Podcast appearances and mentions of max delbr

Die mRNA-Forschung hat die Impfstoffe gegen das Corona-Virus geliefert. Kann die RNA-Technologie irgendwann sogar den Krebs besiegen? Prof. Markus Landthaler arbeitet am Max Delbrück Center daran, die Wirkweise der RNA-bindenden Proteine zu entschlüsseln und nutzbar zu machen. Ein Porträt unseres Gesprächspartners Prof. Markus Landthaler findet ihr hier. >> Artikel zum Nachlesen: https://detektor.fm/wissen/forschungsquartett-mrna-forschung

Die mRNA-Forschung hat die Impfstoffe gegen das Corona-Virus geliefert. Kann die RNA-Technologie irgendwann sogar den Krebs besiegen? Prof. Markus Landthaler arbeitet am Max Delbrück Center daran, die Wirkweise der RNA-bindenden Proteine zu entschlüsseln und nutzbar zu machen. Ein Porträt unseres Gesprächspartners Prof. Markus Landthaler findet ihr hier. >> Artikel zum Nachlesen: https://detektor.fm/wissen/forschungsquartett-mrna-forschung

Die mRNA-Forschung hat die Impfstoffe gegen das Corona-Virus geliefert. Kann die RNA-Technologie irgendwann sogar den Krebs besiegen? Prof. Markus Landthaler arbeitet am Max Delbrück Center daran, die Wirkweise der RNA-bindenden Proteine zu entschlüsseln und nutzbar zu machen. Ein Porträt unseres Gesprächspartners Prof. Markus Landthaler findet ihr hier. >> Artikel zum Nachlesen: https://detektor.fm/wissen/forschungsquartett-mrna-forschung

Der Neurobiologe Gary Lewin erforscht am Max-Delbrück-Zentrum die Geheimnisse unseres Tastsinns und kommt dabei dem Geheimnis, wie unser Fühlen funktioniert, näher. Von Anna Corves

In unseren Körperzellen läuft permanent eine Art Reinigungsprozess ab. Der hält unseren Körper gesund. Es einstehen dabei Abfälle, die sie selbst abbauen. Der Mechanismus dahinter nennt sich Autophagie - wörtlich „Selbstverzehr“. Auf diesem noch recht neuen Forschungsfeld ist Prof. Katja Simon, Leiterin der Arbeitsgruppe Zellbiologie der Immunität am Max-Delbrück-Centrum, unterwegs – und jetzt hier im Gespräch auf radio3.

As part of the US HUPO sponsored "What is a proteomics?" series, Ben and Ben sit down to talk with Dr. Ilaria Piazza, Max Delbrück Center for Molecular Medicine.

Dr. Sebastian Diecke is a Group Leader and Stem Cell Core Director at the Max Delbrück Center, where his research focuses on iPSCs and organoid models. He talks about the early days of iPSC research, developing organoids from endangered rhinoceros, and modeling Huntington's and other diseases.

“Neuroinflammation causes neuronal dysfunction by destabilizing excitatory synapses” and “Antigen-specific T cells in autoimmune inflammatory diseases of the central nervous system” The Anne Klibanski Visiting Lecture Series was created to support and advance the careers of women. These lectures bring together faculty from institutions that have hosted Anne Klibanski Scholars with MGH scholars, on topics that overlap both research areas. Dr. Gillani presented on “Neuroinflammation causes neuronal dysfunction by destabilizing excitatory synapses.”  Dr. Hastermann presented on “Antigen-specific T cells in autoimmune inflammatory diseases of the central nervous system.” Presenters: Rebecca L. Gillani, MD, PhD, Instructor, Neurology, MGH/HMS Maria Hastermann, MD, PhD, Max Delbrück Center, Berlin Learning Objectives for Dr. Gillani's talk: Upon completion of this activity, participants were able to: Understand the contribution of neuronal dysfunction to neurologic disability in people living with multiple sclerosis. Recognize the scope of synaptic dysfunction in people living with multiple sclerosis. Identify potential mechanisms for neuronal dysfunction due to neuroinflammation. Learning Objectives for Dr. Hastermann' talk: Upon completion of this activity, participants were able to: Describe neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Recognize the role of T cells in central nervous system (CNS) inflammation. Review the longitudinal prospective registry study (example BERLimmun). Click here to watch webinar.

Fast jede zweite Person erkrankt im Laufe ihres Lebens an Krebs. Hoffnung macht die Einzelzellen-Biologie. Es sei eine "fundamentale Neuigkeit", so viel besser in Zellen reinschauen zu können, sagt Nikolaus Rajewsky, Direktor des Berliner Instituts für Medizinische Systembiologie des Max Delbrück Center.

We're adding "animal intelligence" to rsr.org/squeeze. The claim that apes should have the highest intelligence in the animal kingdom because we humans supposedly evolved from them turns out to be yet another fail. Did you know, for example, that certains species of birds demonstrate that they know what other birds are thinking? On today's Real Science Radio program Bob Enyart and Fred Williams discuss really fun and hugely significant examples of animal intelligence! Wait till you can hear what the lowly ant does! RSR thanks Answers in Genesis for publishing Dr. Joe Francis' article Smarter Than You Think which we've used as a framework for today's broadcast.  From kgov.com/definitions: These are RSR-styled... - Animal: Excepting humans, a multicellular biological organism with specialized sense organs and voluntary movement. - Mammal: A warm-blooded vertebrate animal with hair or fur, females that secrete milk, and, except for the platypus and spiny anteater, the birth of live young. - Animal Kingdom: The animals of the world collectively, excluding insects and fish (which are more likened to biological robots than to volitional organisms) - Human being: A person, made in God's likeness, with body, soul and spirit (whereas animals have body and soul) - Plant: A biological organism that synthesizes nutrients in its leaves by photosynthesis (possessing a body but neither a soul or spirit). * One minute video of a magpie perceiving what many apes don't:  * Otherwise, this is a great video on mole rats vocalizing: If you ignore the absurd claim made by Dr. Gary Lewin of Berlin's Max Delbrück Center for Molecular Medicine about mole rats and human social behavior, this video announces extraordinary research and an exciting discovery! (If you have a choice, you might want to avoid the Max Delbrück Center for your own medical treatment. Researchers who remain so oblivious to the ubiquitous evidence against Darwinian rsr.org/evolution may also miss the insights needed to save your life.)  

Jim Collins is one of the leading biomedical engineers in the world. He's been elected to all 3 National Academies (Engineering, Science, and Medicine) and is one of the founders of the field of synthetic biology. In this conversation, we reviewed the seminal discoveries that he and his colleagues are making at the Antibiotics-AI Project at MIT.Recorded 5 February 2024, transcript below with audio links and external links to recent publicationsEric Topol (00:05):Hello, it's Eric Topol with Ground Truths, and I have got an extraordinary guest with me today, Jim Collins, who's the Termeer Professor of Medical Engineering at MIT. He also holds appointments at the Wyss Institute and the Broad Institute. He is a biomedical engineer who's been making exceptional contributions and has been on a tear lately, especially in the work of discovery of very promising, exciting developments in antibiotics. So welcome, Jim.Jim Collins (00:42):Eric, thanks for having me on the podcast.Eric Topol (00:44):Well, this was a shock when I saw your paper in Nature in December about a new structure class of antibiotics, the one from 1962 to 2000. It took 38 years, and then there was another one that took 24 years yours, the structural antibiotics. Before I get to that though, I want to go back just a few years to the work you did published in Cell with halicin, and can you tell us about this? Because when I started to realize what you've been doing, what you've been chipping away here, this was a drug you found, halicin, as I can try to understand, it works against tuberculosis, c. difficile, enterobacter that are resistant, acinetobacter that are resistant. I mean, this is, and this is of course in mice models. Can you tell us how did you make that discovery before we get into I guess what's called the Audacious Project?Jim Collins (01:48):Yeah, sure. It's actually a fun story, so it is origins go broadly to institute wide event at MIT, so MIT in 2018 launched a major campus-wide effort focused on artificial intelligence. The institute, which had played a major role in the first wave of AI in the 1950s, 1960s, and a major wave in the second wave in the 1980s found itself kind of at the wheel in this third wave involving big data and deep learning and looked to correct that and to correct it the institute had a symposium and I had the opportunity to sit next to Regina Barzilay, one of our faculty here at MIT who specializes in AI and particularly AI applied to biomedicine and we really hit it off and realized we had interest in applying AI to drug discovery. My lab had focused on antibiotics to then close to 15 years, but primarily we're using machine learning and network biology to understand the mechanism of action of antibiotics and how resistance arise with the goal of boosting what we already had, with Regina we saw there was an opportunity to see if we could use deep learning to get after discovery.(02:55):And notably, as you kind of alluded in your introduction, there's really been a discovery void and the golden age of discovery antibiotics was in the forties, fifties and sixties before I was born and before you had the genomic revolution, the biotech revolution, AI revolution. Anyways, we got together with our two groups, and it was an unfunded project and we kind of cobbled together very small training set of 2,500 compounds that included 1,700 FDA approved drugs and 800 natural compounds. In 2018, 2019, when you started this, if you asked any AI expert should you initiate that study, they would say absolutely not, there's going to be two big data. The idea of these models are very data hungry. You need a million pictures of a dog, a million pictures of a cat to train a model to differentiate between the cat and the dog, but we ignored the naysayers and said, okay, let's see what we can do.(03:41):And we apply these to E. coli, so a model pathogen that's used in labs but is also underlies urinary tract infections. So it's a look to see which of the molecules inhibited growth of the bacteria as evidence for antibacterial activity and we could have measured and we quantified each of their effects, but because we had so few compounds, we just discretized instead, if you inhibited at least 80% of the growth you were antibacterial, and if you didn't achieve that, you weren't antibacterial zero in ones. We then took the structure of each molecule and trained a deep learning model, specifically a graphical neural net that could look at those structures, bond by bond, substructure by substructure associated with whatever features you look to train with. In our case, making for good antibiotic, not for good antibiotic. We then took the train model and applied it to a drug repurposing hub as part of the Broad Institute that consists of 6,100 molecules in various stages of development as a new drug.(04:40):And we asked the model to identify molecules that can make for a good antibiotic but didn't look like existing antibiotics. So part of the discovery void has been linked to this rediscovery issue we have where we just keep discovering quinolones like Cipro or beta-lactams like penicillin. Well, anyways, from those criteria as well as a small tox model, only one molecule came out of that, and that was this molecule we called halicin, which was named after HAL, the killing AI computer system from 2001 Space Odyssey. In this case, we don't want it to kill humans, we want it to kill bacteria and as you alluded, it turned out to be a remarkably potent novel antibiotic that killed off multi-drug resistant extensively drugs, a pan-resistant bacteria went after to infections. It was affected against TB, it was affected against C. diff and acinetobacter baumannii and acted to a completely new mechanism of action.(05:33):And so we were very excited to see how AI could open up possibilities and enable one to explore chemical spaces in new and different ways. We took them model, then applied it to a very large chemical library of 1.5 billion molecules, looked at a subset of about 110 million that would be impossible for any grad student, any lab really to look at that experimentally but we looked at it in a model computer system and in three days could screen those 110 million molecules and identified several new additional candidates, one which we call salicin, which is the cousin of halicin that similes broad spectrum and acts to a novel mechanism of action.Eric Topol (06:07):So before we go further with this initial burst of discovery, for those who are not used to deep neural networks, I think most now are used to the convolutional neural network for images, but what you use specifically here as you alluded to, were graph neural networks that you could actually study the binding properties. Can you just elaborate a little bit more about these GNN so that people know this is one of the tools that you used?Jim Collins (06:40):Yeah, so in this case, the underlying structure of the model can actually represent and capture a graphical structure of a molecule or it might be of a network so that the underlying structure itself of the model will also look at things like a carbon atom connects to an oxygen atom. The oxygen atom connects to a nitrogen atom and so when you think back to the chemical structures we learned in high school, maybe we learned in college, if we took chemistry class in college, it was actually a model that can capture the chemical structure representation and begin to look at sub aspects of it, associating different properties of it. In this case, again, ours was antibacterial, but it could be toxic, whether it's toxic against a human cell and the model, the train model, the graph neural model can now look at new structures that you input them and then make calculations on those bonds so a bond would be a connection between two atoms or substructures, be multiple bonds, interconnecting multiple atoms and assign it a score. Does it make, for example, in our case, for a good antibiotic.Eric Topol (07:48):Right. Now, what's also striking as you set up this collaboration that's interdisciplinary with Regina, who I know of her work through breast cancer AI and not through drug discovery and so this was, I think that new effort and this discovery led to this, I love the name of it, Audacious Project, right?Jim Collins (08:13):Right. Yeah, so a few points on the collaboration then I'll speak to Audacious Project. In addition to Regina, we also brought in Tommi Jaakkola, another AI faculty member and marvelous colleague here at MIT and really we've benefited from having outstanding young folks who were multilingual. We had very rich, deep trained grad students from ML on Regina and Tommi's side who appreciated the biology and we had very richly, deeply trained postdocs, Jon Stokes in particular from the microbiology side on my side, who could appreciate the machine learning and so they could speak across the divide. And so, as I look out in the next few decades in this exciting time of AI coming into biomedicine, I think the groups will make a difference of those that have these multilingual young trainees and two who are well set up to also inject human intelligence with machine intelligence.(09:04):Brings the Audacious Project. Now, prior to our publication of halicin, I was invited by the Audacious Project to submit a proposal, the Audacious Project is a new philanthropic effort run by TED, so the group that does the TED Talks that's run by Chris Anderson, so Chris had the idea that there was a need to bring together philanthropists around the world to go for a larger scale in a collective manner toward audacious projects. I pitched them on the idea that we could use AI to address the antibiotic resistance crisis. As you can appreciate, and many of your listeners can appreciate that we're doomed if we don't actually address this soon, in that the number of resistance strains that are in our communities, in our hospitals has been growing decade upon decade, and yet the number of new antibiotics being developed and approved has been dropping decade upon decade largely because the antibiotic market is broken, it costs just as much to develop an antibiotic as it does a cancer drug or a blood pressure drug.(09:58):But antibiotic you take once or maybe over the course of three to five days, blood pressure, drug cancer drug you might take for months if not for the rest of your life. Pricing points for antibiotics are small dollars, cancer drugs, blood pressure drugs, thousands if not hundreds of thousands. We pitched this idea that we can maybe turn to AI and use the power of AI to address this crisis and see if we could use our wits to outcompete the genes of superbugs and Chris and his team really were taken with this, and we worked with them over the course of nine months and learned how to make the presentations and pulled this together. Chris took our pitches to a number of really active and fantastic philanthropists, and they got behind us and gave us a good amount of money to launch what we have now called the Antibiotics-AI Project at MIT and in conjunction with it and also using funding from the Audacious Project, we've launched a nonprofit called Phare Bio which is French for lighthouse, so our notion is that antibiotics are public good that we need to get behind his community and Phare Bio, which is run by Akhila Kosaraju, she's the CEO and President, is the mission of which is to take the most promising molecules out of the antibiotics AI project and advance them towards the clinic through partnerships with biotech, with pharma, with other nonprofits, with nation states as needed.Eric Topol (11:18):Well, before I get to the next chain of discovery and as explain ability features, which we all like to see when you can explain stuff with AI, did halicin because of this remarkable finding, did it get into clinical trials yet?Jim Collins (11:36):It's being advanced quite nicely and aggressively by Phare Bio. So Phare Bio is in discussions with the Department of Defense and BARDA, and actually on an interesting feature of halicin is that it acts like a flash bomb in the gut, meaning that when delivered orally to the gut, it only acts briefly and very quickly in a fairly narrow spectrum manner as well, so that it can go after pathogens sparing the commensals. One of the challenges our US military face is one of the challenges many militaries face are gut issues when soldiers are first deployed to a new location, and it can disable the soldiers for three to four weeks. And so, there's a lot of excitement that halicin might be effective as a treatment to help prevent gut dysbiosis resulting from new deployments.Eric Topol (12:27):Oh wow. That's another application that I would never have thought of. Interesting, so you then moved on to this really big report in Nature, which I think this is now involving a transformer model as I recall. So you can explain the difference and you made a discovery from a massive, again, number of potential compounds to staph aureus resistant methicillin resistant agents that were very potent in vivo. So how did you make this big jump? This is a whole new structural class of antibiotics.Jim Collins (13:11):Yeah, so we made this jump, this was an effort led by Felix Wong, who's a really talented postdoc in my lab, and we got intrigued of to what extent could we expand the utility of AI and biology of medicine. As you can appreciate that, that many of our colleagues are underwhelmed by the black box nature of many AI models and by black box I mean that when you train your model, you then largely use it as a filter where you'll provide the model with some input. You look at the output and the outputs, what's of interest to you, but you don't really understand in most cases, what guided the model to make the prediction of the output that you look at and that can be very unsatisfactory for biology, interested in mechanism. It can be very unsatisfactory for physicians interested in understanding the underlying disease mechanism.(13:57):It can be unsatisfactory for biotech and drug discoveries that want to understand how drugs act and what maybe underlies meaningful structural features. So with Felix, we decided it'd be interesting if you could open up the box. So could you look inside the model to see what was being learned? We are able to open up, in this case actually, we primarily focused on graph neural nets. We now have a new piece we're just about to submit on transformers, but in this case, we could open up and look to see what were the rationales, what were the chemical substructures that the model was pointing to in each compound that was leading to the high prediction that it could make for a good antibiotic and these rationales we then used as hooks, I should notably say, that we were able to identify the rationales from these large collections using algorithms that would develop by DeepMind as part of their AlphaGo program.(14:51):So AlphaGo was developed by DeepMind as a deep learning platform to play and win go the ancient Asian board game and we used similar approaches called Monte Carlo Tree Search that allowed us to identify these rationales that we effectively then used as hooks and kind of organizing hooks on screens where you can envision or appreciate that most exposed screens give you one-offs. This molecule does what you want and silico screens are similarly designed with these rationales. We could use them as organizing hooks to say, ah, these compounds that are identified as making for very good antibiotics all have the same substructure and thus they likely in the same class and act in similar mechanism and this led us to identify five novel classes, one of which we highlighted in this piece that acts very effectively against MRSA, so methicillin-resistant staph aureus you alluded, which is probably the most famous of the antibiotic resistant pathogens that we even outside infectious are quite familiar with. It be devil's athletes, so NFL players are often hit with MRSA, whether from scraping their limbs on AstroTurf or from actually surgeries to say, for example, correct something at their knee. This new class had great efficacy in animal models, again, acting through a new mechanism.Eric Topol (16:12):Will you bring that forward like halicin through this same entity?Jim Collins (16:17):Yes. We've now provided the molecules to Phare Bio and they're digging in to see which of these might be the most exciting and interesting to advance clinically.Eric Topol (16:26):I mean, it's amazing because this area is so neglected. Maybe you can help explain, since we're talking about existential threats as we get more and more resistant antibiotics and the biopharma industry is basically not into this and it relies on the work that you've been doing perhaps or other groups, I don't know of any that are doing more than you. I mean, it's incredible to me. Is it just because of the financial aspects that there's no business in the life science industry?Jim Collins (17:03):It's an interesting challenge. So I've thought about it. I really haven't come up with a great solution yet, but I think you've got multiple factors at play. One is that I think all of us, every one of your listeners has lost someone to a bacterial infection, but in most cases you don't realize you lost them to a bacterial infection. It might be that your elderly relative went into the hospital with a condition but acquired hospital-based infection and died subsequently from that and happened quite quickly. Another cases, again, it's secondary. Notably, during the pandemic, one out of seven individuals hospitalized for Covid had a bacterial infection and 50% of those who died had a bacterial co-infection. And noted by going back to the Spanish flu of over a hundred years ago. It was as deadly as it was because we didn't have antibiotics and most of the folks that died had a bacterial co-infection.(17:56):So you have this in the backdrop, you then have that, nobody's kind of gotten behind it, so we don't have any major foundation addressing antibiotic resistance. There are no charity walks, there are no charity runs, there is no month, there is no color, there are no ribbons, there are no celebrity behind it, there's just not known so it hasn't captured the public's imagination. AThen you come with that, this backdrop of the broken market where I said shared, it's really expensive to develop a new antibiotic, but if you develop a new antibiotic, the tendency now will be to shelve it until it's desperate so now even the young companies that had developed and gotten an antibiotic through to approval often went bankrupt because the model, the market couldn't provide them with revenue to go after the next one or sustain their efforts. And so you have pharma biotech jumping out. I think we need two-pronged effort going forward. I do think we need nation states to come forward and get behind this, and I think we increasingly need philanthropists to come forward and go after it. As I share your term of existential threat, I think if you speak with most educated individuals, antibiotic resistance broadly, antimicrobial resistance will be on everyone's existential threat list but notably of that list, it's the cheapest one that can be solved.Eric Topol (19:09):Well, you're showing that you've got the most extraordinary candidates that have been found in decades. So that says a lot right there.Jim Collins (19:18):Important step, yeah. So I think we've got additional innovation needed in the models to address this, and until we have that address, then this interesting discoveries we and others are making will not get to patients. So we need to have that additional next step to close this gap.Eric Topol (19:32):Now, obviously this has relied on AI and the progress that's occurring in AI to enable some of your work. I am fascinated by the use of AlphaGo. Most times we hear about using AlphaFold2, but you actually use AlphaGo the original game DeepMind work but there also was the progress of from deep neural networks to transformer models and your ability now to basically exemplify what can be achieved in drug discovery using the progress in multimodal AI. Is this something that is making a difference for you and your group?Jim Collins (20:13):It is, it's huge. I think it's very early in terms of the introduction to these new tools extensively within drug discovery. Machine learning has been used for over two decades, both supervised learning and unsupervised learning. Now we're seeing groups coming in for the deep learning efforts. It's largely data-driven so in fact, with the exception of sequences, most of drug discoveries not yet big data in the big data phase, but it's beginning to change. It's truly been transformative for us, so we've used graph neural nets primarily for our discovery efforts. We're now beginning to incorporate language models as multimodal models along with the graph neural nets as well as to see to what extent pre-trained language models. For example, mobile form from IBM, which was trained on PubChem and the ZINC database could be fine-tuned with small amounts of training data, screening data from a resistant organism.(21:06):Third, and I made an indirect allusion already, we've been looking at using transformers and genetic algorithms in older form of AI tech for design of novel antibiotics so we've been now looking to see using fragments as a starting base, using trained models to build out novel antibiotics that can then be de novo designed. One of the big challenges in that space is how do you synthesize these molecules? So you have both the challenge of can you come up with a small number of steps that enable you to synthesize? And second is could you find somebody to synthesize them? And each of those remains very big challenges. My faculty colleague here at MIT, Connor Coley's probably one of the world leaders, easily, he's in using AI to calculate the synthesized ability of a molecule, but we still have gaps in that we don't have the community resources to make most of what we come up with.Eric Topol (21:58):Well, one of the features of large language models that David Baker at the Protein Design Institute exploited is its ability to hallucinate and come up with proteins that don't exist. Can you do the same thing in your design of antibiotic candidate molecules in a way that is not worrying about the synthesis, but just basically the hallucinatory behavior of large language models?Jim Collins (22:28):It's interesting, so yes and so David's work is marvelous and we're big fans and longtime friends of his work. Yes, so we've been driving these models truly to do de novo synthesis. So based on what has been learned, can you put together molecules that one's never seen before? We're doing it quite successfully. It becomes interesting from the hallucination in that it comes out really more of these models making stuff up and ours it's really more directing the hallucinations, right? Really looking to see can we harness the imagination of the models in order to move them forward in very creative design manners.Eric Topol (23:08):Yeah, I mean, I think most people have a negative connotation of hallucinations, but these are the smart variety potentially. This in many ways you could say there's so much crowded interest in the drug discovery AI world, but what you're doing now seems to be setting the pace in many respects for others to follow such remarkable advances in a short time. By the way, we'll link to that TED talk you gave in April 2020, where in seven minutes you went over what you're doing of course and who would've, and that was in 2020 that where you'd be three or four years later, and that was what you're going to do over the next seven years with seven new classes of new antibiotics. Now, before we wrap up, it isn't just that you're an AI antibiotic, you and your team antibiotic discover and doing compressing in time, what has taken decades that you're doing in months, but also you are a father of figure in the field of synthetic biology and I wonder if you, before we wrap up, can explain not only what synthetic biology is since a lot of people don't really know what that means, but how does that dovetail with your efforts in what we've been discussing?Jim Collins (24:33):Yeah, thanks. So synthetic biology is a relatively new field that's bringing together engineers with biologists to use engineering principles to model design and build synthetic gene networks and other molecular components that can be used to rewire and reprogram living cells and cell-free systems, endowing them with novel functions of a variety of applications. So the circuits, these programmable cells are impacting broad swats of the economy from food and water to health and sustainability of bioenergy to human health. Our focus is primarily human health and we've been advancing the idea that you can reprogram bacteria to detect and treat bacterial infections. So we've shown you can use this to go after cholera, we've shown you can use is to prevent antibiotic induced gut dysbiosis. We've also used synthetic biology to create whole new classes of diagnostics. For example, paper-based ones using RNA sensors for Ebola, for Zika and for Covid.(25:33):How it dovetails with what we talked about is that I think there's a great opportunity now to turn to AI to expand synthetic biology, both expanding the number of parts we have to re-engineer living systems as well as to better infer design principles that can be used to reprogram rewire living systems. We're beginning to advance, we're not yet at the SynBio AI project phase, but very early efforts and David's dominating the protein space and we and others are beginning to now movement to the RNA space. So to what extent can we create large libraries of RNA components, train language-based models, structure-based models that can both predict RNA structure more critically predict RNA function and as you know from your marvelous work and what's happening is that it's the exciting age of RNA of getting after RNA therapeutics, be it mRNA or CRISPR related and we still need to get better at our ability to design those therapeutics with certain functions in mind, and we think AI is going to help get us there faster.Eric Topol (26:34):Well, speaking of that, there was a paper this week in Cell by McCafferty and colleagues, and one of the sentences that struck me, we are standing on the cusp of a new era of biology, where the integration of multimodal structural datasets with multiscale physics-based simulation will enable the development of visible, virtual cells. This is yet another lineage or direction of where we're headed with AI, but this fusion of the advances that are occurring right now in biology with AI that extend in many different directions, it's so exciting and you are basically nailing it. I mean, you're putting points on the board, Jim, and I just have to say, I'm blown away by what you've been accomplishing in a time space that's so incredibly compressed.Jim Collins (27:40):Oh, well thanks. Well, you think back to the early days of molecular biology and physicists like Francis Crick and Max Delbrück played huge pioneering roles and then in the second wave in the eighties or so, you had other physicists like Walter Gilbert playing big roles. I do think physicists computer scientists are starting now to play big roles in this next phase where we need tools like AI in order to really grapple with and harness the complexity, both the biology and the chemistry that underlies living cells. They can kind of expand our intuitions both to understand and to really control these systems for good going forward.Eric Topol (28:15):Well, you're doing it and we're be cheering for the success of these drugs that you've come up with in the clinical trials as they go forward because they look so remarkably promising. You even highlighted ways that I wouldn't have envisioned where they could make a difference, so we'll follow your work, you and your colleagues with great interest. Thanks so much for joining,Jim Collins (28:37):Eric, thanks for having me. Enjoyed our conversation.******************************************************************************Thanks for listening to Ground Truths. Please share if you found this podcast informative.Full video interview will post here Get full access to Ground Truths at erictopol.substack.com/subscribe

Bakteriophagen sind Viren, die Bakterien befallen - und töten. Es sind gute Viren. Sie können wichtige Verbündete sein, im Kampf gegen Bakterien. Und sie sind noch viel mehr. Die Erforschung von Bakteriophagen schaffte die Grundlage für die moderne Molekularbiologie. Und ohne Bakteriophagen wäre die Gentechnik nicht denkbar. Im BiOfunk betrachten wir heute die spannende Entdeckungsgeschichte der Bakteriophagen, die vor gut 100 Jahren begann.Weitere InformationenBuchtipp: "The Good Virus" von Tom IrelandWhy evolution is true: Happy birthday, Max Delbrück!Annual Reviews: Phage Therapy in the Twenty-First CenturyBBC Science Focus: The best way to kill a superbug? Weaponise a virusASM: Phage Therapy - Past, Present and FutureNature Reviews: A century of the phage: past, presentand future

They look like… 'sabre-toothed sausages', they can barely see, they live for a really long time and have a queen who oppresses them.Find out all about the Naked Mole-rat this week and let us know your weirdest animal on earth suggestions at whattheduck@abc.net.au.Featuring:Dr Alison Barker, Max Planck Institute for Brain Research.Adjunct Professor Rochelle Buffenstein, University of Illinois at Chicago.Extra information: Professor Gary R. Lewin, Max Delbrück Center for Molecular Medicine.Production:Ann Jones, Presenter / Producer.Petria Ladgrove, Producer.Additional mastering: Angie GrantThis episode of What the Duck?! was produced on the land of the Wadawarrung and Kaurna people.

Laut WHO leben etwa 55 Millionen Menschen auf der Welt mit Demenz, 70 Prozent davon mit Alzheimer. Darauf soll der Welt-Alzheimer-Tag aufmerksam machen. Professor Erich Wanker vom Max-Delbrück-Center forscht zu neuen Behandlungen. Er sieht Fortschritte, aber auch noch viel Luft nach oben, was die Anstrengungen angeht.

Über die Bedeutung der Vertreibung von Geistesgrößen wie Hannah Arendt, Th. W. Adorno, Max Delbrück, Walter Gropius und vieler mehr aus dem nationalsozialistischen DeutschlandHannah Arendt, Theodor W. Adorno, Walter Gropius, Hans Jonas, Max Delbrück, Curt Stern und viele andere Größen aus Physik, Jura, Geschichtswissenschaften, Theologie, Chemie, Pädagogik und mehr: Die Machtübernahme der Nationalsozialisten war für viele Wissenschaftler:innen verbunden mit Berufsverbot, Bedrohung und Verfolgung. Viele sahen sich gezwungen, Deutschland zu verlassen und zu versuchen, im Exil eine neue Existenz aufzubauen. In Interviews aus den Jahren 1959 und 1960 sprechen 35 Exilant:innen in den USA über die Gründe ihrer Vertreibung und den Neuanfang, über Fluchtwege und Helfer, über neue Hoffnung und Scheitern. Mit: Theodor W. Adorno, Hannah Arendt, Fritz Bamberger, Walter Berendsohn, Albrecht Bethe, Arnold Brecht, Richard Courant, Max Delbrück, Friedrich Dessauer, Tilly Edinger, Friedrich Wilhelm Förster, Walter Friedländer, Kurt Goldstein, Sabine Gova, Walter Gropius, Emil Gumbel, Hajo Holborn, Werner Jaeger, Hans Jonas, Hans Kelsen, Adolf Leschnitzer, Fritz Lipmann, Leo Löwenthal, Karl Landauer, Adolf Leschnitzer, Anna Maenchen, Kurt Pinthus, Hans Rothe, Hans Rothfels Rosenstock-Huessy , Martin Schwarzschild, Else Staudinger, Hans Staudinger, Curt Stern, Paul Tillich und Ernst Toch Annette Vogt studierte Mathematik und Physik an der Universität Leipzig, ist Diplom-Mathematikerin und promovierte Mathematikhistorikerin. Von 1994 bis 2018 war sie research scholar am Max-Planck-Institut für Wissenschaftsgeschichte in Berlin, seitdem research scholar emeriti. Seit 1997 hält sie Lehrveranstaltungen an der Humboldt-Universität zu Berlin, an der Wirtschaftswissenschaftlichen Fakultät der HU Berlin seit 2014 als Honorar-Professorin. Sie ist Mitglied der International Academy for History of Science (2016 Full Member). Sie publizierte mehrere Bücher, über 200 Artikel und ist Mitautorin der Wanderausstellung zu Leben und Werk Emil J. Gumbels (1891-1966), die u. a. in München und Heidelberg gezeigt wurde. Hans Sarkowicz studierte Germanistik und Geschichte in Frankfurt/Main. Seit 1979 arbeitet er beim Hessischen Rundfunk. Er leitete das hr2-Ressort Literatur und Hörspiel und ist Autor von zeitgeschichtlichen und kulturhistorischen Publikationen, unter anderem zur Kunst und Literatur im Nationalsozialismus.

Dr. Angeli Möller, Ph.D, is Head of the Data and Integrations Generating Insights Group (DIGI) at Roche ( https://www.roche.com/ ), which is a fascinating group focused on bringing together data & technology from Roche diagnostics and pharma divisions to enable innovation for patients. Previously, Dr. Möller served as Head of Pharma Informatics International at Roche focused specifically on driving the employment of AI technologies to help get the right treatment to the right patient at the right time. Prior to joining Roche, Dr. Möller led the artificial intelligence workstream and was responsible for the research digital investment strategy at Bayer Pharmaceuticals. Before Bayer, she worked as a data scientist for translational medicine at Thomson Reuters and researcher at Cancer Research UK and the Max Delbrück Center for Molecular Medicine. As a proponent of pre-competitive collaboration, Dr. Möller co-founded the Alliance for Artificial Intelligence in Healthcare (AAIH), where she is Vice Chair and is also a member of the scientific advisory board of Multiomic Health. She also serves as a Member of The Science and Technology Facilities Council (STFC) of UK Research and Innovation (UKRI), which supports research in astronomy, physics and space science, and operates world-class research facilities for the UK. Dr. Möller has her Bachelor of Science (BSc) in Molecular Biology from University of Aberdeen, her Ph.D. in Molecular Biology with an oncology focus, from The University of Edinburgh, and did post-doc work in the neuroproteomics of neurodegeneration at the Max Delbrück Center for Molecular Medicine. Support the show

Neste episódio especial, temos a honra de receber o renomado pesquisador e doutor Marcelo Mori, que nos guia em uma exploração sobre os mistérios do envelhecimento humano e as descobertas científicas relacionadas ao retardo e até mesmo à reversão desse processo, conhecido como rejuvenescimento. Durante nossa conversa, abordamos uma variedade de tópicos, como os diferentes tipos de envelhecimento, o intrigante conceito de relógio epigenético e sua relação com a contagem dos anos biológicos. Exploramos também a importância da homeostase na manutenção da juventude, bem como os efeitos benéficos da dieta e do exercício físico no retardamento do envelhecimento. Falamos sobre os impactos da síndrome metabólica nesse processo e abordamos os estudos laboratoriais que foram capazes de reverter o envelhecimento em ratos, chegando ao ponto de recuperarem a visão. Além disso, mergulhamos em uma discussão sobre os indivíduos que buscam rejuvenescer utilizando seus próprios recursos e exploramos a visão do Dr. Marcelo Mori em relação ao futuro, onde essas ferramentas poderão ser aprimoradas e acessíveis a um número cada vez maior de pessoas. Seremos um dia capaz de reverter por completo o envelhecimento? Quais os impactos disso na nossa sociedade? É impossível não se fazer essas perguntas ao final deste episódio. Possui graduação em Ciências Biológicas (na Modalidade Médica) pela UNIFESP. Doutor em Biologia Molecular também pela UNIFESP, com estágio no instituto Max-Delbrück for Molecular Medicine (Berlim, Alemanha). Pós-doutorado pela Joslin Diabetes Center/Harvard Medical School (EUA). Foi Professor Adjunto e Pesquisador no Departamento de Biofísica da UNIFESP de 2011 a 2016. Atualmente ocupa o cargo de Professor Doutor em Biologia do Envelhecimento no Departamento de Bioquímica e Biologia Tecidual do Instituto de Biologia da UNICAMP. Atua na área de Biologia Molecular com ênfase em Metabolismo, dedicando-se principalmente à investigação dos mecanismos moleculares associados à Síndrome Metabólica e ao Processo de Envelhecimento. ----------- REFERÊNCIAS DO EPISÓDIO ---------- Currículo Lattes - Marcelo Mori Artigos publicados por Marcelo Mori (Vídeo Explicativo) Epigenética e Envelhecimento (acione as legendas em PT) (Livro) Tempo de vida: por que envelhecemos - e por que não precisamos (Livro) A morte da morte: a possibilidade científica da imortalidade (Livro) O fim do envelhecimento: Os avanços que poderiam reverter o envelhecimento humano durante nossa vida ------------------ Apoie o Canal ------------ Apoio mensal: ⁠⁠⁠⁠https://apoia.se/podcastuniversogeneralista⁠⁠⁠⁠ ------------------ Outras Plataformas ------------------ Nosso canal no ⁠⁠⁠⁠YouTube⁠⁠⁠⁠ Nosso perfil no ⁠⁠⁠⁠Instagram⁠⁠⁠⁠ Nossa conta no ⁠⁠⁠⁠Twitter⁠⁠⁠⁠ -------- Tratamento de áudio ----------- Allan Spirandelli: ⁠⁠⁠⁠Instagram⁠⁠⁠⁠ - ⁠⁠⁠⁠Spotify⁠⁠⁠⁠ -------- ASSUNTOS DO EPISÓDIO ------- (0:00) Introdução (0:52) Currículo Marcelo Mori (2:23) O que é envelhecer? (4:40) Dois indivíduos, com a mesma idade, podem envelhecer de formas diferentes? (6:01) Biomarcadores, taxa de envelhecimento e relógio epigenético (11:57) Homeostase e o processo de envelhecimento (15:23) Tipos de estresses e envelhecimento (21:31) Jejum intermitente e exercício físico: o que diz a literatura? (25:48) Há alimentos que afetam diretamente o envelhecimento? (29:24) Evitar picos glicêmicos pode aumentar a longevidade? (32:00) A síndrome metabólica e o processo de envelhecimento (41:23) Controlar o envelhecimento pode evitar as disfunções metabólicas? (43:11) Tecido adiposo, obesidade e expectativa de vida (51:29) Obesidade acelera o processo de envelhecimento? (53:15) Diferenças entre homens e mulheres (56:19) Fatores ambientais e o envelhecimento (57:07) David Sinclair: é realmente possível rejuvenescer? (1:13:29) Recursos para pesquisas sobre rejuvenescimento (1:17:19) Brian Johnson: há avanços na ciência a partir de casos isolados? (1:21:29) Como você imagina o futuro com o rejuvenescimento? --- Send in a voice message: https://podcasters.spotify.com/pod/show/universogeneralista/message

Millionen Deutsche starrten über Monate und Jahre auf die Corona-Zahlen. Dabei waren die stets unvollständig und gaben die Ausbreitung des Virus zeitverzögert wieder. Und vor allem kennt die Wissenschaft längst elegantere und weniger aufwändige Wege, um kurz bevorstehende Wellen einer Virusepidemie zu erkennen oder neue Varianten zu identifizieren. Der Schlüssel liegt in der braunen Brühe, die täglich durch die Rohre der Kanalisation rauscht. Abwasser ist für die Wissenschaft Gold wert. In dieser Folge des ZEIT WISSEN-Podcast spricht Jakob Simmank mit dem Molekularbiologen Emanuel Wyler, der am Max-Delbrück-Centrum für molekulare Medizin forscht. Es geht darum, wie Forscher das Abwasser geschickt durchleuchten, um ein Frühwarnsystem für ansteckende Krankheiten, aber auch die Ausbreitung von Antibiotikaresistenzen zu entwickeln. Ganz entscheidend dafür ist ein Virus, das rote Paprika befällt. Außerdem in dieser Folge: Christoph Drösser fragt in seiner Kolumne, warum warmes Wasser schneller gefriert als kaltes (25:20). Shownotes: Einen Artikel über den noch immer schleppenden Ausbau der Abwasserüberwachung aus der ZEIT lesen Sie hier: https://www.zeit.de/2022/40/grossbritannien-abwasserkontrollen-polioviren-kinderlaehmung-fruehwarnsytem - Der Pandemieradar des Robert Koch-Instituts zeigt inzwischen auch Auswertungen des Abwassers: https://www.rki.de/DE/Content/InfAZ/N/Neuartiges_Coronavirus/Situationsberichte/COVID-19-Trends/COVID-19-Trends.html?__blob=publicationFile#/home - Die US-amerikanische Seuchenschutzbehörde CDC hat den Polio-Fall in New York hier rekonstruiert: https://www.cdc.gov/mmwr/volumes/71/wr/mm7144e2.htm Eine kostenlose Probeausgabe des ZEIT-WISSEN-Magazins erhalten Sie unter zeit.de/wissen-podcast. Wir freuen uns über Kritik, Lob und Themenwünsche an podcast@zeit-wissen.de.

They look like... 'sabre-toothed sausages', they can barely see, they live for a really long time and have a queen who oppresses them. Find out all about the Naked Mole-rat this week and let us know your weirdest animal on earth suggestions at whattheduck@abc.net.au. Featuring: Dr Alison Barker, Max Planck Institute for Brain Research. Adjunct Professor Rochelle Buffenstein,  University of Illinois at Chicago. Extra information: Professor Gary R. Lewin,  Max Delbrück Center for Molecular Medicine. Production: Ann Jones, Presenter / Producer. Petria Ladgrove, Producer. Joel Werner, Script Editor.  Additional mastering: Angie Grant This episode of What the Duck?! was produced on the land of the Wadawarrung and Kaurna people.

They look like... 'sabre-toothed sausages', they can barely see, they live for a really long time and have a queen who oppresses them. Find out all about the Naked Mole-rat this week and let us know your weirdest animal on earth suggestions at whattheduck@abc.net.au. Featuring: Dr Alison Barker, Max Planck Institute for Brain Research. Adjunct Professor Rochelle Buffenstein,  University of Illinois at Chicago. Extra information: Professor Gary R. Lewin,  Max Delbrück Center for Molecular Medicine. Production: Ann Jones, Presenter / Producer. Petria Ladgrove, Producer. Joel Werner, Script Editor.  Additional mastering: Angie Grant This episode of What the Duck?! was produced on the land of the Wadawarrung and Kaurna people.

When we think about gut health, we should be thinking about Fiber and we want you to focus on the fiber that doesn't create mucky bowels so, seeds, beans and nuts are great but to keep things moving we really need to focus on sources of fiber that contain water as well.  These are your fruits and vegetables.  -I provide information on the importance of eating your veggies-What we should focus on when eating whole grains-Ideas for fussy eaters-Tips to help get more vegetables into your dietshow notes:Episode 8: How to Deal with Picky EatersEpisode 6: Healthy Family TipsEp 13: Eat your Greens Berlin research team from theExperimental and Clinical Research Center (ECRC), a joint institution of the Max Delbrück Center for MolecularMedicine (MDC) and Charité -- Universitätsmedizin Berlin, shows why this is the case. Their study has beenpublished in advance online in the journal Circulationhttps://drsearscoachportal.org/wp-content/uploads/2019/01/012319-How-dietary-fiber-and-gut-bacteria-protect-the-cardiovascular-system-ScienceDaily.pdfHarvard article:https://www.health.harvard.edu/blog/should-i-be-eating-more-fiber-2019022115927Head to www.raisinghealthyhumans. com to learn moreJoin our Community:Moms Raising Healthy HumansLearn about our Movement Snack Podcast:5 Minute Mornings (buzzsprout.com)or follow me on IG or Tik Tokcourtney_formfitVoiceover Intro: SJ RockiEditing: SJ Rocki

Die 6. Sendung am 31.12.2022 mit Ricarda Obrikat auf dem tdor2022, mit Pascal Mennen, Wahlkreisabgeordneter im Landtagswahlkreis Lüneburg und mit Dr. Emanuel Wyler, Molekularbiologe beim Max-Delbrück-Centrum in Berlin. Weiterlesen →

Mit Dr. Emanuel Wyler, Molekularbiologe beim Max-Delbrück-Centrum, sprach ich über Geschlechterbiologie im Kontext von trans und konnte nicht widerstehen ihn zu fragen: „Was ist eine Frau?“ Weiterlesen →

The twelfth episode of The Pain Beat is dedicated to Stephen McMahon, PhD, FMedSci (1954-2021). Stephen, affectionately known as “Mac,” was a world class pain researcher, lecturer, and inspiration to many. Our podcast guests pay homage to “Mac” with stories that illustrate his influence on the pain research field, and those in it. He will be remembered not only for his seminal contributions to our understanding of pain, but also for his generous and enthusiastic personal spirit which has left an indelible mark. Podcast participants include: David Bennett, MB, PhD, University of Oxford, UK Gary Lewin, PhD, Max-Delbrück Center for Molecular Medicine, Berlin, Germany Irene Tracey, DPhil, University of Oxford, UK Franziska Denk, DPhil, King's College London, UK (Host)

Was bewegt die Menschen, die unsere Welt weiterdenken und die Grenzen des Wissens verschieben? Darum geht es in den neuen Folgen des Wissenschafts-Talks bei rbbKultur "Gefährliche Gedanken". Zu Gast bei Jörg Thadeusz ist heute der Zellbiologe Nikolaus Rajewsky. Der Direktor des Berliner Instituts für Medizinische Systembiologie am Max-Delbrück-Centrum für Molekulare Medizin arbeitet daran, Krankheiten bereits zu erkennen, während sie in den Zellen entstehen.

Partito dalla penisola sorrentina, Gaetano Gargiulo, 41 anni, oggi è a capo di un gruppo di ricerca oncologica all'istituto Max Delbrück di Berlino, dove studia il glioblastoma, un tumore del cervello per il quale finora non sono state trovate soluzioni efficaci. Una recente scoperta del gruppo di lavoro di Gargiulo però inizia a fare luce sul funzionamento delle cellule di questo tumore. Fare ricerca in questo ambito è fondamentale, ma quando e come la ricerca si traduce in una terapia?

Muscle diseases come in a variety of forms. Among the more common conditions are muscle wasting, which can occur in cancer patients and the elderly. But there are also hundreds of genetically caused muscle diseases as well as local muscle defects that altogether affect more than 15 million in Europe. MyoPax is a muscle stem cell-producing platform for the treatment of muscle defects and genetic muscular dystrophies. It combines its proprietary first-in-class muscle stem cell manufacturing technology with CRISPR/Cas9-based gene repair. The first muscle stem cell product will enter a clinical trial soon (beginning of 2022). The founding of MyoPax as spin-off of the Charité University Medicine and the Max Delbrück Center for Molecular Medicine in Berlin is planned for this year. The group is a pre-spinout group at the Max Delbrueck Center and Charité – Universitätsmedizin in Berlin, Germany, whose work is suppored by https://www.spark-bih.de/ (SPARK Berlin). In this episode of https://www.lifescienceorg.com/bioinnovation (BioInnovation Spotlight @ LifeScience ORG) Verena talks about the impact of muscle disease, MyoPax's technology and how it works, and their plans to spin out.  

Weltweite Untersuchungen belegen, dass Abwasserdaten zeigen können, ob die Inzidenz in einer bestimmten Stadt oder Region zu- oder abnehmen wird. Auch am Max-Delbrück-Zentrums für Molekulare Medizin erforschen Wissenschaftler, was das Abwasser über die Ausbreitung des Corona-Virus verrät. Von Axel Dorloff

Dr Alison J. Barker is a neuroscientist from Max-Delbrück Center for Molecular Medicine in Berlin.   Dr Barker explains the importance of listening with patience over her multi-year study into language and dialects.   During this discussion, Dr Barker explains the importance of listening to yourself, the content and the context.   Using complex computer algorithms to listen, Dr Barker discerned patterns in language faster than a human listening. She explains the limitations of software and where humans hold an advantage.

This week is a Double Feature Circulation on the Run. Please join author Patrick Serruys, editorialist Shamir Mehta, and Associate Editor Emmanouil Brilakis as they discuss their article "Ten-Year All-Cause Death According to Completeness of Revascularization in Patients with Three-Vessel Disease or Left Main Coronary Artery Disease: Insights from the SYNTAX Extended Survival Study" and editorial "Achieving complete revascularization for multi-vessel coronary artery disease." Then, please join author G. Michael Felker, and Associate Editor Mark Link as they discuss the Research Letter "Implantable-Cardioverter-Defibrillator Eligibility after Initiation of Sacubitril/valsartan in Chronic Heart Failure: Insights from PROVE-HF." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts, I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke-National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: So guess what, Greg, we have another double feature this week. First, we need to talk about completeness of revascularization in patients with three-vessel disease or left main coronary artery disease. Always a question, and this time we've got insights from the SYNTAX Extended Survival Study. And then, the next feature talks about implantable cardioverter defibrillator eligibility after initiation of sacubitril/valsartan in heart failure, and these are insights from PROVE-HF. But before we get to that, I suggest, as I pick up my coffee, could you tell us what some of the papers you've spotted? Dr. Greg Hundley: Thanks so much, Carolyn. Sure. So I'm going to start from the world of preclinical science, and the paper comes to us from Dr. Vadim Fedorov from The Ohio State University Wexner Medical Center. Carolyn, up to 50% of the adult human sinoatrial node is composed of dense connective tissue, and cardiac diseases, including heart failure might further increase fibrosis within the sinoatrial node pacemaker complex, leading to impaired automaticity and conduction of electrical activity to the atrium. However, unlike the role of cardiac fibroblasts in pathological fibrotic remodeling and tissue repair, nothing is known about fibroblasts that maintain the inheritantly fibrotic sinoatrial node environment. Dr. Carolyn Lam: That's true. So what did these authors do? Dr. Greg Hundley: Right, Carolyn. So these authors found that increased sinoatrial node-specific fibrosis, with presence of myofibroblasts and CILP-1, and periostin-positive interstitial fibrosis only in heart failure versus non-heart failure human hearts. And comprehensive proteo-transcriptomic profiles of sinoatrial node fibroblasts identified up-regulation of genes and proteins promoting stiffer sinoatrial node extracellular matrix in heart failure hearts. Dr. Greg Hundley: And next, fibroblast specific profiles generated by the team's proteo-transcriptomic analyses of the human sinoatrial node provided a comprehensive framework for future studies to investigate the role of sinoatrial node-specific fibrosis in cardiac rhythm regulation and arrhythmias. So really very interesting preclinical science, Carolyn. Dr. Carolyn Lam: Yeah. Makes me think of arrhythmias and heart failure very differently, too. Thanks Greg. Well, for my next paper, we know that dietary high salt is bad for us. It's associated with mortality and morbidity. Serum sodium can accumulate at sites of inflammation and affect the function of both innate and adaptive immune cells. But how do changes in extracellular sodium actually affect mononuclear phagocytes? Dr. Greg Hundley: Ah. Carolyn, this is really an interesting question, but how would you even set this up or go about investigating this? Dr. Carolyn Lam: Ah, good question, Greg, and these investigators are really smart. So first, let me tell you about the co-corresponding authors, Dr. Kempa from Berlin Institute of Medical Systems Biology at Max Delbrück Center for Molecular Medicine in the Helmholtz Association, and Dr. Müller from the Experimental and Clinical Research Center in Berlin, Germany. Now, guess what they did? They used sea horse technology, pulsed stable isotope-resolved metabolomics and enzyme activity assays to characterize the central carbon metabolism and mitochondrial function of human and murine mononuclear phagocytes under high salt, in vitro. Dr. Carolyn Lam: And what they found was a disturbance of mitochondrial respiration as the initial step by which high salt mechanistically influenced immune cell function. While these functional changes may help to resolve bacterial infections, a shift towards pro-inflammation could accelerate inflammatory cardiovascular disease. A further potential implication is that mitochondrial functional analysis in monocytes and other immune cells upon a high-salt challenge, could serve as a test for salt sensitivity of immune cells in future. Dr. Greg Hundley: Oh wow, Carolyn. We don't often think about salt sensitivity in immune cells. Really informative research. Well, my next paper comes to us from the world of clinical science, and it's from Professor Derek Chew, from the school of medicine, at Flinders University, the Department of Cardiovascular Medicine at Flinders Medical Center. Dr. Greg Hundley: Carolyn, this paper reports results from a multicenter prospective, patient-level, randomized comparison of care informed by unmasked zero to one-hour, high-sensitivity troponin-T protocol, reported as less than five nanograms per liter versus standard-practice, masked high-sensitivity, cardiac troponin T-testing, reported at a value of less than 29 nanograms per liter, assessed at zero to three hours, and followed participants for 12 months. Participants included were those presenting to metropolitan emergency departments with suspected acute coronary syndromes, without ECG evidence of coronary ischemia. And the primary endpoint was timed to all-cause death or myocardial infarction. Dr. Carolyn Lam: Interesting experiment there. So what did they find, Greg? Dr. Greg Hundley: Right, Carolyn. So, while the use of the zero to one-hour, high-sensitivity, cardiac troponin T-protocol expedited discharge of patients presenting to the emergency department, with a low-event rate at 30 days, an increase in death or myocardial infarction was observed at one year in those with unmasked, high-sensitivity, cardiac troponin T-concentrations. Next, among those with intermediate cardiac troponin concentrations, where care was informed by zero to one-hour unmasked, high-sensitivity, cardiac troponin T-protocols, increases in revascularization and reductions in noninvasive cardiac investigation were observed. Dr. Greg Hundley: So these changes in practice that result from the use of rapid-discharge protocols, may be potentially associated with an increase in all-cause death or MI, by 12 months among those low-level troponin elevations. So in summary, Carolyn, this research found that unmasked, high-sensitivity, cardiac troponin T-reporting, deployed within a zero to one hour protocol, did not reduce ischemic events over a 12-month followup, and changes in practice associated with the implementation of this protocol may be associated with an increase in death in MI among those with newly-identified troponin elevations. Dr. Carolyn Lam: Wow, that's very, very interesting and clinically important. Thanks, Greg. Well, let's do a little bit of a tour around what else is available in this week's issue, shall we? I want to talk about a Special Report that I was so privileged to contribute to and was led by Dr. Gemma Figtree. And it's a Call to Action for new global approaches to cardiovascular disease drug solutions. There's also a Research Letter by Dr. Solomon on the prognostic value of natriuretic peptides and cardiac troponins in COVID-19. Dr. Greg Hundley: Great, Carolyn. So I'm going to tell you about an exchange of letters between Professors Correia and Chaitman regarding a prior published article, entitled “Myocardial Infarction in the ISCHEMIA Trial: Impact of Different Definitions on Incidence, Prognosis, and Treatment Comparisons.” Also, there's a very nice Case Series from Professor Shapira entitled, “In the Heart of the Ancient Silk Road: Fever of Unknown Origin, Right Ventricular Mass, and Systemic Vasculitis. And then, finally, Dr. de Boer has a very nice On My Mind piece From Studying Heart Disease and Cancer Simultaneously to Reverse Cardio Oncology. Dr. Carolyn Lam: So interesting. Well, let's get onto our double feature, Greg. Dr. Greg Hundley: Absolutely. Well, listeners, we are here for our first feature discussion today and we have with us really, an very interesting panel. First, Dr. Patrick Serruys from National University-Ireland, Galway, Dr. Shamir Mehta from McMaster University in Ontario, and our own associate editor, Dr. Manos Brilakis, from Minneapolis Heart Institute. Welcome gentlemen. Patrick, we're going to start with you. Could you describe for us the hypothesis that you wanted to test. Dr. Patrick Serruys: Yeah. The hypothesis was that if the surgeon and the interventional cardiologist doesn't achieve a complete revascularization, there will be a penalty. The penalty is we look at the all-cause mortality because that's really a unbiased assessment. Dr. Greg Hundley: And then, tell us the design of your study for us. Dr. Patrick Serruys: So SYNTAXES, which is the extension of the SYNTAX study up to 10 years, had 1,800 patient, and then basically, we took a threshold of eight. If you have a residual SYNTAX for more than eight, you have an incomplete revascularization. We stratify for less than four, four to eight, and above eight. And clearly, the group above eight has a bad outcome, not only with PCI, but also with surgery. The score is a little bit more difficult to establish in surgery, because you don't have an angiography immediately after the procedure. Dr. Patrick Serruys: And then as I said, if you do a complete revascularization by PCI, and that's basically a residual SYNTAX score of zero, then you have an outcome which is comparable to the surgical outcome. What is interesting, if you have above eight, you have to think twice and maybe refer that patient to surgery. It's difficult to anticipate, but of course, bifurcation, total chronic occlusion, small vessel, is the three major reason to have a residual SYNTAX score. Dr. Greg Hundley: Very good. So Shamir, could you help us put these results in context with other studies that have been performed in this sphere of research? Dr. Shamir Mehta: Yeah, sure. I would be happy to. So the SYNTAX study was unique in that they were able to look at the degree of revascularization, and the key finding that PCI was comparable to CABG surgery in terms of outcomes, when complete revascularization was able to be achieved, is a very intriguing finding. In cases where PCI was not able to achieve complete revascularization, it was clear superiority of CABG surgery. And so the question is in this study, this comparison, which is a non-randomized comparison, whether or not there's any type of external validity for these findings. Dr. Shamir Mehta: And, in fact there is. It's a timely publication, because recently we had the 4,000-patient multinational COMPLETE trial, which looked at the issue of complete revascularization versus incomplete revascularization in patients with STEMI, and found that complete revascularization with multi-vessel PCI, in appropriately-chosen patients, reduced hard clinical outcomes, including the composite of cardiac mortality and/or current myocardial infarction. And it reduces it quite substantially, by about 26%, and it's a highly-significant benefit. Dr. Shamir Mehta: I think the caveats to this finding are important, though. Because in the COMPLETE trial, patients were not eligible for recruitment, unless the interventional cardiologists felt that all of the lesions were amenable to PCI. So complete revascularization had to be achieved in the trial. And in fact, over 90% of patients in the trial were able to achieve complete revascularization. So that's absolutely key, and that brings up the importance of having a heart team in evaluating these patients. Dr. Shamir Mehta: The second point is that the SYNTAX score, Patrick had referred to was relatively low in the trial, it was only 4.6. Meaning that the lesions that were attempted were relatively straightforward, meaning that there was a high probability of achieving complete revascularization. So again, I think we're starting to see from the randomized trials and from the observational studies, the types of patients that may be suitable for PCI versus suitable for CABG surgery. Dr. Greg Hundley: Very nice. Well, Manos, Shamir, what an outstanding description in helping us put this paper in context with other research in this space. Manos, I know you see a number of papers come across your desk. Also, for you, what attracted you to this particular study? Dr. Emmanouil (Manos) Brilakis: Yeah, thank you, Greg. And again, congratulations to Patrick for a phenomenal study. I think the main strength of this analysis is the clinical relevance. I think everyone is still debating this question, is complete revascularization the goal in every patient? And all of the data, as mentioned already, have several limitations. Nevertheless, they move us a little bit closer to understanding better on whom complete revascularization should be used. Dr. Emmanouil (Manos) Brilakis: So the clinical relevance is one key. I think this paper does set the stage well for a randomized trial. End of the day, we are still not hundred percent sure if COMPLETE is the best for everyone, because COMPLETE counts as a risk, and the risk is going to be higher in those patients who have more complex anatomy. But that study will give us the definitive answer about which is the best way to go for each individual base. Dr. Greg Hundley: Very nice, Manos. So that's a great segue. So I'll turn to both Shamir and Patrick, and ask them also, as well, what do you think is the next study to be performed in this particular space? Shamir, you first and then we'll finish with Patrick. Dr. Shamir Mehta: Well, I think the concept of complete revascularization has now essentially been proven in multiple trials. And don't forget, if you go back several decades, really the first proof was in the context of CABG surgery. So really, this should be the goal in patients with multi-vessel disease. The next large randomized trial that is going to be starting very soon is the COMPLETE 2 trial where we are actually looking at the lesions physiologically to see whether or not we need to revascularize lesions that are physiologically significant versus anatomically severe. Dr. Shamir Mehta: This is an important question because what it does is it has the potential to reduce the number of lesions that we perform PCI in, by about 50%. We are also looking at plaque composition in that trial with optical coherence tomography. A very, very large number of patients will be receiving that. So that will be trying to target PCI to the actual pathophysiology of the disease, by targeting unstable plaques to perform PCI on. I think this is the whole next era of coronary intervention, where we are now beginning to target our therapies to the actual pathophysiology of the disease, which is a very, very exciting idea. Dr. Greg Hundley: And Patrick, do you have anything to add? Dr. Patrick Serruys: Yeah. I think, that obviously, you have to convert the anatomical SYNTAX Score in a functional SYNTAX Score. You could do that with the pressure wire and hyperemia of diastolic resting gradient. You can also do that by QFR or FFR CT. So we are going in that direction since a few years. The second point is that we have been working on machine learning that, at some point, the segmentation of the coronary segment, the assessment of the narrowing is done. And then, the next step that we are doing right now to is to convert that to the multi-slice CT scan. Dr. Greg Hundley: Very nice. Well, listeners, we want to thank Dr. Patrick Serruys, from National University-Ireland, Galway, Dr. Shamir Mehta from McMaster university in Ontario, and our own associate editor, Dr. Manos Brilakis, from Minneapolis Heart Institute, really bringing to us this paper that, in patients with complex coronary artery disease, incomplete revascularization can be common after PCI. And the degree of incompleteness can be associated with 10-year mortality. And therefore, if it's unlikely that complete or nearly complete revascularization can be achieved with PCI in patient with three-vessel disease, maybe we should be considering coronary artery bypass grafting. Dr. Greg Hundley: Well, again, let's get on now to that second feature discussion. Well, listeners, we are now here for our second feature discussion today, and we have with us Dr. Michael Felker from Duke University, and our own associate editor, Dr. Mark Link, from UT Southwestern. Welcome, gentlemen. And Mike, we'll start with you. Tell us a little bit about the background pertaining to your study and what hypothesis did you want to address? Dr. G. Michael Felker: Great. Thanks, Greg. So I think everybody's very familiar with the concept of favorable ventricular remodeling in patients with heart failure, that we know is something that happens when we treat our patients with guideline-directed medical therapy, like beta blockers, ACE inhibitors, MRAs. Interestingly, with the introduction of sacubitril/valsartan and the landmark PARADIGM trial, we had a drug where we had clearly a major outcome benefit, but we actually had very little understanding about whether that was mediated by remodeling. Dr. G. Michael Felker: And those questions led us to design the PROVE trial, which was a single-arm trial of 794 patients, looking at whether or not patients with heart failure and reduced ejection fraction who met the FDA label for sacubitril/valsartan, the initiation of that therapy will be associated with favorable changes in ventricular structure and function, as well as favorable changes in natriuretic peptide. The current paper's really trying to put those results in a clinical context around some of the things that we make clinical decisions about, in taking care of heart failure patients in this case, whether and when patients qualify for a primary prevention ICD. Dr. Greg Hundley: Fantastic, Mike. And so you've told us a little bit about the study design, and did you have exactly the same number of patients, or what was the study population for this sort of substudy, if you will? Dr. G. Michael Felker: Yeah. So in PROVE, we enrolled people who had chronic heart failure in the EF, less than 40%, because that's the FDA label for sacubitril/valsartan. In this analysis, because we were interested in patients who qualified for ICD therapy, we limited our analysis to those who an EF plus or equal to 35%. Because, as you all know, the guideline for primary prevention ICD is people who have a EF less or equal to 35% after at least three months of optimized heart failure therapy. Dr. G. Michael Felker: And so, one of our questions was in some patients start on sacubitril/valsartan, what happens to their ventricle and how many patients might favorably remodel? This is, obviously, a question that comes up a lot clinically as more and more we're switching people from ACE inhibitors, or ARBs, to sacubitril/valsartan in line with the recommendation that's 1A from the AHA guidelines. Dr. Greg Hundley: Fantastic. ell, we're all listeners waiting to hear your results, Mike. This is very exciting. So what did you find? Dr. G. Michael Felker: I think our results were quite interesting. I mean, for one thing, the patients that were enrolled PROVE were incredibly well-treated at baseline, and they had had heart failure for quite some time, and a average median time of over six years. So this is not patients who are just recently diagnosed. A lot of these are people that you might think, clinically, we're unlikely to go on and have much favorable ventricular modeling, but that's not what we found. We actually found that after the initiation of sacubitril/valsartan, after six months, on average, we had a five point increase in injection faction. Dr. G. Michael Felker: And by 12 months, on average, that was almost 10 points. So quite a bit of favorable remodeling, even in these patients you might think were less likely to do that. And we put that in the context of ICD decision-making. By six months, 32% of the patients who would initially have been eligible based on the guidelines for primary prevention ICD, no longer met those criteria because their EF had risen to greater than 35, and by 12 months, it was up to 62% of those patients. So as we're thinking about decision-making around ICDs, I think these data have some pretty obvious direct clinical relevance to decisions we now make in the care of our patients. Dr. Greg Hundley: Really interesting. So Mark, I know you get several papers coming across your desk, and as associate editor, boy, I think I can see why this paper was attractive to you. Tell us a little bit, how do we put these results from this study into the context of how we decide whether a patient should receive an ICD? Dr. Mark Link: Yeah. The current guidelines are to wait three months after guideline-directed medical therapy, and then repeat the ECHO and see if they still qualify. I think what this study shows us is that patients can continue to improve after three months, and that improvement is somewhat continuous, actually. Because at six months, the improvement in EF was five percent, and at 12 months, it was 10%. So I think that's what this shows, the context is, if you have a patient who has a low EF and they are improving, but still haven't quite made it to 35, let's say when they went from 25 to 30 in three months, I'd probably hold off and wait another three months and repeat the ECHO again. Dr. Greg Hundley: Excellent. Well, Mike, Mark, I'm going to ask you question. And we'll start with you Mike, and then go to Mark. What study would you perform next in this space? Mike, you first. Dr. G. Michael Felker: So, I think it's important to recognize some of the limitations of any study you do, including this one. So this was not a randomized trial. PROVE was a single-arm trial, there wasn't a control group. And the question about the ICD per se was not pre-specified. It was really a post-hoc analysis. So as is often the case, I think these are intriguing and highly-suggestive results, but I think there's clearly an opportunity to confirm them in perspective studies designed to answer this specific question. Dr. G. Michael Felker: So you could imagine a trial where patients who are starting on sacubitril/valsartan who don't have ICDs, get randomized to waiting three months or waiting six months, or 12 months or whatever the interval would be. So I think these are intriguing, and that there definitely opportunities to develop confirmatory results. Dr. Greg Hundley: Excellent. Mark, do you have anything to add to that? Dr. Mark Link: I think the big thing we would really like to know are predictors, predictors of response and predictors of non-response. And that would take a larger trial perspective, and that would be very, very valuable. Because if you could have a predictor of a non-responder, they would get an ICD earlier, and predictors of responders, you might wait a while. Dr. Greg Hundley: Very nice. Well, listeners, we get rate studies here in circulation, and you'll find this one as a research letter, highlighting that in the substudy of the PROVE heart failure study, that in patients with an EF less than or equal to 35%, the introduction of sacubitril/valsartan improved EF to greater than 35%, at 62% of subjects at 12 months. Really an interesting finding, and perhaps further randomized clinical trials as suggested by both Mike and Mark here, are maybe warranted in the future. Dr. Greg Hundley: Well, on behalf of Carolyn and myself, we want to A, thank Dr. Mike Felker and also our associate editor, Mark Link, and wish you, as listeners, a great week, and we will catch you next week On the Run. Dr. Greg Hundley: This program is copyright of the American Heart Association, 2021. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit ahajournals.org.

In this episode, Allison and Sandra continue their conversation with Dr. Sofia Forslund, group leader at the Max Delbrück Center for Molecular Medicine. They discuss the importance of having role models, specifically in someone who is similar to yourself. Sofia talks about what it means to be an ally and how to create an inclusive and welcoming environment in the context of academia. The conversation also focuses on tokenizing, why forced or artificial inclusivity can feel so draining, and the importance of anti-discriminatory policies, with some bright outlook for the future. Check out Sofia's lab at: https://www.mdc-berlin.de/forslund You can follow us on: Twitter: https://twitter.com/MPPhdnetPodcast Instagram: https://www.instagram.com/offspringmagazine_thepodcast Linkedin: https://www.linkedin.com/company/offspring-magazine-the-podcast If you have any feedback, comments or suggestion, reach out to us at offspring.podcasts@phdnet.mpg.de Check out the Offspring-Blog where we publish articles on a regular basis: https://www.phdnet.mpg.de/offspring-blog Intro - Outro music composed by Srinath Ramkumar: https://twitter.com/srinathramkumar Pre-Intro jingle composed by Gustavo Carrizo: https://www.instagram.com/carrizo.gus See you in a week, Stay Safe and Stay Healthy!

Heute geht es mal wieder um Corona. Für viele Menschen beginnt der Tag mit einem Blick auf den aktuellen Inzidenzwert. Forscher auf der ganzen Welt sind im Zuge der Pandemie auf der Suche nach effektiven Frühwarnsystemen für Corona-Ausbrüche. Ins Visier geraten ist dabei das Abwasser. Schließlich hinterlässt der Mensch dort viele Spuren, auch Spuren des SARS-CoV-2-Virus. Im Podcast reden wir darüber mit zwei Fachleuten. Dr. Matthias Staub ist Wasserwirtschaftler und hat im Bereich Umwelttechnik promoviert. Er ist Prokurist und Leiter Kommunalentwicklung bei der Veolia Wasser Deutschland GmbH, sowie mit Molekularbiologe Dr Emanuel Wyler, der in Berlin am Max-Delbrück-Centrum für Molekulare Medizin in der Helmholtz-Gemeinschaft (MDC) forscht.

In this episode, Allison and Sandra talk to Dr. Sofia Forslund, group leader at the Max Delbrück Center for Molecular Medicine. Sofia talks about her journey to becoming a group leader as well as her journey to becoming herself. She shares what it is like to transition while looking for a position in academia, and the consideration that goes into choosing a queer-friendly lab, institute, or even the city. Together, our hosts and Sofia discuss what it means to be a woman and the societal expectations connected to it, and talk about gender dysphoria, feminism, and toxic masculinity. Check out Sofia's lab at: https://www.mdc-berlin.de/forslund You can follow us on: Twitter: https://twitter.com/MPPhdnetPodcast Instagram: https://www.instagram.com/offspringmagazine_thepodcast Linkedin: https://www.linkedin.com/company/offspring-magazine-the-podcast If you have any feedback, comments or suggestion, reach out to us at offspring.podcasts@phdnet.mpg.de Check out the Offspring-Blog where we publish articles on a regular basis: https://www.phdnet.mpg.de/offspring-blog Intro - Outro music composed by Srinath Ramkumar: https://twitter.com/srinathramkumar Pre-Intro jingle composed by Gustavo Carrizo: https://www.instagram.com/carrizo.gus See you in a week, Stay Safe and Stay Healthy!

Solid tumors make up 90% of the cases in cancer patients worldwide but the standard of care has not changed in decades. Chemotherapies are still widely used and are non-specific, often with a wide range of negative side effects for the patient. To address this, Dr Felix Lorenz and his team started the Captain T-Cell project. Based at the Max Delbrück Center in Berlin and supported by https://www.go-bio.de/en/index.html (GO-Bio) and https://www.spark-bih.de/ (SPARK Berlin), they are developing a T-cell receptor (TCR) therapy for tackling solid tumors in a targeted and safe manner for cancer patients. TCRs have the ability to target a wide range of antigens and can be expressed intracellularly, which is important for recognizing those antigens that are not transported to the cell surface. Their technology relies on engineering a patient's own T-cells to recognize specific antigens for solid tumors and reinfused back to the patient where they can find and kill the tumor with high specificity. Initially, they are targeting Epstein-Barr Virus antigens that are expressed throughout tumors called by this disease. In this episode of the BioInnovation Spotlight podcast, we ask Felix what technology lies behind the Captain T-Cell project, how it can help transform cancer therapy for patients, and why he wanted to start a company.

Lycopene is a promising nutrient that can prevent gastric diseases associated with H. pylori Yonsei University (Japan), April 30, 2021 Helicobacter pylori is a spiral-shaped bacterium that grows in your digestive tract. An opportunistic pathogen, it is considered to be the most successful colonizer of the human gastrointestinal tract, infecting the stomachs of roughly 60 percent of the world’s adult population. In a recent study, researchers at Yonsei University in South Korea found that lycopene, a bioactive pigment with powerful antioxidant properties, can help prevent gastric diseases associated with H. pylori infection. Lycopene is a non-provitamin A carotenoid commonly found in bright red and orange produce, such as tomatoes, watermelons, papaya and pink grapefruit. This beneficial compound is extensively studied for its remarkable ability to scavenge free radicals, the unstable byproducts of cellular metabolism responsible for causing oxidative stress. How lycopene prevents H. pylori-induced gastric cancer According to studies, H. pylori infection promotes the hyperproliferation of gastric epithelial cells — the very cells that make up the stomach lining — by increasing the production of free radicals called reactive oxygen species (ROS). ROS then activates two signaling pathways — Wnt/B-catenin and JAK1/Stat3 — that influence cell fate decisions. While Wnt/B-catenin signaling is involved in the regulation of the self-renewal processes of cells, JAK1/Stat3 signaling is said to play a role in conferring malignant properties to cancer cells. Due to the involvement of ROS, the South Korean researchers hypothesized that lycopene, which has antioxidant and anti-cancer properties, may be able to suppress H. pylori-induced hyperproliferation by inhibiting the activation of Jak1/Stat3 and Wnt/B-catenin signaling, as well as the expression of B-catenin target genes. B-catenin is a protein that accumulates due to the aberrant activation of Wnt/B-catenin signaling. The buildup of this protein promotes the expression of cancer genes (oncogenes) and the progression of tumors. In an earlier study published in The American Journal of Clinical Nutrition, German researchers reported that lycopene is the most effective scavenger of singlet oxygen, a very strong oxidant and one of the major ROS produced by cells. To determine if it can prevent ROS-mediated hyperproliferation, South Korean researchers treated H. pylori-infected gastric epithelial cells with lycopene.  They measured the cells’ ROS levels and viability before and after treatment. The researchers found that lycopene effectively reduced ROS levels and inhibited not only the activation of Jak1/Stat3 and Wnt/B-catenin signaling but also the expression of B-catenin target oncogenes and the proliferation of H. pylori-infected gastric epithelial cells. In addition, lycopene inhibited the increase in Wnt-1 (an oncogenic protein) and lipoprotein-related protein 5 (a protein involved in cancer progression) expression caused by H. pylori infection. Based on these findings, the researchers concluded that lycopene can be used to prevent H. pylori-associated gastric cancer, thanks to its inhibitory effects on gastric cell hyperproliferation.   Too much salt suppresses phagocytes Max Delbrück Center for Molecular Medicine (Germany), May 4, 2021 For many of us, adding salt to a meal is a perfectly normal thing to do. We don't really think about it. But actually, we should. As well as raising our blood pressure, too much salt can severely disrupt the energy balance in immune cells and stop them from working properly. Back in 2015, the research group led by Professor Dominik Müller of the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC) and the Experimental and Clinical Research Center (ECRC) found that elevated sodium concentrations in the blood affect both the activation and the function of patrolling monocytes, which are the precursors to macrophages. "But we didn't know exactly what was happening in the cells," says Dr. Sabrina Geisberger of the Berlin Institute for Medical Systems Biology (BIMSB) at the MDC. She is lead author of the study of an international research team led by MDC scientists together with colleagues from University of Regensburg and from Flanders Institute for Biotechnology (VIB) /Hasselt University in Belgium. It was funded by the German Center for Cardiovascular Research (DZHK) and has now been published in the journal Circulation.  Salt disrupts the respiratory chain in cells Working with biochemist and metabolomics expert Dr. Stefan Kempa of BIMSB, the researchers began in the lab by looking at the metabolism of immune cells that had been exposed to high salt concentrations. Changes appeared after just three hours. "It disrupts the respiratory chain, causing the cells to produce less ATP and consume less oxygen," explains Geisberger. ATP (adenosine triphosphate) is the universal fuel that powers all cells. It provides energy for the "chemical work" - synthesizing proteins and other molecules - required for muscle power and metabolic regulation. ATP is produced in the mitochondria, the cell's "power plant," using a complex series of biochemical reactions known as the respiratory chain. "Salt very specifically inhibits complex II in the respiratory chain." This has consequences: The lack of energy causes the monocytes to mature differently. "The phagocytes, whose task is to identify and eliminate pathogens in the body, were able to fight off infections more effectively. But this could also promote inflammation, which might increase cardiovascular risk," explains Müller.  Effects of salt are reversible Professor Markus Kleinewietfeld of Hasselt University and VIB, and Professor Jonathan Jantsch of Universität Regensburg, were heavily involved in the work investigating human monocytes and macrophages. They were able to show that salt affects the functioning of human phagocytes in the same way. Researchers at the ECRC, which is run jointly by the MDC and Charité - Universitätsmedizin Berlin, then conducted a study in which healthy male participants supplemented their usual diets with six grams of salt in tablet form every day for 14 days. In another clinical study, the researchers investigated a familiar scenario: eating a pizza delivered by an Italian restaurant. They then analyzed the monocytes in the participants' blood. The findings showed that the dampening effect on mitochondria doesn't just occur after an extended period of increased salt intake - it also happens after a single pizza. Data from the pizza experiment showed how long the effect lasted: Blood was taken from the participants after three and eight hours, and the effect was barely measurable in the second sample. "That's a good thing. If it had been a prolonged disturbance, we'd be worried about the cells not getting enough energy for a long time," says Müller. The mitochondrial activity is therefore not permanently inhibited. That said, the continuous risk of sodium on mitochondrial function if a person eats very salty food several times a day cannot be ruled out, but needs to be tested in the future. The pizza, incidentally, contained ten grams of salt. Nutrition experts recommend that adults limit their daily intake to five or six grams at most. The calculation includes the salt that is hidden in processed foods. Small ion, big effect "The fundamental finding of our study is that a molecule as small as the sodium ion can be extremely efficient at inhibiting an enzyme that plays a crucial role in the respiratory chain," says Kempa. "When these ions flood into the mitochondria - and they do this under a variety of physiological conditions - they regulate the central part of the electron transport chain." It therefore appears to be a very fundamental regulatory mechanism in cells. Now the task is to investigate whether salt can also influence this mechanism in other types of cells. Kleinewietfeld believes that this is extremely likely because mitochondria aren't just present in immune cells; with the exception of red blood cells, they exist in every cell of the body. They can be found in particularly high numbers wherever a lot of energy is consumed - in muscle cells, neurons, receptors, and egg cells.  It is still not fully elucidated how different cell types regulate the influx of sodium into the mitochondria. Nevertheless, the study confirms that consuming too much salt can be bad for our health. "Of course the first thing you think of is the cardiovascular risk. But multiple studies have shown that salt can affect immune cells in a variety of ways. If such an important cellular mechanism is disrupted for a long period, it could have a negative impact - and could potentially drive inflammatory diseases of the blood vessels or joints, or autoimmune diseases," says Kleinewietfeld.     Ginkgo biloba extract improves cognitive function and increases neurogenesis by reducing amyloid beta pathology  Xuzhou Medical University (China), May 1, 2021 According to news reporting from Jiangsu, People’s Republic of China, research stated, “Previous studies have indicated that the generation of newborn hippocampal neurons is impaired in the early phase of Alzheimer’s disease (AD). A potential therapeutic strategy being pursued for the treatment of AD is increasing the number of newborn neurons in the adult hippocampus.” The news correspondents obtained a quote from the research from Xuzhou Medical University, “Recent studies have demonstrated that ginkgo biloba extract (EGb 761) plays a neuroprotective role by preventing memory loss in many neurodegenerative diseases. However, the extent of EGb 761’s protective role in the AD process is unclear. In this study, different doses of EGb 761 (0, 10, 20, and 30 mg/kg; intraperitoneal injections once every day for four months) were tested on 5xFAD mice. After consecutive 4-month injections, mice were tested in learning memory tasks, A beta, and neurogenesis in the dentate gyrus (DG) of hippocampus and morphological characteristics of neurons in DG of hippocampus. Results indicated that EGb 761 (20 and 30 mg/kg) ameliorated memory deficits. Further analysis indicated that EGb 761 can reduce the number of A beta positive signals in 5xFAD mice, increase the number of newborn neurons, and increase dendritic branching and density of dendritic spines in 5xFAD mice compared to nontreated 5xFAD mice.” According to the news reporters, the research concluded: “It was concluded that EGb 761 plays a protective role in the memory deficit of 5xFAD mice.” This research has been peer-reviewed.     Fasting lowers blood pressure by reshaping the gut microbiota Baylor College of Medicine, April 30 2021 Nearly half of adults in the United States have hypertension, a condition that raises the risk for heart disease and stroke, which are leading causes of death in the U. S. At Baylor College of Medicine, Dr. David J. Durgan and his colleagues are dedicated to better understand hypertension, in particular the emerging evidence suggesting that disruption of the gut microbiota, known as gut dysbiosis, can have adverse effects on blood pressure. "Previous studies from our lab have shown that the composition of the gut microbiota in animal models of hypertension, such as the SHRSP (spontaneously hypertensive stroke-prone rat) model, is different from that in animals with normal blood pressure," said Durgan, assistant professor of anesthesiology at Baylor. The researchers also have shown that transplanting dysbiotic gut microbiota from a hypertensive animal into a normotensive (having a healthy blood pressure) one results in the recipient developing high blood pressure. "This result told us that gut dysbiosis is not just a consequence of hypertension, but is actually involved in causing it," Durgan said. "This ground work led to the current study in which we proposed to answer two questions. First, can we manipulate the dysbiotic microbiota to either prevent or relieve hypertension? Second, how are the gut microbes influencing the animal's blood pressure?" Can manipulating the gut microbiota regulate blood pressure? To answer the first question, Durgan and his colleagues drew on previous research showing that fasting was both one of the major drivers of the composition of the gut microbiota and a promoter of beneficial cardiovascular effects. These studies, however, had not provided evidence connecting the microbiota and blood pressure. Working with the SHRSP model of spontaneous hypertension and normal rats, the researchers set up two groups. One group had SHRSP and normal rats that were fed every other day, while the other group, called control, had SHRSP and normal rats with unrestricted food availability. Nine weeks after the experiment began, the researchers observed that, as expected, the rats in the SHRSP control had higher blood pressure when compared to the normal control rats. Interestingly, in the group that fasted every other day, the SHRSP rats had significantly reduced blood pressure when compared with the SHRSP rats that had not fasted. "Next, we investigated whether the microbiota was involved in the reduction of blood pressure we observed in the SHRSP rats that had fasted," Durgan said. The researchers transplanted the microbiota of the rats that had either fasted or fed without restrictions into germ-free rats, which have no microbiota of their own. Durgan and his colleagues were excited to see that the germ-free rats that received the microbiota of normally fed SHRSP rats had higher blood pressure than the germ-free rats receiving microbiota from normal control rats, just like their corresponding microbiota donors. "It was particularly interesting to see that the germ-free rats that received microbiota from the fasting SHRSP rats had significantly lower the blood pressure than the rats that had received microbiota from SHRSP control rats," Durgan said. "These results demonstrated that the alterations to the microbiota induced by fasting were sufficient to mediate the blood pressure-lowering effect of intermitting fasting." How the microbiota regulates blood pressure The team proceeded to investigate the second question of their project. How does the gut microbiota regulate blood pressure? "We applied whole genome shotgun sequence analysis of the microbiota as well as untargeted metabolomics analysis of plasma and gastrointestinal luminal content. Among the changes we observed, alterations in products of bile acid metabolism stood out as potential mediators of blood pressure regulation," Durgan said. The team discovered that the SHRSP hypertensive animals that were fed normally had lower bile acids in circulation than normotensive animals. On the other hand, SHRSP animals that followed an intermittent feeding schedule had more bile acids in the circulation. "Supporting this finding, we found that supplementing animals with cholic acid, a primary bile acid, also significantly reduced blood pressure in the SHRSP model of hypertension," Durgan said. Taken together, the study shows for the first time that intermittent fasting can be beneficial in terms of reducing hypertension by reshaping the composition of gut microbiota in an animal model. The work also provides evidence that gut dysbiosis contributes to hypertension by altering bile acid signaling. "This study is important to understand that fasting can have its effects on the host through microbiota manipulation," Durgan said. "This is an attractive idea because it can potentially have clinical applications. Many of the bacteria in the gut microbiotaare involved in the production of compounds that have been shown to have beneficial effects as they make it into the circulation and contribute to the regulation of the host's physiology. Fasting schedules could one day help regulate the activity of gut microbial populations to naturally provide health benefits.   Study: Following healthy diets found to reduce the risk of acquired hearing loss by 30% Brigham and Women's Hospital, April 30, 2021 A study published in the American Journal of Epidemiology suggests that following a healthy diet may help ward off acquired hearing loss. A team led by Brigham and Women’s Hospital researchers examined middle-aged women and found that the odds of developing hearing loss is 30 percent lower in those who adhere to a healthy diet. Adherence to a healthy diet linked to lower risk of hearing loss Acquired hearing loss refers to the total or partial inability to hear sounds that develop after birth. It occurs for various reasons, including ear infection, meningitis, measles, head injury, exposure to loud noise and aging. Past studies linked higher intake of certain nutrients such as beta-carotene (found in carrots, legumes and other foods) and omega-3 fatty acids (found in fatty fish) to a lower risk of self-reported hearing loss. The researchers wished to learn more about this connection by tracking people’s diets and measuring changes in their hearing sensitivity over a long period of time. To do so, the researchers studied 20 years of dietary intake information from over 3,000 women with a median age of 59 who were included in the Nurses’ Health Study II. Using this information, they examined how closely the women’s long-term diets resembled the Alternate Mediterranean diet (AMED), Dietary Approaches to Stop Hypertension (DASH diet) and Alternate Healthy Index-2010 (AHEI-2010).  AMED is a version of the Mediterranean diet adapted to reflect eating patterns that are linked to a lower risk of chronic disease, while the DASH diet is intended to control and prevent high blood pressure. On the other hand, AHEI-2010 is based on the 2010 U.S. Department of Agriculture’s Dietary Guidelines for Americans and shares similar components with AMED and the DASH diet. Past studies linked adherence to these diets to a lower risk of heart disease, stroke, diabetes, hypertension and premature death. To measure the participants’ hearing sensitivity over the course of three years, the team put up 19 testing sites across the country and trained audiologists to measure changes in the participants’ pure-tone hearing thresholds – the lowest and highest pitch (frequency of a sound) that a person can detect in one ear. The researchers found that the odds of hearing loss in the mid-frequencies were nearly 30 percent lower in the women whose dietary patterns resembled the three diets, compared to those whose diets least resembled them. Meanwhile, the odds of hearing loss in higher frequencies were up to 25 percent lower. The frequencies encompassed in these associations, according to the researchers, are critical for speech understanding. “We were surprised that so many women demonstrated hearing decline over such a relatively short period of time,” said Sharon Curhan, a professor of medicine at Harvard Medical School and the lead researcher of the study. After only three years, nineteen percent of the participants had low-frequency hearing loss, 38 percent had mid-frequency hearing loss, while nearly half had high-frequency hearing loss. (Related: Age-related hearing loss halted with folate nutrient.) “The mean age of the women in our study was 59 years; most of our participants were in their 50s and early 60s. This is a younger age than when many people think about having their hearing checked,” she added. The researchers plan to continue tracking the participants with repeated hearing tests and are currently investigating ways to collect high-quality information for future studies across diverse populations.   Thai ginseng found to improve erectile function in men Life Extension Foundation, April 28, 2021 American researchers examined the effects of an ethanol extract derived from Kaempferia parviflora, also known as Thai ginseng, on erectile function in healthy middle-aged and older men. Their findings were published in the Journal of Integrative Medicine. Sexual health positively correlates with overall well-being. Current strategies that are meant to enhance male sexual health are limited by many factors, such as responsiveness, adherence and adverse effects. Researchers understand the need for safe and effective interventions that could help preserve male sexual function. K. parviflora, a plant from the Zingiberaceae (ginger) family, has been found to support cardiovascular health and has shown signs that it could ameliorate erectile dysfunction. To investigate this, the researchers conducted an open-label, one-arm study involving 14 generally healthy males aged 50 to 68 years with self-reported mild erectile dysfunction. The participants received 100 mg of an extract obtained from the rhizome of K. parviflora daily for 30 days. Primary efficacy analyses included the International Index of Erectile Function (IIEF), while secondary efficacy analyses included the Global Assessment Question about erectile function. The researchers reported that 13 of the 14 participants completed the study. Supplementation of the K. parviflora ethanol extract induced statistically significant improvements in erectile function, intercourse satisfaction and total scores on IIEF questionnaire. The extract was well-tolerated by the participants and exhibited an excellent safety profile. Based on these findings, the researchers concluded that K. parviflora can improve erectile function in healthy middle-aged and older men.     Curcumin Reduces Anxiety and Depression Even In People With Major Depression Texas Christian University and University of Arkansas, May 1, 2021   Dietary supplements formulated with highly bioavailable curcumin may allow for faster recovery after competition-level training, and blunt training-related decreases in performance , says new data presented at Experimental Biology.   Powdered turmeric has been used for centuries to treat a host of illnesses. It inhibits inflammatory reactions, has anti-diabetic effects, reduces cholesterol among other powerful healtheffects. A recent study led by a research team in Munich showed that it can also inhibit formation of metastases.  Dietary supplements formulated with highly bioavailable curcumin may allow for faster recovery after competition-level training, and blunt training-related decreases in performance , says new data presented at Experimental Biology. Using OmniActive's supplement ingredient, scientists reported that supplementation for eight weeks resulted in significant reductions in levels of creatine kinase, a marker of muscle damage, while self-reported pain scores were also significantly lower 24 hours post-exercise. A daily 200 mg dose of curcuminoids (in the form of 1,000 mg supplement) was also associated with a decrease in performance declines observed during "These data suggest that high dose bioavailable curcumin (200 mg curcuminoids) attenuates performance decrements following downhill running, eccentric loading, which may improve subsequent adaptations to chronic training," wrote the researchers in the FASEB Journal . Dr Ralf Jager from Wisconsin-based Increnovo and co-author on the study reports, explained that curcumin's sports nutrition benefits were linked to its antioxidant and anti-inflammatory potential. Muscle Damage Study The researchers recruited 59 moderately trained men and 29 women with an average age of 21 to participate in their double-blind, randomized, placebo controlled parallel design study. The participants were randomly assigned to receive 250 mg or 1,000 mg of supplement or placebo per day for eight weeks. The data indicated that, following muscle-damaging exercise, the high dose curcumin group experienced significantly lower pain scores, while increases in creatine kinase (CK) levels were also significantly reduced compared to placebo, when the baseline CK value is held constant at the mean. "These data demonstrate curcuminoids reduce muscle damage and improve muscle soreness in healthy young subjects following a bout of muscle damaging exercise. Faster recovery allows for consistent training at competition intensity and might lead to enhanced adaptation rate and performance," they wrote in the FASEB Journal . Performance A separate analysis was done with 62 men and women randomly assigned to 250 mg or 1,000 mg of supplement per day or placebo. After eight weeks the subjects performced downhill running, which promotes muscle damage. The results showed that performance declined significantly in both the placebo and low-dose curcumin group, but such declined were attenuated in the high-dose curcumin group. "Further study is warranted in other exercise types (i.e. resistance training) and chronically," wrote the researchers.

In today’s episode, Prof Ana Pombo, group leader at the Max Delbrück Center for Molecular Medicine in Berlin, is interviewed by PhD student Vasiliki Salameti. Ana talks about her pioneering work that enabled scientists to dissect how the genome is packaged inside cells and how this method is evolving with new single-cell technologies. She shares her view on future technology development which should help us make predictions. She discusses collaboration in science and the importance of timing in making research decisions. To learn more about Ana’s work check out the following link: https://www.mdc-berlin.de/pombo

 Perspectives on the Pandemic | "The Illusion of Evidence Based Medicine"  Leemon McHenry 10 mins   Leemon McHenry is Emeritus Professor in the Department of Philosophy , California State University, Northridge. Leemon does research in Philosophy of Science, Metaphysics and Bioethics. His current project is 'Evidence Based Medicine'.   Vitamin A for nerve cells University Medical Center Freiburg (Germany), April 1, 2021 Neuroscientists agree that a person's brain is constantly changing, rewiring itself and adapting to environmental stimuli. This is how humans learn new things and create memories. This adaptability and malleability is called plasticity. "Physicians have long suspected that remodeling processes also take place in humans at the contact points between nerve cells, i.e. directly at the synapses. Until now, however, such a coordinated adaptation of structure and function could only be demonstrated in animal experiments," says Prof. Dr. Andreas Vlachos from the Institute of Anatomy and Cell Biology at the University of Freiburg. But now Vlachos, together with Prof. Dr. Jürgen Beck, head of the Department of Neurosurgery at the University Medical Center Freiburg, has provided experimental evidence for synaptic plasticity in humans. In addition to Vlachos and Beck, the research team consists of Dr. Maximilian Lenz, Pia Kruse and Amelie Eichler from the University of Freiburg, Dr. Jakob Strähle from the University Medical Center Freiburg and colleagues from Goethe University Frankfurt. The results were presented in the scientific journal eLife. In the experiments, the team investigated whether so-called dendritic spines change when exposed to a vitamin A derivative called retionic acid. Dendritic spines are the parts of the synapse that receive, process and transmit signals during communication between neurons. As such, they play a crucial role in brain plasticity and are constantly adapting to everyday experience. For example, learning can change the number and shape of dendritic spines. However, a transformation in the number or shape of the spines is also found in diseases such as depression or dementia. The research shows that retinoic acid not only increases the size of dendritic spines, but also strengthens their ability to transmit signals between neurons. "We have concluded from our results that retinoic acids are important messengers for synaptic plasticity in the human brain. Thus, this finding contributes to the identification of key mechanisms of synaptic plasticity in the human brain and could support the development of new therapeutic strategies for brain diseases, such as depression," says Vlachos. To experimentally demonstrate that synaptic plasticity also exists in humans, the researchers use tiny samples of human cerebral cortex, which must be compulsorily removed during neurosurgical procedures for therapeutic reasons. The removed brain tissue was then treated with retinoic acid before functional and structural properties of neurons were analyzed using electrophysiological and microscopic techniques.       Study: Chemical compound in certain essential oils promotes wound healing Indiana University, April, 2021 A study from Indiana University revealed that a chemical compound in essential oils may enhance wound healing, especially when applied topically. According to co-author Sachiko Koyama, essential oils – like those from lavender, rosemary, ylang-ylang and black pepper – contain a chemical compoundcalled beta-caryophyllene. This contributes to improved wound healing, based on a murine model. “This is the first finding at the chemical-compound level showing improved wound healing in addition to changes in gene expression in the skin,” said Koyama. Beta-caryophyllene may decrease inflammation and accelerate re-epithelialization. The latter refers to the restoration of structure and function of injured tissues. During this process, epithelial cells at the wound start to migrate and cover the injured area. The researchers added that beta-caryophyllene may prevent cell death, allowing cells to survive and proliferate. “I thought maybe wound healing would be accelerated if inflammation was suppressed, stimulating an earlier switch from the inflammatory stage to the next stage,” she added. The team also noted increased gene expression of hair follicle stem cells in the treated tissue. This potentially indicate that there’s more to wound-healing activity of beta-caryophyllene than just activating genes. “It’s possibly more complicated,” she added. “Our findings suggest the involvements of some other routes in addition to CB2. I hope to clarify the mechanisms of action in the near future.” Koyama, a social neuroscientist at Indiana University, said that she wasn’t interested in studying essential oils at first, as her field of expertise was in pheromone and social status. However, her interest was sparked when she saw students working on the wound healing process in mice. She knew from experience that beta-caryophyllene can also activate cannabinoid receptor 2 (CB2), which has anti-inflammatory and analgesic properties. Healing beyond smell Most people know essential oils by way of aromatherapy. These are often used with diffusers, aromatic spritzers, inhalers, facial steamers and clay masks to bring out the aroma coming from the oil. Essential oils, in particular, may help with asthma, insomnia, fatigue and depression, among others. In the study, the researchers did not find any relationship between the sense of smell and the healing properties of beta-caryophyllene. (Related: Curcumin found to aid in the healing of skin wounds.) Koyama also offered a caveat for those looking to use essential oils for treatment, in particular, warning against the use of any essential oils. In the study, the researchers used essential oils that underwent purification processes to achieve that result. “It’s not very precise to use the essential oils themselves because there are differences,” she added. “Even if you say you used lavender, when the lavender was harvested, where it was harvested, how it was stored—all of this makes a difference in the chemical composition.” The team is also hopeful that their results will warrant further studies to determine an exact chemical composition for beta-caryophyllene that can be used to treat skin wounds. “There are many things to test before we can start using it clinically, but our results are very promising and exciting; someday in the near future, we may be able to develop a drug and drug delivery methods using the chemical compounds found in essential oils,” she added.     Exercise may help slow cognitive decline in some people with Parkinson's disease Hallym University (South Korea), April 1, 2021 For people with Parkinson's disease, problems with thinking and memory skills are among the most common nonmotor symptoms of the disease. A new study shows that exercise may help slow cognitive decline for some people with the disease. The study is published in the March 31, 2021, online issue of Neurology. Research has suggested that people with Parkinson's who have the gene variant apolipoprotein E e4, or APOE e4, may experience faster cognitive decline and earlier in the disease than people without the variant. APOE e4 is known as a genetic risk factor for Alzheimer's disease. The study looked at whether exercise could play a role in slowing cognitive decline for people with APOE e4. "Problems with thinking skills and memory can have a negative impact on people's quality of life and ability to function, so it's exciting that increasing physical activitycould have the potential to delay or prevent cognitive decline," said study author Jin-Sun Jun, M.D., of Hallym University in Seoul, Korea. The study involved 173 people with early Parkinson's disease who were on average 63 years old at the time and 59 years old when they developed the disease. A total of 27% had the APOE e4 gene variant. People reported their physical activity with a questionnaire on how much activity they had in the previous week through leisure activities such as walking or biking, household activities such as dusting or yard work and work activities for pay or as a volunteer. People took a test of their thinking skills at the beginning of the study and then one and two years later. Overall, scores at the beginning of the study averaged 26 points. For people with the APOE e4 gene variant, test scores declined by an average of 1.33 points by the end of the study compared to those without the variant. But researchers also found that greater physical activity at the start of the study lessened APOE e4-related cognitive decline two years later by an average of 0.007 points. "Additional research is needed to confirm our findings, but these results would support the use of interventions that target physical activity as a way to delay cognitive decline in people with early Parkinson's who have the APOE e4 gene variant," Jun said. A limitation of the study was that participants reported their own levels of physical activity, so there is the possibility that they would not remember their levels exactly.   Time to shift from 'food security' to 'nutrition security' to increase health and well-being Tufts and Georgetown Universities, April 1, 2021   In the 1960s, a national focus on hunger was essential to address major problems of undernutrition after World War II. In the 1990s, the nation shifted away from hunger toward "food insecurity" to better capture and address the challenges of food access and affordability. Now, a new Viewpoint article argues that today's health and equity challenges call for the U.S. to shift from "food insecurity" to "nutrition insecurity" in order to catalyze appropriate focus and policies on access not just to food but to healthy, nourishing food. The Viewpoint, by Dariush Mozaffarian of the Friedman School of Nutrition Science & Policy at Tufts University, Sheila Fleischhacker of Georgetown Law School, and José Andrés of World Central Kitchen, was published online in JAMA this week. The concept of food security focuses on access to and affordability of food that is safe, nutritious, and consistent with personal preferences. In reality, however, the "nutritious" part often has been overlooked or lost in national policies and solutions, with resulting emphasis on quantity, rather than quality, of food, say the authors. "Food is essential both for life and human dignity. Every day, I see hunger, but the hunger I see is not only for calories but for nourishing meals. With a new focus on nutrition security, we embrace a solution that nourishes people, instead of filling them with food but leaving them hungry," said Chef José Andrés, founder of World Central Kitchen. The authors define nutrition security as having consistent access to and availability and affordability of foods and beverages that promote well-being, while preventing -- and, if needed, treating -- disease. Nutrition security provides a more inclusive view that recognizes that foods must nourish all people. "'Nutrition security' incorporates all the aims of food security but with additional emphasis on the need for wholesome, healthful foods and drinks for all. COVID-19 has made clear that Americans who are most likely to be hungry are also at highest risk of diet-related diseases including obesity, diabetes, heart disease, and many cancers - a harsh legacy of inequities and structural racism in our nation. A new focus on nutrition security for all Americans will help crystallize and catalyze real solutions that provide not only food but also well-being for everyone," said first author Dariush Mozaffarian, dean of the Friedman School of Nutrition Science & Policy at Tufts University. "It's the right time for this evolution," said Sheila Fleischhacker, adjunct professor at Georgetown Law School, who has drafted food, nutrition and health legislation and campaign positions at the local, state, tribal and federal levels. "By prioritizing nutrition security, we bring together historically siloed areas - hunger and nutrition - which must be tackled together to effectively address our modern challenges of diet-related diseases and disparities in clinical care, government food and food assistance policies, public health investments, and national research." "The current approach is not sufficient," the authors write, and "traditionally marginalized minority groups as well as people living in rural and lower-income counties are most likely to experience disparities in nutrition quality, food insecurity, and corresponding diet-related diseases."     Fasting acts as diet catalyst in those with metabolic syndrome Max Delbruck Center for Molecular Medicine (Germany), March 30, 2021 One in four Germans suffers from metabolic syndrome. Several of four diseases of affluence occur at the same time in this 'deadly quartet': obesity, high blood pressure, lipid metabolism disorder and diabetes mellitus. Each of these is a risk factor for severe cardiovascular conditions, such as heart attack and stroke. Treatment aims to help patients lose weight and normalise their lipid and carbohydrate metabolism and blood pressure. In addition to exercise, doctors prescribe a low-calorie and healthy diet. Medication is often also required. However, it is not fully clear what effects nutrition has on the microbiome, immune system and health.  A research group led by Dr Sofia Forslund and Professor Dominik N. Müller from the Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC) and the Experimental and Clinical Research Center (ECRC) has now examined the effect a change of diet has on people with metabolic syndrome. The ECRC is jointly run by the MDC and Charité Universitätsmedizin Berlin. "Switching to a healthy diet has a positive effect on blood pressure," says Andras Maifeld, summarising the results. "If the diet is preceded by a fast, this effect is intensified." Maifeld is the first author of the paper, which was recently published in the journal "Nature Communications". Broccoli over roast beef Dr Andreas Michalsen, Senior Consultant of the Naturopathy Department at Immanuel Hospital Berlin and Endowed Chair of Clinical Naturopathy at the Institute for Social Medicine, Epidemiology and Health Economics at Charité - Universitätsmedizin Berlin, and Professor Gustav J. Dobos, Chair of Naturopathy and Integrative Medicine at the University of Duisburg-Essen, recruited 71 volunteers with metabolic syndrome and raised systolic blood pressure. The researchers divided them into two groups at random.  Both groups followed the DASH (Dietary Approach to Stop Hypertension) diet for three months, which is designed to combat high blood pressure. This Mediterranean-style diet includes lots of fruit and vegetables, wholemeal products, nuts and pulses, fish and lean white meat. One of the two groups did not consume any solid food at all for five days before starting the DASH diet. On the basis of immunophenotyping, the scientists observed how the immune cells of the volunteers changed when they altered their diet. "The innate immune system remains stable during the fast, whereas the adaptive immune system shuts down," explains Maifeld. During this process, the number of proinflammatory T cells drops, while regulatory T cells multiply.  A Mediterranean diet is good, but to also fast is better The researchers used stool samples to examine the effects of the fast on the gut microbiome. Gut bacteria work in close contact with the immune system. Some strains of bacteria metabolise dietary fibre into anti-inflammatory short-chain fatty acids that benefit the immune system. The composition of the gut bacteria ecosystem changes drastically during fasting. Health-promoting bacteria that help to reduce blood pressure multiply. Some of these changes remain even after resumption of food intake. The following is particularly noteworthy: "Body mass index, blood pressure and the need for antihypertensive medication remained lower in the long term among volunteers who started the healthy diet with a five-day fast," explains Dominik Müller. Blood pressure normally shoots back up again when even one antihypertensive tablet is forgotten.  Blood pressure remains lower in the long term - even three months after fasting Together with scientists from the Helmholtz Centre for Infection Research and McGill University, Montreal, Canada, Forslund's working group conducted a statistical evaluation of these results using artificial intelligence to ensure that this positive effect was actually attributable to the fast and not to the medication that the volunteers were taking. They used methods from a previous study in which they had examined the influence of antihypertensive medication on the microbiome. "We were able to isolate the influence of the medication and observe that whether someone responds well to a change of diet or not depends on the individual immune response and the gut microbiome," says Forslund.  If a high-fibre, low-fat diet fails to deliver results, it is possible that there are insufficient gut bacteria in the gut microbiome that metabolise fibre into protective fatty acids. "Those who have this problem often feel that it is not worth the effort and go back to their old habits," explains the scientist. It is therefore a good idea to combine a diet with a fast. "Fasting acts as a catalyst for protective microorganisms in the gut. Health clearly improves very quickly and patients can cut back on their medication or even often stop taking tablets altogether." This could motivate them to stick to a healthy lifestyle in the long term.   Rice bran adds microbiome diversity, slows growth of colon cancer cells University of Colorado, April 5, 2021    At the American Association for Cancer Research (AACR) Annual Meeting, University of Colorado Cancer Center researchers at Colorado State University present results of a phase II clinical trial of 29 people exploring the effects of adding rice bran or navy beans to the diets of colorectal cancer survivors. After the 4-week randomized-controlled trial during which people added rice bran, navy bean powder or neither, both the rice bran and navy bean groups showed increased dietary fiber, iron, zinc, thiamin, niacin, vitamin B6, folate, and alpha-tocopherol. The rice bran group also showed increased microbiome richness and diversity. When researchers treated colorectal cancer cells with stool extracts from these groups, they saw reduced cell growth from the groups that had increased rice bran and navy bean consumption.   Previous work shows the ability of these diets to decrease colorectal cancer risk in animal models. The current trial confirms that people can eat enough bean- and rice bran-enhanced foods to promote gut health at levels shown to prevent colorectal cancer in animals. Guidelines from the American Institute for Cancer Research recommend reducing the risk of cancer by eating more vegetables, fruits, whole grains and legumes, such as beans. Ryan has established from these studies that eating a half-cup of beans and 30 grams of rice bran per day is enough to see changes in small molecules that can confer protection against colorectal cancer.   "The simple message is, 'Food is medicine,' and we are looking at how to simplify that and make it apply to our everyday lives," says study co-author Regina Brown, MD, assistant professor at the CU School of Medicine and oncologist for CUHealth.   Brown is long-time collaborator of CU Cancer Center investigator and CSU assistant professor, Elizabeth Ryan, PhD. The Ryan Lab in the CSU College of Veterinary Medicine and Biomedical Sciences studies the potential power of navy beans and rice bran to promote digestive health and to prevent metabolic alterations in obesity, heart disease and certain cancers.   "The evidence is there in animals and we can now study this in people. The question is, what are we doing to achieve adequate levels of intake of these foods?" Ryan said. "It's not enough to say 'I eat them once in a while.' That's not going to work, particularly if you are at higher risk. You have to meet a dose, just like you need a dose of a certain drug, you need to reach intake levels and consume increased amounts of these foods, and that's where people, including me, are challenged. Not everyone wants to open up a can of beans and eat them every day."   The two met about 10 years ago, when Ryan was a researcher in CSU professor Henry Thompson's Cancer Prevention Lab, and Brown was practicing medicine in Fort Collins and caring for her mother, who had uterine cancer. "It was kind of a novel partnership and had we not dug in our heels it could have died, but I told Elizabeth, 'Your work is so interesting and so valuable. We have to take this translational research from the benchtop to the clinic.' I guarantee, nine out of 10 of my patients, the first thing they ask is about their diet," Brown said.   The study's lead author is Erica Borresen, Ryan's research associate and study coordinator, who worked with colorectal cancer survivors to make sure they ate their beans and rice bran provided in meals and snacks, and that they filled out their food logs and gastrointestinal health questionnaires. It was sometimes intimate and awkward, but so is getting a colonoscopy and being treated for colorectal cancer. "Our participants donated their time and effort, and I want to make sure they understand they are appreciated," said Borresen, who earned her Master of Public Health at the Colorado School of Public Health, and plans to become a physician's assistant. "I came to realize I love the patient interaction - that's one of my favorite parts about coordinating our studies."   The next phase of Ryan's research examines effects of the cooked navy bean powder and rice bran on the colon tissue of people who have already had colorectal cancer and are at high risk for recurrence. "I really feel that there's hope in this being a practical solution to improve gut health and specifically colorectal cancer prevention," says Ryan.       Research suggests L-tryptophan supplements might help prevent impulsivity associated with psychological disorders University of California Berkeley, April 2, 2021 According to news reporting originating from Berkeley, California, research stated, “Emotion-related impulsivity, defined as the tendency to say or do things that one later regret during periods of heightened emotion, has been tied to a broad range of psychopathologies. Previous work has suggested that emotion-related impulsivity is tied to an impaired function of the serotonergic system.” Our news editors obtained a quote from the research from the University of California Berkeley, “Central serotonin synthesis relies on the intake of the essential amino acid, tryptophan and its ability to pass through the blood brain barrier. The aim of this study was to determine the association between emotion-related impulsivity and tryptophan intake. Undergraduate participants (N = 25, 16 women, 9 men) completed a self-rated measure of impulsivity (Three Factor Impulsivity Index, TFI) and daily logs of their food intake and exercise. These data were coded using the software NutriNote to evaluate intakes of tryptophan, large neutral amino acids, vitamins B6/B12, and exercise. Correlational analyses indicated that higher tryptophan intake was associated with significantly lower scores on two out of three subscales of the TFI, Pervasive Influence of Feelings scores r = -.502, p< .010, and (lack-of) Follow-Through scores, r = -.407, p< .050. Findings provide further evidence that emotion-related impulsivity is correlated to serotonergic indices, even when considering only food habits.” According to the news editors, the research concluded: “It also suggests the need for more research on whether tryptophan supplements might be beneficial for impulsive persons suffering from a psychological disorder.” This research has been peer-reviewed.         Nutritional supplementation in preconception and pregnancy linked to reduced risk of preterm birth University of Southampton (UK), March 30, 2021 Increasing evidence suggests that a mother's nutritional status at the onset of pregnancy has an important influence on the growth and development of her baby, and that a good nutritional status during pregnancy may help reduce the risk of pregnancy complications. A specific blend of nutrients and probiotics was tested in an international multicentre double blind randomized controlled trial NiPPeR (Nutritional Intervention Preconception and during Pregnancy to maintain healthy glucosE levels and offspRing health). Researchers from the international EpiGen Global Research Consortium, an academic group of clinicians and scientists including from around the world, including the University of Southampton, specifically assessed the effects of a nutritional intervention, a combination of myo-inositol, probiotics and micronutrients, consumed both before and during pregnancy, on maintaining healthy blood sugar levels in pregnancy and sustaining a healthy pregnancy and delivery. As published in the journal Diabetes Care, (Myo-inositol, Probiotics and Micronutrient Supplementation from Preconception for Glycemia in Pregnancy: the NiPPeR study involved 1,729 women from the UK, New Zealand and Singapore who were planning pregnancy—one of the largest international preconception randomized controlled trials of its type. While the study found that the intervention did not influence the mother's blood sugar levels or birthweights of the 585 babies born, the nutritional supplement decreased the incidence of preterm birth, particularly the cases associated with preterm pre-labor rupture of membranes. "Preterm delivery is a serious, common and costly public health problem worldwide that continues to increase in incidence," said Professor Keith Godfrey from the MRC Lifecourse Epidemiology Unit at the University of Southampton. "Preterm pre-labor rupture of membranes is a major cause of preterm birth. Our study presents for the first time a clinical trial of a novel non-pharmacological approach that started preconception and extended throughout pregnancy, through the innovative use of a combination of nutritional ingredients. The study findings highlight the potential value of the mix of nutrients and probiotics in reducing the risk of preterm birth and supporting a timely delivery," Professor Godfrey continued.  Associate Professor Shiao-Yng Chan, a principal investigator on the study from the Yong Loo Lin School of Medicine, National University of Singapore, deputy executive director at the Singapore Institute for Clinical Sciences, A*STAR, and Senior Consultant, Department of Obstetrics & Gynaecology, National University Hospital, commented "One of the strengths of our study is the diversity of its participants as we have involved women of multiple ethnicities from the general population across three countries, which means that the outcomes have wide relevance to women planning for pregnancy. Additionally, the study included blinded intervention and control groups, so bias is minimized." Sharing his thoughts, Professor Wayne Cutfield, principal investigator on the study from the University of Auckland, New Zealand, said, "The importance of the preconception period on maternal and offspring health is being increasingly recognized, but there are very few randomized control trials seeking to optimize preconception nutrition." Dr. Isabelle Bureau-Franz, Head of Nestlé Research, who partnered with EpiGen for this academic-led trial, says, "We are focused on discovering science-based solutions for mothers and their infants during preconception, pregnancy and while breastfeeding. The NiPPeR study is a great example of how a public-private partnership can build scientific evidence on nutritional interventions in a largely understudied group."

Aujourd'hui : nous partons en Afrique pour un voyage sous la surface, à la rencontre du mal-aimé rat-taupe nu. Ce petit rongeur à la peau glabre compense son manque de charme par toute une série de super pouvoirs qui en font un favori des chercheurs. Mais si nous nous intéressons aujourd'hui à lui, c'est parce que les rats-taupes nus ne parlent pas tous le même dialecte, même lorsqu'ils vivent à proximité les uns des autres.« Mais pourquoi donc s'embêter à parler des langues différentes ? », nous demanderez-vous. Pour le savoir, il vous faudra écouter ce nouvel épisode de Bêtes de Science.

Wissenschaftler sehen die Pandemie-Entwicklungen weiter mit Sorge. Auf dem Corona-Symposium, das auf Einladung des Max-Delbrück-Centrums in Berlin stattfand, präsentierten internationale Experten neueste wissenschaftliche Forschungen rund um Covid-19. Von Thomas Prinzler

Der Charité-Virologe Christian Drosten und weitere führende Wissenschaftler aus aller Welt werden in einem Online-Symposium neueste Forschungen rund um Corona präsentieren. Gastgeber Prof. Klaus Rajewsky vom Max-Delbrück Centrum sieht momentan die absolute Priorität in einer Durchimpfung der Bevölkerung.

本期节目的嘉宾是我们的朋友黄宇翔。黄宇翔是美国密歇根大学安娜堡分校分子、细胞与发育生物学的博士学生，主要研究方向是细胞代谢。他也是科学新媒体"知识分子"的撰稿人，目前正在创作《科研外史》，一部以科学史为主题，以武侠为风格的非虚构文集。“有人的地方就有江湖。”作为一门实验科学，生物科研的江湖是什么样的？为什么在黄宇翔看来，生物化学法和遗传学法分别对应降龙十八掌、掷暗器这样的绝顶武功？如果科研史是一部武侠小说，它的精神内核是什么？如果说做研究也是修行，研究者以什么为目标、如何理解自己的角色？在广为人知的科学结论背后往往是无数次失败的经历，而这些探索的过程恰恰构成了科学的基石。为什么这些经历值得被记录、为什么科普写作是重要的？在传递事实信息之外，科普写作又如何传递知识？从高中生物与生物学研究的区别讲起，黄宇翔和我们在这期节目中聊到了科研观、研究者身份、科研武侠、科普写作等话题。本期嘉宾黄宇翔内容提要+精彩预告01:15 生物科学的研究和高中生物课程有什么区别？“说生命科学是文科是完全错误的概念。生物学是一门实验科学，高中生物学课本上的每一个概念背后都有实验支持。高中生物学课本上过度强调了结论性的东西，使得很多人对生物失去了兴趣。”“本科生物学训练强调知识是怎么来的这一过程。”“十九世纪以前的生物学研究叫natural history，自然史或者博物学，是非常描述性的研究。这和当代强调逻辑和抽象概念的生物学研究有所不同。”“生物学上没有百分之百确定的东西，都是在限定条件下的结论。”06:40 生物医学的原创性和重要性“真正开创领域的工作在刚刚发现的时候大部分人无法认识到其重要性。”“作为细胞自噬这个现象最最早发现的人之一，我的导师在90年代观察到这个现象的时候还觉得很郁闷，因为人们不觉得它重要。直到90年代末，人们发现细胞自噬与癌症发病原因的关系，才意识到这个生理学过程的重要意义。”10:58 什么事值得研究的？-不同科学家的科研观“分子生物学的先驱Max Delbrück说过Don't follow the fashion science. 一个科研问题如果大部分人都知道它重要了，那就不要去研究他了。因为有没有你，也会有人能做出来。”“生物学研究的很多竞争很像武侠小说中的华山论剑。大家都想争取第一，但是通过不同的途径。”“生物化学途径像降龙十八掌，是非常霸道的外家功夫，从上百升的培养液中提取中不同的组份进行实验。思路比较简单，但是比较消耗内力。”“遗传学像剑或是暗器，通过化学物质诱发随机突变探索克隆基因的方法。”“两种方法思路非常不一样，但是殊途同归，几乎是同一时间把同一基因克隆出来并一起获得了2001年的诺贝尔生理学奖。”20:20 对武侠的兴趣：做研究也是修行“生物学研究大部分时候是很重复且枯燥的。研究是Re-search，需要你一次又一次的去探索。”“关于武侠的联想是我在科研中找乐子的方法。”“科研大部分时候还是很艰苦的。探究知识的边界大多会以失败收尾，给自己找一些正反馈就很重要。”29:20 生物医学武侠的精神内核：“为苍生的健康谋福利”“从大的学科角度说生物医学研究以科学为手中的宝剑，以愚昧无知作为敌人，为苍生的健康谋福利。从个人的角度说，武侠小说是成年人的童话。我未必能成为封号斗罗或绝世大侠，我也没有天资聪颖，可能放在武侠小说里就是路人甲。我能做到的就是努力把自己的武功练扎实，能做到无愧于心，不要浪费有限的武功，不要让时光虚度掉。做些有益的事情，在过程中充实自己享受过程。”32:00 从《斯通纳》一个本关于学者的一生的小说中获得的启发“不是每个人都要成为那个站在山顶上的人。做自己的英雄，去做一些有益于社会事情。焚膏油以继晷，恒兀兀以穷年。也是一种很好的人生选择。”34:00 对科普写作的兴趣“最开始写科学史科普的时候是出于对学术文章背后科研探索过程的好奇。”“文章是很清晰的，但是探索的过程是曲折的。”“在接近崩溃的时候，如何通过身边人的鼓励而坚持下来。”“一个项目可能六七年前就开始做了，研究幕后的故事细节可能研究者本人都不太记得。但艰苦的奋斗过程如果不记录下来就太可惜了，这都是人类奋斗的经历”39:32 科普写作与播客节目“科普写作和播客都是希望记录冷冰冰的研究背后生动的人和事”“写科普也是希望把理性的科学逻辑传递给大家。”“研究的意义可能在回顾的时候才能够更加清楚，借助导师的见解也很重要。”“科学的前沿是通过武艺的切磋，互相的批评而推进的。“45:40 生物科学科学所理解的科学是什么样的？“生物科学的底层逻辑是必要性、充分性。”46:40 科普不是什么？“科普不是fact，是knowledge：科学中的结论是怎么来的，如何把fact整合成knowledge的过程是科普真正想传递的。这些科学思维可以帮助我们更理性地思考一些现象。”“有人给你展现了一段推理的过程，你可以思考它是不是有道理。这是科普想要传达的思维。”“我们要明白这个结论在什么条件下才成立。一个结论常常只是在一个很小的范围内才成立的。写科普的一大动力是希望大家能以更批判的角度看待问题。”50:40 做科普的感受“做科普写作对自己最直接的影响是增长了自己的科研修养，武器库，扩充了自己的科研思路。”“通过采访老科学家一路的科研生涯也拓宽了我对于科学作为一种职业的的理解。”52:40 总结“科学是一个过程，它的背后是很多有血有肉、像我们一样普通的平凡人。”54:00 书籍推荐Li, J. J. (2006). Laughing gas, Viagra, and Lipitor: The human stories behind the drugs we use. Oxford University Press. “药物发现背后的故事”Sinclair, D. A., & LaPlante, M. D. (2019). Lifespan: Why We Age—and Why We Don't Have To. Atria Books. “明星科学家实验室背后的故事；关于衰老医学的见解。”Ribatti, D. (2018). Judah Folkman: A Biography. Springer. “一位医生科学家的传记。”参考资料黄宇翔在知识分子发表的文章列表：http://zhishifenzi.com/u/2425.html李少峰. (2017年09月28日). "知乎大v王立铭:相信伪科学只需要本能". 长江日报. Retrieved from: http://www.cjrbapp.cjn.cn/p/1694.html片头片尾音乐《Sunrise at Seaside》by 王乾-----------双重意识是一档「让我们认识到那些我们以为此时此刻与我们生活需求没有关联的东西其实和我们紧密相关」的播客节目。你可以在苹果播客, 喜马拉雅，网易云音乐，荔枝fm，小宇宙APP和Spotify搜索"双重意识DoubleConsciousness"找到我们，关注我们并收听我们的节目。欢迎大家在微信后台或是微博(@双重意识DoubleConsciousness)等各大平台给我们留言、提供反馈意见。

In der Wissenschaft scheint die Luft nach oben auf der Karriereleiter für Frauen ziemlich dünn zu sein. Bis auf einige Ausnahmen, zu denen beispielsweise die beiden Chemikerinnen und Nobelpreisträgerinnen Emmanuelle Charpentier und ihre US-amerikanische Kollegin Jennifer Doudna gehören, bekleiden Frauen in der Wissenschaft selten Führungspositionen. Bei einer internationalen Tagung des Max Delbrück Zentrums (MDC) für Molekular-Medizin in Berlin geht es um diesesThema. Auf rbbKultur vorab Informationen von Dr. Christiane Nolte, Frauenvertreterin am MDC.

We're adding "animal intelligence" to rsr.org/squeeze. The claim that apes should have the highest intelligence in the animal kingdom because we humans supposedly evolved from them turns out to be yet another fail. Did you know, for example, that certains species of birds demonstrate that they know what other birds are thinking? On today's Real Science Radio program Bob Enyart and Fred Williams discuss really fun and hugely significant examples of animal intelligence! Wait till you can hear what the lowly ant does! RSR thanks Answers in Genesis for publishing Dr. Joe Francis' article Smarter Than You Think which we've used as a framework for today's broadcast. Also, February is our annual telethon month and our goal is $50,000 so we can really use your help! We're only at a couple thousand dollars so far. So if you can, please check out kgov.com/store or call us at 1-800-8Enyart (836-9278) to purchase materials, sign up for a subscription, or to make a one-time or monthly donation. Thanks so much! From kgov.com/definitions: These are RSR-styled... - Animal: Excepting humans, a multicellular biological organism with specialized sense organs and voluntary movement. - Mammal: A warm-blooded vertebrate animal with hair or fur, females that secrete milk, and, except for the platypus and spiny anteater, the birth of live young. - Animal Kingdom: The animals of the world collectively, excluding insects and fish (which are more likened to biological robots than to volitional organisms) - Human being: A person, made in God's likeness, with body, soul and spirit (whereas animals have body and soul) - Plant: A biological organism that synthesizes nutrients in its leaves by photosynthesis (possessing a body but neither a soul or spirit). * One minute video of a magpie perceiving what many apes don't:  * Otherwise, this is a great video on mole rats vocalizing: If you ignore the absurd claim made by Dr. Gary Lewin of Berlin's Max Delbrück Center for Molecular Medicine about mole rats and human social behavior, this video announces extraordinary research and an exciting discovery! (If you have a choice, you might want to avoid the Max Delbrück Center for your own medical treatment. Researchers who remain so oblivious to the ubiquitous evidence against Darwinian rsr.org/evolution may also miss the insights needed to save your life.)  

On its first day, the new Biden administration announced plans to recalculate the social cost of carbon—a way of estimating the economic toll of greenhouse gases. Staff Writer Paul Voosen and host Sarah Crespi discuss why this value is so important and how it will be determined.  Next up, Alison Barker, a postdoctoral researcher at the Max Delbrück Center for Molecular Medicine, talks with Sarah about the sounds of naked mole-rats. You may already know naked mole-rats are pain and cancer resistant—but did you know these eusocial mammals make little chirps to identify themselves as colony members? Can these learned local dialects make naked mole-rats a new research model for language learning? This week's episode was produced with help from Podigy. Listen to previous podcasts. About the Science Podcast Download a transcript (PDF). [Image: Smithsonian's National Zoo/Flickr; Music: Jeffrey Cook] Authors: Sarah Crespi; Paul Voosen See omnystudio.com/listener for privacy information.

On its first day, the new Biden administration announced plans to recalculate the social cost of carbon—a way of estimating the economic toll of greenhouse gases. Staff Writer Paul Voosen and host Sarah Crespi discuss why this value is so important and how it will be determined.  Next up, Alison Barker, a postdoctoral researcher at the Max Delbrück Center for Molecular Medicine, talks with Sarah about the sounds of naked mole-rats. You may already know naked mole-rats are pain and cancer resistant—but did you know these eusocial mammals make little chirps to identify themselves as colony members? Can these learned local dialects make naked mole-rats a new research model for language learning? This week's episode was produced with help from Podigy. Listen to previous podcasts. About the Science Podcast Download a transcript (PDF). [Image: Smithsonian's National Zoo/Flickr; Music: Jeffrey Cook] Authors: Sarah Crespi; Paul Voosen See omnystudio.com/listener for privacy information.

On its first day, the new Biden administration announced plans to recalculate the social cost of carbon—a way of estimating the economic toll of greenhouse gases. Staff Writer Paul Voosen and host Sarah Crespi discuss why this value is so important and how it will be determined.  Next up, Alison Barker, a postdoctoral researcher at the Max Delbrück Center for Molecular Medicine, talks with Sarah about the sounds of naked mole-rats. You may already know naked mole-rats are pain and cancer resistant—but did you know these eusocial mammals make little chirps to identify themselves as colony members? Can these learned local dialects make naked mole-rats a new research model for language learning? This week’s episode was produced with help from Podigy. Listen to previous podcasts. About the Science Podcast Download a transcript (PDF).

Jonathan Hankins (Bassetti Foundation Foreign Scientific Correspondent) at Berlin Science Week’s Open Science Café, hosted by ORION Open Science and the Max Delbrück Centre for Molecular Medicine. On the road to Berlin, November 4, 2020 Video and synthesis in our site: https://www.fondazionebassetti.org/en/focus/2021/01/orion_open_science_train_the_t.html

Auch bei der Entwicklung von Covid19-Impfstoffen wird mit Tierversuchen gearbeitet. Diese werden in Berlin von der Tierschutzkommission überwacht. In dieser könnten demnächst erstmals mehr Tierschützer als Wissenschaftler sitzen. Warum jene davon nicht begeistert sind, erklärt Thomas Sommer vom Max-Delbrück-Zentrum für molekulare Medizin.

Am Sonntag beginnt die Berlin Science Week, auf der viele Vorträge und Diskussionen aus der Berliner Wissenschaft präsentiert werden. 2020 findet die Science Week nun virtuell statt - so auch die Veranstaltung, die Luiza Bengtsson vom Max-Delbrück-Centrum für molekulare Medizin mitinitiiert hat. "Real oder Fake" heißt die Wissenschafts-Show für kritisches Denken.

Ende Januar 2020 – also noch bevor Corona in unseren Breitengraden zum Thema Nummer eins wurde – veranstaltete die Berlin-Brandenburgischen Akademie der Wissenschaften ein eintägiges Symposium über die unterschiedlichen Verständnisse von Gesundheit. Wir dokumentieren einen Vortrag des Medizinhistorikers und Literaturwissenschaftlers Philip van der Eijk. Einleitend spricht der Gründungsdirektor des Max-Delbrück-Centrums für Molekulare Medizin, Detlev Ganten.

Salvador Luria and Max Delbrück travelled a long road to finally meet each other. Little did they know, their collaboration would change how bacterial genetics was conducted. From attending summer camp for geniuses to gaining "enemy alien" status together, Salvador and Max formed an unlikely yet productive friendship. Join us as we fluctuate with this pair and find out if we're worthy of joining Max's "tiny island" phage cult.  Special guest vocals by Mariela's cat, Masapan.  --- Support this podcast: https://anchor.fm/bunsenburnerpod/support

Um das SARS-CoV-2-Virus wirksam bekämpfen zu können, muss es gründlich erforscht werden – und da gibt es noch viel zu tun. Zum Beispiel am Max-Delbrück-Centrum für Molekulare Medizin in Berlin. Wissenschaftsredakteur Thomas Prinzler hat mit den dortigen Forschern gesprochen.

Baris Tursun ist Molekularbiologe, promoviert an der Columbia University in New York und Foschungsgruppenleiter am Max Delbrück Centrum in Berlin. In unserem Gespräch tauchen wir ein in die Welt der Wissenschaft und der Grundlagenforschung in der Gentechnik. Er erklärt uns seine Sicht auf aktuelle Themen wie den Corona Virus, das Klonen von Lebewesen, Gedanken zum gesunden Altern, die Zukunft der Menschheit und Bewusstsein nach dem Tod. Bitte schreibt uns Kommentare und Anregungen. Viel Spass beim Anhören.

In this Episode of the Epigenetics Podcast our guest Ana Pombo from the Max-Delbrück-Center in Berlin provides insight in her work on the interplay between gene regulation and genome architecture. To do so she and her team use different state of the art methods, including cryo-sectioning to unravel this regulatory network. In 2006, they proposed the Interchromatin Network Model of chromosome organization which postulates that chromosome folding is driven by contacts between different genomic regions and between chromatin and nuclear landmarks, such as the nuclear lamina. And later on they used polymer physics modeling to study those mechanisms, which lead to the development of the Strings & Binders Switch (SBS) model. And this is just a glimpse of the topics that are discussed in this Episode.   References Miguel R. Branco, Ana Pombo (2006) Intermingling of Chromosome Territories in Interphase Suggests Role in Translocations and Transcription-Dependent Associations (PLOS Biology) DOI: 10.1371/journal.pbio.0040138  Robert A. Beagrie, Ana Pombo (2016) Gene activation by metazoan enhancers: Diverse mechanisms stimulate distinct steps of transcription (BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology) DOI: 10.1002/bies.201600032  Emily Brookes, Inês de Santiago, … Ana Pombo (2012) Polycomb Associates Genome-wide with a Specific RNA Polymerase II Variant, and Regulates Metabolic Genes in ESCs (Cell Stem Cell) DOI: 10.1016/j.stem.2011.12.017  Mario Nicodemi, Ana Pombo (2014) Models of chromosome structure (Current Opinion in Cell Biology) DOI: 10.1016/j.ceb.2014.04.004 - Robert A. Beagrie, Antonio Scialdone, … Ana Pombo (2017) Complex multi-enhancer contacts captured by genome architecture mapping (Nature) DOI: 10.1038/nature21411   Contact https://twitter.com/activemotif https://twitter.com/epigenetics_pod https://www.linkedin.com/company-beta/35651/ https://www.facebook.com/ActiveMotifInc/ eurotech@activemotif.com

Bundespressekonferenz, Berlin, 09.04.2019 Saubere Luft ‒ Stickstoffoxide und Feinstaub in der Atemluft: Grundlagen und Empfehlungen mit -Prof. Dr. Martin Lohse, Vize-Präsident der Nationalen Akademie der Wissenschaften Leopoldina & Wissenschaftlicher Vorstand des Max-Delbrück-Centrums für Molekulare Medizin (MDC) -Prof. Dr. Manfred Hennecke, ehemaliger Präsident der Bundesanstalt für Materialforschung und -prüfung (BAM) - Prof. Dr. Jos Lelieveld, Direktor am Max-Planck-Institut für Chemie Bitte unterstützt unsere Arbeit finanziell: Jung IBAN: DE36700222000072410386 BIC: FDDODEMMXXX Verwendungszweck: Jung & Naiv PayPal ► http://www.paypal.me/JungNaiv

Helmut Fink spricht mit Prof. Dr. Ernst Peter Fischer über seinen Weg von der Physik über die Molekularbiologie zur Wissenschaftsvermittlung. Der bekannte Sachbuchautor erzählt davon, wie Einsteins Biografie sein Leben beeinflusste, von der ebenso Publikations- wie Party-reichen Doktorandenzeit bei Nobelpreisträger Max Delbrück und wie es kam, dass er es war, der Delbrücks Biografie schrieb.

In der heutigen Folge beschäftigen wir uns mit den Aminosäuren, jagen wilde Mäuse, benutzen CAR-T-Zellen und stellen euch den Nobelpreisträger Max Delbrück vor.

Dr. Carolyn Lam:               Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center, and Duke National University of Singapore.                                                 In just a moment, we will take a deep dive into the issue of age and its association with outcomes of primary prevention ICDs in patients with non-ischemic systolic heart failure.                                                 Yes, a long-awaited discussion from the Danish trial. That, in just a moment. First, here's your summary of this week's Journal.                                                 The first original paper provides evidence of a true association between disturbed genetic imprinting and Preeclampsia. This paper is from co-first authors, Dr. Zadora, and Dr. Singh, and co-corresponding authors, Dr. Izsvak, from the Max Delbrück Center for Molecular Medicine; Dr. Hurst, from the University of Bath; and Dr. Dechend, from the Experimental and Clinical Research Center of Berlin.                                                 These authors performed an unbiased analysis of genome-wide molecular data on raw characterized patient material, from normal controls, and patients with  Preeclampsia, and identified DLX-5 as an imprinted target gene, with novel placental function in Preeclampsia. Due to loss of imprinting, DLX5 was upregulated in 69% of placentas from Preeclampsia patients. Levels of DLX5 correlated with the classical Preeclampsia markers.                                                 DLX5 was expressed in human, but not in urine trophoblast, underlying the known human specificity of Preeclampsia. Finally, DLX5-induced overexpression if trophoblasts faithfully modeled Preeclampsia in a cell culture system. In summary, this paper shows that disturbed imprinting is common, and may play a causal role in Preeclampsia.                                                 The next study affirms that stenosis severity is better discriminated using coronary invasive physiologic indices, than using coronary angiographic assessment. First author, Dr. Lee, corresponding author Dr. Koo, colleagues of Seoul National University Hospital, studied 115 patients with left anterior descending artery stenosis, who underwent both ammonia positron emission tomography, or PET, an invasive physiologic measurement.                                                 Myocardial blood flow measured using PET, and invasively measured coronary pressures, were used to calculate microvascular resistance, and stenosis resistance. They found that both fractional flow reserve, or FFR, and instantaneous weight free ratio, or IFR, decreased as angiographic stenosis severity, resistance, and pressure gradient increased, and hyperemic myocardial blood flow decreased.                                                 When the presence of myocardial ischemia was defined by both low hyperemic myocardial blood flow, and low coronary flow reserve, the diagnostic accuracy of FFR and IFR did not differ, regardless of cutoff values for hyperemic myocardial blood flow, and CFR. However, at any given stratum of a given stenosis, physiologic classification of stenosis severity using FFR or IFR showed better discrimination of a unique relationship between absolute myocardial blood flow, and pressure gradient, than anatomic classification using angiographic percentage.                                                 In summary, by demonstrating coronary physiologic responses to coronary stenosis, these authors showed that stenosis severity is better discriminated, using invasive physiologic indices, than using angiographic assessment.                                                 The next paper identifies a previously unknown angiogenic growth factor that can be enhanced therapeutically to repair the heart after myocardial infarction. This novel growth factor is endoplasmic reticulum membrane complex, Subunit 10, or EMC10, which the authors previously identified by bioinformatic secretome analysis in bone marrow cells.                                                 In the current paper, from co-first authors Dr. [Rabel 00:04:35], and [Krof Clengobill 00:04:37], and corresponding author Dr. Wollert, from Hanover Medical Center, and colleagues, the authors investigated the angiogenic potential of EMC10, and its mouse homologue, in cultured endo fetal cells and infarcted heart explants. They found that EMC10 and its mouse homologue signal a virus, small GTAPases; p21-activated kinase; and p38 mitogen-activated protein kinase, to promote endothelial cell migration.                                                 In mice with acute myocardial infarction, bone marrow derived monocytes and macrophages produced EMC10 endogenously, to enhance infarct vascularization, tissue repair, and heart function. Furthermore, subcutaneous treatment with recombinant EMC10 for one week, after myocardial infarction, augmented infarct vascularization and repair, and led to a sustained improvement in heart function and survival.                                                 The next study is the first prospective randomized trial of screening for atrial fibrillation, with a smartphone-based, single-lead, electrocardiographic system in 1,001 patients, aged 65 years and above, with a CHA2DS2-VASc score of two and above, and without a history of atrial fibrillation.                                                 In this paper, from first and corresponding author Dr. Halcox, from Swansea University Medical School, in the United Kingdom, and colleagues, patients were randomized, either to biweekly electrocardiographic recordings with the iPhone device, or to routine over a 12-month period.                                                 The smartphone-based electrocardiographic approach was at least three times more likely to identify incident atrial fibrillation, than routine care, and at a cost of just over $10,000 per case identified, and was judged to be a highly acceptable approach in this group of patients. These results support consideration of evaluation in an appropriately-powered, event-driven randomized trial, to confirm the clinical and cost effectiveness of such an approach to stroke prevention in atrial fibrillation.                                                 Well, that wraps it up for your summaries. Now for our feature discussion. The Danish trial really created a huge splash last year, when it was reported that a primary prevention ICD in patients with non-ischemic systolic heart failure, may not actually reduce all cause mortality. Something that we had, perhaps, taken for granted, and in fact, entered our guidelines.                                                 Now, however, there was a pre-specified subgroup analysis at the time, that suggested a possible age-dependent association, between ICD and mortality, in the Danish trial. This week, we are so pleased to be discussing an in-depth analysis of the association between age and outcomes in the Danish trial.                                                 I'm so pleased to have the first author of today's featured paper, Dr. Marie Bayer Elming, of Copenhagen, Denmark, as well as Dr. Sana Al-Khatib, who's not only an associate editor of circulation, but also the author of an accompanying, and she is from Duke, Durham, North Carolina. Welcome, ladies! Dr. Bayer Elming:              Thank you. Happy to be here. Dr. Sana Al-Khatib:          Thank you so much. Dr. Carolyn Lam:               Sana, could you start by framing why this paper is so important, and why we've been looking forward in anticipation to these results? Dr. Sana Al-Khatib:          Absolutely. As you know, data on the outcomes of primary prevention ICDs in patients with non-ischemic cardiomyopathy started emerging in the early 2000s, or so. Then in 2005, the sudden cardiac deaths and heart failure trial was published, that included a large number of patients with non-ischemic cardiomyopathy, and absolutely showed survival benefits from primary prevention ICDs in those patients. Of course, there were also patients with ischemic cardiomyopathy.                                                 But really, that trial formed the basis of the guidelines, recommendations, that have informed our practice for the last 12 years, that basically tell us that we should consider implanting a primary prevention ICD in patients with non-ischemic cardiomyopathy, who have an EF of 35% or less, who have Class II or III heart failure symptoms. As long as they are on optimal care at the end, they have a reasonable life expectancy.                                                 So that's what's we've been doing for years, and then, the Danish trial was published this past year, that really called into question the prior findings, and the current practice. Because Danish, as you stated, showed no survival benefit with primary prevention ICDs, but there are many aspects about the trial that people need to pay attention to, to put the results in perspective.                                                 The fact that 58% of patients in the trial, in those arms, received cardiac resynchronization therapy ... the fact that the trial required that patients have an elevated NTproBMB level, to be considered for enrollment ... that may have biased the results toward a higher risk of non-sudden cardiac deaths, so on, so forth.                                                 I think what was really interesting, and caught people's attention, when the paper was published, was this subgroup analysis that showed that younger patients may benefit more than older patients. I think, many of us, Carolyn, were really awaiting the results of a more dedicated analysis, looking at age in Danish, and Dr. Elming and her colleagues did a great job looking at this very closely in their paper, and showed great results, and probably will let Dr. Elming share those results with us. Dr. Carolyn Lam:               Yes, absolutely, Sana. Actually, I just wanted to echo how surprised everyone was, and the immediate thing was, "Oh, my goodness. What do we do with the guidelines?" Maybe we should get back to that later, and Marie, please share with us, what did you do, and what did you find this time? Dr. Bayer Elming:              The reason why we did this study was that, in this main Danish trial, age was the only one of the 13 pre-specified subgroups that had a significant treatment by a subgroup interaction. This suggested that a younger patient might have a survival benefit from ICD ... the implication, even though the overall study was neutral. So we wanted to further investigate this relationship between age and effective ICD implantation.                                                 What we did was to look at the relation between age and effective ICD, and we found that there was this linear relation, for each year of younger age, that was associated with a reduction, a 3% reduction in the hazard ratio, for the benefit of ICD.                                                 Also, we did this selection impact curve, which is a bit technical, but what it does is to describe the expected survival for the population, on as a whole, for the different age cutoffs for ICD treatments.                                                 So, if we take into account, both the patients receiving an ICD, and those who did not, we could see why we would get the highest survival for the population as a whole. What we found was that, when no one in the population received an ICD, around 70% would survive.                                                 If everyone in the population received an ICD, only 72% would survive, but if we chose 70 years as the age cutoff ... so, patients younger than 70 years received an ICD, and patients older than 70 years did not receive an ICD, we got the highest survival for the population, and 75% would survive. Dr. Carolyn Lam:               Thank you, Marie. What important results. So, maybe, still consider ICDs for primary prevention ... in our non-ischemic systolic heart failure, patients were less than 70 years old. Is it as simple as that, Sana? You wrote a beautiful editorial. Tell us, what are the clinical implications? Dr. Sana Al-Khatib:          This is an important question. Danish was an important trial, but in my mind, it truly doesn't refute the role of primary prevention ICDs in patients with non-ischemic cardiomyopathy. As I mentioned earlier, the majority of patients enrolled in Danish received a CRT device. And so, you end up questioning, what does that actually mean, for those patients who are not eligible for cardiac resynchronization therapy?                                                 So, I actually believed that, and as you know, Carolyn, and maybe Marie knows, as well, there have been several meta analyses that have been published, combining data on patients with non-ischemic cardiomyopathy only, and excluding patients with cardiac resynchronization therapy from Danish, that have actually now shown, consistently, a significant improvement in survival, with a primary prevention ICD ... including one that was done by our group.                                                 So, no, I don't think that, based on the results, we should say, "No, we shouldn't be offering primary prevention ICDs to patients with non-ischemic cardiomyopathy," and this beautiful analysis that was done by Marie and her group actually shows that, at least for those patients who are 70 years of age and younger, I think we should absolutely continue to consider them for the therapy, and offer them the therapy, if they're appropriate candidates.                                                 Then, of course, if the patients are older than 70,, and they meet criteria for cardiac resynchronization therapy, I think it will be important for us to be talking to the patients about ... is the RTD with a defibrillator, versus a CRTP only, with a pacemaker, and talking about the pros and cons, and everything else? But in those patients who are older than 70, who don't meet criteria for CRT, I think more research is needed, to really understand the role of primary prevention ICDs in those patients. We definitely need more data there. Dr. Bayer Elming:              I definitely agree that, of course, for the patients older than 70 years were not candidates for CRT treatment. These patients, we do not know very much about 'em, and this study that we did, do not answer that question. Based on the Danish study, and this further analysis of the age inspection, the guidelines in Denmark also state that patients younger than, we say, 68 years, because that was the age cutoff used in the '08 Danish trial, you should definitely think of giving patients with non-ischemic cardiomyopathy an ICD.                                                 But for the older patients, it depends on a variety of co-factors, such as co-morbidity, or frailty, and it should be an individual assessment of the patient. So, I agree with you, Sana. Dr. Carolyn Lam:               That's wonderful. Hey, just one more question. Sana, I'd like you to put on your AE hat, now, and sort of think with me. In circulation, we don't ... well, we're careful about publishing subgroup analyses, so to speak, right, of results. You articulated, in your editorial, reasons why this, perhaps subgroup analysis, may be different from others. Could you elaborate on that a bit? Dr. Bayer Elming:              Yeah, and absolutely, that's a great question. As you pointed out, I mean, you really ... the conventional wisdom in clinical research is to be careful, interpreting subgroup analyses. I think there are some strengths in this particular analysis, as Marie stated: "Here's what we specified." The other thing is, I believe that Marie and her group then came, and did their very robust statistical methods, and really, probably most importantly, if you look at their findings, they actually really align well, and support their main conclusion.                                                 For example, looking at the fact that older patients had the higher presence of co-morbidities, that they had a higher level of [Co-BMP 00:17:00], they had had a longer duration of heart failure ... I mean, all those things most likely had an impact on their mode of death, really making it more likely for those patients to succumb to non-sudden cardiac death. I think the whole story makes a lot of sense. Dr. Bayer Elming:              If I can elaborate a bit on this, I think one of the important findings from the study is that we show that mode of death varied according to age. So, the rates of sudden cardiac death were almost similar, between the younger and the older part of the population. But the rates of non-sudden death were almost twice as high in the older part of the population. This is a really good explanation why the ICD implantations have less impact in the older patients. Dr. Carolyn Lam:               Yeah, because ICDs would definitely not be expected to reduce non-sudden cardiac deaths. Really, really, well put. Oh, thank you so much, Marie. We're so proud to be publishing your beautiful paper, as well as your editorial, Sana, and thank you for this great conversation.                                                 Well, listeners, I'm sure you enjoyed that as much as I did. Thank you for joining us this week, and don't forget to tune in next week.

Das Max-Delbrück-Centrum für Molekulare Medizin (MDC) betreibt biomedizinische Grundlagenforschung. Hier wird versucht, die Ursachen von Krankheiten auf molekularer Ebene aufzuspüren.