Podcasts about cortical

Today, you'll learn about why you may want to consider letting yourself daydream, how a sense of humor might protect you from depression and anxiety, and the effects of caffeine on the performance of soccer players. Daydream Brain •“What Happens in the Brain While Daydreaming?” by Catherine Caruso. 2023. •“Is the role of sleep in memory consolidation overrated?” by Mohammad Dastgheib, et al. 2022. •“Cortical reactivations predict future sensory responses.” by Nghia D. Nguyen, et al. 2023. •“Why Daydreaming Is Good For Us.” by David B. Feldman Ph.D. 2017. Power of a Laugh •“Your type of humor might say something about your risk of depression and anxiety.” by Eric W. Dolan. 2023. •“Understanding the Association Between Humor and Emotional Distress: The Role of Light and Dark Humor in Predicting Depression, Anxiety, and Stress.” by Alberto Dionigi, et al. 2023. Caffeine & Soccer •“Caffeine highs and lows footballers should be aware of.” n.a. 2023. •“The effects of acute caffeine ingestion on decision-making and pass accuracy in young soccer players: A preliminary randomized controlled trial.” by Negar Jafari, et al. 2023. Hosted on Acast. See acast.com/privacy for more information.

Contact and collision athletes face a higher risk of recurrent anterior shoulder instability after surgical stabilization. The Latarjet procedure is often preferred given the high incidence of bony lesions. However, this stabilizing procedure, performed either open or arthroscopically, is met with concerns regarding complications and revision surgery rates.   In conclusion, the arthroscopic Latarjet procedure with suture button fixation allowed 82% of athletes with recurrent anterior shoulder instability to return to contact or collision sports. Patients with severe humeral bone defects have a higher risk of persistent anterior apprehension and decreased RTS. The arthroscopic-guided procedure with suture button fixation is safe; accurate, with a high rate of anatomic graft positioning and healing; and reliable, with a low recurrence rate.     Click here to read the article.

Join me for a summary looking into the increasingly popular topic of paediatric obstructive sleep apnoea, a review of orthodontic treatments available, and how effective they are in this growing field of both medicine and dentistry. This episode is a summary of Alberto Capriglio's lecture from the AAO and Carlos Flores Mir's lecture at the IOF earlier this year.     OSA - Defined upper airway dysfunction causing complete or partial airway obstruction during sleep   Sleep = Slow wave sleep – constructive phase of sleep (recuperation of the mind) ·      Growth hormones secreted ·      Glial cells within brain restored ·      Cortical synapses increase in number – Moberget 2019   Outcomes to paediatric patients of SDB: (AASM) ·      delays in development,  Poor academic performance, Aggressive behaviour, attention- deficit/hyperactivity disorder, , emotional problems in adolescence   First line medical treatment – adenotonsillectomy  ·      40% residual  OSA       Effect palatal expansion 1.        Roof the mouth = base of the nose - Increase in nasal airway volume - Reduction in OSA, if obstruction in naso-pharynx, 2.        Short term reduction in OSA (not cure AASM) a.        20% improvement in AHI, 85% of cases Villa 2015 b.        15% got worse by 20% c.        57.5% residual AHI greater than 1 - not resolution 3.        Caprioglio 2019 long term AHI return to initial scores, from 7 to 5 long term 4.        Change in metabolism when combined with Vit D3 a.        Vit D3 with RME increases reduction in AHI, sustained long term, Caprioglio 2019 AHI 61.9% Vs 35.5% long term     Expansion other outcomes -  school performance  Bariani 2024 ·      AJODO – RME improves academic performance – o   BEHAVOUR 1 of 8 parameters improved only for academic performance  - change small 0.68 o   COGNITIVE 1 in 8 improve       Mandibular advancement Move mandible forwards and open space behind the tongue – oropharynx ·      Anatomical – increase size of oropharangeal airway ·      YAnyAn 2019 mandibular advancement for pOSA systematic review:  1.75 AHI reduction (CI) −2.07, −1.44) – modest change ·      However long term use required of the paediatric patient     Orofacial features in children with obstructive sleep apnea.  Fagundes Flores-Mir 2022 o   No craniofacial features specific to pOSA – ANB, o   However medical diagnosis through polysomnography may under-estimate incidence, o   Broader diagnosis such as snoring, may over-estimate OSA   AADSM 2024 – consensus statement ·      Expansion o   Prevention: No consensus o   Management: No consensus o   Cure: Insufficient ·      Mandibular advancement o   Prevention, management, cure – unclear   More about OSA? To hear more about OSA, please check out the last interview on orthodontics in interview with Sanjivan Kandasamy, where we had a deep dive into OSA and where we are in our understanding today from the research Interview with Sanjivan Kandasamy on OSA                          

Fiser's work taught me how to think about grounding computational models in biologically plausible implementations.

In this episode, we're exploring the various ways stress affects your brain, both positively and negatively.We'll discuss the key differences between eustress (the beneficial kind) and distress (the harmful kind), and reveal practical strategies to manage chronic stress for better cognitive health.Whether you're dealing with daily pressures or long-term stress, this episode will arm you with knowledge to protect your brain and help you build resilience.What to Listen For:The key differences between eustress (positive stress) and distress (chronic stress).How chronic stress leads to memory loss, emotional difficulties, and increased Alzheimer's risk.The role of cortisol and the HPA axis in stress responses and brain health.How eustress boosts cognitive function, memory, and neuroplasticity.The dangers of prolonged cortisol exposure on brain structures like the hippocampus and amygdala.A study from Frontiers in Behavioral Neuroscience showing how moderate stress improves learning and memory.How chronic stress can trigger brain inflammation and accelerate cognitive decline.Practical strategies for reducing chronic stress: mindfulness meditation, social connections, and reframing stress as a positive force.The effects of chronic stress on the amygdala, prefrontal cortex, and hippocampus.Three actionable tips to protect your brain from the long-term effects of stress.Research Studies Referenced:McEwen BS (2007). "Physiology and neurobiology of stress and adaptation: central role of the brain." Physiol Rev, 87(3), 873-904. This paper explores how stress affects brain function and structure.Lupien SJ, et al. (2009). "Effects of stress throughout the lifespan on the brain, behaviour and cognition." Nat Rev Neurosci, 10(6), 434-445.Sousa N, et al. (2016). "Cortical and hippocampal circuitry changes under chronic stress: Implications for mood and cognition." Prog Neuropsychopharmacol Biol Psychiatry, 67, 1-14.Wilson, R. S., et al. (2007). "Chronic distress and incidence of mild cognitive impairment." JAMA Psychiatry, 68(2), 211-218Tang YY, et al. (2015). "The neuroscience of mindfulness meditation." Nat Rev Neurosci, 16(4), 213-225.RESOURCES: Access the FREE Masterclass: How To Optimize Your Sleep Order Amy's book Thoughts Are Habits Too: Master Your Triggers, Free Yourself From Diet Culture, and Rediscover Joyful Eating. Join our private Facebook group: Moxie Club Meetup Follow Amy on Instagram @habitwhisperer

Rachel Bennett travelled a path that many mothers with a child with Cortical/cerebral Visual Impairment (CVI) encountered. The diagnosis was a long time coming and when it was discovered new world opened up for her son, Henry. Now Rachel helps to support and advocate for other families like hers through CVI Now at the Perkins School for the Blind. Listen as Dr. Cathy encourages Rachel to tell her story as the first episode of Season Four on Feeling This Life.     Want to learn more about CVI Now and their resources?   CVI Now Website: CVINow.org  CVI Now on Instagram: @cvinow   Subscribe to the monthly CVI Now newsletter    Please give us your feedback using this survey link: ⁠https://educationutah.co1.qualtrics.com/jfe/form/SV_39OmBvMih6MlgNw⁠   Make a Donation to-   VIPS: ⁠https://secure.vips.org/np/clients/vips/donation.jsp?forwardedFromSecureDomain=1&campaign=495⁠   Anchor Center: ⁠https://www.anchorcenter.org/get-involved/donate/⁠     Get in touch with us!   Follow us on Facebook @Feelingthislifepodcast and Instagram @Feelingthislife   Email: ⁠feelingthislife@vips.org⁠   ⁠www.anchorcenter.org⁠   ⁠www.vips.org 

Radiology read to you! Frank reads Radiopaedia's focal cortical dysplasia article and does a little link surfing at the same time. Plus, Olympics closing ceremony, Tom Cruise, Snoop Dogg, Frank Steps Down, new Epileptogenic Brain Tumours Course and a chat about buzzwords.   Radiopaedia's FCD article  ► https://radiopaedia.org/articles/focal-cortical-dysplasia Epileptogenic Brain Tumour Course ► https://radiopaedia.org/courses/epileptogenic-brain-tumours-learning-pathway Radiopaedia 2024 Census ► https://bit.ly/r-census2024   Richard Feynamn on names ► https://www.youtube.com/watch?v=lFIYKmos3-s Radiopaedia Community chat ► http://radiopaedia.org/chat Become a supporter ► https://radiopaedia.org/supporters Get an All-Access Pass ► https://radiopaedia.org/courses/all-access-course-pass Andrew's X ► https://twitter.com/drandrewdixon Frank's X ► https://twitter.com/frankgaillard Ideas and Feedback ► podcast@radiopaedia.org   The Reading Room is a radiology podcast intended primarily for radiologists, radiology registrars and residents. 

How can we help people with prosthetic legs walk more easily and with less effort? In this episode of Neurocareers: Doing the Impossible!, we explore this question with Giacomo Valle, PhD, a leading researcher in the field of biomimetic brain-computer interfaces (BCIs) and bionic legs. Dr. Valle and his colleagues at ETH Zürich have developed an innovative biomimetic BCI that uses peripheral nerve stimulation to convey naturalistic touch sensations in bionic legs. This groundbreaking work has earned them a spot as one of the 12 finalists for the BCI Award 2023. Dr. Valle's research focuses on creating artificial communication with the brain through peripheral nerve stimulation, providing a more intuitive and natural sensory experience. His team developed a biomimetic neurostimulation framework inspired by nature, capable of "writing" physiologically plausible information back into the peripheral nervous system. Using an in-silico model of mechanoreceptors, they created biomimetic stimulation policies, which were tested alongside mechanical touch and common linear neuromodulations. In clinical trials, these techniques have shown significant improvements in mobility and reduced mental effort compared to traditional approaches. The neural responses produced by this innovative approach resemble those naturally induced, marking a significant advancement in assistive neurotechnologies. Dr. Valle's project, "Biomimetic BCI Conveys Naturalistic Touch Sensations via Peripheral Nerve Stimulation for Bionic Legs," represents a major leap forward in neuroengineering and bionics. With an educational background that includes a B.S. in Biomedical Engineering and an M.S. in Bioengineering from the University of Genoa, and a Ph.D. in Biorobotics from the Scuola Superiore Sant'Anna, Dr. Valle has extensive experience in this field. His career journey includes research positions at the École Polytechnique Fédérale de Lausanne and ETH Zurich, where he contributed to significant innovations in neuroprosthetics. As a co-founder of the medtech startup MYNERVA and now a Tenure-track Assistant Professor in Bionics at Chalmers University of Technology in Sweden, Dr. Valle's research focuses on neuroengineering and computational models aimed at restoring sensory feedback and understanding somatosensory processing and neural control of movements. Join us as Dr. Valle shares insights into his research, discusses his career path, and offers valuable advice for a successful BCI Award submission. Whether you're interested in the latest advancements in neuroengineering or seeking inspiration for your own scientific endeavors, this episode is packed with fascinating insights and expert guidance. About the Podcast Guest: Dr. Giacomo Valle holds  a position as an Assistant Professor in Bionics, Head of the Neural Bionics Laboratory at the Department of Electrical Engineering  | Life Bionics Chalmers University of Technology in Hörsalsvägen 11, SE - 412 96, Gothenburg, Sweden Sahlgrenska Universitetssjukhuset R-huset, plan 7, Länsmansgatan 28, 431 80 Mölndal Other Dr. Valle's affiliations: Cortical Bionics Research Group, USA: https://www.corticalbionics.com/ Co-founder MYNERVA  Wyss Zurich Translational Center | ETH Zurich, Weinbergstrasse 35, WEH 8092 Zurich Switzerland Contact Information: E-mail: valleg@chalmers.se  @NeuralBionicsLab socials: LinkedIn, X.   Open Positions: The Neural Bionics Lab (PI: Giacomo Valle) has available projects (6-12 months) starting this fall and next spring on: - Bidirectional neuroprosthetics - Implantable Brain-Computer Interfaces - Somatosensation & Touch - Neural stimulation for sensory restoration - Cortical & peripheral interfacing - Mechatronics for neurotechnology - Human neurophysiology Please contact us here or at valleg@chalmers.se sending your CV, transcript of records (Bachelor and Master) and motivation letter. Info about the projects on https://sirop.org/app/ Our projects are done in collaboration with Biological Sciences Division at the University of Chicago, CBRG, University of Zurich and MYNERVA. hashtag About the Podcast Host: The Neurocareers podcast is brought to you by The Institute of Neuroapproaches (https://www.neuroapproaches.org/) and its founder, Milena Korostenskaja, Ph.D. (Dr. K), a neuroscience educator, research consultant, and career coach for people in neuroscience and neurotechnologies. As a professional coach with a background in the field, Dr. K understands the unique challenges and opportunities job applicants face in this field and can provide personalized coaching and support to help you succeed. Here's what you'll get with one-on-one coaching sessions from Dr. K: Identification and pursuit of career goals Guidance on job search strategies, resume, and cover letter development Neurotech / neuroscience job interview preparation and practice Networking strategies to connect with professionals in the field of neuroscience and neurotechnologies Ongoing support and guidance to help you stay on track and achieve your goals You can always schedule a free neurocareer consultation/coaching session with Dr. K at https://neuroapproaches.as.me/free-neurocareer-consultation Subscribe to our Nerocareers Newsletter to stay on top of all our cool neurocareers news at updates https://www.neuroapproaches.org/neurocareers-news

In this episode, we delve into the impact of the new groundbreaking research uncovering the RNU4-2 genetic variant linked to neurodevelopmental conditions. The discovery, made possible through whole genome sequencing, highlights a genetic change in the RNU4-2 gene that affects about 1 in 200 undiagnosed children with neurodevelopmental conditions, making it more prevalent than previously thought. This discovery represents one of the most common single-gene genetic causes of such conditions. Our host, Naimah Callachand, Head of Product Engagement and Growth at Genomics England, is joined by Lindsay Pearse who shares her journey through the diagnosis of her son Lars. They are also joined by Sarah Wynn, CEO of Unique, and Emma Baple, Clinical Genetics Doctor and Professor of Genomic Medicine in the University of Exeter and the Medical Director of the Southwest NHS Genomic Laboratory Hub. We also hear from the 2 research groups who independently discovered the findings: Dr Andrew Mumford, Professor of Haematology at the University of Bristol Link to the research paper: https://www.nature.com/articles/s41591-024-03085-5  Assistant Professor Nicky Whiffin, Big Data Institute and Centre for Human Genetics at the University of Oxford Link to the research paper: https://www.nature.com/articles/s41586-024-07773-7 To access resources mentioned in this podcast:  Unique provides support, information and networking to families affected by rare chromosome and gene disorders - for more information and support please visit the website. Connect with other parents of children carrying a variation in RNU4-2 on the Facebook group.   "I think one of the things we really hope will come out of diagnoses like this is that we will then be able to build up more of that picture about how families are affected. So, that we can give families more information about not only how their child is affected but how they might be affected in the future."   You can read the transcript below or download it here: https://www.genomicsengland.co.uk/assets/documents/Podcast-transcripts/How-has-a-groundbreaking-genomic-discovery-impacted-thousands-worldwide.docx  Naimah: Welcome to Behind the Genes. Lindsay: So, this feeling that like we've been on this deserted island for eight years and now all of a sudden, you're sort of looking around through the branches of the trees. It's like, wait a minute, there are other people on this island and in this case actually there's a lot more people on this island. Yeah, it's very exciting, it's validating. It gives us a lot of hope and, you know, it has been quite emotional too and also a bit of an identity shift. Being undiagnosed had become quite a big part of our identity, and so now that's kind of shifting a little bit that we have this new diagnosis and are part of a new community. Naimah: My name is Naimah Callachand and I'm Head of Product Engagement and Growth at Genomics England. On today's episode, I'm joined by Lindsay Pearse whose son Lars recently received a genetic diagnosis, made possible by research using data from the National Genomic Research Library, Sarah Wynn CEO of Unique, and Emma Baple, a clinical genetics doctor. Today we'll be discussing the impact of recent research findings which have found a genetic change in the non-coding RNU4-2 gene, to be linked to neurodevelopmental conditions. If you enjoy today's episode, we'd love your support. Please like, share and rate us on wherever you listen to your podcasts. Naimah: And first of all, I would like everyone to introduce themselves. So, Lindsay, maybe if we could come to you first. Lindsay: Great, thank you. So, thank you for having me. I'm Lindsay Pearse, I live outside of Washington DC and I'm a mum to 3 boys. My oldest son Lars who is 8, he was recently diagnosed with the de novo variant in the RNU4-2 gene. Naimah: Thank you. And Emma? Emma: My name is Emma Baple. I'm a Clinical Genetics Doctor which means I look after children and adults with genetic conditions. I'm also a Professor of Genomic Medicine in the University of Exeter and the Medical Director of the Southwest NHS Genomic Laboratory Hub. Naimah: And Sarah? Sarah: Hi, thank you for having me. I'm Sarah Wynn, I'm the CEO of a patient organisation called Unique, and we provide support and information to all those affected by rare genetic conditions. Naimah: Great, thank you. It's so great to have you all here today. So, first of all Lindsay, I wonder if we could come to you. So, you mentioned in your introduction your son Lars has recently been diagnosed with the de novo variant. I wondered if you could tell us a bit about your story, and what it's been like up until the diagnosis. Lindsay: Sure, yeah. So, Lars is, he's a wonderful 8 year-old boy. With his condition, his main symptoms he experiences global developmental delays, he's non-verbal. He's had hypertonia pretty much since birth and wears AFO's to support his walking. He has a feeding disorder and is fed by a G-Tube. Cortical vision impairments, a history of seizures and slow growth, amongst other things. So, that's just a bit of a picture of what he deals with day to day. But he's my oldest child, so first baby. When I was pregnant, we were given an IUGR diagnosis. He was breech, he had a hernia soon after birth, wouldn't breastfeed. But all of these things aren't terribly uncommon, you know. But once he was about 3 or 4 months old, we noticed that he wasn't really able to push up like he should, and we were put in touch with early intervention services for an assessment. So, we went ahead and did that when he was about 4 or 5 months old. And as parents, we could just kind of tell that something was off from the assessors. And, you know, they were very gentle with us, but we could just get that sense that okay, something is off, and they're worried here. So, that kind of kickstarted me into making appointments left, right and centre with specialists. The first specialist that we saw was a neurologist. And yeah, again, that's another appointment that I'll never forget. She referred us to genetics and to get an MRI and some lab work but at the end of the appointment, she said to us, ‘Just remember to love your child.' And, you know, that was quite shocking to us at the time because it wasn't something that had ever crossed our mind that we wouldn't do or felt like we needed to be told to do this. But on the other hand, it certainly set off a lot of worry and anxiety of okay, well, what exactly are we dealing with here? So, fast forward, we saw genetics and that was about when Lars was about 8 months old. We went through a variety of genetic testing, a chromosomal micro-array, a single gene testing, then the whole exome testing. Everything came back negative, but it was explained to us that what was going on was likely an overarching genetic diagnosis that would explain his like, multi-system symptoms. And so meanwhile as he was getting older his global delays were becoming more pronounced and we were also in and out of the hospital a lot at this time. At first, he was in day care and, you know, any sort of cold virus would always turn into like a pneumonia for him. So, we were just in and out of hospital seeing a myriad of specialists, trying to put together this puzzle of what's going on and it was really hard to accept that nobody could figure it out. That was just, you know, sort of mind-blowing to us I guess. So, we applied for and were accepted into the Undiagnosed Diseases Programme at the National Institute of Health over here. The NIH as it's commonly referred to. So, we first went there when Lars was 2. He was one of their youngest patients at the time. But that was a really great experience for us because we felt like they were looking at him holistically and across a bunch of all of his systems, and not just seeing a specialist for sort of each system. So, we really appreciated that. We also did the whole genome sequencing through this research study. Although that also came back negative and so at that point, we were told to kind of keep following up symptomatically. Keep seeing the specialists and eventually maybe one day we'll find an overarching diagnosis, but that science just hadn't quite caught up to Lars. It was hard for me again to believe that and to sort of wrap my head around that. But certainly, it was an education from all of the doctors and geneticists and everyone we saw at NIH, to realise like how far there still was to go in terms of genetic research. How it wasn't also that uncommon to be undiagnosed in the rare disease community. I would say that being undiagnosed sort of became part of our identity. And it's, you know, it was something that, you know, you had to explain to like insurance companies and to his school, and it became part of our advocacy around him. Because without being able to say oh, it's this specific thing and if it was someone who hadn't met Lars before, trying to explain to them that, you know, yeah, within the range of this community you can be undiagnosed, and they just haven't found it yet, but I promise you there is something going on here. And I'd say the other thing too without a diagnosis you have no prognosis, right? And so, trying to figure out what the future would look like. Also, family planning. We waited 5 and a half years before we had another child and, you know, it was certainly an anxiety ridden decision. Ultimately after seeing as many specialists as we possibly could, we still were left with the same answer of well, we just don't really know if it will happen again. So, that was a big decision to make. But again, it just kind of became part of our identity and something that you did eventually accept. But I would say in my experience I feel like the acceptance part also of Lars' disabilities perhaps took me a little bit longer. Because again, I didn't have a prognosis, so I didn't exactly know what we were dealing with. Only as he has become older and, you know, you're sort of getting a better sense of what his abilities might be than being able to understand, okay, this is what I'm dealing with. I need to accept that and do what I can to care for him and our family in the best way that we can. Naimah: Thanks so much for sharing that, Lindsay. I feel like you've touched on a lot of really, you know, a lot of complications and difficulties for your family. Especially, you know, with regards to keeping hopeful and things about the prognosis as well, I'm sure it was really difficult. You've mentioned that Lars was able to be diagnosed recently due to recent research efforts. So, Sarah, I wonder if you can tell us a bit more about these and what the findings have meant for patients with neurodevelopmental conditions. Sarah: Yes. So, I think we know that there are lots of families that are in Lindsay and Lars' position where they know that there is almost certainly an underlying genetic condition, and it just hasn't been found yet. And so, I think we know that lots of researchers are working really hard to try and find those causes. I think over time we know that as time goes on and research goes on, we'll find more of these new genetic causes for neurodevelopmental conditions. I think particularly as we start to look at regions of the genome that we haven't looked at so much so far. But I think one of the things that's really extraordinary about this one is that actually it turns out to be much more common than we might have expected, for one of these new conditions that we haven't found before. But I think it's about one in 200 of those undiagnosed children with neurodevelopmental conditions, have this diagnosis so that's not a small number. That's not a rare finding at all actually, that's much more common than we could ever have anticipated. But I think one of the things that we do know is that as we look further and deeper into that genomic sequence, so, we've started off looking at the bits of the sequence that are genes that code for proteins. This changes in a gene that actually doesn't code for protein, so it's less obvious that it would be important but clearly it is important in development because we know when it has a spelling mistake in it, it causes this neurodevelopmental condition. But there will be as researchers look more and more at these kinds of genes, and also the other part of the genome that is not genes at all, we'll find out more and more the underlying genetic causes of these neurodevelopmental conditions. I think it's also really important to stress why this is so important to find these genetic changes and it's because families really need a diagnosis. Lindsay talked quite eloquently and a lot about that knowing something was off and really wanting to know the reason why. Getting these diagnoses might change care management or treatment, but actually really importantly it just gives an answer to families who have often been looking for an answer for a really long time. Naimah: I just wanted to go back to the point that Sarah made that actually this genetic change is relatively common. Emma, I wondered if you could tell us a bit more about maybe why it took us so long to discover it? Emma: That's an interesting question actually. I suppose the sort of slightly simplified answer to that question is we haven't been able to sequence the whole of a person's genetic information for that long. And so, children like Lars would have had, as Lindsay described lots and lots of genetic tests up until they had a whole genome sequencing which is what Sarah was talking about. The types of tests that we had up until the whole genome sequencing wouldn't have allowed us to look at that bit of the genetic code where this RNU4-2 gene can be found. So, we can only really find that using whole genome sequencing. So, before that existed, we wouldn't have been able to find this cause of developmental condition. Naimah: Okay, thanks Emma. Naimah: Now we're going to hear from one of the two research groups who are responsible for these research findings. First of all, let's hear from Nicky Whiffin. (Clip - Nicky Whiffin) Naimah: How were the findings possible using the Genomics England dataset? Nicky: So, most previous studies have only looked at genetic variants that, in genes that make proteins, but only a subset of our genes actually do makes proteins. The Genomics England dataset we have sequencing information on the entire genome, not just on these protein coding genes and that means we can also look at variants in other genes. So, those that make molecules other than proteins. And RNU4-2 for example, makes an RNA molecule. Naimah: These findings translated to direct patient benefit for patients like Lars who were able to receive support from Unique. How does this demonstrate the value of the dataset? Nicky: Yes. So, it was incredible that we could find so many patients with RNU4-2 variants so quickly. This was enabled by access to Genomics England data but also to other large sequencing datasets around the world. So, we worked with people in the US, in Australia and also in mainland Europe. These large datasets enabled us to spot consistent patterns in the data and by looking across multiple datasets we can also make sure that our findings are robust. When we realised how significant this was and how many families would be impacted, we very quickly contacted Sarah at Unique to see if we could direct patients to them for support. (End of clip) Emma: There's one thing I wanted to raise. It's important to recognise the way that was discovered was through the National Genomic Research Library that Genomics England hosts. To highlight the value of that, and the value of having this centralised resource where families have been kind enough really to allow their data to be shared with some limited clinical information that allowed these researchers to be able to pull this out. And I think it highlights the power of the National Health Service in that we were able to create such a resource. It's really quite astounding that we've found such a common cause of a rare genetic condition, and it wouldn't have happened in the same timescale or in this way without that resource. And then to just say that as Sarah talked about the fact that we've been able to get that information out there, also the researchers were able to get out there and contact the NIH and all of these other programmes worldwide. In Australia, America, everywhere in the world and quickly identify new patients who had this condition and get those diagnoses out really rapidly to people. But all that came from that power of sharing data and being able to have that all in one place and making it accessible to very clever people who could do this work and find these answers. It's so important for families like Lindsay's, and all the families in England and around the world that have got these answers. So, I guess it's a big plug for the value of data sharing and having a secure place where people feel that it's trusted and safe, that enables these diagnoses to be made. Lindsay: If I could just echo that, we're so grateful that that exists in the UK. Just acknowledging like the privilege here that we have had to be able to, I mean for our family in the US, that we've been able to, you know, get ourselves into the NIH study and into the study at Children's National. That takes a lot of work. I feel like not everybody has that opportunity to be able to spend the time to do these applications and to go to all the appointments and get the testing done and have the insurance to cover it. So, very grateful that the system exists in a way in the UK that made this sort of research possible. I just hope that that can be replicated in other places, and also to what Emma was saying earlier, come up with a lower cost test as well for this to further the growth of the community and of course then the corresponding research. Sarah: I think firstly we have to sort of thank all of those families that took part and do share their data, because I think it's not always clear why you might want to do that as a family. I think this is really a powerful example of the benefit of that. I also think the data sharing goes one stage further. So, it's partly about getting the diagnosis, but the data sharing going forward about how this condition impacts families, both clinically and sort of day to day lived experience, is how we'll be able to learn more about these conditions. And so, when families get this diagnosis next week or next year, not only will they get a diagnosis, but they'll get a really good idea about what the condition is and how it might impact their child. Naimah: And Lindsay, coming back to you. So, we've talked about, you know, what it meant for your family before the diagnosis, but what has it meant to have a diagnosis and how did you feel? And what happened whenever you received the diagnosis? Lindsay: Sure. Lars was again part of the NIH Undiagnosed Diseases Research study. So, once you attend this programme and if you are not diagnosed like at the end of your stay, they keep your details on file and you're part of this database at the NIH Undiagnosed Diseases Programme. So, if you're undiagnosed after your sort of week-long work up, your samples stay within the research programme. We were also part of a research programme at Children's National Medical Centre, the Rare Disease Institute. So, our samples were sort of on file there in their database as well. And so, at the end of March I was really quite shocked to receive a call from our long time and trusted geneticist at Children's National that they had found a diagnosis. It was quite emotional. I really kind of didn't believe it. I just kept asking, you know, ‘Are you sure? Is this it?' you know, ‘How confident are we?' Because I think in my head, I sort of always thought that we would eventually find a diagnosis, but I thought that Lars would be, you know, a 30- or 40-year-old adult. I thought it would be decades from now. Like I felt like for whatever reason we had to wait decades for the science to sort of catch up to him. So, we were very, very grateful. It felt very validating, I guess. I had always kind of had this intuition feeling that we were sort of missing something and it's more that the science just hadn't quite caught up yet. But, you know, it was validating to know that okay, Lars is not the only person in the entire world with this, it is something that is relatively common in fact within the rare disease community. That is also very exciting to me personally because I'm hopeful that that will lead more researchers to be interesting in this, given how, quote on quote, common it is. I've sort of been describing it as like a mass diagnosis event but also more so this feeling that like we've been on this deserted island for eight years and now all of a sudden, you're sort of like looking around through the branches of the trees. It's like, wait a minute, there are other people on this island ad in this case, there's actually a lot more people on this island. Yeah, it's very exciting, it's validating. It gives us a lot of hope. And, you know, it has been quite emotional too and also a bit of an identity shift. Because I spoke earlier about how like being undiagnosed had become quite a big part of our identity. So, now that's kind of shifting a little bit that we have this new diagnosis and are part of a new community. But yeah, we're just very grateful that the research had continued. And, you know, I think sometimes you sort of have this feeling of okay, our files are up on a shelf somewhere, you know, collecting dust and are people really looking at them? And actually, it turns out that the research was ongoing and yeah, we're just very grateful for that. Naimah: Thanks so much for sharing, Lindsay. It sounds like it's been a real rollercoaster of emotions for your family and I'm glad to hear that, you know, you've got some hope now that you've got a diagnosis as well. So, moving onto the next question. Emma, I wanted to ask you then, how will these findings improve clinical diagnostic services for those for neurodevelopmental conditions? Emma: So, you asked me earlier about why it had taken so long to find this particular cause of neurodevelopmental condition, and I gave you a relatively simple answer. The reality is one of the other reasons is that almost eight out of ten children and adults who have RNU4-2 related neurodevelopmental condition have exactly the same single letter spelling change in that gene. So, actually that in itself means that when researchers are looking at that information, they might think that it's actually a mistake. Because we know that when we sequence genetic information, we can see mistakes in that sequencing information that are just because the machine has, and the way that we process that data, it's not perfect. So, sometimes we find these little mistakes and they're not actually the cause of a person's problems, they're just what we call an artefact or an issue with the way that that happens. So, that is part of the reason for why it was tricky for us to know whether this was, or rather the researchers to know whether this was or was not the cause of this particular condition. But that in itself is quite helpful when we think about how we might identify more people who have this going forwards. Because unlike in Lars' case where we didn't know what the cause was and so we were still searching, and we didn't know where to look in the billions of letters that make up the genetic code to find that answer, we now know that this is really very common. It's unbelievably common. I think we didn't think we would be finding a cause of a rare genetic condition that was this commonly occurring at this stage. But the fact that it's just a single, it's commonly this one single change in the gene means that we can set up pretty cheap diagnostic testing. Which means that if you were somewhere where you wouldn't necessarily have access to whole genome sequencing, or a more comprehensive testing in that way, we could still be able to pick up this condition. And it's common enough that even if you didn't necessarily recognise that a person had it, you could still have this as part of your diagnostic tool kit for patients who have a neurodevelopmental condition. It's common enough that just doing a very simple test that could be done in any diagnostic lab anywhere in the world, you would be able to identify the majority of people who have this. Naimah: Now let's hear from the other research group who are responsible for these findings. Here is Dr Andrew Mumford. (Clip - Dr Andrew Mumford) Naimah: Why are these research findings significant? Andrew: It offers genetic diagnosis not just for a handful of families but potentially for many hundreds of families, who we all know have been searching often for many, many years for a genetic diagnosis. But actually, there are other gains from understanding how this gene causes neurodevelopmental disorder. We know that there's GRNU4-2 in codes, not a protein actually, but a small nuclear RNA which is unusual for rare, inherited disorders. It's a component of a very complicated molecule called the spliceosome which in turn regulates how thousands of other genes are regulated, how they're made into proteins. So, fundamentally this discovery tells us a lot about the biology of how the spliceosome works. We already know that some other components of the spliceosome can go wrong, and result in diseases like neurodevelopmental disorders. This gives us an extra insight and actually opens the door to, I hope, a whole load of more discoveries of genetic diagnosis possible from other components of this complicated molecule. Naimah: Your research group used a mathematical modelling approach. Can you tell me a bit about this, and what this means for other rare conditions, Andrew? Andrew: So, identifying relationships between changes in individual genes and different kinds of rare, inherited disease is notoriously difficult because of the volume of data that's involved and the need to be absolutely certain that observed genetic changes are actually the cause of different rare, inherited disease. So, applying statistics to that kind of problem isn't new. But what my collaboration group have achieved here, is to develop, actually developed some years ago a completely new approach to applying statistics to genetic data. We call that BeviMed and we've been working for many years on the genes in code that make individual proteins. Most rare disorders are caused by genetic changes in genes that make proteins. What this discovery comes from is actually we've applied the BeviMed statistical technique to genes that don't make proteins, they're non-coding genes. For example, genes that make small nuclear RNA, it's just like RNU4-2. What's unusual about the BeviMed approach is that it's very sensitive to detecting links between genetic changes and rare diseases, and it can detect statistical associations really driven by very, very small numbers of families. So, we apply it to datasets like the 100,00 Genomes dataset and identify associations using statistics that have got a very high probability of association. Other members of the team then seek to corroborate that finding by looking at if we can see the association in other datasets, and we certainly achieve that with RNU4-2. But also, assessing biological plausibility by investigating what we understand already about in this case, a small nuclear RNA, and how it can possibly result in a disease. And we normally try and employ other independent evidence such as experimental investigation. Or going back to our families and asking for additional data to help really test this sort of theory that changes in this particular gene have resulted in a problem with neurodevelopment. (End of clip) Naimah: Emma, are there any other ways that we can identify these conditions based on their clinical presentation? Emma: So, Lindsay and I were talking with you just yesterday, wasn't it? And I asked Lindsay about what sorts of things Lars had in common with other children and adults who have been diagnosed with this condition? I actually think Lindsay probably gives a better summary than I would, so I might ask you to maybe repeat what you said to me yesterday. But the bit of it that really stood out to me was when you said to us that a lot of parents have said, ‘I'm not sure how we weren't all put together in the first place because you notice so many things that were in common.' So, maybe if you can give that summary and then I can translate that back into medical terms, if that's okay Lindsay. Lindsay: Sure, of course. Yeah, it been again, kind of mind blowing, some of the similarities. Especially as we've exchanged pictures and such, and baby pictures especially where some of the children like look like siblings. So, definitely some similarities in facial features, you know, everyone seems to experience some of the slow growth, so a short stature or quite skinny. There's feeding issues also that seem to be quite common. Also, you know, things like the global developmental delays, that's certainly across the board and histories of seizures, that's also quite common. Some people have experienced also some, like, bone density issues, that's not something that we've experienced so far, but that also seems to be quite common. But then also, behaviourally, there's a lot of similarities which has been, I think, quite exciting to a lot of us because you've always thought okay, so this is just my child. And of course, some of that is true but it's also interesting to find out some of these other things that are, you know, are quite similar. So, a lot of people have mentioned their child having, like, an interesting sense of humour. Kind of like a very slapstick sense of humour which is quite interesting. Or everyone seems to love water, everybody loves swimming pools and bathtime, and all of that. Lars loves a windy day. Something about the wind, he just loves it and plane noises and things like that have also come up with other people. So, yeah, it's been really interesting and cool to see. Emma: So, I guess Lindsay's sort of very beautifully summed up what is written in the research publication. So, there's only two research publications so far on this condition, it's all really new. And I am definitely not claim to be a clinical expert on this condition, and I don't think there are any yet. It will take people time to see lots of children and adults who have this particular condition. But ultimately what Lindsay summarised was the common clinical features that have been described by parents. In my job as a clinical genetics doctor, part of what we look at is a person's appearance. So, Lindsay described the photographs of children particularly when they were little, looked very similar. In the photographs that I've seen, I would agree with that. And so obviously those children look like their mum and dad, but they have other features that are in common. They have a characteristic appearance and that helps doctors like me to have an idea as to whether a child or an adult might have a particular condition. Then put together with the sorts of information that Lindsay gave us around the low tone, so being a little bit floppier particularly when they're little. The slow growth and growth problems, problems with eating, also with seizures. Those are all common things that were pulled out of both of the two research publications on this condition and putting that all together into one picture helps doctors to have an idea whether somebody may have a particular condition. That would help us in this case to potentially request that simple test I was talking about, if maybe we were practicing in a part of the world where we wouldn't have the resources that we thankfully do have in the United Kingdom, and in the USA. Naimah: So, Sarah, just coming to you next. How does this research spread awareness and help other patients with these conditions? Sarah: So, I think one of the things that's been really great about research now is that we are able to, you know, social media and things like that mean that we can spread this information really quickly across the world basically. I think what that does is that as well as helping bring people together that they've got this diagnosis, what it does is I think it provides hope for all of those people that Lindsay was talking about at the beginning who don't have a diagnosis. So, that piece around people are still looking, the researchers are working hard and that even if you don't have a diagnosis today you might get one in the future. Lindsay talked about your sample being dusty and not being looked at. I think it gives lots of families, not just those that get this diagnosis but all of those that haven't got a diagnosis, hope, that hopefully in the future they will get a diagnosis. I think one of the things we really hope will come out of diagnoses like this is that we will then be able to build up more of that picture about how families are affected. So, that we can give families more information about not only how their child is affected but how they might be affected in the future. That prognosis information that Linsday said is really missing when you don't have a diagnosis. And I think the other thing that hopefully is the next stage in this journey with this discovery is that those two science publications that Emma talked about, what we will want to do here at Unique working with the researchers and those families that have got a diagnosis, is to produce a patient family friendly information leaflet about this condition. One of the things we know is really important about those patient leaflets is including the photos. Because as both Emma and Lindsay have said that idea that they have facial features in common. And so, if you look at a leaflet and you can recognise your child in it, and you can see others that look like it, that can be a really sort of quite heartwarming experience in what often is a lonely experience with a rare condition. Naimah: And I think kind of on that point about it being a lonely experience, I wondered Lindsay if you could talk a bit more if this research has allowed you to connect with other parents and families who have received a diagnosis, and what impact that's had on your family? Lindsay: Yeah. I mean, and I think everything that Sarah has said was spot on. It's wonderful to have resources like Unique to connect families and have those diagnoses on the platform, so other clinicians can look for it and sort of grow this group. I think that has definitely been the highlight of getting this diagnosis at this stage, right. Because there's not much more you can do with it, with someone so brand new so being able to connect with the other families has been wonderful. One amazing mum who with this diagnosis set up a Facebook group, RNU4-2 Family Connect. And, you know, it's just been amazing to see people from all over the world joining this as they receive this diagnosis, you know, sharing their stories. We've spent countless hours on the weekends over the past couple of months on Zoom calls with total strangers, but just you find that you can just talk for hours and hours because you have so much in common. It's great to see what has worked well for other families and, you know, what has not worked. Sharing resources, just kind of all learning together. Also seeing the spectrum of this diagnosis, I think most genetic disorders have a spectrum and this seems to be the same here. So, that's been very interesting. And of course, our son is 8, Lars is 8. There's now a 33-year-old and a 29-year-old in the Facebook group. Speaking for me personally it's just amazing to see them and like it's very cool to see where they're at. That sort of helps you answer some of those questions about that before were quite unknown when you were thinking about the future. Obviously, everybody's development whether you have a genetic disorder or not, it is going to be what it's going to be, and everybody is going to do their own thing. But being able to see what a path might look like is just so helpful. And, you know, we all want community and connection, and so this has been really, really great to have that now. Sarah: I don't think there's much more that I can add because Lindsay articulated so well. But it's really heartwarming for us to hear the benefits of those connections because that's really why Unique and other support groups exist. Is to provide, partly to provide information, but I think predominantly to put families in touch with other families so that they can find a new home and connect and share experiences. And, you know, stop feeling as alone as they might have done before. Naimah: Okay, we'll wrap up there. Thank you to our guests, Lindsay Pearce, Sarah Wynn and Emma Baple for joining me today as we discussed the research findings which found a genetic change in the RNU4-2 gene which has been linked to neurodevelopmental conditions. If you'd like to hear more like this, please subscribe to Behind the Genes on your favourite podcast app. Thank you for listening. I've been your host and producer, Naimah Callachand, and this podcast was edited by Bill Griffin of Ventoux Digital.

A discussion of disorders of cortical visual processing with Drs. Kevin Yan, Vanessa Veloso and Jeremy Moeller. Special thanks for Drs. Sashank Prasad and Marc Dinkin for providing the inspiration and a framework for this discussion.Note: This podcast is intended solely as an educational tool for learners, especially neurology residents. The contents should not be interpreted as medical advice.

This is part 1 of my conversation with Stephanie Duesing. She shares how her son was diagnosed with Cerebral/Cortical Visual Impairment (CVI) as a teenager, and how this diagnosis has impacted their family. If you have an idea for a topic we should discuss on the podcast e-mail us: OurView4Life@gmail.com Learn More about CVI: https://www.nei.nih.gov/about/news-and-events/news/vision-loss-children-whose-eyesight-may-be-2020-requires-new-diagnostic-and-teaching-strategies https://www.optometrytimes.com/view/getting-to-the-heart-of-pediatric-vision-loss-and-blindness https://www.sciencedirect.com/science/article/abs/pii/S0028393221002359 https://www.npr.org/sections/health-shots/2014/05/26/314621545/the-blind-woman-who-sees-rain-but-not-her-daughters-smile#:~:text=You%20can%27t%20see%20a,stroke%20at%2029%20years%20old. https://cviscotland.org/  

  Phil Starr is a Professor of Neurological Surgery at University of California, San Francisco and a developer of implantable brain devices. At UCSF, he co-directs a multidisciplinary neurology/neurosurgery movement disorders clinic together with Dr. Jill Ostrem. I've been a long-time admirer of Phil's work and in this conversation we blaze through quite a few of his numerous publications. One key breakthrough and invention of Phils work has been to include Ecog recordings – both intraoperatively but also chronically – to investigate brain signals in various states. We talk about the Open Mind Consortium, Mentorship and the cross-pollination between academia and industry. One key highlight of Phils work is a paper which was accepted for publication in Nature Medicine, at the time of recording this just yesterday. In it, the three co-first authors Carina Oehrn, Stephanie Cernera and Lauren Hammer demonstrate the chronic use of a newly identified cortical physiomarker, which is now referred to as the finely tuned gamma activity. I hope you enjoy this conversation as much as I did, and thank you for tuning into Stimulating Brains!

Dr. Tesha Monteith and Dr. Messoud Ashina discuss the comparison between cortical morphometry to a large sample of people with migraine and healthy controls, as well as across migraine subtypes.  Show reference: https://www.neurology.org/doi/10.1212/WNL.0000000000209305  This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.

Dr. Tesha Monteith talks with Dr. Messoud Ashina about the comparison between cortical morphometry to a large sample of people with migraine and healthy controls, as well as across migraine subtypes. Read the related article in Neurology. This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information. Disclosures can be found at Neurology.org.

Ein Thema, das in schlechten SV Trainings total fehlt und in super schlechten jedes Mal stattfindet. Klingt spannend genug, dass Tobi eine Stunde lang drüber redet und dir alles erklärt, was auf Arbeitsebene dazugehört: Was ist Schmerz, wieso ist Schmerz und was machen wir jetzt damit im Selbstschutz? Literatur: Grant, J. A., Courtemanche, J., Duerden, E. G., Duncan, G. H., & Rainville, P. (2010). Cortical thickness and pain sensitivity in zen meditators. Emotion, 10(1), 43-53. https://doi.org/10.1037/a0018334 Gross, J. J. (2002). Emotion regulation: Affective, cognitive, and social consequences. Psychophysiology, 39(3), 281-291. https://doi.org/10.1017/S0048577201393198 Hamilton, N. A., Zautra, A. J., & Reich, J. W. (2007). Self-regulation and positive affect in chronic pain populations. Cognitive Therapy and Research, 31(4), 457-470. https://doi.org/10.1007/s10608-006-9006-8 Jacobson, E. (1938). Progressive Relaxation. Chicago: University of Chicago Press. Kalso, E., Edwards, J. E., Moore, R. A., & McQuay, H. J. (2004). Opioids in chronic non-cancer pain: Systematic review of efficacy and safety. Pain, 112(3), 372-380. https://doi.org/10.1016/j.pain.2004.09.019 Seppälä, E. M., Nitschke, J. B., Tudorascu, D. L., Hayes, A., Goldstein, M. R., Nguyen, D. T., Perlman, D., & Davidson, R. J. (2014). Breathing-based meditation decreases posttraumatic stress disorder symptoms in U.S. military veterans: A randomized controlled longitudinal study. Journal of Traumatic Stress, 27(4), 397-405. https://doi.org/10.1002/jts.21936 Tracey, I., & Mantyh, P. W. (2007). The cerebral signature for pain perception and its modulation. Neuron, 55(3), 377-391. https://doi.org/10.1016/j.neuron.2007.07.012 Villemure, C., & Bushnell, M. C. (2002). Cognitive modulation of pain: How do attention and emotion influence pain processing? Pain, 95(3), 195-199. https://doi.org/10.1016/S0304-3959(02)00007-6 Zeidan, F., Grant, J. A., Brown, C. A., McHaffie, J. G., & Coghill, R. C. (2012). Mindfulness meditation-related pain relief: Evidence for unique brain mechanisms in the regulation of pain. Neuroscience Letters, 520(2), 165-173. https://doi.org/10.1016/j.neulet.2012.03.082 Einspieler: Musik im Intro: Home Base Groove von Kevin MacLeod unterliegt der Creative-Commons-Lizenz "Namensnennung 4.0". https://creativecommons.org/licenses/by/4.0/ Quelle: http://incompetech.com/music/royalty-free/index.html?isrc=USUAN1100563  Künstler: ⁠http://incompetech.com/⁠ Musik im Outro: Eyes Gone Wrong von Kevin MacLeod unterliegt der Creative-Commons-Lizenz "Namensnennung 4.0". https://creativecommons.org/licenses/by/4.0/ Quelle: http://incompetech.com/music/royalty-free/index.html?isrc=USUAN1100362 Künstler: http://incompetech.com/

The powerful new generation of AI tools that has come out over the past few years —  DALL-E, ChatGPT, Claude, Gemini, and the rest — have blown away our old ideas about what AI can do and raised questions about what it means for computers to start acting... intelligent?This week, we ask what the rise of these systems might teach us about our own biological intelligence — and vice versa. What does modern neuroscience have to say about how AI could become as flexible, efficient, and resilient as the human brain. Few people are better positioned to speak to the intersection of neuroscience and AI than today's guest: Surya Ganguli. Ganguli's lab produced some of the first diffusion models — which are at the foundation of today's AI revolution — and is now working to understand how complex emergent properties arise from biological and artificial neural networks. Ganguli is a member of the Neuroscience Theory Center at the Wu Tsai Neurosciences Institute, a Senior Fellow at Stanford's Institute for Human-Centered Artificial Intelligence (HAI), and an associate professor in Stanford's Department of Applied Physics. Further ReadingInterpreting the retinal neural code for natural scenes: From computations to neurons (Neuron, 2023)Beyond neural scaling laws: beating power law scaling via data pruning (arXiv, 2023)Cortical layer-specific critical dynamics triggering perception (Science, 2019)Stanford team stimulates neurons to induce particular perceptions in mice's minds (Stanford Medicine, 2019)What DALL-E reveals about human creativity (Wu Tsai Neurosciences Institute, 2023)Visit us!Want to learn more about AI and Neuroscience? Join us at Wu Tsai Neuro's annual symposium on October 17, 2024, which will showcase the frontiers of biological and artificial intelligence research. (More details coming soon!)Episode creditsThis episode was produced by Michael Osborne at 14th Street Studios, with production assistance by Morgan Honaker. Our logo is by Aimee Garza. The show is hosted by Nicholas Weiler at Stanford's Wu Tsai Neurosciences Institute. Send us a text!Thanks for listening! If you're enjoying our show, please take a moment to give us a review on your podcast app of choice and share this episode with your friends. That's how we grow as a show and bring the stories of the frontiers of neuroscience to a wider audience. Learn more about the Wu Tsai Neurosciences Institute at Stanford and follow us on Twitter, Facebook, and LinkedIn.

Aprender, repetir a informação para ensinar uma nova via sináptica, tudo isso pela plasticidade cortical. Quantas palavras complicadas! Nesse curto vídeo te explico um pouco sobre esses conceitos e suas interações. ATENÇÃO: no início do vídeo tivemos um problema com o microfone, o problema é solucionado nos segundos que seguem. Esse foi o assunto desse video, que foi ao ar AO VIVO no dia 31de agosto 2022 pelo JTT no canal do Youtube do Portal Desacato:  @PortalDesacato  Com Dra. Juliana Barcellos de Souza, PhD

This “MOGcast” edition of the “Ask the Expert” podcast series is a collaborative episode titled, “MOGcast 2: Understanding Cortical Encephalitis.” Dr. Eoin Flanagan and Dr. Cristina Valencia Sanchez joined Julia Lefelar of The MOG Project and Dr. GG deFiebre of SRNA to discuss cortical encephalitis, its symptoms, and the connection to MOG antibody disease (MOGAD) [00:04:21]. Audience members asked about the distinction between ADEM and cerebral cortical encephalitis, their treatments, diagnostic methods, and long-term impacts [00:35:34]. Dr. Flanagan and Dr. Sanchez agreed that the preventive treatment approach remains similar regardless of the MOGAD phenotype [00:40:36]. The discussion touched on recent studies on the diagnostic utility of MOG antibody testing in cerebrospinal fluid, and ongoing research on treatments, including clinical trials for developing FDA-approved medications for MOGAD [00:43:05]. Dr. Flanagan and Dr. Sanchez addressed community questions on fulminant cortical involvement cases [00:50:00], the long-term effects of Rituximab treatment [00:51:23], anxiety attacks and mood swings in ADEM [00:53:34], and treatment decisions based on antibody levels [00:54:49]. Eoin Flanagan, MB, BCh is a Professor of Neurology and Consultant in the departments of Neurology and Laboratory Medicine and Pathology at the Mayo Clinic (Rochester, MN). He completed his medical school training at University College Dublin in Ireland in 2005. He did a medical residency in Ireland and then completed neurology residency, fellowships in neuroimmunology and a masters in clinical and translational science at Mayo Clinic (Rochester, MN). He works in the Autoimmune Neurology and Multiple Sclerosis Clinics and the Neuroimmunology Laboratory at the Mayo Clinic. His clinical expertise and research are focused on inflammatory myelopathies and their imaging patterns, myelin oligodendrocyte glycoprotein (MOG) antibody associated disorder, neuromyelitis optica spectrum disorders, autoimmune encephalitis, paraneoplastic neurologic disorders, and multiple sclerosis. He is principal investigator on an NIH RO1 grant studying MOG antibody associated disorder. Cristina Valencia Sanchez, MD, PhD is an Assistant Professor of Neurology and Senior Associate Consultant in the Department of Neurology at the Mayo Clinic (Phoenix, AZ). She completed her medical school training and PhD in Neuroscience at the Universidad Complutense de Madrid. She did a Neurology residency in the Hospital Universitario Clinico San Carlos and then completed Neurology residency and fellowships in ARZ Multiple Sclerosis and RST Autoimmune Neurology at the Mayo School of Graduate Medical Education, Mayo Clinic College of Medicine, in Arizona and Minnesota. The research interests of Dr. Valencia Sanchez focus on autoimmune disorders involving the central nervous system. These include neuromyelitis optica spectrum disorders, myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), autoimmune encephalitis, and paraneoplastic neurological syndromes. She is particularly interested in the neurological complications of immune checkpoint inhibitor cancer immunotherapy. The clinical trials that she leads at Mayo Clinic in Arizona are among the first studies that may lead to approval of new targeted therapies for MOGAD and autoimmune encephalitis. Additionally, Dr. Valencia Sanchez's clinical research allows for increased recognition of autoimmune neurological disorders. Also, her work is helping to avoid misdiagnosing autoimmune encephalitis in the clinical setting. Her research leads to earlier diagnosis and appropriate treatment to ultimately improve patient outcomes.

Dr. Pierre Vanderhaeghen is a Professor and Principal Investigator at VIB-KU Leuven Center for Brain & Disease Research. His lab studies the mechanisms of cortical development and brain evolution. He talks about species-specific neuronal development, human neuron excitability, and playing in a rock cover band!

*Texas Panhandle ranchers are recovering from the wildfires.  *National Sorghum Producers is accepting entries for the National Sorghum Yield Contest.   *The Texas NRCS announced an additional signup for the National Water Quality Initiative.  *Fed cattle prices remain strong, but Texas feedyards are finding it challenging to make a profit.*Agriculture cybersecurity was the topic of a recent House Ag Committee hearing.  *The 2024 hurricane season is expected to be strong.  *The Rolling Plains wheat crop is heading, and it looks pretty good.  *Cortical steroids are the most common drugs injected into the joints of performance horses.  

Leah Krubitzer | MacArthur Fellow   Professor of Psychology | University of California, Davis"Combinatorial Creatures: Cortical Plasticity Within and Across Lifetimes" The neocortex is one of the most distinctive structures of the mammalian brain, yet also one of the most varied in terms of both size and organization. Multiple processes have contributed to this variability including evolutionary mechanisms (i.e., changes in gene sequence) that alter the size, organization and connections of the neocortex, and activity dependent mechanisms that can also modify these same features over shorter time scales. Because the neocortex does not develop or evolve in a vacuum, when considering how different cortical phenotypes emerge within a species and across species over time, it is also important to consider alterations to the body, to behavior, and the environment in which an individual develops. Thus, changes to the neocortex can arise via different mechanisms, and over multiple time scales. Brains can change across large, evolutionary time scales of thousands to millions of years; across shorter time scales such as generations; and across the life of an individual – day-by-day, within hours, minutes and even on a time scale of a second. The combination of genetic and activity dependent mechanisms that create a given cortical phenotype allows the mammalian neocortex to rapidly and flexibly adjust to different body and environmental contexts, and in humans permits culture to impact brain construction during development.

EMERGENCE OF THE CORTICAL ENCODING OF PHONETIC FEATURES IN THE FIRST YEAR OF LIFEGiovanni M. Di Liberto, Adam Attaheri, Giorgia Cantisani, Richard B. Reilly, Áine Ní Choisdealbha, Sinead Rocha, Perrine Brusini & Usha Goswami   Nature Communications volume 14, Article number: 7789 (2023)   Abstract  Even prior to producing their first words, infants are developing a sophisticated speech processing system, with robust word recognition present by 4–6 months of age.   These emergent linguistic skills, observed with behavioural investigations, are likely to rely on increasingly sophisticated neural underpinnings. The infant brain is known to robustly track the speech envelope, however previous cortical tracking studies were unable to demonstrate the presence of phonetic feature encoding.  Here we utilise temporal response functions computed from electrophysiological responses to nursery rhymes to investigate the cortical encoding of phonetic features in a longitudinal cohort of infants when aged 4, 7 and 11 months, as well as adults.   The analyses reveal an increasingly detailed and acoustically invariant phonetic encoding emerging over the first year of life, providing neurophysiological evidence that the pre-verbal human cortex learns phonetic categories. By contrast, we found no credible evidence for age-related increases in cortical tracking of the acoustic spectrogram.

There are a lot of confusing things you can see on an MRI report, on an x-ray report or an ultrasound report when you're a runner with pain that you think might be a stress fracture.  One of those findings that may be reported on your medical imaging study is a thing called "cortical thickening." I want to explain what that is so you can better understand it in case you happen to see it on an MRI report, x-ray report or in your doctor's notes. What is cortical thickening that precedes a stress fracture?  Well, that's what we're talking about today on the Doc On The Run Podcast.   

Dr. David Fitzpatrick is Chief Executive Officer, Scientific Director, and Research Group Leader at the Max Planck Florida Institute for Neuroscience. The brain is important for so many aspects of our daily experiences, including what we perceive, what we think about, how we move, the decisions we make, and more. However, we still know relatively little about how the brain works and how it develops. David's goal is to dive deep into these basic science questions of how the brain works and how it develops. When David isn't hard at work at Max Planck, he spends his time hiking, biking, kayaking, and immersing himself in nature. He has also become a keen photographer, capturing captivating photos of the natural world and memorable moments in his life. David received his B.S. degree in Biology from Pennsylvania State University and his PhD in Psychology and Neuroscience from Duke University. He conducted postdoctoral research at the Medical University of South Carolina and then returned to Duke University as a member of the faculty. Before accepting his current positions at the Max Planck Florida Institute, David was the James B. Duke Professor of Neurobiology and Director of the Institute for Brain Sciences at Duke University. David has received numerous awards and honors over the course of his career for his outstanding research and teaching, including the 2011 Ellis Island Medal of Honor from the National Ethnic Coalition of Organizations, the Alfred P. Sloan Research Award, the Cajal Club Cortical Discoverer Award, the McKnight Neuroscience Investigator Award, and the Excellence in Basic Science Teaching Award from Duke University School of Medicine. David joined us for an interview to share his experiences in life and science.

Neurology Today Editor-in-chief Joseph E. Safdieh, MD, FAAN, discusses a new study showing retinal vascular perfusion as a migraine biomarker, clinical and pathophysiological correlates of posterior cortical atrophy, and advances in gene therapies for neuromuscular disorders.

MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: January 25, 2018 We expose our soft spot this week on the show. Lindsay Raab and John Best join Jim Siegler in the studio to discuss their own personal struggles with residency and patient care and how they've battled hard to overcome them. Produced by John Best and Lindsay Raab. Senior producer, Jim Siegler. Music by Daniel Birch, Little Glass Men, The New Valleys, Rod Hamilton, Chris Zabriskie, and Jon Watts. Voiceovers by David Manly, Erika Mejia, and Pat Green. BrainWaves' podcasts and online content are intended for medical education only. If you're in healthcare and feeling burnt out, maybe this episode will be insightful. But please do not misconstrue this as advice. REFERENCES Thomas NK. Resident burnout. JAMA 2004;292(23):2880-9. PMID 15598920  We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.

Today, you'll learn about why you may want to consider letting yourself daydream, how a sense of humor might protect you from depression and anxiety, and the effects of caffeine on the performance of soccer players. Daydream Brain “What Happens in the Brain While Daydreaming?” by Catherine Caruso. 2023. “Is the role of sleep in memory consolidation overrated?” by Mohammad Dastgheib, et al. 2022. “Cortical reactivations predict future sensory responses.” by Nghia D. Nguyen, et al. 2023. “Why Daydreaming Is Good For Us.” by David B. Feldman Ph.D. 2017. Power of a Laugh “Your type of humor might say something about your risk of depression and anxiety.” by Eric W. Dolan. 2023. “Understanding the Association Between Humor and Emotional Distress: The Role of Light and Dark Humor in Predicting Depression, Anxiety, and Stress.” by Alberto Dionigi, et al. 2023. Caffeine & Soccer “Caffeine highs and lows footballers should be aware of.” n.a. 2023. “The effects of acute caffeine ingestion on decision-making and pass accuracy in young soccer players: A preliminary randomized controlled trial.” by Negar Jafari, et al. 2023. Follow Curiosity Daily on your favorite podcast app to get smarter with Calli and Nate — for free! Still curious? Get exclusive science shows, nature documentaries, and more real-life entertainment on discovery+! Go to https://discoveryplus.com/curiosity to start your 7-day free trial. discovery+ is currently only available for US subscribers. Hosted on Acast. See acast.com/privacy for more information.

Robert T. Fremeau, Jr., Ph.D., delves into Rett syndrome, a complex neurological condition. His research with brain organoids unveils its origins and progression. Fremeau uncovers disease markers and innovative treatments, offering insight into the pursuit of breakthrough therapies. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Science] [Show ID: 39167]

Robert T. Fremeau, Jr., Ph.D., delves into Rett syndrome, a complex neurological condition. His research with brain organoids unveils its origins and progression. Fremeau uncovers disease markers and innovative treatments, offering insight into the pursuit of breakthrough therapies. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Science] [Show ID: 39167]

Robert T. Fremeau, Jr., Ph.D., delves into Rett syndrome, a complex neurological condition. His research with brain organoids unveils its origins and progression. Fremeau uncovers disease markers and innovative treatments, offering insight into the pursuit of breakthrough therapies. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Science] [Show ID: 39167]

Robert T. Fremeau, Jr., Ph.D., delves into Rett syndrome, a complex neurological condition. His research with brain organoids unveils its origins and progression. Fremeau uncovers disease markers and innovative treatments, offering insight into the pursuit of breakthrough therapies. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Science] [Show ID: 39167]

Robert T. Fremeau, Jr., Ph.D., delves into Rett syndrome, a complex neurological condition. His research with brain organoids unveils its origins and progression. Fremeau uncovers disease markers and innovative treatments, offering insight into the pursuit of breakthrough therapies. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Science] [Show ID: 39167]

Robert T. Fremeau, Jr., Ph.D., delves into Rett syndrome, a complex neurological condition. His research with brain organoids unveils its origins and progression. Fremeau uncovers disease markers and innovative treatments, offering insight into the pursuit of breakthrough therapies. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Science] [Show ID: 39167]

Robert T. Fremeau, Jr., Ph.D., delves into Rett syndrome, a complex neurological condition. His research with brain organoids unveils its origins and progression. Fremeau uncovers disease markers and innovative treatments, offering insight into the pursuit of breakthrough therapies. Series: "Autism Tree Project Annual Neuroscience Conference" [Health and Medicine] [Science] [Show ID: 39167]

*Texas winter wheat planting is almost finished.   *Texas A&M is doing research on coronavirus in cattle.  *USDA has appointed two Texans to serve on the United Soybean Checkoff's board of directors.  *Wildfires are a big threat to rangelands across Texas.  *Companies are developing technology to improve soil fertilization for farmers here in Texas and around the world.  *Leaves are falling across Texas.  *Cortical steroids are commonly injected into equine joints.  *300,000 rainbow trout are being stocked in water bodies across Texas.  

Moderator: James P. Rathmell, M.D. Participants: Phillip Vlisides, M.D. and Patrick L. Purdon, Ph.D. Articles Discussed: Electroencephalographic Biomarkers, Cerebral Oximetry, and Postoperative Cognitive Function in Adult Non-Cardiac Surgical Patients: a Prospective Cohort Study Charting a Cognitive Course: Can Electroencephalographic or Oximetry Biomarkers Predict Postoperative Cognitive Function? Transcript

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Perceived Moral Value of Animals and Cortical Neuron Count, published by WillemSleegers on August 25, 2023 on The Effective Altruism Forum. Publication note We initially drafted a writeup of these results in 2019, but decided against spending more time to finalize this draft for publication, given the large number of other projects we could counterfactually be working on, and given that our core results had already been reported (with permission) by Scott Alexander, which seemed to capture a large portion of the value of publishing. We're now releasing a lightly edited version of our initial draft, by request, so that our full results can be cited. As such, this is a 'blog post', not a research report, meaning it was produced quickly and is not to Rethink Priorities' typical standards of substantiveness and careful checking for accuracy. Summary Scott Alexander reported the results of a small (n=50) experiment on a convenience sample of his Tumblr followers suggesting that the moral value assigned to animals of different species closely tracks their cortical neuron count (Alexander, 2019a). If true, this would be a striking finding suggesting that lay people's intuitions about the moral values of non-human animals are highly attuned to these animals' neurological characteristics. However, a small replication on Amazon Mechanical Turk (N=263) by a commenter called these findings into question by reporting very different results (Alexander, 2019b). We ran a larger study on MTurk (n=526) (reported in Alexander, 2019c)) seeking to explain these differences. We show how results in line with either of these two studies could be found based on different choices about how to analyze the data. However, we conclude that neither of these approaches are the most informative way to interpret the data. We present our own analyses showing that there is enormous variance in the moral value assigned to each animal, with large numbers of respondents assigning each animal equal value with humans or no moral value commensurable with humans, as well as many in between. We discuss implications of this and possible lines of future research. Introduction Scott Alexander previously published the results of a small survey (n=50, recruited from Tumblr) asking individuals "About how many [of different non-human animals] are equal in moral value to one adult human?" (Alexander, 2019a) A response that 1 animal of a given species was of the same moral value as 1 adult human, could be construed as assigning animals of this species and humans equal moral value. Conversely, a response that >1 individuals of a given species were of the same moral value as 1 adult human, could be construed as suggesting that those animals have lower moral value than humans. In principle, this could also tell us how much moral value individuals intuitively assign to different non-human animals relative to each other (e.g. pigs vs cows). Alexander reported that the median value assigned by respondents to animals of different species seemed to track the cortical neuron count (see Alexander 2019d) of these animals conspicuously closely (as shown in Figure 1) and closer than for other potential proxies for moral value, such as encephalization quotient. This apparent correlation between the moral value assigned to animals of different species and their cortical neuron count is particularly striking given that Alexander (2019d) had argued in a previous post that cortical neuron count, specifically, was strongly associated with animal intelligence. Thus it might seem that the intuitive moral value assigned to animals of different species was closely linked to the intelligence of the animals. If so this would potentially, as Alexander put it, add "at least a little credibility" to intuitive judgments about the moral value of no...

In The Hidden Spring, our guest Mark Solms does not dive too deeply into Karl Friston's mathematics. As you will discover, he summarises its implications, describing Friston's free energy as a quantifiable measure of how a system models the world and how it behaves. This notion leads to a very different idea of consciousness from Descartes's reason-centric version that set up the puzzling dualism of “mind” and “matter”, a la Damasio's Descartes Error. Mark explores the “cortical fallacy,” which refers to his view that neuroscientists who have argued that the “seat of consciousness” is in the cortex are wrong. Recent neuroscience has shed light on where this is. As Mark points out, damage to just two cubic millimetres of the upper brainstem will “obliterate all consciousness.”   So where does it "Spring" from?   00:00:00 Intro 00:00:12 Teeing Up “The Cortical Fallacy” with hydranencephaly, a rare condition in which the brain's cerebral hemispheres are absent and replaced by sacs filled with cerebrospinal fluid. 00:02:37 “The Cortical Fallacy”  00:18:14 The Report-ability Problem of Consciousness 00:31:00 Chemical and Pharmacological Probes 00:37:00 1949 discovery of the Reticular Activating System  00:55:25 The Reticular Activating System: Salience, Filtering, Gratitude, Law of Attraction 00:58:00 The Mr. W joke and The Global Workspace Theory

When we look at how to be an impactful teacher, I notice that the best teachers only focus on 3 key areas. In this conversation, Diyana Ahmad, a visionary TVI in Malaysia shows us how she helps her learners with Cortical and Cerebral Visual Impairments (CVI) in unique ways. We also share: How she balances work & pleasure while traveling A Tiered system for creating tactile graphics What a day in the life of a teacher of students with visual impairments in Malaysia looks like. SAVE THE DATE! Our upcoming webinar, "What's Working for TVI's: Students with Multiple Impairments" is happening July 20th. The TVI Online Symposium is coming up on September 21-22, 2023. Register for the waitlist to be the first to get information on both the webinar and the conference as they come up! FOLLOW DIYANA ON INSTAGRAM! FOLLOW Allied Independence on Instagram and Facebook!

In this episode, Dr. Renee is joined by Stephanie Duesing, author, speaker, and international advocate for people who have cerebral/cortical visual impairment as they explore the condition of CVI including such things as its prevalence, symptoms and testing.    Libido Code Waitlist: https://drrenee.mykajabi.com/the-libido-code    To connect with Stephanie Duesing, links mentioned in today's episode, and so much more, visit: https://www.drreneewellenstein.com/the-real-heal-podcast/episode-169

JAACAP May 2023: Contributing Editor Dr. Nicole King Cotton interviews Drs. Adriana Fortea and Gisela Sugranyes on how transitions to psychosis in adolescence are associated with changes in longitudinal trajectory of brain cortical surface area.

JAACAP May 2023: Contributing Editor Dr. Nicole King Cotton interviews Drs. Adriana Fortea and Gisela Sugranyes on how transitions to psychosis in adolescence are associated with changes in longitudinal trajectory of brain cortical surface area.

Dr Jack Kruse joins me for a deep exploration of WATER. He explains the role of water in mitochondrial respiration, the impacts of light on water, mitochondrial heteroplasmy, why non-native electromagnetic fields (EMFs) accelerate disease and aging, the problems with in the somatic gene mutation paradigm of disease, and much, much more.This is Part II of the Jack Kruse Series. In these conversations we explore Dr Kruse's paradigm of health centered on Light, Water and Magnetism, mitochondrial and circadian function and how these are impacted to influence human health and disease.Dr Jack Kruse is a practicing neurosurgeon, biophysicist and health optimisation researcher. He has done extensive research into the causes of human disease with a highly unique perspective grounded in bio-physics.TIMESTAMPS00:00:00 Dr Max's intro00:03:14 Podcast begins00:05:45 Mitochondria produce water as part of oxidative metabolism00:07:30 Water created inside the mitochondrial matrix is deuterium depleted00:11:45 Light changes the physics of water00:16:50 Water is NOT homogeneous, and changes its physics based on its environment 00:23:05 Dr Max's summary of first 20 minutes00:26:05 Water content of the mammals decreases with age related to mitochondrial heteroplasmy00:24:14 What is mitochondrial heteroplasmy and how does it relate to disease?00:28:15 Animal based diet is superior to plant-based diet based on the body's ability to generate mitochondrial water00:31:58 Dr Max: genetics might load the gun, but environment pulls the trigger and mitochondrial dysfunction is key 00:33:58 Astronaut kelly developed accelerated disease in the space station because of unshielded, sun-derived EMF exposure which impaired his mitochondrial water production causing mitochondrial heteroplasmy 00:36:43 Environment is the most important cause of disease, and since the 1950s humans have created terrestrial sources of non-native EMF in the form of telecommunications devices/networks00:41:50 Water is the carrier of electromagnetic information from the sun into cells00:45:55 Dr Max's empahsises the previous 20 minutes of discussion00:57:15 The flaws of the neo-Darwinist paradigm00:59:11 Microwaves and non-native EMF cause harm through cellular dehydration and mechanisms of impaired mitochondrial water production 01:07:21 Dr Max summaries the harms of non-native EMFs01:09:30 Story Steve Jobs and his exposure to non-native EMF01:17:00 Dr Max explains why keeping your device in your pocket is so harmful for fertility01:19:13 The origin of the Black Swan nomenclature01:21:20 On the harms of sunscreen and sunglasses 01:26:00 Closing thoughts----------------------------------------------------------------------------FURTHER READING2023 MELANIN-LEPTIN Rx UPDATE on Jack Kruse Patreon - https://www.patreon.com/posts/2023-melanin-rx-78628253CPC #65: "CELL PHONE" BURN & CANCER on Jack Kruse Patreon - https://www.patreon.com/posts/cpc-65-cell-burn-70790447Somatotopic brain organization (Cortical homunculus) - https://en.wikipedia.org/wiki/Cortical_homunculusCircumventricular organs - https://en.wikipedia.org/wiki/Circumventricular_organsSteve Jobs' retroperitoneal cancer - https://www.scientificamerican.com/article/pancreatic-cancer-type-jobs/Victor Schauberger - https://en.wikipedia.org/wiki/Viktor_SchaubergerAlexander Gurwitsch - https://en.wikipedia.org/wiki/Alexander_Gurwitsch----------------------------------------------------------------------------FOLLOW DR KRUSEPatreon: https://www.patreon.com/DrJackKruse/Website: https://jackkruse.com/Twitter: https://twitter.com/DrJackKruse

Ellen brings you summaries of 8 abstracts from November 2022, all about functional connectivity and imaging in the context of Alzheimer's disease. There are a variety of brain regions covered in today's episode, including cortical regions, subcortical structures, and the hippocampus. Spanning studies in both humans and animals, this episode is sure to have something of interest to you and your research!  Sections in this episode:  Cortical regions (3:39)  Subcortical forebrain regions (8:57)  Hippocampus (14:30) -------------------------------------------------------------- To find the numbered bibliography with all the papers covered in this episode, click here, or use the link below:https://drive.google.com/file/d/1vpN33jcSgeoS-9QrcNiSJaYDFQY23CeW/view?usp=share_linkTo access the folder with ALL our bibliographies, follow this link (it will be updated as we publish episodes and process bibliographies), or use the link below:https://drive.google.com/drive/folders/1bzSzkY9ZHzzY8Xhzt0HZfZhRG1Gq_Si-?usp=sharingYou can also find all of our bibliographies on our website: amindr.com. --------------------------------------------------------------Follow-up on social media for more updates!Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastFacebook:  AMiNDR  Youtube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us spread the word about AMiNDR to your friends, colleagues, and networks! And if you could leave us a rating and/or review on your streaming app of choice (Apple Podcasts, Spotify, or wherever you listen to the podcast), that would be greatly appreciated! It helps us a lot and we thank you in advance for leaving a review! Don't forget to subscribe to hear about new episodes as they come out too. Thank you to our sponsor, the Canadian Consortium of Neurodegeneration in Aging, or CCNA, for their financial support of this podcast. This helps us to stay on the air and bring you high quality episodes. You can find out more about the CCNA on their website: https://ccna-ccnv.ca/. Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted, hosted, and edited by Ellen Koch, and reviewed by Anusha Kamesh. The bibliography was created by Anjana Rajendran and the wordcloud was made by Lara Onbasi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For November 2022, the sorters were Sarah Louadi, Eden Dubchak, Ben Cornish, Christy Yu, Dana Clausen, Kevin Nishimura, Anelya Gandy, Salodin Al-Achkar, Ellen Koch, and Elyn Rowe. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Lara Onbasi, Joseph Liang, and Judy Cheng, for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

Today we discuss how using gas stoves has caused a huge uptick in childhood asthma, how motor memory is developed while we sleep, and how scientists are working to save the larvae of coral reefs! Gasthma“Population Attributable Fraction of Gas Stoves and Childhood Asthma in the United States” by Talor Gruenwald et al.https://www.mdpi.com/1660-4601/20/1/75“Gas stove pollution causes 12.7% of childhood asthma, study finds” by Maxine Joselow and Vanessa Montalbanohttps://www.washingtonpost.com/politics/2023/01/06/gas-stove-pollution-causes-127-childhood-asthma-study-finds/Sleep Memory “During sleep, brain regions synchronize to create motor memory” by UNIVERSITY OF CALIFORNIA - SAN FRANCISCOhttps://www.eurekalert.org/news-releases/974905“Cortical–hippocampal coupling during manifold exploration in motor cortex” by Jaekyung Kim et al.https://www.nature.com/articles/s41586-022-05533-zFrozen Reefs “Scientists freeze Great Barrier Reef coral in world-first trial” By Jill Gralowhttps://www.reuters.com/lifestyle/science/scientists-freeze-great-barrier-reef-coral-world-first-trial-2022-12-19/“Scientists pioneer ‘game-changing' freezing technique that could save the Great Barrier Reef's coral” by Charlotte Eltonhttps://www.euronews.com/green/2022/12/19/scientists-pioneer-game-changing-freezing-technique-that-could-save-the-great-barrier-reef“Scientists Freeze Great Barrier Reef Coral” by GKTodayhttps://www.gktoday.in/topic/scientists-freeze-great-barrier-reef-coral/“What is coral bleaching?” by National Ocean Servicehttps://oceanservice.noaa.gov/facts/coral_bleach.html“SCIENTISTS HAVE MADE A HUGE BREAKTHROUGH IN CRYOGENICS” by June Javelosahttps://futurism.com/neoscope/4-scientists-have-found-a-way-to-rapidly-thaw-cryopreserved-tissue-without-damageFollow Curiosity Daily on your favorite podcast app to get smarter with Calli and Nate — for free! Still curious? Get exclusive science shows, nature documentaries, and more real-life entertainment on discovery+! Go to https://discoveryplus.com/curiosity to start your 7-day free trial. discovery+ is currently only available for US subscribers.Find episode transcripts here: 

If you've ever had a migraine, you know that the symptoms — splitting headache, nausea, sensitivity to light — mean you're going to want to spend some time in bed, in a dark room. Migraines are flat out debilitating, and the statistics back this up.Migraines are the third most common neurological disorder. They affect as many as a billion people around the world, making them one of the world's 10 most disabling diseases according to the World Health Organization. But for all the misery for those who suffer from migraines, it's been a long haul for scientists to figure out what actually causes these episodes, and more importantly, how to provide relief.We spoke this week with  Gabriella Muwanga, a Stanford graduate student who studies what's actually going on in the brain during a migraine. And for good reason —  Muwanga has suffered from regular migraines herself since childhood and hopes to contribute to finding better treatments for them in the future.LinksMuwanga's research profileThe Tawfik lab at Stanford MedicineThe Airan lab at Stanford MedicineStanford headache specialist demystifies migraine auras (Stanford Scope Blog, 2017)Migraine Treatment Has Come a Long Way (New York Times Well Blog, 2022)ReferencesAhn, A.H. and Basbaum, A.I. Where do triptans act in the treatment of migraine? Pain. 2005 May; 115(1-2): 1–4.Charles, A., Baca, S. Cortical spreading depression and migraine. Nat Rev Neurol 9, 637–644 (2013). Weatherall, M.W. The diagnosis and treatment of chronic migraine. Ther Adv Chronic Dis. 2015 May; 6(3): 115–123.Hoffmann, J.,  Baca, S. M., and  Akerman, S. Neurovascular mechanisms of migraine and cluster headache. J Cereb Blood Flow Metab. 2019 Apr; 39(4): 573–594.Episode CreditsThis episode was produced by Michael Osborne, with production assistance by Morgan Honaker and Christian Haigis, and hosted by Nicholas Weiler. Cover art by Aimee Garza.Thanks for listening! Learn more about the Wu Tsai Neurosciences Institute at Stanford and follow us on Twitter, Facebook, and LinkedIn.

Today, we talk all about neuroimaging, with 7 papers that use various imaging modalities in humans, animals, and computational modeling, to study how the brain changes in Alzheimer's disease. Tune in to learn more!  Sections in this episode:  Hippocampus (3:50)  Hypothalamus (8:15)  Cortical regions (10:29)  Nucleus basalis (15:57)  Pineal gland (18:40) -------------------------------------------------------------- To find the numbered bibliography with all the papers covered in this episode, click here, or use the link below:https://drive.google.com/file/d/1I3kmmULxiu1EG1CoEtIMsFQzZIs8zSbO/view?usp=share_linkTo access the folder with ALL our bibliographies, follow this link (it will be updated as we publish episodes and process bibliographies), or use the link below:https://drive.google.com/drive/folders/1bzSzkY9ZHzzY8Xhzt0HZfZhRG1Gq_Si-?usp=sharingYou can also find all of our bibliographies on our website: amindr.com. --------------------------------------------------------------Follow-up on social media for more updates!Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastFacebook:  AMiNDR  Youtube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us spread the word about AMiNDR to your friends, colleagues, and networks! And if you could leave us a rating and/or review on your streaming app of choice (Apple Podcasts, Spotify, or wherever you listen to the podcast), that would be greatly appreciated! It helps us a lot and we thank you in advance for leaving a review! Don't forget to subscribe to hear about new episodes as they come out too. Thank you to our sponsor, the Canadian Consortium of Neurodegeneration in Aging, or CCNA, for their financial support of this podcast. This helps us to stay on the air and bring you high quality episodes. You can find out more about the CCNA on their website: https://ccna-ccnv.ca/. Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted, hosted, and edited by Ellen Koch, and reviewed by Anusha Kamesh. The bibliography and wordcloud were created by Lara Onbasi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For October 2022, the sorters were Sarah Louadi, Eden Dubchak, Ben Cornish, Christy Yu, Dana Clausen, Kevin Nishimura, Salodin Al-Achkar, and Elyn Rowe. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Lara Onbasi, Joseph Liang, and Judy Cheng, for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

Today we speak with Dr. Wendy Kelso about a clinical case – this is a woman with posterior cortical atrophy, or PCA. Wendy is a senior clinical neuropsychologist and coordinator of neuropsychology services at the Royal Melbourne Hospital in Victoria, Australia.   Show notes are available at www.NavNeuro.com/111 _________________ If you'd like to support the show, here are a few easy ways: 1) Get APA-approved CE credits for listening to select episodes: www.NavNeuro.com/INS  2) Tell your friends and colleagues about it 3) Subscribe (free) and leave an Apple Podcasts rating/review: www.NavNeuro.com/itunes   Thanks for listening, and join us next time as we continue to navigate the brain and behavior! [Note: This podcast and all linked content is intended for general educational purposes only and does not constitute the practice of psychology or any other professional healthcare advice and services. No professional relationship is formed between hosts and listeners. All content is to be used at listeners' own risk. Users should always seek appropriate medical and psychological care from their licensed healthcare provider.]

Dr. Christian Cordano discusses his paper, "Differences in Age-related Retinal and Cortical Atrophy Rates in Multiple Sclerosis". Show references: https://n.neurology.org/content/99/15/e1685 This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.

Dr. Justin Abbatemarco talks with Dr. Christian Cordano about differences in age-related retinal and cortical atrophy rates in multiple sclerosis. Read the full article in Neurology. This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information.