcast. You can find it by searching for it or selecting it from your library. Just note that you'll have to go to the series page which shows all the episodes, not just the page for a single episode.3.Scroll down to find the subhead titled "Ratings & Reviews."4.Under one of the highlighted reviews, select "Write a Review."5.Next, select a star rating at the top — you have the option of choosing between one and five stars. 6.Using the text box at the top, write a title for your review. Then, in the lower text box, write your review. Your review can be up to 300 words long.7.Once you've finished, select "Send" or "Save" in the top-right corner. 8.If you've never left a podcast review before, enter a nickname. Your nickname will be displayed next to any reviews you leave from here on out. 9.After selecting a nickname, tap OK. Your review may not be immediately visible.Full TranscriptHarry Glorikian: I'm Harry Glorikian, and this is MoneyBall Medicine, the interview podcast where we meet researchers, entrepreneurs, and physicians who are using the power of data to improve patient health and make healthcare delivery more efficient. You can think of each episode as a new chapter in the never-ending audio version of my 2017 book, “MoneyBall Medicine: Thriving in the New Data-Driven Healthcare Market.” If you like the show, please do us a favor and leave a rating and review at Apple Podcasts.Harry Glorikian: We talk a lot on the show about how computation and data are changing the way we develop new medicines and the way we deliver healthcare. Some executives in the drug discovery business speak of the computing and software side of the business as the “dry lab” —to set it apart from the “wet labs” where scientists get their hands dirty working with actual cells, tissues, and reagents.But the thing is, recent progress on the wet lab side of biotech has been just as amazing as progress in areas like machine learning. And this week, my friend Kevin Davies is here to talk about the most powerful tool to come along in the last decade, namely, precise gene editing using CRISPR.Of course, CRISPR-based gene editing has been all over the news since Jennifer Doudna and Emmanuel Charpentier published a groundbreaking Science paper in 2012 describing how the process works in the lab. That work earned them a Nobel Prize in medicine just eight years later, in 2020.But what's not as well-known is the story of how CRISPR was discovered, how it was turned into an easily programmable tool for cutting and pasting stretches of DNA, how most of the early pioneers in the field have now formed competing biotech companies, and how the technology is being used to help patients today—and in at least one famous case, misused.Kevin put that whole fascinating story together in his 2020 book Editing Humanity. And as the executive editor of The CRISPR Journal, the former editor-in-chief of Bio-IT World, the founding editor at Nature Genetics, and the author of several other important books about genomics, Kevin is one of the best-placed people in the world to tell that story. Here's our conversation.Harry Glorikian: Kevin, welcome to the show. Kevin Davies: Great to see you again, Harry. Thanks for having me on.Harry Glorikian: Yeah, no, I mean, I seem to be saying this a lot lately, it's been such a long time since, because of this whole pandemic, nobody's really seeing anybody on a regular basis. I want to give everybody a chance to hear about, you had written this book called Editing Humanity, which is, you know, beautifully placed behind you for, for product placement here. But I want to hear, can you give everybody sort of an overview of the book and why you feel that this fairly technical laboratory tool called CRISPR is so important that you needed to write a book about it?Kevin Davies: Thank you. Yes. As you may know, from some of my previous “bestsellers” or not, I've written about big stories in genetics because that's the only thing I'm remotely qualified to write about. I trained as a human geneticist in London and came over to do actually a pair of post-docs in the Boston area before realizing my talents, whatever they might be, certainly weren't as a bench researcher. So I had to find another way to stay in science but get away from the bench and hang up the lab coats.So moving into science publishing and getting a job with Nature and then launching Nature Genetics was the route for me. And over the last 30 years, I've written four or five books that have all been about, a) something big happening in genomics, b) something really big that will have both medical and societal significance, like the mapping and discovery of the BRCA1 breast cancer gene in the mid-90s, the Human Genome Project at the turn of the century, and then the birth and the dawn of consumer genetics and personalized medicine with The $1,000 Genome. And the third ingredient I really look for if I'm trying to reach a moderately, significantly large audience is for the human elements. Who are they, the heroes and the anti heroes to propel the story? Where is the human drama? Because, you know, we all love a good juicy, gossipy piece of story and rating the good guys and the bad guys. And CRISPR, when it first really took off in 2012, 2013 as a gene editing tool a lot of scientists knew about this. I mean, these papers are being published in Science in particular, not exactly a specialized journal, but I was off doing other things and really missed the initial excitement, I'm embarrassed to say. It was only a couple of years later, working on a sequel to Jim Watson's DNA, where I was tasked with trying to find and summarize the big advances in genomic technology over the previous decade or whatever, that I thought, well, this CRISPR thing seems to be taking off and the Doudnas and the Charpentiers are, you know, winning Breakthrough Prizes and being feted by celebrities. And it's going on 60 Minutes. They're going to make a film with the Rock, Dwayne Johnson. What the heck is going on. And it took very little time after that, for me to think, you know, this is such an exciting, game-changing disruptive technology that I've got to do two things. I've gotta, a) write a book and b) launch a journal, and that's what I did. And started planning at any rate in sort of 2016 and 17. We launched the CRISPR Journal at the beginning of 2018. And the book Editing Humanity came out towards the end of 2020. So 2020, literally one day before the Nobel Prize—how about that for timing?—for Doudna and Charpentier for chemistry last year. Harry Glorikian: When I think about it, I remember working with different companies that had different types of gene editing technology you know, working with some particularly in the sort of agriculture space, cause it a little bit easier to run faster than in the human space. And you could see what was happening, but CRISPR now is still very new. But from the news and different advances that are happening, especially here in the Boston area, you know, it's having some real world impacts. If you had to point to the best or the most exciting example of CRISPR technology helping an actual patient, would you say, and I've heard you say it, Victoria Gray, I think, would be the person that comes to mind. I've even, I think in one of your last interviews, you said something about her being, you know, her name will go down in history. Can you explain the technology that is helping her and what some of the similar uses of CRISPR might be?Kevin Davies: So the first half of Editing Humanity is about the heroes of CRISPR, how we, how scientists turned it from this bizarre under-appreciated bacterial antiviral defense system and leveraged it and got to grips with it, and then figured out ways to turn it into a programmable gene editing technology. And within a year or two of that happening that the classic Doudna-Charpentier paper came out in the summer of 2012. Of course the first wave of biotech companies were launched by some of the big names, indeed most of the big names in CRISPR gene editing hierarchies. So Emmanuel Charpentier, Nobel Laureate, launched CRISPR Therapeutics, Jennifer Doudna co-founded Editas Medicine with several other luminaries. That didn't go well for, for reasons of intellectual property. So she withdrew from Editas and became a co-founder of Intellia Therapeutics as well as her own company, Caribou, which just went public, and Feng Zhang and others launched Editas Medicine. So we had this sort of three-way race, if you will, by three CRISPR empowered gene editing companies who all went public within the next two or three years and all set their sights on various different genetic Mendelian disorders with a view to trying to produce clinical success for this very powerful gene editing tool. And so, yes, Victoria Gray is the first patient, the first American patient with sickle cell anemia in a trial that is being run by CRISPR Therapeutics in close association with Vertex Pharmaceuticals. And that breakthrough paper, as I think many of your listeners will know, came out right at the end of 2020 published in the New England Journal of Medicine. Doesn't get much more prestigious than that. And in the first handful of patients that CRISPR Therapeutics have edited with a view to raising the levels of fetal hemoglobin, fetal globin, to compensate for the defective beta globin that these patients have inherited, the results were truly spectacular.And if we fast forward now to about two years after the initial administration, the initial procedures for Victoria Gray and some of her other volunteer patients, the results still look as spectacular. Earlier this year CRISPR Therapeutics put out of sort of an update where they are saying that the first 20 or 24 patients that they have dosed with sickle cell and beta thallasemia are all doing well. There've been little or no adverse events. And the idea of this being a once and done therapy appears very well founded. Now it's not a trivial therapy. This is ex-vivo gene editing as obviously rounds of chemotherapy to provide the room for the gene edited stem cells to be reimplanted into the patient. So this is not an easily scalable or affordable or ideal system, but when did we, when will we ever able to say we've pretty much got a cure for sickle cell disease? This is an absolutely spectacular moment, not just for CRISPR, but for medicine, I think, overall. And Victoria Gray, who's been brilliantly profiled in a long running series on National Public Radio, led by the science broadcaster Rob Stein, she is, you know, we, we can call her Queen Victoria, we can call it many things, but I really hope that ,it's not just my idea, that she will be one of those names like Louise Brown and other heroes of modern medicine, that we look and celebrate for decades to come.So the sickle cell results have been great, and then much more recently, also in the New England Journal, we have work led by Intellia Therapeutics, one of the other three companies that I named, where they've been also using CRISPR gene editing, but they've been looking at a rare liver disease, a form of amyloidosis where a toxic protein builds up and looking to find ways to knock out the production of that abnormal gene.And so they've been doing in vivo gene editing, really using CRISPR for the first time. It's been attempted using other gene editing platforms like zinc fingers, but this is the first time that I think we can really say and the New England Journal results prove it. In the first six patients that have been reported remarkable reductions in the level of this toxic protein far, not far better, but certainly better than any approved drugs that are currently on the market. So again, this is a very, very exciting proof of principle for in vivo gene editing, which is important, not just for patients with this rare liver disorder, but it really gives I think the whole field and the whole industry enormous confidence that CRISPR is safe and can be used for a growing list of Mendelian disorders, it's 6,000 or 7,000 diseases about which we know the root genetic cause, and we're not going to tackle all of them anytime soon, but there's a list of ones that now are within reach. And more and more companies are being launched all the time to try and get at some of these diseases.So as we stand here in the summer of 2021, it's a really exciting time. The future looks very bright, but there's so much more to be done. Harry Glorikian: No, we're just at the beginning. I mean, I remember when I first saw this, my first question was off target effects, right? How are we going to manage that? How are they going to get it to that place that they need to get it to, to have it to that cell at that time, in the right way to get it to do what it needs to do. And you know, all these sorts of technical questions, but at the same time, I remember I'm going to, trying to explain this to my friends. I'm like, “You don't understand, this can change everything.” And now a high school student, I say this to people and they look at me strangely, a high school student can order it and it shows up at your house.Kevin Davies: Yeah, well, this is why I think, and this is why one reason why CRISPR has become such an exciting story and receives the Nobel Prize eight years after the sort of launch publication or the first demonstration of it as a gene editing tool. It is so relatively easy to get to work. It's truly become a democratized or democratizing technology. You don't need a million-dollar Illumina sequencer or anything. And so labs literally all around the world can do basic CRISPR experiments. Not everyone is going to be able to launch a clinical trial. But the technology is so universally used, and that means that advances in our understanding of the mechanisms, new tools for the CRISPR toolbox new pathways, new targets, new oftware, new programs, they're all coming from all corners of the globe to help not just medicine, but many other applications of CRISPR as well.Harry Glorikian: Yeah. I always joke about like, there, there are things going on in high school biology classes now that weren't, available, when I was in college and even when we were in industry and now what used to take an entire room, you can do on a corner of a lab bench.Kevin Davies: Yeah. Yeah. As far as the industry goes we mentioned three companies. But you know, today there's probably a dozen or more CRISPR based or gene editing based biotech companies. More undoubtedly are going to be launched before the end of this year. I'm sure we'll spend a bit of time talking about CRISPR 2.0, it seems too soon to be even thinking about a new and improved version of CRISPR, but I think there's a lot of excitement around also two other Boston-based companies, Beam Therapeutics in Cambridge and Verve Therapeutics both of which are launching or commercializing base editing. So base editing is a tool developed from the lab of David Lu of the Broad Institute [of MIT and Harvard]. And the early signs, again, this technology is only five or six years old, but the early signs of this are incredibly promising. David's team, academic team, had a paper in Nature earlier this year, really reporting successful base editing treatment of sickle cell disease in an animal model, not by raising the fetal globin levels, which was sort of a more indirect method that is working very well in the clinic, but by going right at the point mutation that results in sickle cell disease and using given the chemical repertoire of base editing.Base editing is able to make specific single base changes. It can't do the full repertoire of single base changes. So there are some limitations on researchers' flexibility. So they were unable to flip the sickle cell variant back to the quote unquote wild type variants, but the change they were able to make is one that they can live with, we can live with because it's a known benign variant, a very rare variant that has been observed in other, in rare people around the world. So that's completely fine. It's the next best thing. And so that looks very promising. Beam Therapeutics, which is the company that David founded or co-founded is trying a related approach, also going right at the sickle cell mutation. And there are other companies, including one that Matthew Porteus has recently founded and has gone public called Graphite Bio.So this is an exciting time for a disease sickle cell disease that has been woefully neglected, I think you would agree, both in terms of basic research, funding, medical prioritization, and medical education. Now we have many, many shots on goal and it doesn't really, it's not a matter of one's going to win and the others are going to fall by the wayside. Just like we have many COVID vaccines. We'll hopefully have many strategies for tackling sickle cell disease, but they are going to be expensive. And I think you know the economics better than I do. But I think that is the worry, that by analogy with gene therapies that have been recently approved, it's all, it's really exciting that we can now see the first quote, unquote cures in the clinic. That's amazingly exciting. But if the price tag is going to be $1 million or $2 million when these things are finally approved, if and when, that's going to be a rather deflating moment. But given the extraordinary research resources that the CRISPRs and Intellias and Beams and Graphites are pouring into this research, obviously they've got to get some return back on their investment so that they can plow it back into the company to develop the next wave of of gene editing therapies. So you know, it's a predicament Harry Glorikian: One of these days maybe I have to have a show based on the financial parts of it. Because there's a number of different ways to look at it. But just for the benefit of the listeners, right, who may not be experts, how would you explain CRISPR is different from say traditional gene therapies. And is CRISPR going to replace older methods of, of gene therapy or, or will they both have their place? Kevin Davies: No, I think they'll both have their place. CRISPR and, and these newer gene editing tools, base editing and another one called prime editing, which has a company behind it now called Prime Medicine, are able to affect specific DNA changes in the human genome.So if you can target CRISPR, which is an enzyme that cuts DNA together with a little program, the GPS signal is provided in the form of a short RNA molecule that tells the enzyme where to go, where to go in the genome. And then you have a couple of strategies. You can either cut the DNA at the appropriate target site, because you want to inactivate that gene, or you just want to scramble the sequence because you want to completely squash the expression of that gene. Or particularly using the newer forms of gene editing, like base editing, you can make a specific, a more nuanced, specific precision edit without, with one big potential advantage in the safety profile, which is, you're not completely cutting the DNA, you're just making a nick and then coaxing the cell's natural repair systems to make the change that you sort of you're able to prime.So there are many diseases where this is the way you want to go, but that does not in any way invalidate the great progress that we're making in traditional gene therapy. So for example today earlier today I was recording an interview or for one of my own programs with Laurence Reid, the CEO of Decibel Therapeutics, which is looking at therapies for hearing loss both genetic and other, other types of hearing disorders.And I pushed him on this. Aren't you actually joinomg with the gene editing wave? And he was very circumspect and said, no, we're very pleased, very happy with the results that we're getting using old fashioned gene replacement therapy. These are recessive loss of function disorders. And all we need to do is get the expression of some of the gene back. So you don't necessarily need the fancy gene editing tools. If you can just use a an AAV vector and put the healthy gene back into the key cells in the inner ear. So they're complimentary approaches which is great.Harry Glorikian: So, you know, in, in this podcast, I try to have a central theme when I'm talking to people. The relationships of big data, computation, advances in new drugs, and other ways to keep people healthy. So, you know, like question-wise, there's no question in my mind that the whole genomics revolution that started in the ‘90s, and I was happy to be at Applied Biosystems when we were doing that, would have been impossible in the absence of the advances in computing speed and storage in the last three decades. I think computing was the thing that held up the whole human genome, which gave us the book of life that CRISPR is now allowing us to really edit. But I wonder if you could bring us sort of up-to-date and talk about the way CRISPR and computation are intertwined. What happens when you combine precision of an editing tool like CRISPR with the power of machine learning and AI tools to find meaning and patterns in that huge genetic ball? Kevin Davies: Yeah. Well, yeah. I'm got to tread carefully here, but I think we are seeing papers from some really brilliant labs that are using some of the tools that you mentioned. AI and machine learning with a view to better understanding and characterizing some of the properties and selection criteria of some of these gene editing tools. So you mentioned earlier Harry, the need to look out for safety and minimize the concern of off-target effects. So I think by using some of these some algorithms and AI tools, researchers have made enormous strides in being able to design the programmable parts of the gene editing constructs in such a way that you increase the chances that they're going to go to the site that you want them to go to, and nnot get hung up latching onto a very similar sequence that's just randomly cropped up on the dark side of the genome, across the nucleus over there. You don't want that to happen. And I don't know that anybody would claim that they have a failsafe way to guarantee that that could never happen. But the you know, the clinical results that we've seen and all the preclinical results are showing in more and more diseases that we've got the tools and learned enough now to almost completely minimize these safety concerns. But I think everyone, I think while they're excited and they're moving as fast as they can, they're also doing this responsibly. I mean, they, they have to because no field, gene therapy or gene editing really wants to revisit the Jesse Gelsinger tragedy in 1999, when a teenage volunteer died in volunteering for a gene therapy trial at Penn of, with somebody with a rare liver disease. And of course that, that setback set back the, entire field of gene therapy for a decade. And it's really remarkable that you know, many of the sort of pioneers in the field refuse to throw in the towel, they realized that they had to kind of go back to the drawing board, look at the vectors again, and throw it out. Not completely but most, a lot of the work with adenoviruses has now gone by the wayside. AAV is the new virus that we hear about. It's got a much better safety profile. It's got a smaller cargo hold, so that's one drawback, but there are ways around that. And the, the explosion of gene therapy trials that we're seeing now largely on the back of AAV and now increasingly with, with non-viral delivery systems as well is, is very, very gratifying. And it's really delivery. I think that is now the pain point. Digressing from your question a little bit, but delivery, I think is now the big challenge. It's one thing to contemplate a gene therapy for the eye for rare hereditary form of blindness or the ear. Indeed those are very attractive sites and targets for some of these early trials because of the quantities that you need to produce. And the localization, the, the physical localization, those are good things. Those help you hit the target that you want to. But if you're contemplating trying something for Duchenne muscular dystrophy or spinal muscular atrophy, or some of the diseases of the brain, then you're going to need much higher quantities particularly for muscular disorders where, you run into now other challenges, including, production and manufacturing, challenges, and potentially safeguarding and making sure that there isn't an immune response as well. That's another, another issue that is always percolating in the background.But given where we were a few years ago and the clinical progress that we've talked about earlier on in the show it, I think you can safely assume that we've collectively made enormous progress in, in negating most, if not all of these potential safety issues.Harry Glorikian: No, you know, it's funny, I know that people will say like, you know, there was a problem in this and that. And I look at like, we're going into uncharted territories and it has to be expected that you just…you've got people that knew what they were doing. All of these people are new at what they are doing. And so you have to expect that along the way everything's not going to go perfectly. But I don't look at it as a negative. I look at it as, they're the new graduating class that's going to go on and understand what they did right. Or wrong, and then be able to modify it and make an improvement. And, you know, that's what we do in science. Kevin Davies: Well, and forget gene editing—in any area of drug development and, and pharmaceutical delivery, things don't always go according to plan. I'm sure many guests on Moneyball Medicine who have had to deal with clinical trial failures and withdrawing drugs that they had all kinds of high hopes for because we didn't understand the biology or there was some other reaction within, we didn't understand the dosing. You can't just extrapolate from an animal model to humans and on and on and on. And so gene editing, I don't think, necessarily, should be held to any higher standard. I think the CRISPR field has already in terms of the sort of market performance, some of the companies that we've mentioned, oh my God, it's been a real roller coaster surprisingly, because every time there's been a paper published in a prominent journal that says, oh my God, there's, there's a deletion pattern that we're seeing that we didn't anticipate, or we're seeing some immune responses or we're seeing unusual off target effects, or we're seeing P53 activation and you know, those are at least four off the top of my head. I'm sure there've been others. And all had big transient impact on the financial health of these companies. But I think that was to be expected. And the companies knew that this was just an overreaction. They've worked and demonstrated through peer review publications and preclinical and other reports that these challenges have been identified, when known about, pretty much completely have been overcome or are in the process of being overcome.So, you know, and we're still seeing in just traditional gene therapy technologies that have been around for 15, 20 years. We're still seeing reports of adverse events on some of those trials. So for gene editing to have come as far as it's common, to be able to look at these two big New England Journal success stories in sickle cell and ATTR amyloidosis, I don't think any very few, except the most ardent evangelists would have predicted we'd be where we are just a few years ago. [musical transition]Harry Glorikian: I want to pause the conversation for a minute to make a quick request. If you're a fan of MoneyBall Medicine, you know that we've published dozens of interviews with leading scientists and entrepreneurs exploring the boundaries of data-driven healthcare and research. And you can listen to all of those episodes for free at Apple Podcasts, or at my website glorikian.com, or wherever you get your podcasts.There's one small thing you can do in return, and that's to leave a rating and a review of the show on Apple Podcasts. It's one of the best ways to help other listeners find and follow the show.If you've never posted a review or a rating, it's easy. All you have to do is open the Apple Podcasts app on your smartphone, search for MoneyBall Medicine, and scroll down to the Ratings & Reviews section. Tap the stars to rate the show, and then tap the link that says Write a Review to leave your comments. It'll only take a minute, but it'll help us out immensely. Thank you! And now back to the show.[musical transition]Harry Glorikian:One of your previous books was called The $1,000 Genome. And when you published that back in 2010, it was still pretty much science fiction that it might be possible to sequence someone's entire genome for $1,000. But companies like Illumina blew past that barrier pretty quickly, and now people are talking about sequencing individual genome for just a few hundred dollars or less. My question is, how did computing contribute to the exponential trends here. And do you wish you'd called your book The $100 Genome?Kevin Davies: I've thought about putting out a sequel to the book, scratching out the 0's and hoping nobody would notice. Computing was yes, of course, a massive [deal] for the very first human genome. Remember the struggle to put that first assembly together. It's not just about the wet lab and pulling the DNA sequences off the machines, but then you know, the rapid growth of the data exposure and the ability to store and share and send across to collaborators and put the assemblies together has been critical, absolutely critical to the development of genomics.I remember people were expressing shock at the $1,000 genome. I called the book that because I heard Craig Venter use that phrase in public for the first time in 2002. And I had just recently published Cracking the Genome. And we were all still recoiling at the billions of dollars it took to put that first reference genome sequence together. And then here's Craig Venter, chairing a scientific conference in Boston saying what we need is the $1,000 genome. And I almost fell off my chair. “what are you? What are you must you're in, you're on Fantasy Island. This is, there's no way we're going to get, we're still doing automated Sanger sequencing. God bless Fred Sanger. But how on earth are you going to take that technology and go from billions of dollars to a couple of thousand dollars. This is insanity.” And that session we had in 2002 in Boston. He had a local, a little episode of America's Got Talent and he invited half a dozen scientists to come up and show what they had. And George Church was one of them. I think Applied Biosystems may have given some sort of talk during that session. And then a guy, a young British guy from a company we'd never heard of called Celexa showed up and showed a couple of pretty PowerPoint slides with colored beads, representing the budding DNA sequence on some sort of chip. I don't know that he showed any data. It was all very pretty and all very fanciful. Well guess what? They had the last laugh. Illumina bought that company in 2006. And as you said, Harry you know, I think when, when they first professed to have cracked the $1,000 dollar genome barrier, a few people felt they needed a pinch of salt to go along with that. But I think now, yeah, we're, we're, we're well past that. And there are definitely outfits like BGI, the Beijing Genomics Institute being one of them, that are touting new technologies that can get us down to a couple of hundred. And those were such fun times because for a while there Illumina had enormous competition from companies like 454 and Helicose and PacBio. And those were fun heady times with lots and lots of competition. And in a way, Illumina's had it a little easy, I think over the last few years, but with PacBio and Oxford Nanopore gaining maturity both, both in terms of the technology platforms and their business strategy and growth, I think Illumina' gonna start to feel a little bit more competition in the long read sequence space. And one is always hearing whispers of new companies that may potentially disrupt next-gen sequencing. And that would be exciting because then we'd have an excuse to write another book. Harry Glorikian: Well, Kevin, start writing because I actually think we're there. I think there are a number of things there and you're right, I think Illumina has not had to bring the price down as quickly because there hasn't been competition. And you know, when I think about the space is, if you could do a $60 genome, right, it starts to become a rounding error. Like what other business models and opportunities now come alive? And those are the things that excite me. All right. But so, but you have a unique position as editor of the journal of CRISPR and the former editor of a lot of prominent, you know, publications, Nature Genetics, Bio-IT World, Chemical & Engineering News. Do you think that there's adequate coverage of the biological versus the computing side of it? Because I, I have this feeling that the computing side still gets a little overlooked and underappreciated. Kevin Davies: I think you're right. I mean I think at my own company Genetic Engineering News, we still have such deep roots in the wet lab vision and version of biotechnology that it takes a conscious effort to look and say, you know, that's not where all the innovation is happening. Bio-IT World, which you mentioned is interesting because we launched that in 2002. It was launched by the publisher IDG, best-known from MacWorld and ComputerWorld and this, this whole family of high-tech publications.And we launched in 2002 was a very thick glossy print magazine. And ironically, you know, we just couldn't find the advertising to sustain that effort, at least in the way that we'd envisioned it. And in 2006 and 2007, your friend and mine Phillips Kuhl, the proprietor of Cambridge Healthtech Institute, kind of put us out of our misery and said, you know what I'll, take the franchise because IDG just didn't know what to do with it anymore. But what he really wanted was the trade show, the production. And even though at the magazine eventually we fell on our sword and eventually put it out of its misery, the trade show went from strength to strength and it'll be back in Boston very soon because he had the vision to realize there is a big need here as sort of supercomputing for life sciences.And it's not just about the raw high-performance computing, but it's about the software, the software tools and data sharing and management. And it's great to go back to that show and see the, you know, the Googles and Amazons and yeah, all the big household names. They're all looking at this because genome technology, as we've discussed earlier has been one of the big growth boom areas for, for their services and their products.Harry Glorikian: Right. I mean, well, if you look at companies like Tempus, right. When I talked to Joel Dudley over there on the show it's, they want to be the Amazon AWS piping for all things genomic analysis. Right. So instead of creating it on your own and building a, just use their platform, basically, so it's definitely a growth area. And at some point, if you have certain disease states, I don't see how you don't get you know, genomic sequencing done, how a physician even today in oncology, how anybody can truly prescribe with all the drugs that are being approved that have, you know, genomic biomarkers associated with them and not use that data.Kevin Davies: On a much lower, lo-fi scale, as I've been doing a lot of reading about sickle cell disease lately, it's clear that a lot of patients who are, of course, as you, as you know, as your listeners know, are mostly African-American because the disease arose in Africa and the carrier status gives carriers a huge health advantage in warding off malaria. So the gene continues to stay, stay high in in frequency. Many African-American patients would benefit from some generic drugs that are available in this country that provide some relief, but aren't aware of it and maybe their physicians aren't completely aware of it either. Which is very sad. And we've neglected the funding of this disease over many decades, whereas a disease like cystic fibrosis, which affects primarily white people of Northern European descent that receives far more funding per capita, per head, than than a disease like sickle cell does. But hopefully that will begin to change as we see the, the potential of some of these more advanced therapies.I think as far as your previous comment. I think one of the big challenges now is how we tackle common diseases. I think we're making so much progress in treating rare Mendelian diseases and we know thousands of them. But it's mental illness and asthma and diabetes you know, diseases that affect millions of people, which have a much more complicated genetic and in part environmental basis.And what can we learn, to your point about having a full genome sequence, what can we glean from that that will help the medical establishment diagnose and treat much more common diseases, not quite as simple as just treating a rare Mendelian version of those diseases? So that's, I think going to be an important frontier over the next decade.Harry Glorikian: Yeah. It's complicated. I think you're going to see as we get more real-world data that's organized and managed well, along with genomic data, I think you'll be able to make more sense of it. But some of these diseases are quite complicated. It's not going to be find one gene, and it's going to give you that answer.But I want to go back to, you can't really talk about CRISPR without talking about this specter of germline editing. And a big part of your book is about this firestorm of criticism and condemnation around, you know, the 2018 when the Chinese researcher He Jankui, I think I said it correctly.Yep.Kevin Davies: He Jankui is how I say it. Close. Harry Glorikian: He announced that he had created twin baby girls with edits to their genomes that were intended to make them immune to HIV, which sort of like—that already made me go, what? But the experiment was, it seems, unauthorized. It seems that, from what I remember, the edits were sloppy and the case spurred a huge global discussion about the ethics of using CRISPR to make edits that would be inherited by future generations. Now, where are we in that debate now? I mean, I know the National Academy of Sciences published a list of criteria, which said, don't do that. Kevin Davies: It was a little more nuanced than that. It wasn't don't do that. It was, there is a very small window through which we could move through if a whole raft of criteria are met. So they, they refuse to say hereditary genome editing should be banned or there should be a moratorium. But they said it should not proceed until we do many things. One was to make sure it is safe. We can't run before we can walk. And by that, I mean, we've got to first demonstrate—because shockingly, this hasn't been done yet—that genome editing can be done safely in human embryos. And in the last 18 months there've been at least three groups, arguably the three leading groups in terms of looking at genetic changes in early human embryos, Kathy Niakan in London, Shoukhrat Mitalipov in Oregon, and Dieter Egli in New York, who all at roughly the same time published and reports that said, or posted preprints at least that said, when we attempt to do CRISPR editing experiments in very early human embryos, we're seeing a mess. We're seeing a slew of off-target and even on-target undesirable edits.And I think that says to me, we don't completely understand the molecular biology of DNA repair in the early human embryo. It may be that there are other factors that are used in embryogenesis that are not used after we're born. That's speculation on my part. I may be wrong. But the point is we still have a lot to do to understand, even if we wanted to.And even if everybody said, “Here's a good case where we should pursue germline editing,” we've gotta be convinced that we can do it safely. And at the moment, I don't think anybody can say that. So that's a huge red flag.But let's assume, because I believe in the power of research, let's assume that we're going to figure out ways to do this safely, or maybe we say CRISPR isn't the right tool for human embryos, but other tools such as those that we've touched on earlier in the show base editing or prime editing, or maybe CRISPR 3.0 or whatever that is right now to be published somewhere. [Let's say ] those are more safe, more precise tools. Then we've got to figure out well, under what circumstances would we even want to go down this road? And the pushback was quite rightly that, well, we already have technologies that can safeguard against families having children with genetic diseases. It's called IVF and pre-implantation genetic diagnosis. So we can select from a pool of IVF embryos. The embryos that we can see by biopsy are safe and can therefore be transplanted back into the mother, taken to term and you know, a healthy baby will emerge.So why talk about gene editing when we have that proven technology? And I think that's a very strong case, but there are a small number of circumstances in which pre-implantation genetic diagnosis will simply not work. And those are those rare instances where a couple who want to have a biological child, but have both of them have a serious recessive genetic disease. Sickle cell would be an obvious case in point. So two sickle cell patients who by definition carry two copies of the sickle cell gene, once I have a healthy biological child preimplantation genetic diagnosis, it's not going to help them because there are no healthy embryos from whatever pool that they produce that they can select. So gene editing would be their only hope in that circumstance. Now the National Academy's report that you cited, Harry, did say for serious diseases, such as sickle cell and maybe a few others they could down the road potentially see and condone the use of germline gene editing in those rare cases.But they're going to be very rare, I think. It's not impossible that in an authorized approved setting that we will see the return of genome editing, but that's okay. Of course you can can issue no end of blue ribbon reports from all the world's experts, and that's not going to necessarily prevent some entrepreneur whose ethical values don't align with yours or mine to say, “You know what, there's big money to be made here. I'm going offshore and I'm going to launch a CRISPR clinic and you know, who's going to stop me because I'll be out of the clutches of the authorities.” And I think a lot of people are potentially worried that that scenario might happen. Although if anyone did try to do that, the scientific establishment would come down on them like a ton of bricks. And there'll be a lot of pressure brought to bear, I think, to make sure that they didn't cause any harm.Harry Glorikian: Yeah. It's funny. I would like to not call them entrepreneurs. I like entrepreneurs. I'd like to call them a rogue scientist. Kevin Davies: So as you say, there's the third section of four in Editing Humanity was all about the He Jankui debacle or saga. I had flown to Hong Kong. It's a funny story. I had a little bit of money left in my travel budget and there were two conferences, one in Hong Kong and one in China coming up in the last quarter of 2018. So I thought, well, okay, I'll go to one of them. And I just narrowed, almost a flip of a coin, I think. Okay, let's go to the Hong Kong meeting.It's a bioethics conference since I don't expect it to be wildly exciting, but there are some big speakers and this is an important field for the CRISPR Journal to monitor. So I flew there literally, you know, trying to get some sleep on the long flights from New York and then on landing, turn on the phone, wait for the new wireless signal provider to kick in. And then Twitter just explode on my feed as this very, very astute journalists at MIT Technology Review, Antonio Regalado, had really got the scoop of the century by identifying a registration on a Chinese clinical trial website that he and only he had the foresight and intelligence to sort of see. He had met He Jankui in an off the record meeting, as I described in the book, about a month earlier. A spider sense was tingling. He knew something was up and this was the final clue. He didn't know at that time that the Lulu and Nana, the CRISPR babies that you mentioned, had actually been born, but he knew that there was a pregnancy, at least one pregnancy, from some of the records that he'd seen attached to this registration document. So it was a brilliant piece of sleuthing. And what he didn't know is that the Asociated Press chief medical writer Marilynm Marchion had confidentially been alerted to the potential upcoming birth of these twins by an American PR professional who was working with He Jankui in Shenzhen. So she had been working on an embargoed big feature story that He Jankui and his associates hoped would be the definitive story that would tell the world, we did this quote unquote, “responsibly and accurately, and this is the story that you can believe.” So that story was posted within hours.And of course the famous YouTube videos that He Jankui had recorded announcing with some paternal pride that he had ushered into the world these two gene edited, children, screaming and crying into the world as beautiful babies I think was [the phrase]. And he thought that he was going to become famous and celebrated and lauded by not just the Chinese scientific community, but by the world community for having the ability and the bravery to go ahead and do this work after Chinese researchers spent the previous few years editing human embryos. And he was persuaded that he had to present his work in Hong Kong, because he'd set off such a such an extraordinary firestorm. And I think you've all seen now you're the clips of the videos of him nervously walking onto stage the muffled, the silence, or the only sound in the front row, the only sound in the big auditorium at Hong Kong university—[which] was absolutely packed to the rim, one side of the auditorium was packed with press photographers, hundreds of journalists and cameras clicking—and the shutters clattering was the only, that was the applause that he got as he walked on stage.And to his credit, he tried to answer the questions directly in the face of great skepticism from the audience. The first question, which was posed by David Liu, who had traveled all the way there, who just asked him simply, “What was the unmet medical need that you are trying to solve with this reckless experiment? There are medical steps that you can do, even if the couple that you're trying to help has HIV and you're trying to prevent this from being passed on. There are techniques that you can use sperm washing being one of them. That is a key element of the IVF process to ensure that the no HIV is transmitted.”But he was unable to answer the question in terms of I'm trying to help a family. He'd already moved out and was thinking far, far bigger. Right? And his naiveté was shown in the manuscript that he'd written up and by that point submitted to Nature, excerpts of which were leaked out sometime later.So he went back to Shenzhen and he was put under house arrest after he gave that talk in Hong Kong. And about a year later was sentenced to three years in jail. And so he's, to the best of my knowledge that's where he is. But I often get asked what about the children? As far as we know, there was a third child born about six months later, also gene-edited. We don't even know a name for that child, let alone anything about their health. So one hopes that somebody in the Chinese medical establishment is looking after these kids and monitoring them and doing appropriate tests. The editing, as you said, was very shoddily performed. He knocked out the gene in question, but he did not mimic the natural 32-base deletion in this gene CCR5 that exists in many members of the population that confers, essentially, HIV resistance. So Lulu and Nana on the third child are walking human experiments, sad to say. This should never have been done. Never should have been attempted. And so we hope that he hasn't condemned them to a life of, you know, cancer checkups and that there were no off-target effects. They'll be able to live, hopefully, with this inactivated CCR5 gene, but it's been inactivated in a way that I don't think any, no other humans have ever been recorded with such modifications. So we, we really hope and pray that no other damage has been done. Harry Glorikian: So before we end, I'd love to give you the chance to speculate on the future of medicine in light of CRISPR. Easy, fast, inexpensive genome sequencing, give us access to everybody's genetic code, if they so choose. Machine learning and other forms of AI are helping understand the code and trace interactions between our 20,000 genes. And now CRISPR gives us a way to modify it. So, you know, it feels like [we have] almost everything we need to create, you know, precise, targeted, custom cures for people with genetic conditions. What might be possible soon, in your view? What remaining problems need to be solved to get to this new area of medicine? Kevin Davies: If you know the sequence that has been mutated to give rise to a particular disease then in principle, we can devise a, some sort of gene edit to repair that sequence. It may be flipping the actual base or bases directly, or maybe as we saw with the first sickle cell trial, it's because we understand the bigger genetic pathway. We don't have to necessarily go after the gene mutation directly, but there may be other ways that we can compensate boost the level of a compensating gene.But I think we, we should be careful not to get too carried away. As excited as I am—and hopefully my excitement comes through in Editing Humanity—but for every company that we've just mentioned, you know, you can go on their website and look at their pipeline. And so Editas might have maybe 10 diseases in its cross hairs. And CRISPR [Therapeutics] might have 12 diseases. And Intellia might have 14 diseases and Graphite has got maybe a couple. And Beam Therapeutics has got maybe 10 or 12. And Prime Medicine will hasn't listed any yet, but we'll hopefully have a few announced soon. And so I just reeled off 50, 60, less than a hundred. And some of these are gonna work really, really well. And some are going to be either proven, ineffective or unviable economically because the patient pool is too small. And we've got, how many did we say, 6,000 known genetic diseases. So one of the companies that is particularly interesting, although they would admit they're in very early days yet, is Verve Therapeutics. I touched on them earlier because they're looking at to modify a gene called PCSK9 that is relevant to heart disease and could be a gene modification that many people might undergo because the PCSK9 gene may be perfectly fine and the sequence could be perfectly normal, but we know that if we re remove this gene, levels of the bad cholesterol plummet, and that's usually a good thing as far as heart management goes. So that's an interesting, very interesting study case study, I think, to monitor over the coming years, because there's a company looking at a much larger patient pool potentially than just some of these rare syndromes with unpronounceable names. So the future of CRISPR and gene editing is very bright. I think one of the lessons I took away from CRISPR in Editing Humanity is, looking at the full story, is how this technology, this game-changing gene-editing technology, developed because 25 years ago, a handful of European microbiologists got really interested in why certain microbes were thriving in a salt lake in Southeastern Spain. This is not exactly high-profile, NIH-must-fund-this research. There was a biological question that they wanted to answer. And the CRISPR repeats and the function of those repeats fell out of that pure curiosity, just science for science's sake. And so it's the value of basic investigator-driven, hypothesis-driven research that led to CRISPR being described and then the function of the repeats.And then the story shifted to a yogurt company in Europe that was able to experimentally show how having the right sequence within the CRISPR array could safeguard their cultures against viral infection. And then five years of work people in various groups started to see, were drawn to this like moths to a flame. Jennifer Doudna was intrigued by this from a tip-off from a coffee morning discussion with a Berkeley faculty colleagues, Jill Banfield, a brilliant microbiologist in her own. And then she met meets Emmanuelle Charpentier in Puerto Rico at a conference, and they struck up a friendship and collaboration over the course of an afternoon. And that, why should that have worked? Well, it did, because a year later they're publishing in Science. So it's serendipity and basic research. And if that can work for CRISPR, then I know that there's another technology beginning to emerge from somewhere that may, yet trump CRISPR.And I think the beauty of CRISPR is its universal appeal. And the fact is, it's drawn in so many people, it could be in Japan or China or South Korea or parts of Europe or Canada or the U.S. or South America. Somebody is taking the elements of CRISPR and thinking well, how can we improve it? How can we tweak it?And so this CRISPR toolbox is being expanded and modified and updated all the time. So there's a hugely exciting future for genome medicine. And you know, whether it's a new form of sequencing or a new form of synthetic biology, you know, hopefully your show is going to be filled for many years to come with cool, talented, young energetic entrepreneurs who've developed more cool gadgets to work with our genome and other genomes as well. We haven't even had time to talk about what this could do for rescuing the wooly mammoth from extinction. So fun things, but maybe, maybe another time. Harry Glorikian: Excellent. Well, great to have you on the show. Really appreciate the time. I hope everybody got a flavor for the enormous impact this technology can have. Like you said, we talked about human genome, but there's so many other genomic applications of CRISPR that we didn't even touch. Kevin Davies: Yup. Yup. So you have to read the book. Harry Glorikian: Yeah. I will look forward to the next book. So, great. Thank you so much. Kevin Davies: Thanks for having me on the show, Harry. All the best.Harry Glorikian: Take care.Harry Glorikian: That's it for this week's show. You can find past episodes of MoneyBall Medicine at my website, glorikian.com, under the tab “Podcast.” And you can follow me on Twitter at hglorikian.  Thanks for listening, and we'll be back soon with our next interview.

5G ist das wahre Virus, die Corona-Impfung ist ansteckend, an Masken kann man ersticken: In der Pandemie wimmelt es von Fake News. Dabei tappen wir gedanklich in Fallen, die die Forschung längst kennt: Kausalfehler, Bestätigungsfehler, Framing, Dunning Kruger-Effekt. Der Kognitionspsychologe Markus Knauff erklärt im Gespräch mit Wissenschaftsredakteurin Korinna Hennig, was Falschnachrichten mit unserem Denken machen, was ihre Verbreitung mit Aufmerksamkeit zu tun hat und wie man kognitive Verzerrungen vermeiden kann. Die Hintergrundinformationen • Fake News, Social Media und Aufmerksamkeit | Gordon Pennycook et al: Shifting attention to accuracy can reduce misinformation online: "Shifting attention to accuracy can reduce misinformation online", erschienen im März 2021 auf Nature • Übersichtsartikel zu Falschnachrichten und Kognitionspsychologie, mit vielen Quellenverweisen | Gordon Pennycook et al: The Psychology of Fake News. Trends in Cognitive Science Vol.25, No.5/2021 (Cell Press): "The Psychology of Fake News", erschienen im März 2021 bei Cell • So erkennen Sie, welche Nachrichten zum Coronavirus stimmen. Ein Gastbeitrag von Markus Knauff. Zeit Online, 15. Januar 2021: "So erkennen Sie, welche Nachrichten zum Coronavirus stimmen", erschienen im Januar 2021 bei Zeit Online Vertrauen vor Kontrolle. Fälschung in Wissenschaft und Dokumentarfilmen | Markus Knauff: "Vertrauen vor Kontrolle", erschienen in Forschung & Lehre im Juni 2021 • Artikel über Verschwörungstheorien | Markus Knauff: "Gegen Irrationalität gibt es auch Impfstoffe", erschienen in der Frankfurter Allgemeinen Zeitung im Februar 2021

5G ist das wahre Virus, die Corona-Impfung ist ansteckend, an Masken kann man ersticken: In der Pandemie wimmelt es von Fake News. Dabei tappen wir gedanklich in Fallen, die die Forschung längst kennt: Kausalfehler, Bestätigungsfehler, Framing, Dunning Kruger-Effekt. Der Kognitionspsychologe Markus Knauff erklärt im Gespräch mit Wissenschaftsredakteurin Korinna Hennig, was Falschnachrichten mit unserem Denken machen, was ihre Verbreitung mit Aufmerksamkeit zu tun hat und wie man kognitive Verzerrungen vermeiden kann. Die Hintergrundinformationen • Fake News, Social Media und Aufmerksamkeit | Gordon Pennycook et al: Shifting attention to accuracy can reduce misinformation online: "Shifting attention to accuracy can reduce misinformation online", erschienen im März 2021 auf Nature • Übersichtsartikel zu Falschnachrichten und Kognitionspsychologie, mit vielen Quellenverweisen | Gordon Pennycook et al: The Psychology of Fake News. Trends in Cognitive Science Vol.25, No.5/2021 (Cell Press): "The Psychology of Fake News", erschienen im März 2021 bei Cell • So erkennen Sie, welche Nachrichten zum Coronavirus stimmen. Ein Gastbeitrag von Markus Knauff. Zeit Online, 15. Januar 2021: "So erkennen Sie, welche Nachrichten zum Coronavirus stimmen", erschienen im Januar 2021 bei Zeit Online Vertrauen vor Kontrolle. Fälschung in Wissenschaft und Dokumentarfilmen | Markus Knauff: "Vertrauen vor Kontrolle", erschienen in Forschung & Lehre im Juni 2021 • Artikel über Verschwörungstheorien | Markus Knauff: "Gegen Irrationalität gibt es auch Impfstoffe", erschienen in der Frankfurter Allgemeinen Zeitung im Februar 2021

Professor Susan Bailey from CSU's Department of Environmental & Radiological Health Sciences joins us to discuss her project with the NASA Twins Study, an investigation of identical twin astronauts Scott and Mark Kelly that aims to identify factors in spaceflight that influence human health in preparation for human space exploration to the Moon or Mars.Bailey tells us what her study reveals about aging in space, particularly how telomeres, the caps of our chromosomes, change with spaceflight — and what this means for aging on Earth and in orbit.Read about Bailey's preliminary findings on telomeres in space here.Find the Twins Study' scientists first publication in Science here.Read the latest update on "The Biology of Spaceflight," a package of papers from 200 NASA Twins Study investigators, published in Cell Press in November 2020, here.

Ron and Matt are joined by a great friend and just a wonderful person, PQ of Cell Press, to chat about The Sliver Mt. Zion Memorial Orchestra & Tra-la-la Band/Choir - This Is Our Punk Rock, Thee Rusted Satellites Gather+Sing.

Can selection act on ecosystems, societies, or planets such that some persist and others disappear? Must such systems reproduce to evolve? On this episode of Big Biology, we talk to Tim Lenton, Director of the Global Systems Institute (@GSI_Exeter) and a Professor of Climate Change and Earth System Science at the University of Exeter. In his 2021 Trends in Ecology & Evolution paper “Survival of the Systems,” Tim outlined his idea that large, complex systems--such as grasslands, coral reefs, and even human economies--are subject to a kind of natural selection based on their ability to persist. Tim argues that systems better able to extract and recycle resources will spread across landscapes and outcompete other such systems. This episode is produced in collaboration with Trends in Ecology & Evolution (@Trends_Ecol_Evo). TREE, published by Cell Press, is a monthly review journal that contains polished, concise and readable Reviews and Opinions in all areas of ecology and evolutionary science. It aims to keep scientists informed of new developments and ideas across the full range of ecology and evolutionary biology--from the pure to the applied, and from the molecular to the global. Visit: http://www.cell.com/trends/ecology-evolution. --- Send in a voice message: https://anchor.fm/bigbiology/message

Nesse episódio, a Cris fala um pouco sobre a importância dos estudos relacionados a biotecnologia azul para a bioeconomia. Para isso, ela se baseou no artigo entitulado de: "Cinquenta tons de azul: Como a biotecnologia azul molda a bioeconomia". Referência: Helena Vieira, Miguel Costa Leal & Ricardo Calado. Fifty Shades of Blue: How Blue Biotechnology is Shaping the Bioeconomy. Cell Press, Trends in Biotechnology (2020).

Mark is the drummer of Cell Press. He has also played with The Chariot, I Hate Sally and more. https://cellpress.bandcamp.com/album/cell-press https://www.facebook.com/cellpressmtl/ This podcast is powered by ZenCast.fm

Oh hello, 11th best metal podcast in the world here (more on that in the show). This week...well it's all the regular stuff really. We get some great MESSAGES and become underwear models. We talk NEW RELEASES from Cell Press, Alpha Male Tea Party, Genus Ordinis Dei, Allt, Alitor, Firing Squad, Cult of Luna and Every Time I Die. We take you through our super super groups in HOMEWORK and of course the universally loved BAND NAME GENERATOR. Episode playlist containing over 2.5 hours of music from bands we mention in the show available over on our Instagram page @maycontainmetalpod https://blog.feedspot.com/metal_music_podcasts/

Pipeman interviews Cell Press. In this great interview, you will hear topics such as prison conditions, hockey, events happening in the U.S., that there are a lot of great musicians that come out of Canada, people who wear masks incorrectly, the pandemic, how we miss live shows with our metal family, and monster brand tour water.The Adventures of Pipeman Radio Show is broadcast live every day 10am ET- Noon ET on W4CY Radio (www.w4cy.com), W4VET Radio, and K4HD Radio (www.k4hd.com) part of Talk 4 Radio (www.talk4radio.com) on the Talk 4 Media Network (www.talk4media.com). This podcast is also available on Talk 4 Podcasting (www.talk4podcasting.com).

Pipeman interviews Cell Press. In this great interview, you will hear topics such as prison conditions, hockey, events happening in the U.S., that there are a lot of great musicians that come out of Canada, people who wear masks incorrectly, the pandemic, how we miss live shows with our metal family, and monster brand tour water.Pipeman in the Pit is a segment of The Adventures of Pipeman Radio Show (#pipemanradio) broadcast live on W4CY Radio (www.w4cy.com), W4VET Radio, and K4HD Radio - Hollywood Talk Radio (www.k4hd.com) part of Talk 4 Radio (www.talk4radio.com) on the Talk 4 Media Network (www.talk4media.com). This podcast is also available on Talk 4 Podcasting (www.talk4podcasting.com).

Pipeman interviews Cell Press. In this great interview, you will hear topics such as prison conditions, hockey, events happening in the U.S., that there are a lot of great musicians that come out of Canada, people who wear masks incorrectly, the pandemic, how we miss live shows with our metal family, and monster brand tour water.Pipeman's Power of Music is a segment of The Adventures of Pipeman Radio Show (#pipemanradio) broadcast live on W4CY Radio (www.w4cy.com), W4VET Radio, and K4HD Radio - Hollywood Talk Radio (www.k4hd.com) part of Talk 4 Radio (www.talk4radio.com) on the Talk 4 Media Network (www.talk4media.com). This podcast is also available on Talk 4 Podcasting (www.talk4podcasting.com).

pomeさんをゲストに迎え、ボストン界隈を中心としたCRISPR関連のバイオスタートアップについて話を伺いました。Show notes Top CRISPR Startup Companies Changing the Future of Biotech and Medicine … CRISPR関連スタートアップまとめ Researchat.fm, ep76 … ゲノム編集特集回 Researchat.fm, ep77 … ゲノム編集特集回 Researchat.fm, ep2 … CRISPR特集回 Researchat.fm, ep77 Researchat.fm, ep47 … SHERLOCKについて話しました。 Boston MIT … マサチューセッツ工科大学。Kendall Station近くに位置する。厳密にはボストン市ではなく、ケンブリッジ市である。 Harvard University … ハーバード大学。こちらもメインキャンパスはケンブリッジ市。Oxford Stに位置する建物もあるため、Oxford St., Cambridgeと住所的には何が何だかわからないところもある。 Boston University … BU University of Massachusetts … UMass Tufts University Berklee College of Music … いつもバークリーなのかバークレーなのかわからなくなる。有名な音楽学校。 NOVARTIS Takeda Biogen Bayer Cell Press … いわゆるCell誌。MIT,ハーバードの目と鼻の先にある。 カリフォルニア州 マサチューセッツ州 ニューヨーク州 ニュージャージー州 Akamai Feng Zhang David Liu Researchat.fm, Ep60 … 培養肉などについて話しました。 GMO …Genetically modified organism Plantedit FAD2 Solive … by Plantedit spCas9 Cas12 Cas13 Inscripta mad7 nuclease Unreal Engine Unity C4U BioPallete Cas3 モダリス Beam Therapeutics Researchat.fm, ep22 … Base editorやTarget AIDについて話しました。 in vivo ex vivo 鎌状赤血球 CRISPR Therapeutics 造血幹細胞 CD34+ ヘモグロビン BCL11A eGenesis Bio George Church 胚盤胞置換法 Living cell technologies (LCT) Diatranz Otsuka CAR-T レンチウイルス AAV HIV ゾルゲンスマ TLO … Technology License Organizationの略 Wyss Institute Wyss Instituteのポッドキャスト … めちゃくちゃ良い。tadasuはリピートしまくって聞いている時期が度々ある。 Peng Yin Researchat.fm, ep74 … DNA Origamiについて話しました。 Cambridge Innovation Center (CiC) Venture Cafe Venture Cafe Tokyo … 虎ノ門ヒルズ内にある。木曜日にイベントをやっているようです。 CiC Tokyo … 虎ノ門ヒルズ内にある。 Cambridge City, MA … ケンブリッジ市 スタンフォード大学のパテントに関する資料 … Stanford UniversityのOTLによる資料。 lab central Johnson & Johnson Roche Job Description 四行教授 … とあるブログ様を引用させていただきました。当時修士のtadasuに四行教授や「履歴書を汚せ」と説いた人物は黒川清先生です。 Researchat.fm, ep75 … I’m not sure though. Editorial notes とっても楽しいおしゃべりでした。仕事と関係ないマニアックな話をできる場はあんまりないので貴重です。またやりましょう。(pome) 後編もお楽しみに〜 (soh) 同じ地区に住んでいるのに何にも活かせていません…(tadasu) (coela)

Welcome to Essential Insights: A Podcast for Healthcare Professionals. Hosted by Sidnie Kane, Program Coordinator for the Hospice & Homecare Webinar Network. My goal is to bring the listener, the essential worker, the latest information and high-quality education on critical topics that healthcare professionals are facing on a daily basis. The first episode covers the next COVID-19 wave. What we know, what we can expect. and how to prepare. Chris Moore, Senior Director and Head of Immunology and Kathy Ahearn of Ahearn Advisement tackle this challenging topic. They deliver industry expert insights to essential workers to keep them safe and to prepare them for the next COVID-19 wave. Check out these links for more info! Kathy's latest webinar on Marketing & Community Outreach for Fall 2020: Challenges & Opportunities for Hospice & Palliative Care: https://bit.ly/3gE6ws2 HHWN COVID-19 Resource Page: https://bit.ly/32bCuaS Follow us on LinkedIn: https://www.linkedin.com/company/hhwn Give us a like on Facebook: https://www.facebook.com/hhwnwebinars Chris Moore is an Immunology group leader experienced in the discovery and development of novel antivirals and immunomodulators. Proven track record of building transformative pipelines with years of experience in leading multidisciplinary matrix teams, managing biologists and chemists, and developing scientific strategy and business plans. Experience leading programs from inception through clinical proof of concept. Numerous high impact publications in journals such as Nature and Cell Press. Kathy Ahearn has a Bachelor's in both Nursing and Social Work, and owns Ahearn Advisement Partners. With over 30 years working and serving the healthcare community the combination of nursing and social work has served her well. She has worked in a variety of post-acute care settings with an emphasis on home health and hospice, home infusion, homecare, and skilled nursing as a PICC and compliance expert. Kathy has a unique ability to identify agency challenges and opportunities, quickly providing education, support, and mentoring to organizations, guiding them to a new level of operation.

Currently working as a Scientific Editor at Cell Press, Amsterdam, Dr. Rituparna Chakrabarti's interdisciplinary work has taken her between Germany and the USA. We talked to her about her journey, as well as transferable skills for future generations.

No expresso dessa semana, o William Leonel (@wl_leonel) fala sobre uma tecnologia promissora para o estudo de órgãos e mecanismos de citotoxicidade de fármacos e cosméticos, em muitos casos evitando o uso de animais para as pesquisas. Essa tecnologia é o órgão-em-chip. Entre em contato conosco em: E-mail: contato@cafecomnano.com Twitter: twitter.com/cafecomnano Instagram: instagram.com/cafecomnano/ Facebook: facebook.com/cafecomnano/ Membros nesse programa: Bruno Lima – twitter.com/BHRLima9 William Leonel - twitter.com/wl_leonel O programa foi embasado a partir de diversos estudos, dentre eles os principais são: RONALDSON-BOUCHARD, K.; VUNJAK-NOVAKOVIC, G. Organs-on-a-Chip: A Fast Track for Engineered Human Tissues in Drug Development, Cell Press, 2018. ZHANG, M.; XU, C.; JIANG, L.; QIN, J. A 3D human lung-on-a-chip model for nanotoxicity testing. Toxicology Research, [s. l.], v. 7, n. 6, p. 1048–1060, 2018. --- Send in a voice message: https://anchor.fm/cafecomnano/message

科学論文の探し方、読み方とその楽しみ、そして理想の論文について三人で熱っぽく話しました。Shownotes Nature Review Cancer…Natureが出版しているレビュー誌の一つで、がん研究に関連する論文を取り扱う。 Nature Review Genetics…Natureが出版しているレビュー誌の一つ、遺伝学に関連する論文を取り扱う。 Boston Chromatin Club Blog Karl Deisseroth (Wikipedia)…光遺伝学の開祖 DNA microscopy, researchat.fm…これについては、エピソード16で解説しています。 物体にデータをエンコードできる「モノのDNA」の時代が、小さなウサギのフィギュアから始まった (WIRED) Eric Lander (Wikipedia)…Genomicsを作った重鎮のうちの一人。 Leonard Adleman (Wikipedia)…AdlemanはDNA computingという分野を作った。これについては、エピソード24で紹介しています。 Researchmap OCRID…研究者に固有のidを付与することで業績と人物を関連させるためのIDシステムとそのwebサイト。 Gene to Cells…日本分子生物学会の発行する論文誌 Cold Spring Harbor Lab Press ABC予想の京大 望月先生のホームページ abc予想の主張を理解する (Youtube)…教育系Youtuberヨビノリさんのこの解説動画はとてもわかり易くてよかったです。 Cell Press, STAR Methods ripgrep-all (Github)…“rga: ripgrep, but also search in PDFs, E-Books, Office documents, zip, tar.gz, etc.”とのこと。めちゃ便利そうですね。 fzf（fuzzy finder）の便利な使い方をREADME, Wikiを読んで学ぶ…コマンドラインから曖昧検索をするツール エスペラント語…一般社団法人日本エスペラント協会なんてものがあるんですね。 形式言語の構文と意味 Unix哲学 (Wikipedia) Betweenness centrality…グラフにおけるノードの重要性を評価する指標の一つ。 researchat.fm ep4 … 情報収集について話しました。 Editorial notes 名言？が多い回でした。論文に貴賎なしとはとてもいい言葉だと思いました (soh) きれいごとを話しすぎた感があります。自分の行動にも矛盾ありまくりなのがよくわかりました。論文に貴賎なしですが、いい/おもしろいと思う論文があるのも事実です。立川談志師匠の落語論について思い出しました。(tadasu) 色々熱が入ってしまいました。全然関係ないですが最近sfvでスーパーゴールドになりました(coela)

Dr. Sheila Chari is the Editor-in-Chief at the journal Cell Stem Cell, and Executive Editor at Cell Press. As the Editor-in-Chief, Dr. Chari’s primary responsibilities are knowing and publishing the top stem cell discoveries, driving journal publishing strategy, and managing a global editorial staff.

This #DataFemme episode features Dr. Sarah Callahan, the Editor in Chief of Cell Press's new Data Science Journal, Patterns.Listen to this episode to figure out the many ways in which YOU can contribute to Patterns. Stay tuned for the official release in April at www.cell.com/patterns. Do you like getting the heads up of what’s going on in the data science industry? Ensure you always do by becoming a patron of #DataFemme at www.patreon.com/DataFemme

I talk about my Thanksgiving, Trumpism, voting this year and reading about termites:) Cell Press. "4,000-year-old termite mounds found in Brazil are visible from space." ScienceDaily. ScienceDaily, 20 November 2018. . Background Music: pyramidskeme.com/tracks : 18th Floor --- Send in a voice message: https://anchor.fm/the-dope-science-show/message