Podcasts about phenotypic

duckDNA recently concluded its second season, which brought continued enthusiasm from hunters and several never-before-seen hybrids! On this episode, Dr. Mike Brasher is joined by conservation science assistants, Kayci Messerly and Katie Tucker, and Dr. Phil Lavretsky to share initial results from season 2 while discussing genetic mysteries uncovered through the analysis of several unique hybrid ducks. Also discussed are behind-the-scenes interactions with participating hunters and the potential future of duckDNA. Thanks to hunters for their support and participation and a special thanks to our year 2 funding partners -- Pinola Conservancy, Rice Pond Preserve, and Brian Hornung.Listen now: www.ducks.org/DUPodcastSend feedback: DUPodcast@ducks.org

14e émission de la 60e session...Cette semaine, jazz moderne, freebop et free jazz! En musique: Devin Gray sur l'album Melt All The Guns II  (Rataplan, 2024); Travis Reuter sur l'album Quintet Music  (Indépendant, 2024); Patrick Wolff sur l'album You Can't Stand Still  (Phenotypic, 2024); Dennis Gonzalez Legacy Band sur l'album Live at the Texas Theatre  (Astral Spirits, 2024); AALY Trio sur l'album Sustain  (Silkheart, 2024); Painkiller sur l'album Samsara  (Tzadik, 2024)...

The menstrual cycle is known to affect things like mood and changes in pain. But there can also be symptoms that have a serious impact on a person's function, ability to work, ability to maintain friendships and romantic relationships. This is a rare condition known as premenstrual dysphoric disorder. But it's not the only psychiatric condition that can worsen with changes in the menstrual cycle. For instance, nearly 60 percent of menstruating patients with depression can experience cyclical worsening similar to PMDD. Conditions such as these are generally referred to as menstrual cycle affective change. Menstrual cycle affective change is more common in those with chronic psychiatric disorders. The authors are interested in reframing the conversation around menstrual cycle affective change to be something that is a more fundamental process that we can study across disorders, across categories, and identify biomarkers that might help us predict who's going to have those symptoms in more complex ways than we might be able to do with categories. This paper represents how can we take this dimensional way of thinking about menstrual cycle affective change and talk about the specific ways that we can be precise in looking at the time the time characteristics of that, the specific mechanisms, et cetera. Tory Eisenlohr-Moul is an associate professor of psychiatry at the University of Illinois at Chicago in the department of psychiatry, and she's one of the authors. Jordan Barone is an MD/PhD candidate at the University of Illinois at Chicago, and she's another author. Hosted on Acast. See acast.com/privacy for more information.

BUFFALO, NY- November 20, 2024 – This #review was #published by Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), in Volume 16, Issue 17, titled, “A systematic review of phenotypic and epigenetic clocks used for aging and mortality quantification in humans.” This systematic review by Brandon Warner, Edward Ratner, Anirban Datta and Amaury Lendasse from Verseon International Corporation, University of Houston and Missouri University of Science and Technology, explores how biological clocks measure aging and predict mortality. These clocks are tools scientists use to track the body's aging process by identifying specific changes over time. This review analyzes 33 biological clocks proposed over the last decade, offering key insights into their design, accuracy, and clinical applications. The study categorizes these clocks into two types: epigenetic clocks, which track cellular aging through DNA changes, and phenotypic clocks, which assess physical biomarkers like blood pressure and cholesterol. These findings highlight the transformative potential of biological clocks in aging research and preventive healthcare. Epigenetic clocks have demonstrated impressive precision in estimating chronological age by analyzing DNA methylation, a key marker of cellular aging. These tools are also linked to age-related diseases, offering valuable insights into the aging process. Phenotypic clocks, which rely on common clinical measures, have been shown to better predict mortality and health outcomes. As the study highlights: “Phenotypic clocks have shown to be better predictors of mortality than chronological age and do so using easily measurable clinical variables.” Their affordability and ease of implementation make them especially practical for healthcare settings. The review also explores how advancements in technology, such as artificial intelligence and machine learning, are enhancing the accuracy and utility of these clocks. For example, newer models now use neural networks to improve predictive performance and identify key aging biomarkers. Understanding biological age can help detect diseases earlier, tailor interventions, and encourage lifestyle changes to slow aging. By providing a clearer picture of individual aging processes, these clocks could lead the way toward personalized healthcare and improved health outcomes. The researchers call for further studies to make epigenetic clocks more affordable and expand the integration of phenotypic clocks into routine healthcare. In conclusion, this review underscores the transformative potential of biological clocks to redefine our understanding and management of aging. By addressing gaps in current research, it paves the way for future advancements in aging science and healthcare. DOI - https://doi.org/10.18632/aging.206098 Corresponding author - Brandon Warner - bwarner@verseon.com Video short - https://www.youtube.com/watch?v=rrqk5HrljQ0 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Introducing Why dementia could start in your blood vessels with Dr. William Li from ZOE Science & Nutrition.Follow the show: ZOE Science & Nutrition 55 million people suffer dementia worldwide with numbers expected to double every 20 years. Understanding the link between our heart health and brain function is critical, illuminating the profound impact that heart health has on preventing dementia.Dr. William Li, an expert in cardiovascular and metabolic health. He reveals how caring for our heart is not just about longevity but maintaining sharp, effective brain function as we age. His groundbreaking work has impacted more than seventy diseases including diabetes, heart disease, and obesity. Dr. Li is also a New York Times best-selling author.In today's episode, Dr. Li explains how simple lifestyle choices in diet, exercise and sleep can drastically shape our brain's health and stave off dementia.

Introducing Why dementia could start in your blood vessels with Dr. William Li from ZOE Science & Nutrition.Follow the show: ZOE Science & Nutrition 55 million people suffer dementia worldwide with numbers expected to double every 20 years. Understanding the link between our heart health and brain function is critical, illuminating the profound impact that heart health has on preventing dementia.Dr. William Li, an expert in cardiovascular and metabolic health. He reveals how caring for our heart is not just about longevity but maintaining sharp, effective brain function as we age. His groundbreaking work has impacted more than seventy diseases including diabetes, heart disease, and obesity. Dr. Li is also a New York Times best-selling author.In today's episode, Dr. Li explains how simple lifestyle choices in diet, exercise and sleep can drastically shape our brain's health and stave off dementia.

Marfan Surgery   Guest: Alberto Pochettino, M.D. Hosts: Paul A. Friedman, M.D.   Marfan syndrome is a genetic abnormality where the fibrillin protein is abnormal. That affects all collagen structures within a given individual. Phenotypic features involve ocular abnormalities such as lens dislocation and a higher risk of retinal detachment, as well as diffuse musculoskeletal abnormalities such as scoliosis, joints abnormalities, and the diffuse hyper extension of all joints. By far the most life-threatening feature in Marfan syndrome is aortic abnormality.   Topics Discussed: Which patients with Marfan syndrome should be evaluated for aortic disease? Do all Marfan patients develop aortic aneurysm? What other cardiovascular abnormalities are noted in Marfan syndrome? What preventive operations are available, and what are the expected outcomes from such operations? If a Marfan patient develops a type B dissection what is the appropriate management?   Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. LinkedIn: Mayo Clinic Cardiovascular Services Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

55 million people suffer dementia worldwide with numbers expected to double every 20 years. Understanding the link between our heart health and brain function is critical, illuminating the profound impact that heart health has on preventing dementia.Dr. William Li, an expert in cardiovascular and metabolic health. He reveals how caring for our heart is not just about longevity but maintaining sharp, effective brain function as we age. His groundbreaking work has impacted more than seventy diseases including diabetes, heart disease, and obesity. Dr. Li is also a New York Times best-selling author.In today's episode, Dr. Li explains how simple lifestyle choices in diet, exercise and sleep can drastically shape our brain's health and stave off dementia.If you want to uncover the right foods for your body, head to zoe.com/podcast, and get 10% off your membership.Follow ZOE on InstagramTimecodes00:00 Introduction01:23 Quickfire questions03:30 Understanding dementia and Alzheimer's disease04:50 Dementia versus ageing06:35 The role of blood vessels in brain health07:55 How circulation affects brain function09:23 What causes blood clots and strokes?11:06 The importance of maintaining healthy blood vessels12:15 The impact of lifestyle choices on brain health15:01 What happens in our brains when we sleep?19:35 What is the glymphatic system?22:40 Vascular dementia may be the most common form of dementia24:35 The role of glucose in brain function27:10 What causes dementia and why does it happen when we get older?29:00 Preventing dementia with lifestyle changes31:10 What are healthy blood vessels like?37:50 The surprising role of EPCs in brain repair41:30 Can you slow down or reverse dementia?52:08 The connection between gut health and brain health51:40 The importance of exercise for brain health56:30 How to avoid dementia01:01:16 The link between mental health and cardiovascular diseaseRelevant studies:A human brain vascular atlas reveals diverse mediators of Alzheimer's risk, published in NatureHeart-brain connections: Phenotypic and genetic insights from magnetic resonance images, published in ScienceCocoa flavanol consumption improves cognitive function, blood pressure control, and metabolic profile in elderly subjects: the Cocoa, Cognition, and Aging (CoCoA) Study—a randomized controlled trial, published in The American Journal of Clinical NutritionDr. William Li's books:Eat to Beat Your DietEat to Beat Disease Is there a nutrition topic you'd like us to explore? Email us at podcast@joinzoe.com, and we'll do our best to cover it. Episode transcripts are available here.

In this week's episode, Jonathan is joined by Stephanie Hanna, a Research Fellow for the Diabetes Research and Wellness Foundation, in the Division of Infection and Immunity, at Cardiff University's School of Medicine, Wales, UK. In this fascinating episode, the pair discuss all things diabetes, including immunotherapy, the future of diagnosis, and how to predict your diabetes risk. Use the following timestamps to navigate the content in this episode:  (00:00)-Introduction (01:22)-Getting into Type 1 diabetes (T1D) (02:23)-Stages of T1D (05:04)-Biomarkers of T1D (07:01)-Phenotypic analysis of T and B-cells (08:24)-Diabetes progression (10:11)-Immunotherapy for T1D (14:00)-Challenges in measuring immune response (16:22)-Some thoughts on artificial intelligence (18:11)-How to get involved in a study (19:27)-Checking your own antibody status (23:51)-Thyroid eye disease (25:19)-Risks of overlooking T1D (27:34)-Three wishes for the future of healthcare

Commentary by Dr. Valentin Fuster

An arms race between newts and snakes means biological warfare.  Become a Patreon: https://www.patreon.com/herphighlights Merch: https://www.redbubble.com/people/herphighlights/shop Full reference list available here: http://www.herphighlights.podbean.com Main Paper References: Gilbert AL, Cabrera S, Hague MTJ, Stokes AN, Feldman CR, Hanifin CT, Brodie ED, Brodie ED. 2023. Phenotypic outcomes of predator–prey coevolution are predicted by landscape variation in climate and community composition. Functional Ecology 37:2170–2180. DOI: 10.1111/1365-2435.14360. Other Mentioned Papers/Studies: Calhoun, D. M., Bucciarelli, G. M., Kats, L. B., Zimmer, R. K., & Johnson, P. T. (2017). Noxious newts and their natural enemies: Experimental effects of tetrodotoxin exposure on trematode parasites and aquatic macroinvertebrates. Toxicon, 137, 120-127. Williams, B. L., Hanifin, C. T., Brodie, E. D., & Brodie III, E. D. (2010). Tetrodotoxin affects survival probability of rough-skinned newts (Taricha granulosa) faced with TTX-resistant garter snake predators (Thamnophis sirtalis). Chemoecology, 20, 285-290. Editing and Music: Podcast edited by Emmy – https://www.fiverr.com/emmyk10  Intro/outro – Treehouse by Ed Nelson Species Bi-week theme – Michael Timothy Other Music – The Passion HiFi, https://www.thepassionhifi.com

References Immunity. 2018 Oct 16;49(4):695-708 Front Immunol. 2019; 10: 14 Front. Immunol., 24 July 2017 Vol 8. Sec. T Cell Biology --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

In this podcast, Contributing Editor Berkeley Limketkai, MD, PhD, interviews Dr. Octavia Pickett-Blakely on the article “A Phenotypic Approach to Obesity Treatment” published in the October 2023 issue of NCP. Business Corporate by Alex Menco | alexmenco.net Music promoted by www.free-stock-music.com Creative Commons Attribution 3.0 Unported License creativecommons.org/licenses/by/3.0/deed.en_US October 2023

BJ and his wife give each other Christmas lists every year. This year BJ's wife wants a guitar string bracelet made from John Mayer's used guitar strings. Colorado is the first state to approve gambling on paintball! Mathew Perry was laid to rest over the weekend. Phenotypic age is a measure of biological age that can tell you if you are physiologically younger or older than your chronological age. Do you feel older or younger than your chronological age? Black Friday deals are starting up soon! We miss the days of tickle me Elmo and Walmart fights. Willie Nelson was inducted into the hall of fame. Some snow storms are headed this way and could hit the metro as soon as Wednesday. The Las Vegas Culinary union could be going on strike this Friday. This is all before F1 is set to start on the 17th. Carson is trying to convince Jamie to use the Kroger Boost Membership, but she can't remember her password to login to the Kroger app. Jamie is OVER the iPhone.

Hour 3 - Phenotypic age is a measure of biological age that can tell you if you are physiologically younger or older than your chronological age. Do you feel older or younger than your chronological age? Black Friday deals are starting up soon! We miss the days of tickle me Elmo and Walmart fights. Willie Nelson was inducted into the hall of fame. 

Phenotypic age is a measure of biological age that can tell you if you are physiologically younger or older than your chronological age. Do you feel older or younger than your chronological age? 

Dr Rodrigo Starosta describes the management of a challenging presentation of PIGO-CDG and discusses insights into this rare GPI-anchor disorder. PIGO-CDG: A case study with a new genotype, expansion of the phenotype, literature review, and nosological considerations Rodrigo Tzovenos Starosta, et al https://doi.org/10.1002/jmd2.12396

Dante and Tommy are back to talk about Cat out of the Bag 2.7 & 2.8!  Read along with us: https://twigserial.wordpress.com/category/story/arc-2-cat-out-of-the-bag/2-07/ Discussion question (continued from last time): Tell us about a story in which the characters' abilities are simultaneously an advantage and a disadvantage. Bonus discussion question: Tell us the full official name of the academy in Radham. Totally legit contest: Send us a sound byte to use for the Monster Corner (or any other segment). The winner gets to hear their sound byte in future episodes! Bio fact citation: Joanna Wolfe, Javier Luque, & Heather Bracken-Grissom: “How to become a crab: Phenotypic constraints on a recurring body plan” (2021) https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202100020

Guests: Dr. Jimena Laporta, University of Wisconsin-MadisonCovering the topic of Fetal Hyperthermia, Dr. Jimena Laporta of the University of Wisconsin is the second podcast at the 2022 Tri-State Dairy Conference. This makes up part two of the conference series.Heat stress is known to be a significant issue for dairy cattle with both global temperatures and sensitivity of dairy cattle to heat rising. Dr. Laporta adds that negative effects of heat stress last for multiple generations and lactations. 1:16While heat stress affects all cattle, Dr. Laporta focuses on dry cows and their offspring, to provide a more holistic view of its effects. Beginning with the dry cow, she notes that heat stress lessens milk production, as it derails involution and redevelopment. 3:59Epigenetics play a role in fetal development in the dry cow - fetal hyperthermia creates changes in the DNA of the fetus, altering the epigenome. 11:22What are the effects of fetal hyperthermia short term and long term, as well as across generations?Dr. Laporta details many short term hallmarks of prenatal heat stress: the dam experiences a reduction in gestation length leading to a premature calf that has organ alterations, less of an immune response, less feed intake, and a higher core body temperature. 16:31Analyzing a large data set of cattle affected by fetal hyperthermia, Dr. Laporta finds long term effects. The daughters had lower survival rates and less production each lactation, which carried over to the next 2-3 generations. Heat stress effects cost the dairy industry $1.4 billion. 23:08Turning her focus to the molecular signature of heat stress, Dr. Laporta discusses her findings from inspecting a mammary gland, concluding that heat stress causes a lower cell proliferative capacity and negatively impacts protein synthesis. Both lead to compromised milk storage and synthetic capacity. 29:28Wrapping up, Dr. Laporta states that heat stress negatively affects growth, organ development, immune function, survival, longevity, and milk yield for multiple generations. However, she believes that management and nutritional intervention can reduce such effects. 36:58Please subscribe and share with your industry friends to bring more people to join us around the Real Science Exchange virtual pub table.  If you want one of our new Real Science Exchange t-shirts, screenshot your rating, review, or subscription, and email a picture to anh.marketing@balchem.com. Include your size and mailing address, and we'll get a shirt in the mail to you.

Dr Emma Glamuzina of the National Metabolic Service in New Zealand, describes a neonatal presentation of CARS2- related mitochondrial disease and the diagnostic challenges this brought in a pre-exome/genome era. Severe neonatal onset neuroregression with paroxysmal dystonia and apnoea: Expanding the phenotypic and genotypic spectrum of CARS2-related mitochondrial disease Jessie Poquérusse, et al https://doi.org/10.1002/jmd2.12360

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.27.550845v1?rss=1 Authors: Davies, J., Hoerder-suabedissen, A., Musaelyan, K., Torroba, M., Daubney, J., Untermoser, N., Carter, T., Bauer, U., Walker, R., Harris, K. S., Bromhead, L., Suresh, M., Fouka, P., Li, Y., Davies, S., Webber, C., Bannerman, D., Terstappen, G., Russell, A., Szele, F. Abstract: Stem cells and neurogenesis persist in the postnatal and adult brain. Adult brain stem cells can be neuroprotective in disease and augment hippocampal-dependent cognitive function and thus are an important therapeutic target. Although many molecules have been discovered that regulate neurogenesis, few studies have attempted to amplify the process pharmacologically as a therapeutic goal. To address this gap, we used murine neurosphere cultures from the two major stem cell niches: the subventricular zone (SVZ) and the subgranular zone (SGZ). We screened compounds sharing pharmacophores with known inducers of neurogenesis and found several dozen proneurogenic compounds in an in vitro phenotypic screen. One, OXS-N1 was stable, and had acceptable absorption, distribution, metabolism, and excretion profiles in animal studies. OXS-N1 could increase neurogenesis in the SVZ and SGZ in WT mice after both intraperitoneal and oral administration. The number of newborn neurons (BrdU+/NeuN+) was increased; however, the number of activated stem cells (BrdU+/GFAP+) was not, suggesting an effect on neurogenesis independent of stem cell activation. This was supported by OXS-N1 increasing neurosphere differentiation but not proliferation. OXS-N1 also increased neurogenesis and improved performance in a Y maze cognitive task in PDGF-APPSw,Ind mice, a model of Alzheimer's disease. RNAseq of SVZ and SGZ neurospheres in turn showed that genes associated with synaptic function were significantly increased by OXS-N1. Our study demonstrates the utility of phenotypic screening for the identification of molecules that increase neurogenesis and might be of therapeutic relevance. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.23.546309v1?rss=1 Authors: Xuan, W., Cheng, F., Han, X., Tipparaju, S., Ashraf, M. Abstract: Background: Extensive studies have been conducted in skeletal muscle and myocardium affected by Duchenne Muscular Dystrophy (DMD) disease but there is a significant gap of research in the role of vascular smooth muscle cells (VSMCs) in DMD. Here, we investigated the role of dystrophin deficiency in the maintenance of VSMCs contractile phenotype. Methods: 12-14 months old mdx mice and DMD induced pluripotent stem cells (iPSC) derived VSMCs were used as disease models. Morphological and immunohistochemistry analyses were performed to determine histological changes and the expression of contractile markers. Transmission Electron Microscopy (TEM) was used to assess ultrastructural changes in the VSMCs. Mito-tracker staining and TUNEL staining were performed to determine mitochondria fission-fusion and apoptosis respectively. mRNA Sequencing for normal iPSC derived VSMCs (WT-VSMCs) and DMD iPSC derived VSMCs (DMD-VSMCs) with or without oxidative stress was performed. KEGG signaling pathway enrichment, Go function enrichment and Gene set enrichment analysis (GESA) were conducted to explore the potential mechanism responsible for these changes. In addition, transcription factor enrichment analysis was performed to unravel mechanistic pathways of regulatory networks. Results: Spontaneous abnormal VSMCs proliferation, loss of vascular structure and degenerative changes occurred in VSMCs in aorta from 12-14 months old mdx mice. The DMD-VSMCs showed maturation defect, loss of mitochondrial hemostasis, and increased vulnerability to oxidative stress compared with WT-VSMCs. Transcriptome analysis revealed dysregulation of smooth muscle proliferation, differentiation, and vascular development in DMD-VSMCs. Transcriptional factor, target, and motif discovery analysis of the dysregulated gene set suggested potential contributions of transcriptional factors GADD45A, SOX9, TIA1, RBBP9 and FOXM to the phenotypes of DMD-VSMCs. Under oxidative stress, initiation of apoptotic process was significantly enhanced in DMD-VSMCs while their response to hypoxia and oxidative stress was downregulated. Conclusions: Dystrophin deficiency induced VSMCs phenotype switching and disrupted mitochondrial metabolism. The findings in this study underscore the importance of vascular dysfunction in DMD disease and therapeutic interventions to restore VSMC phenotype may ameliorate the propensity of disease progression. It is suggested that the transcriptome analysis may allow the discovery of potential signaling pathways involved in the dysregulation of transcription factors. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

My guest today is Leroy Hood, a world-renowned scientist and recipient of the National Medal of Science in 2011. He co-founded the Institute for Systems Biology (ISB) in 2000, served as its first President from 2000-2017, and is a Professor and Chief Strategy Officer. Dr. Hood was a faculty member at Caltech, serving for 10 years as the Chair of Biology. During this period, he and his colleagues developed four sequencer and synthesizer instruments that paved the way for the Human Genome Project's successful mapping and understanding of the human genome. He and his students also deciphered many of the complex mechanisms of antibody diversification. In 1992, Dr. Hood founded and chaired the Department of Molecular Biotechnology at the University of Washington, the first academic department devoted to cross-disciplinary biology. The topic is his book The Age of Scientific Wellness. In this episode of Trend Following Radio we discuss: Health care opportunities Phenotypic traits
 Three components of health trajectory
 Genome discussion Obesity
 Jump in! --- I'm MICHAEL COVEL, the host of TREND FOLLOWING RADIO, and I'm proud to have delivered 10+ million podcast listens since 2012. Investments, economics, psychology, politics, decision-making, human behavior, entrepreneurship and trend following are all passionately explored and debated on my show. To start? I'd like to give you a great piece of advice you can use in your life and trading journey… cut your losses! You will find much more about that philosophy here: https://www.trendfollowing.com/trend/ You can watch a free video here: https://www.trendfollowing.com/video/ Can't get enough of this episode? You can choose from my thousand plus episodes here: https://www.trendfollowing.com/podcast My social media platforms: Twitter: @covel Facebook: @trendfollowing LinkedIn: @covel Instagram: @mikecovel Hope you enjoy my never-ending podcast conversation!

My guest today is Leroy Hood, a world-renowned scientist and recipient of the National Medal of Science in 2011. He co-founded the Institute for Systems Biology (ISB) in 2000, served as its first President from 2000-2017, and is a Professor and Chief Strategy Officer. Dr. Hood was a faculty member at Caltech, serving for 10 years as the Chair of Biology. During this period, he and his colleagues developed four sequencer and synthesizer instruments that paved the way for the Human Genome Project's successful mapping and understanding of the human genome. He and his students also deciphered many of the complex mechanisms of antibody diversification. In 1992, Dr. Hood founded and chaired the Department of Molecular Biotechnology at the University of Washington, the first academic department devoted to cross-disciplinary biology. The topic is his book The Age of Scientific Wellness. In this episode of Trend Following Radio we discuss: Health care opportunities Phenotypic traits
 Three components of health trajectory
 Genome discussion Obesity
 Jump in! --- I'm MICHAEL COVEL, the host of TREND FOLLOWING RADIO, and I'm proud to have delivered 10+ million podcast listens since 2012. Investments, economics, psychology, politics, decision-making, human behavior, entrepreneurship and trend following are all passionately explored and debated on my show. To start? I'd like to give you a great piece of advice you can use in your life and trading journey… cut your losses! You will find much more about that philosophy here: https://www.trendfollowing.com/trend/ You can watch a free video here: https://www.trendfollowing.com/video/ Can't get enough of this episode? You can choose from my thousand plus episodes here: https://www.trendfollowing.com/podcast My social media platforms: Twitter: @covel Facebook: @trendfollowing LinkedIn: @covel Instagram: @mikecovel Hope you enjoy my never-ending podcast conversation!

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.09.536174v1?rss=1 Authors: Gregory, E. F., Kalra, S., Brock, T., Bonne, G., Luxton, G. G., Hopkins, C., Starr, D. A. Abstract: Striated muscle laminopathies caused by missense mutations in the nuclear lamin gene LMNA are characterized by cardiac dysfunction and often skeletal muscle defects. Attempts to predict which LMNA variants are pathogenic and to understand their physiological effects lags behind variant discovery. We created Caenorhabditis elegans models for striated muscle laminopathies by introducing pathogenic human LMNA variants and variants of unknown significance at conserved residues within the lmn-1 gene. Severe missense variants reduced fertility and/or motility in C. elegans. Nuclear morphology defects were evident in the hypodermal nuclei of many lamin variant strains, indicating a loss of nuclear envelope integrity. Phenotypic severity varied within the two classes of missense mutations involved in striated muscle disease, but overall, variants associated with both skeletal and cardiac muscle defects in humans lead to more severe phenotypes in our model than variants predicted to disrupt cardiac function alone. We also identified a separation of function allele, lmn-1(R204W), that exhibited normal viability and swimming behavior but had a severe nuclear migration defect. Thus, we established C. elegans avatars for striated muscle laminopathies and identified LMNA variants that offer insight into lamin mechanisms during normal development. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This is part 2 of a two part series. Dr. Rachael Liesman goes over scenarios where genotypic and phenotypic testing do not match and what to do. What do you do when your molecular instrument detects mec-A and Staphylococcus aureus but your susceptibility report shows oxacillin susceptible? What about VanA and Enterococcus? As Medical Laboratory Scientists in Microbiology, we encounter this type of situations. Tune in to find out how to troubleshoot these discrepancies. Link to Dr. Patricia Simner's article: https://journals.asm.org/doi/full/10.1128/JCM.00138-20

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.17.532588v1?rss=1 Authors: Patir, A., Barrington, J., Szymkowiak, S., Straus, D., Alfieri, A., Lefevre, L., Henderson, N. C., Horsburgh, K., Ramachandran, P., McColl, B. W. Abstract: Acute stroke causes substantial mortality and morbidity and provokes extensive changes to myeloid immune cell populations in the brain that may be targets for limiting brain damage and enhancing brain repair. The most effective immunomodulatory approaches will require precise manipulation of discrete myeloid cell phenotypes in time and space to avoid harmful effects of indiscriminate neuroimmune perturbation. We sought to define how stroke alters the composition and phenotypes of mononuclear myeloid cells with particular attention to how cell ontogeny and spatial organisation combine to expand myeloid cell diversity across the brain after stroke. Multiple reactive microglial states and dual monocyte-derived populations contributed to an extensive repertoire of myeloid cells in post-stroke brain. We identified important overlap and distinctions among different cell types and states that involved ontogeny- and spatial-related properties. Notably, brain connectivity with infarcted tissue underpinned the pattern of local and remote altered cell accumulation and reactivity. Our discoveries suggest a global but anatomically-governed brain myeloid cell response to stroke that comprises diverse phenotypes arising through intrinsic cell ontogeny factors interacting with exposure to spatially-organised brain damage and neuroaxonal cues. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Those of you that work in Clinical Microbiology have seen at one point that a molecular test detects a gene for antimicrobial resistance and the susceptibility profile does not match. What do we do then? In this episode Dr. Rachael Liesman joins to the podcast to talk about this. What is genotypic testing? What is phenotypic testing? How do we perform these in the lab? How do we troubleshoot these discrepancies? Tune in to this episode which is the first of a two part series to find out.Link to Dr. Liesman's presentation: https://drive.google.com/file/d/1dphVN79alVfQERTL_rTihUA-zlqBOJfY/view?usp=share_link

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.24.529858v1?rss=1 Authors: Godoy-Corchuelo, J. M., Ali, Z., Martins-Bach, A. B., Garcia-Toledo, I., Fernandez-Beltran, L. C., Nair, R. R., Spring, S., Nieman, B., Jimenez-Coca, I., Bains, R. S., Forrest, H., Lerch, J., Miller, K., Fisher, E. M. C., Cunningham, T. J., Corrochano, S. Abstract: FUS (Fused in sarcoma) is a ubiquitously expressed RNA binding protein, which is mislocalized and aggregated in some forms of frontotemporal dementia (FTD), whilst mutations in FUS cause aggressive juvenile forms of amyotrophic lateral sclerosis (ALS), as in the case with the FUSDelta14 mutation. Most studies have focused on the role of FUS in motor neuron degeneration, although it is unknown whether FUS mutations affect other cell and tissue types, and the neurodevelopmental impact of FUS mutation on the nervous system is unclear. Here we studied pleiotropic phenotypes in a physiological knock-in mouse model carrying a partially humanised FUSDelta14 mutation in homozygosity. We performed RNA sequencing of six different tissues (frontal cortex, spinal cord, tibialis anterior muscle, white and brown adipose tissue and liver) and found that the genes and pathways affected were generally tissue-specific and showed few commonalities. Phenotypic assessment of homozygous FUSDelta14 mice revealed systemic metabolic alterations related to the pathway changes identified. Homozygous FUSDelta14 brains displayed significant morphological alterations including a thinner cortex, reduced neuronal number and increased gliosis, which correlated with fatal seizures in early adult life. Altogether, our data supports a wide-ranging role for FUS, and suggests that the disease aetiology of FUS mutation can include developmental and pleiotropic phenotypes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.21.529372v1?rss=1 Authors: Han, Y., Liu, Y., Tian, X., Zhang, X., Liu, D., Yan, C. Abstract: Aortic aneurysm (AA) is a potentially fatal disease with the possibility of rupture, causing high mortality rates with no effective drugs for the treatment of AA. The mechanism of AA, as well as its therapeutic potential to inhibit aneurysm expansion, has been minimally explored. Small non-coding RNA (miRNAs and miRs) is emerging as a new fundamental regulator of gene expression. This study aimed to explore the role and mechanism of miR-193a-5p in abdominal aortic aneurysms (AAA). In AAA vascular tissue and Angiotensin II (Ang II)-treated vascular smooth muscle cells (VSMCs), the expression of miR-193a-5 was determined using real-time quantitative PCR (RT-qPCR). Western blotting was used to detect the effects of miR-193a-5p on PCNA, CCND1, CCNE1, and CXCR4. To detect the effect of miR-193a-5p on the proliferation and migration of VSMCs, CCK-8, and EdU immunostaining, flow cytometry, wound healing, and Transwell Chamber analysis were performed. In vitro results suggest that overexpression of miR-193a-5p inhibited the proliferation and migration of VSMCs, and its inhibition aggravated their proliferation and migration. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.08.527682v1?rss=1 Authors: Balint, B., Bernstorff, I. G. L., Schwab, T., Schäfers, H.-J. Abstract: Background: Aortic complications are more likely to occur in patients with ascending aortic aneurysms and concomitant aortic regurgitation (AR). AR may have a negative impact on the aortic wall structure even in patients with tricuspid aortic valves and absence of aortic dilatation. It is unknown whether smooth muscle cell (SMC) changes are a feature of AR-associated aortic remodeling. Methods: Non-dilated aortic samples were harvested intra-operatively from individuals with normal aortic valves (n=10) or those with either predominant aortic stenosis (AS; n=20) or AR (n=35). Tissue from each patient was processed for immunohistochemistry or used for the extraction of medial SMCs. Tissue and cells were stained for markers of SMC contraction (alpha-smooth muscle actin; ASMA), synthesis (vimentin) and senescence (p16/p21). Replicative capacity was analyzed in cultured SMCs from AS- and AR-associated aortas. A sub-analysis compared SMCs from individuals with either TAVs or BAVs to rule out the effect of aortic valve morphology. Results: In aortic tissue samples, AR was associated with decreased ASMA and increased vimentin, p16 and p21 compared to normal aortic valves and AS. In cell culture, SMCs from AR-aortas had decreased ASMA and increased vimentin compared to SMCs from AS-aortas. AR-associated SMCs had increased p16 and p21 expression, and they reached senescence earlier than SMCs from AS-aortas. In AR, SMC changes were more pronounced with the presence of a BAV. Conclusions: AR itself negatively impacts SMC phenotype in the ascending aortic wall, which is independent of aortic diameter and aortic valve morphology. These findings provide insight into the mechanisms of AR-related aortic remodeling, and they provide a model for studying SMC-specific therapies in culture. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.06.527281v1?rss=1 Authors: Jones, I., Vargas, P. P., Garcia, M. A., Sero, J. E., Bakal, C. Abstract: Protein concentrations are not constant across cell sizes; many dilute or concentrate in response to growth. Through quantitative analysis of ~400,000 single cells across ten cell breast epithelial cell lines (including tumour and non-tumour cells), we show that the cytoplasmic and total concentrations of YAP/TAZ, decreases as a function of cell size in G1 and G2. Degradation of YAP/TAZ alone could not explain this phenomenon. Near S-Phase, YAP/TAZ was synthesised in a ploidy and size dependent manner. Theoretical modelling of YAP/TAZ concentration distributions demonstrated the rate of dilution with cell size relates to YAP/TAZ heterogeneity across the population. YAP/TAZ dilution in the cytoplasm was largely robust to perturbations in Rho GTPase and LATS1/2 signalling, whereas the YAP/TAZ nuclear cytoplasmic (n/c) ratio, was not. Alterations to the n/c ratio following perturbation were more commonly driven by cytoplasmic dilution rather than nuclear enrichment. Together, this work reveals how size scaling phenomena may influence the subcellular distribution of transcription factors, and more generally, relates protein dilution to the emergence of non-genetic heterogeneity in cell populations. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Save 50% on my Initial Consultation during the month of January 2023. Use this link to save! Follow, rate and review your favorite episodes to let me know the things you like so I can keep delivering great content that brings value to your life and health. Check out my online DIY programs for thyroid, gut health and detox.  https://www.drnoseworthy.com/store Follow us on social media Facebook Instagram You can also listen on Apple and Spotify - and all other major podcast platforms.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.16.520302v1?rss=1 Authors: Beri, P., Woo, Y. J., Schierenbeck, K., Chen, K., Barnes, S. W., Ross, O., Krutil, D., Quackenbush, D., Fang, B., Walker, J., Barnes, W., Toyama, E. Abstract: COPD is the third leading cause of death worldwide, but current therapies for COPD are only effective at treating the symptoms of the disease rather than targeting the underlying pathways that are driving the pathogenic changes. The lack of targeted therapies for COPD is in part due to a lack of knowledge about drivers of disease progression and the difficulty in building relevant and high throughput models that can recapitulate the phenotypic and transcriptomic changes associated with pathogenesis of COPD. To identify these drivers, we have developed a cigarette smoke extract (CSE)-treated bronchosphere assay in 384-well plate format that exhibits CSE-induced decreases in size and increase in luminal secretion of MUC5AC. Transcriptomic changes in CSE-treated bronchospheres resemble changes that occur in human smokers both with and without COPD compared to healthy groups, indicating that this model can capture human smoking signature. To identify new targets, we ran a small molecule compound deck screening with diversity in target mechanisms of action and identified hit compounds that attenuated CSE induced changes, either decreasing spheroid size or increasing secreted mucus. This work provides insight into the utility of this bronchosphere model in examining human respiratory diseases, the pathways implicated by CSE, and compounds with known mechanisms of action for therapeutic development. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.12.520139v1?rss=1 Authors: Liu, P. W., Zhang, H., Werley, C. A., Pichler, M., Ryan, S., Lewarch, C., Jacques, J., Grooms, J., Ferrante, J., Li, G., Zhang, D., Bremmer, N., Barnett, A., Chantre, R., Elder, A. E., Cohen, A. E., Williams, L. A., Dempsey, G. T., McManus, O. B. Abstract: Chronic pain associated with osteoarthritis (OA) remains an intractable problem with few effective treatment options. New approaches are needed to model the disease biology and to drive discovery of therapeutics. Here, we present an in vitro model of OA pain, where dorsal root ganglion (DRG) sensory neurons were sensitized by a defined mixture of disease-relevant inflammatory mediators, here called Sensitizing PAin Reagent Composition or SPARC. OA-SPARC components showed synergistic or additive effects when applied in combination and induced pain phenotypes in vivo. To measure the effect of OA-SPARC on neural firing in a scalable format for drug discovery, we used a custom system for high throughput all-optical electrophysiology. This system enabled light-based membrane voltage recordings from hundreds of neurons in parallel with single cell resolution and a throughput of up to 500,000 neurons per day, with patch clamp-like single action potential resolution. A computational framework was developed to construct a multiparameter OA-SPARC neuronal phenotype and to quantitatively assess phenotype reversal by candidate pharmacology with different mechanisms of action. We screened ~3000 approved drugs and mechanistically focused compounds, yielding data from over 1.2 million individual neurons with detailed assessment of both functional OA-SPARC phenotype rescue and orthogonal 'off-target' effects. Analysis of confirmed hits revealed diverse potential analgesic mechanisms including well-known ion channel modulators as well as less characterized mechanisms including MEK inhibitors and tyrosine kinase modulators, providing validation of the platform for pain drug discovery. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Despite the large human and societal costs of neuropsychiatric disorders, many of these conditions have poor or no treatment options. And there has been a dearth of new mechanisms to treat major neuropsychiatric disorders for decades. PsychoGenics is seeking to change that with its unique approach to drug discovery for these conditions. Rather than rely on a target-based approach, the company has created high-throughput phenotypic screens using validated mouse models and artificial intelligence to detect behavioral changes. We spoke to Mark Varney, chief scientific officer of PsychoGenics, about the company's use of phenotypic screens to discover new drugs for neuropsychiatric disorders, how it works, and the case for this approach.

In this latest episode of the In Conversation With series, DDW's Megan Thomas speaks with Dr Mark Varney, the Chief Scientific Officer at PsychoGenics, who discusses both his and the company's work on CNS drug discovery in more detail.  PsychoGenics has taken a novel approach to CNS drug discovery, as its phenotypic approach can deliver treatments that work via novel, unknown or multiple mechanisms. Phenotypic screening has accurately predicted better therapeutic activity with fewer side effects for CNS disorders, leading to the identification of some of the most efficacious drug candidates. PsychoGenics' phenotypic drug discovery significantly reduces the time and cost to reaching approved Investigational New Drug (IND) status, resulting in the identification of a viable drug candidate from a few hundred analogs tested in lead optimisation in just over a year.  

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.08.515730v1?rss=1 Authors: Kwasa, J., Peterson, H. M., Jones, L., Karrobi, K., Parker, T., Nickerson, N., Wood, S. Abstract: Functional near-infrared spectroscopy (fNIRS) promises to be a leading non-invasive neuroimaging method due to its portability and low cost. However, concerns are rising over its inclusivity of all skin tones and hair types (Parker and Ricard 2022, Webb et al 2022). Functional NIRS relies on direct contact of light-emitting optodes to the scalp, which can be blocked more by longer, darker, and especially curlier hair. Additionally, NIR light can be attenuated by melanin, which is accounted for in neither fNIRS hardware nor analysis methods. Recent work has shown that overlooking these considerations in other modalities like EEG leads to the disproportionate exclusion of individuals with these phenotypes - especially Black people - in both clinical and research literature (Bradford et al 2022, Choy 2020). In this article, we sought to determine if (1) biomedical optics developers and researchers report fNIRS performance variability between skin tones and hair textures, (2a) fNIRS neuroscience practitioners report phenotypic and demographic details in their articles, and thus, (2b) is a similar pattern of participant exclusion found in EEG also present in the fNIRS literature. We present a literature review of top Biomedical Optics and Human Neuroscience journals, showing that demographic and phenotypic reporting is unpopular in both fNIRS development and neuroscience applications. We conclude with a list of recommendations to the fNIRS community including examples of Black researchers addressing these issues head-on, inclusive best practices for fNIRS researchers, and recommendations to funding and regulatory bodies to achieve an inclusive neuroscience enterprise in fNIRS and beyond. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.04.515203v1?rss=1 Authors: Merrihew, G. E., Park, J., Plubell, D., Searle, B. C., Keene, C. D., Larsen, E. B., Bateman, R., Perrin, R. J., Chhatwal, J. P., Farlow, M. R., McLean, C. A., Ghetti, B., Newell, K. L., Frosh, M. P., Montine, T., MacCoss, M. J. Abstract: Alzheimers disease (AD) is a looming public health disaster with limited interventions. Progress in therapeutic development requires a more detailed understanding of molecular pathogenesis. Most data for AD pathogenesis in humans is from standard neuropathologic assessments, e.g., neuritic plaques and neurofibrillary tangles or biochemical measurement of a limited number of analytes related to neuropathologic features, e.g., amyloid-{beta} peptides and hyperphosphorylated tau. Standard neuropathologic evaluation is highly valuable as it provides assessment of diseases that afflict an individual brain, but it also is limited in its ability to investigate molecular pathogenesis. Modern mass spectrometry-based proteomics enable quantitative insight into the protein phenotype in brains with AD neuropathology. Careful selection of specimens enabled us to investigate protein signatures specific to autosomal dominant AD dementia (ADD), sporadic ADD with minimal comorbidities, individuals without dementia who had high histopathologic burden of AD, and cognitively normal individuals with no or minimal AD histopathologic burden. All data are deposited in the ProteomeXchange proteomic data repositories (ID: PXD034525). Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Podcast 30: Developing standards and quality metrics for clinical phenotypic using EHR data by NIA IMPACT Collaboratory

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.14.512051v1?rss=1 Authors: Stier, A., Gilberto, S., Mohamed, W. I., Helenius, J., Mikicic, I., Sajic, T., Beli, P., Mueller, D. J., Peter, M. Abstract: The cullin-4 paralogs CUL4A and CUL4B assemble E3 ubiquitin ligase complexes regulating multiple chromatin-associated cellular functions. Although they are structurally similar, we found that the unique N-terminal extension of CUL4B is heavily phosphorylated during mitosis, and the phosphorylation pattern is perturbed in the CUL4B-P50L mutation causing X-linked intellectual disability (XLID). Phenotypic characterization and mutational analysis revealed that CUL4B phosphorylation is required for efficient progression through mitosis, controlling spindle positioning and cortical tension. Interestingly, while CUL4B phosphorylation triggers chromatin exclusion, it critically promotes binding to actin regulators and two previously unrecognized, CUL4B-specific DCAFs, LIS1 and WDR1. Indeed, co-immunoprecipitation experiments and biochemical analysis revealed that LIS1 and WDR1 interact with DDB1, but their binding requires the phosphorylated N-terminal domain of CUL4B. Together, our study uncovers previously unrecognized DCAFs relevant for mitosis and brain development that specifically bind CUL4B, but not the CUL4B-P50L patient mutant, by a phosphorylation-dependent mechanism. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Commentary by Dr. Valentin Fuster

In this episode, Amy speaks with guest Karen Warkentin, a Professor of Biology and a Professor of Women's, Gender, & Sexuality Studies at Boston University.They open by discussing the adaptive value of phenotypic plasticity, particularly at critical moments in complex life cycles. Then, they dig into the mechanisms underlying environmentally-cued hatching in red-eyed treefrogs (Agalychnis callidryas), and they talk about experimental approaches Karen has used to test hypotheses within this system. After the break, they discuss Karen's dual appointments in both Biology and Women's, Gender, & Sexuality Studies at BU, including the value and necessity of integrating these fields. This week's Two-Minute Takeaway comes from Juleyska Vazquez-Cardona (@JuleyskaV), a graduate student in The Birdsong Lab at the University of Lethbridge. Her work explores vocal communication in Adelaide's warblers (Setophaga adelaidae), a tropical songbird.Papers relevant to today's show:1. Karen & collaborators (2017) compare escape-hatching onset in Red-eyed treefrog embryos in response to hypoxia and mechanosensory cues. Developmental onset of escape-hatching responses in red-eyed treefrogs depends on cue type Animal Behaviour2. Karen's former PhD student Dr. Julie Jung leads this paper (2022) parsing the vibration properties that embryos use to discern predation risk. Frog embryos use multiple levels of temporal pattern in risk assessment for vibration-cued escape hatching Animal CognitionCredits:The Animal Behavior Podcast is created by a team of animal behavior researchers and audio professionals. Come meet us here! We receive production support from the Cornell Broadcast studio directed by Bert Odom-Reed, and financial support from the Animal Behavior Society.

Today we'll learn more about the risk of subsequent malignancies in patients treated with genetically modified immune effector cells, discuss how p53 immunohistochemistry can be a global readout for TP53 alterations in AML, and uncover the role of CD19-negative CD22-positive B-cell progenitors in immune escape from CD19-directed therapies.

4-29-22 AJ DailyPhenotypic Data in a Genomic WorldAdapted from an article by Miranda Reiman, Angus JournalFarmers Union Donates $125,000 to Help Humanitarian and Agricultural Crisis in UkraineAdapted from a release by Lyndsey Medsker, National Farmers UnionAmerica's Farmers are Reducing Greenhouse Gas EmissionsAdapted from a release by the American Farm Bureau FederationCAB Insider: Fed-cattle Market Chasing GradeAdapted from a release by Paul Dykstra, Certified Angus Beef LLCCompiled by Paige Nelson, field editor, Angus Journal. For more Angus news, visit angusjournal.net. 

Welcome to

This episode features an interview with Dr. Robin Patel and Dr. Audrey Schuetz to discuss an article titled "Phenotypic and Genomic Profiling of Staphylococcus argenteus in Canada and the United States and Recommendations for Clinical Result Reporting". They are Co-Directors of the Bacteriology Laboratory at the Mayo Clinic in Minnesota. Challenges in identifying this organism are discussed. Staphylococcus argenteus is part of the Staphylococcus aureus complex, and is very similar to S. aureus, including morphology, biochemicals and clinical manifestations. See links for the article.

Integrating plant functioning at organ scale can simulate the phenotypic plasticity of plants. You can read this post online at https://www.botany.one/2022/01/simulating-grass-phenotypic-plasticity-as-an-emergent-property You can read the original research at https://doi.org/10.1093/insilicoplants/diab034

Are triploid Butomus umbellatus plants more plastic to nutrient availability than diploid plants and does this make them more invasive? Read the post online at https://www.botany.one/2021/10/phenotypic-plasticity-to-nutrient-availability-in-a-wetland-invasive-species/ You can read the original research at https://doi.org/10.1093/aobpla/plab045

This episode covers viral phenotypic mixing!