Podcasts about Golgi

https://darienchiropractor.com › your-health-matters-to-uswww.darienchiropractor.comIn this episode of Core Health Darien's podcast, Dr. Brian McKay dives deep into the fascinating world of muscle spindle cells, Golgi tendon organs, and their critical role in modifying pain signals through afferent nerve pathways. These specialized sensory receptors are key players in the body's ability to regulate muscle tension, movement, and pain perception. Dr. McKay explains how the integration of Trigenics, a neurological treatment system, with chiropractic adjustments can amplify the body's natural ability to heal and function.By targeting muscle spindle cells and Golgi tendon organs, Trigenics leverages afferent nerve signaling to “reboot” how the brain communicates with the body. This approach not only reduces pain but also improves functional movement and restores control over areas affected by dysfunction. Dr. McKay explores the brain's pivotal role in pain modulation and how enhancing brain-body communication leads to more sustainable results for patients.Listeners will learn how patients at Core Health Darien benefit from combining Trigenics with chiropractic adjustments to achieve functional enhancements that go beyond pain relief—supporting improved mobility, strength, and long-term recovery. Whether you're a patient, a health professional, or simply curious about innovative pain management techniques, this podcast provides valuable insights into how cutting-edge treatments can unlock the body's potential to heal naturally.Tune in to discover how Core Health Darien is revolutionizing pain relief by bridging the gap between brain control, neurology, and functional health!Core Health Darien-Dr.Brian Mc Kay 551 Post RoadDarien CT 06820203-656-3636https://goo.gl/maps/js6hGWvcwHKBGCZ88https://www.youtube.com/my_videos?o=Uhttps://www.linkedin.com/in/darienchiropractorhttps://www.facebook.com/ChiropractorBrianMckayhttps://sites.google.com/view/corehealthdarien/https://www.google.com/maps?cid=9052981016823215070&hl=enhttps://youtu.be/CTa85YpYBiwhttps://darienchiropractor.com/spinal-decompression/https://maps.app.goo.gl/kbjVbvCn2cAqYZQn6This podcast welcomes your feedback here are several ways to reach out to me. If you have a topic you would like to hear about send me a message. I appreciate your listening. Dr. Brian Mc Kayhttps://twitter.com/DarienChiro/https://www.facebook.com/ChiropractorBrianMckayhttps://chiropractor-darien-dr-brian-mckay.business.sitehttps://podcasts.apple.com/us/podcast/not-just-chiropractor-for-stamford-darien-norwalk-new/id1503674397?uo=4Core Health Darien-Dr.Brian Mc Kay 551 Post RoadDarien CT 06820203-656-363641.0833695 -73.46652073GMP+87 Darien, Connecticuthttps://youtu.be/WpA__dDF0O041.0834196 -73.46423349999999https://darienchiropractor.comhttps://darienchiropractor.com/darien/darien-ct-understanding-pain/Find us on Social Mediahttps://chiropractor-darien-dr-brian-mckay.business.site https://www.youtube.com/channel/UCNHc0Hn85Iiet56oGUpX8rwhttps://docs.google.com/spreadsheets/d/1nJ9wlvg2Tne8257paDkkIBEyIz-oZZYy/edit#gid=517721981https://goo.gl/maps/js6hGWvcwHKBGCZ88https://www.youtube.com/my_videos?o=Uhttps://www.linkedin.com/in/darienchiropractorhttps://www.facebook.com/ChiropractorBrianMckayhttps://sites.google.com/view/corehealthdarien/https://sites.google.com/view/corehealthdarien/home

What do you know about prokaryote structure and the gram stain? Bacteria are members of a unique taxonomic kingdom consisting of prokaryotic unicellular organisms. Prokaryote is a term from ancient Greek meaning “before the kernel.” The kernel in this case is a nucleus, which prokaryotes lack. Prokaryotes also do not have any membrane-bound organelles. In fact, many of the organelles found in eukaryotes—like an endoplasmic reticulum, mitochondria, Golgi apparatus, lysosomes, and peroxisomes—are completely absent in prokaryotes. Bacteria first began to be identified by a “defective method.” Or so its Danish inventor, a recent medical school grad named Hans Christian Gram, deemed it in 1884. Gram was working with lung tissue from cadavers who had died of infections from Streptococcus pneumoniae and Klebsiella pneumoniae when he discovered that those organisms reacted differently to certain substances under the microscope, and—voilà—the Gram stain was born, to identify gram-positive bacteria. The defect he mentioned was overcome by German pathologist Carl Weigert, who added a final step to Gram's procedure and gave us the method to identify gram-negative bacteria. We're still using the same techniques more than 130 years later! After listening to this AudioBrick, you should be able to: Describe the structure of prokaryotic cells. Discuss the physiologic niche of bacteria and their growth characteristics. Describe the staining characteristics and classification and identification of bacteria. To learn more about prokaryote structure and the gram stain, check out the original brick on Gastrointestinal Regulatory Substances from our Gastrointestinal collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/

Sit back, leave behind the cares of the day and take a sonic journey with Dr Michael Mosley. In this new podcast series, designed to help you let go and unwind, each episode focuses on a scientifically-proven technique for activating the body's built-in relaxation response, and takes a deep dive to explore what's happening inside as we find stillness and calm.Deliberately tensing and then relaxing groups of muscles all through the body is a potent technique for engaging your body's relaxation response. We also encounter the magnificently-named Golgi tendon organ afferent nerve cells, and the interconnected nodes of the brain.Guest: Ian Robertson, professor at Trinity College Dublin.Series Producer, sound design and mix engineer: Richard Ward Researcher: William Hornbrook Editor: Zoë Heron Specially composed music by Richard Atkinson (Mcasso) A BBC Studios Audio production for BBC Sounds / BBC Radio 4.

Dr. Lindsey Hughey // #ClinicalTuesday // www.ptonice.com  In today's episode of the PT on ICE Daily Show, Extremity Division Leader Lindsey Hughey reviews the anatomy of the latissimus dorsi muscle, its relevance to overhead movement, and discusses two ways to begin to improve long-term functional mobility. Lindsey also provides a rehabilitation every minute on the minute (rEMOM) program to begin to use for an HEP for patients who need to improve their own lat mobility. Take a listen to the episode or check out the full show notes on our blog at www.ptonice.com/blog. If you're looking to learn more about our Extremity Management course or our online physical therapy courses, check our entire list of continuing education courses for physical therapy including our physical therapy certifications by checking out our website. Don't forget about all of our FREE eBooks, prebuilt workshops, free CEUs, and other physical therapy continuing education on our Resources tab. EPISODE TRANSCRIPTION INTRODUCTION Hey everybody, Alan here, Chief Operating Officer at ICE. Thanks for listening to the PTonICE Daily Show. Before we jump into today's episode, let's give a big shout out to our show sponsor, Jane. in online clinic management software and EMR. The Jane team understands that getting started with new software can be overwhelming, but they want you to know that you're not alone. To ensure the onboarding process goes smoothly, Jane offers free data imports, personalized calls to set up your account, and unlimited phone, email, and chat support. With a transparent monthly subscription, you'll never be locked into a contract with Jane. If you're interested in learning more about Jane, or you want to book a personalized demo, head on over to jane.app.switch. And if you do decide to make the switch, don't forget to use our code ICEPT1MO at sign up to receive a one month free grace period on your new Jane account.LINDSEY HUGHEY PT on Ice daily show. How are you? I am Dr. Lindsay Hughey from our extremity division, here with you today on a clinical Tuesday to share some pearls of how we'll get after our LAT mobility. So I first wanna just briefly unpack the function of the LAT, so a little anatomy review, and then I wanna discuss two ways to really get after mobility access, demo those two ways, and then suggest them in a rehab EMOM sequence for you all, so you can directly use it yourselves, or use it with your patients in the clinic. A lot of our overhead athletes, our weightlifters, our crossfitters, maybe even just our stiff shoulders need more access to lat mobility. REVIEW OF THE LATS So let's first just review what is the lat and where is it? Well, the latissimus dorsi is responsible for internal rotation of the arm, arm adduction, arm extension, and it even assists in respiration. in both inhalation and exhalation. It spans quite a big area of our extrinsic superficial back muscles. So we have a vertebral part that goes from our spinous processes and converges into the thoracolumbar fascia, goes all the way down to our iliac crest. There are even connections into that inferior angle of the scapula, and then even 9 through 12 ribs. So it spans quite a bit of area. The reason we review all of those areas is when you're doing your mobility work, you really want to make sure you hit all of those and make sure to challenge them. TWO WAYS TO ADDRESS LAT MOBILITY So I'm going to show you how we can do two versions, a way where we fix the arms overhead and move the body away to traction the lats from below. And then I'm going to review how you can fix from below and then move lats from above. What we won't do this morning, though, is just a static hold stretch. So before I review these two with you, I want you to know that purposely these two moves are so effective because in the first we're going to use a hold relax technique. So we're going to actually use isometric contraction, hold, and then lengthen tissue longer. And what we see with our ISOs, as long as you hold it at least six to seven seconds, I'm gonna make you all push to 10, but we see this increase in neural drive and we get those Golgi tendon organs to chill out and make that agonist, the deltoid relax so that we can actually gain more lat access. The second exercise, we're gonna actually go after eccentric training. So the reason we choose eccentrics as we see constant and ongoing research links to improve strength and length and even greater cortical excitability when we train in eccentric fashion versus just like a static hold or even doing concentric work for our lats. So without further ado, let me show you these two exercises. So number one, we're going to fix from above by putting our elbows on a surface. I'm going to show you on a bench here today, but it could be a bar. It could be a foam roller, whatever feels good for your body. It could even be the counter or a wall surface. So we're going to put our elbows in like a goalpost position, and then we're going to fix our arms here. And we're going to lean our hips back, but we're going to actively contract our arms down for a hold of 10 seconds, then relax and push our hips away. So we get this tractional effect from below. So it'll look like this. So elbows down, and we're going to push into the object while we push our head down. And we're going to push down for 10 seconds. and then access greater length. So you'll notice that I push my hips back and away as I gain access to new length, but that key piece is activate for 10 seconds into the surface, pushing down, and then move away. To fully maximize this particular movement, we're also going to tie our breath work, because remember I said function of lats is helpful in inhalation and exhalation, And then we have links directly to those ribs. So we're going to pair our breath with this. So we'll do it one more time, but this time we're going to link that isometric hold with an inhalation. And then on our exhalation, we're going to move away. So it looks like so we're going to go hold for 10 seconds, pushing down and then exhale and push the body away. And then we would do another rep pushing down 10 seconds. Inhale. And then exhale. For those that are just listening to this this morning, I do suggest watching the video so you get the visual. But we would repeat that for at least five to six reps. I'm going to show you how we'll do that in a rehab EMOM. But we really want to get at least a six to seven second hold of that isometric where we're pushing down before we lengthen. The key parts here being tie breathwork with it. And then don't forget to access more length and maintain it. So that next isometric hold where you're pushing down in the hold relax sequence should be in that newer length. The second exercise we are going to review today is eccentric training. So we are going, I'm going to lay in either hook lying position or you can put your legs up to put further tension on the thoracolumbar fascia. My palms are going to face toward the ceiling and I'm going to slowly lower a bar. Right now I just have a PVC pipe with a plate on it and I'm going to slowly lower eccentrically. I want the slowly lower to be three to four seconds and then a hold for three seconds at the bottom. And you'll repeat this with a goal of eight to 20 reps or what in extremity management we would call our rehab dose. Keys being that eccentric slowly lowering on the way down and the hold at the bottom. So we want about three to four seconds in each of those parts. Don't care as much about that concentric raising portion. Appreciate this eccentric could be done with dumbbells as well or kettlebells. I love starting with a PVC pipe and just a five pound change plate for those that are new to lat access. So we have two things that we've reviewed so far. We are going to do Number one, our ISO hold, where we get into a position where our lats are on tension and you push and drive the elbows down for 10 seconds. And then after that 10 seconds of inhalation and pushing down, you'll exhale and lengthen those lats into a new mobility access area. The second one is that eccentric overhead with the either Dow or PVC pipe and weight. Just these two things done. MAKE MOBILITY EFFICIENT: THE rEMOM So if you do each of these for a minute and you do three rounds, you have yourself a very efficient six minute rehab EMOM to attack lap mobility access. Nothing gets more bang for the buck when you combine both of these and you'll get relaxation. Start subbing your static hold stretches that either you're doing or that you're doing for your patients and really get the neuromuscular system on board to see change more rapidly. From a frequency perspective, at least two to three days a week is something I would recommend for my patients to get after and even using it as like a precursor before they do some overhead work because we know what will solidify this even more is then to actually load it and do some functional meaningful thing. SUMMARY If you want to learn more about how to even test if your patient has lat mobility tightness, if you want to dive a little bit more into dosage and the rationale behind eccentrics and why we don't use static stretches in our course at extremity management, Mark, Cody, and I and our extremity team would love to see you on the road. Um, and literally we have courses all throughout this year, almost every month in May, May 18th, 19th, I'll be in Bellingham, Washington, and our director of marketing say will be with me. So if you want to join us, that is sure to be a blast. And then June 1st and 2nd, we have two offerings, one in Wisconsin and then one in Texas. So check us out on ptlnice.com. if you want to learn more about how we think and treat the lats. Thanks for tuning in with me today. And if you're listening, be sure to watch the video later. Take care, everybody. OUTROHey, thanks for tuning in to the PT on Ice daily show. If you enjoyed this content, head on over to iTunes and leave us a review and be sure to check us out on Facebook and Instagram at the Institute of Clinical Excellence. If you're interested in getting plugged into more ice content on a weekly basis while earning CUs from home, check out our virtual ice online mentorship program at ptonice.com. While you're there, sign up for our Hump Day Hustling newsletter for a free email every Wednesday morning with our top five research articles and social media posts that we think are worth reading. Head over to ptonice.com and scroll to the bottom of the page to sign up.

Benjamin Ehrlich is the author of the recent biography of Santiago Ramon y Cajal (The brain in search of itself), and The Dreams of Santiago Ramon y Cajal. We talk about Cajal's life and work, Cajal's unlikely beginnings in a rural Spain, how he discovered that neurons were separate from each other, leading to the neutron doctrine, how Cajal became famous seemingly overnight, Cajal's rivalry with Camillo Golgi, the relationship between art and science, how to write a biography of someone whose autobiographical writings were heavily influenced by picaresque novels, and much more.BJKS Podcast is a podcast about neuroscience, psychology, and anything vaguely related, hosted by Benjamin James Kuper-Smith.Support the show: https://geni.us/bjks-patreonTimestamps0:00:00: Why Cajal is worth talking about0:01:42: Cajal's father 0:04:48: Cajal's childhood0:17:22: Cajal's early work on the brain, and the status of neuroscience in the 1880s0:23:45: The conference that made Cajal famous0:29:42: Cajal's years as a famous scientist0:35:33: Cajal's personality0:41:14: Cajal & Golgi's rivalry0:45:48: del Rio and the discovery of glia cells0:49:13: Picaresque novels and the difficulty of trusting Cajal's stories of himself1:02:52: A book or paper more people should read1:04:14: Something Ben wishes he'd learnt sooner1:04:57: Advice for PhD students/postdocs - people in a transitory periodPodcast linksWebsite: https://geni.us/bjks-podTwitter: https://geni.us/bjks-pod-twtBen (Ehrlich)'s linksWebsite: http://www.benehrlich.com/Twitter: https://twitter.com/benehrlich11Ben (Kuper-Smith)'s linksWebsite: https://geni.us/bjks-webGoogle Scholar: https://geni.us/bjks-scholarTwitter: https://geni.us/bjks-twtReferences & linksKölliker: https://en.wikipedia.org/wiki/Albert_von_K%C3%B6llikerGolgi: https://en.wikipedia.org/wiki/Camillo_Golgidel Rio: https://en.wikipedia.org/wiki/P%C3%ADo_del_R%C3%ADo_HortegaCalvino (1972). Invisible cities.Ehrlich (2017). The Dreams of Santiago Ramón y Cajal.Ehrlich (2022). The brain in search of itself: Santiago Ramón y Cajal and the story of the neuron.Pitlor & Lee (editors). The Best American Short Stories 2023 .

The nerds compete in head-to-head NBA and NFL trivia, diving into Patrick Mahomes' career with the Kansas City Chiefs, the most prominent trades in NBA history starring Kevin Durant and Kyrie Irving, and the Golgi apparatus. #VolumeSee omnystudio.com/listener for privacy information.

The nerds compete in head-to-head NBA and NFL trivia, diving into Patrick Mahomes' career with the Kansas City Chiefs, the most prominent trades in NBA history starring Kevin Durant and Kyrie Irving, and the Golgi apparatus. #VolumeSee omnystudio.com/listener for privacy information.

In Episode 60 of "The Art of Aging Mindfully Podcast," we delve into how different durations of yoga practice can cater to personal goals while respecting the body's natural protective mechanisms, such as the stretch reflex and the Golgi tendon organ reflex. This episode offers insights into selecting the optimal practice length and cadence to progress safely in yoga. It emphasizes the importance of honoring our body's signals to prevent overstretching and injury, thereby ensuring a sustainable and enriching yoga journey.To support The Art of Aging Mindfully  Podcast go to patreon:The Art of Aging Mindfully Podcast PatreonThe Art of Aging Mindfully Podcast is sponsored by Viome, Acorn Biolabs and Whoop, your personal digital fitness tracker.To Harvest Your Own Stem Cells, for Future Use, with Acorn Biolabs:https://www.acorn.me/affiliate/the-art-of-aging-mindfullyTo test your full body and gut intelligence with Viome:http://viomehq.sjv.io/eKnAO1Use The $110 discount code: ARTOFAGINGOrder your whoop strap with Jai's Unique Link:https://join.whoop.com/376818To train with Jai, and learn about his yoga classes and massage therapy treatments:https://theartofagingmindfully.com/

Hey Science Enthusiasts!

Welcome to "The New Student Pharmacist's Podcast," where emerging science meets curiosity! In this captivating episode, we dive into the mesmerizing world of the Golgi Apparatus - a cellular cornerstone often overshadowed yet crucial in our biological understanding. Join our host, the inquisitive and passionate New Student Pharmacist, as they guide you through the labyrinthine pathways of this cellular powerhouse. From its discovery over a century ago to its complex roles in cell physiology, we explore how the Golgi Apparatus is pivotal in both health and disease. In "The Majestic Golgi Apparatus Unveiled," we dissect its intriguing structure and function - envision stacks of cisternae bustling with molecular traffic. Discover its critical role in protein and lipid modification, sorting, and packaging, and how these functions are indispensable to cell survival and function. This episode also brings to light the Golgi's significant role in medical research. We delve into its involvement in neurodegenerative diseases, cancer research, and the development of targeted therapies. Our special guests, renowned molecular biologists and neuroscientists, share their latest findings and insights into how understanding the Golgi could revolutionize treatment approaches. In addition, we take a deep dive into the neuroscience perspective - linking the Golgi's functions to neural health and exploring its role in synaptic transmission and regeneration. "The New Student Pharmacist's Podcast" isn't just about facts; it's about making connections. We blend complex science with engaging narratives, ensuring both budding scientists and curious minds alike can grasp the wonders of the cellular world. So, whether you're a student, a professional, or just a science enthusiast, tune in for an enthralling journey into the heart of cellular biology. Discover the unseen yet majestic world of the Golgi Apparatus in a way you've never heard before! Subscribe now and join us in unveiling the secrets of the Golgi Apparatus - the unsung hero of the cellular universe!

Researchers define a protocol for narrow nanoneedle fabrication and high-resolution imaging of living cells using AFM  Transcript of this podcastHello and welcome to the NanoLSI podcast. Thank you for joining us today. In this episode we feature the latest research by Takehiko Ichikawa and Takeshi Fukuma at the Kanazawa University NanoLSI.The research described in this podcast was published in STAR Protocols in September 2023 Kanazawa University NanoLSI websitehttps://nanolsi.kanazawa-u.ac.jp/en/Researchers define a protocol for narrow nanoneedle fabrication and high-resolution imaging of living cells using AFM Researchers at Kanazawa University report in STAR Protocols procedural details and tips for nanoendoscopy-AFM, for capturing images of nanoscale structures inside living cells. Images of nanoscale structures inside living cells are in increasing demand for the insights into cellular structure and function they can reveal. So far, the tools for capturing such images have been limited in various ways, but researchers led by Takeshi Fukuma and Takehiko Ichikawa at Kanazawa University have now devised and reported a full protocol for using atomic force microscopy (AFM) to image inside living cells. AFM was first developed in the 1980s and uses the changes in the forces between a sample surface and a nanoscale tip attached to a cantilever to “feel” surfaces and produce images of the topography with nanoscale resolution. The technique has grown increasingly sophisticated for extracting information about samples and at speeds sufficient for the tool to capture moving images of dynamics at the nanoscale. However, so far, it has been limited to surfaces. Other techniques exist that can provide a view of the inside of a cell but with limitations. For instance, there is electron microscopy, which is capable of resolving details at the nanoscale and smaller, but the required operating conditions are not compatible with living cells. Alternatively, fluorescence microscopy is regularly used on living cells, but while fluorescence techniques exist to increase the resolution, there are practical challenges that inhibit fluorescence imaging at the nanoscale. AFM suffers from neither limitation and by embellishing the tool with a nanoneedle to penetrate cells, Fukuma, Ichikawa and their collaborators have recently demonstrated the capability to image inside cells at the nanoscale, which they describe as nanoendoscopy-AFM.So how does it work?In their protocol, the researchers break down the method for nanoendoscopy-AFM into 4 stages. The first few steps involve cell preparation and staining with a fluorescent dye and checking the fluorescence, which is used to identify the imaging area quickly. Next is the fabrication of the nanoneedles themselves, for which there are two options – either etching away a nanoneedle structure with a focused ion beam or building one up with electron beam deposition. Then comes the nanoendoscopy stage itself, and in the report, the researchers describe the approach for both 2D  and 3D nanoendoscopy. There are even details outlined to describe the best way to clean up after the nanoendoscopy images are captured before finally outlining the data processing needed to visualize the measured data. The method is replete with tips for successfully accomplishing each stage, as well as a guide for troubleshooting when things are not quite working out. This technique should be suitable for the observation of intact intracellular structures, including mitochondria, focal adhesions, endoplasmic reticulum, lysosomes, Golgi apparatus, organelle connections, and liquid-liquid phase-separated structures. They conclude, “This protocol can NanoLSI Podcast website

Dr. John Lewis discusses The Benefits of Polysaccharides with Dr. Ben Weitz. [If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on my WeitzChiro YouTube page.]    Podcast Highlights 13:26  Polysaccharides.  Polysaccharides are complex sugars and some of them have unique health promoting properties, including those that come from aloe vera and from rice bran.  Aloe vera is 99% water, so you have to extract the polysaccharides out of the aloe vera plant and this acetylated polymannose has amazing properties. 20:25  Polymannose.  Dr. Lewis met Dr. Reg McDaniel who had been working on the aloe plant since the 1980s at the Texas A & M vet school, who is still doing research at 87 years of age.  Dr. McDaniel shared studies that these aloe derived polysaccharides were anti-inflammatory, antioxidant, antiproliferative, and have wound healing benefits.  He found that in addition to the wound healing and stem cell production boosting function of aloe vera, this polymannose is a key sugar when the endoplasmic reticulum and the Golgi of the cell are communicating with each other and making other bioactive compounds that you need.  This polymannose is similar to d-mannose, which is often recommended as part of a protocol along with L-carnitine and CoQ10 for supporting the heart muscle in patients with congestive heart failure, though Dr. Lewis's research was more focused on brain health. 25:51  Aloe polymannose multinutrient complex.  In their study on the polysaccharides for Alzheimer's patients, Dr. Lewis and colleagues used an aloe polymannose multinutrient complex, including aloe polymannose, rice bran, larch tree, cysteine, lecithin, tart cherry, inositol hexaphosphate, yam, flax seed, citric acid, and glucosamine.  They gave the patients this nutritional supplement four times per day in a powdered form that put into a liquid to drink. For the Alzheimer's study, they took patients with moderate to severe disease, which means the sickest of the sick and this group is the hardest to see improvements with.  The neuropsychological testing showed a significant improvement at nine and twelve months. 35:06  Alzheimer's study lab results. The lab results showed statistically significant reductions in VEGF and TNF alpha.  There was an improvement in CD4 to CD8 ratio, which obviously is very important for all of us.  They also showed an improvement of just under 300% in CD14 cells, which is a marker of adult stem cells.  And the average age of these patients were 79.9 years of age.  They theorized that these adult stem cells migrated to the brain and created new neurons, new synapses, and repaired damage to neurons.  Also BDNF levels went up by 11%, though this was not considered to be statistically significant.  They did not ask these Alzheimer's patients to change their diet or to exercise or do anything else to improve their lifestyles.  We can only imagine how much more benefit might have been derived if this nutritional intervention were used as part of a Functional Medicine approach that also put them on a healthy diet and had them perform vigorous exercise and do brain stimulating exercises as well, such as the approach used by Dr. Dale Bredesen. [The Effect of an Aloe Polymannose Multinutrient Complex on Cognitive and Immune Functioning in Alzheimer's Disease.] 44:45  MS study. These patients with relapsing remitting MS were placed on a similar aloe polymannose multinutrient complex four times per day for 12 months.  The FAMS (Functional Assessment for MS) questionaire was used for functional assessment and results showed very significant improvements in every scale.  MS patients frequently get infections and these patients who took the nutritional intervention had much fewer infections.  Serum biomarkers, quality of life, symptom severity, and functioning also improved.

Ever wondered how a combat infantry Marine squad leader turned PhD leverages his intense experiences to improve veterans' mental health? How can 30 minutes of brisk walking daily make a difference for people with PTSD? Dive into this episode as Robert Huseth reveals the transformative power of physical activity through exercise science!In this episode, Robert recounts his journey of wanting to join the military since age three and deploying to Afghanistan at 21, where he became a Sergeant SWAT leader. Hear how Corbett used mixed martial arts training and combat conditioning coordination to help him transition back into civilian life while dedicating his volunteer time to helping veterans' mental health through physical activity and exercise. Learn about the importance of aftercare for veterans post-deployment and how physical activity, such as walking briskly for 30 minutes, can help improve mental health issues like PTSD. This episode will surely be inspiring and leave you feeling empowered![00:00 - 08:14] Opening SegmentIntroducing Robert to the showLeveraging education and experience to help businesses establish and maintain their PMOsHe also got a doctorate in health and human performance from MTSU[08:15 - 19:05] The Impact of Physical Activity on Mental HealthMany police officers were former military struggling with substance abuse and suicidesFinding the next mission was essential to focus onExercise science research has been underestimated within the community[19:06 - 29:52] Exploring the Differences Between Hypertrophy and Strength TrainingHypertrophy Training is a minimally invasive approach to helping individuals with PTSDVolume, sets, reps, and weights are essential for an optimized trainingStrength training focuses on activating muscle spindles and suppressing Golgi tendon organsNutrition should be tailored to the individual[29:53 - 35:05] Balancing Fitness, Physique, and Strength with a Busy LifestyleCalorie intake should be monitored to ensure fat loss and muscle gain2-3 hours of training per day is required for bodybuildingHealthy eating choices such as chicken, fish, and red meat are important[35:06 - 38:38] Closing SegmentQuotes:"It doesn't matter if you just got out of Afghanistan or Iraq or you're from the Vietnam era; these things are real. And they're there, and we have to wrestle with them. And we can't just push them under the rug." - Robert Huseth"Physical activity is critical. It's family, work, everything. Those are going to be higher on our scale." - Robert HusethConnect with Robert!LinkedIn: https://www.linkedin.com/in/corbitt-huseth-ph-d-pmp-43a30212b/ https://www.excelsiorgp.com/download/Connect with me on LinkedIn!LIKE, SUBSCRIBE, AND LEAVE US A REVIEW on Apple Podcasts, Spotify, Google Podcasts, or whatever platform you listen on. Thank you for tuning in, and Stay Tuned for the Next Episode COMING SOON! Hosted on Acast. See acast.com/privacy for more information.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.08.03.551802v1?rss=1 Authors: Tojima, T., Suda, Y., Jin, N., Kurokawa, K., Nakano, A. Abstract: Cargo traffic through the Golgi apparatus is mediated by cisternal maturation, but it remains largely unclear how the cis-cisternae, the earliest Golgi sub-compartment, is generated. Here, we use high-speed, high-resolution confocal microscopy to analyze the spatiotemporal dynamics of a diverse set of proteins that reside in and around the Golgi in budding yeast. We find many mobile punctate structures that harbor yeast counterparts of mammalian endoplasmic reticulum (ER)-Golgi intermediate compartment (ERGIC) proteins, which we term "yeast ERGIC". It occasionally attaches onto the ER exit sites and gradually matures into the cis-Golgi. Upon treatment with the Golgi-disrupting agent brefeldin A, the ERGIC proteins form larger aggregates corresponding to the Golgi entry core compartment in plants, while cis- and medial-Golgi proteins are absorbed into the ER. We further analyze the dynamics of several late Golgi proteins. Together with our previous studies, we demonstrate a detailed spatiotemporal profile of the cisternal maturation process from ERGIC to Golgi and further to the trans-Golgi network. 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/2023.07.28.550940v1?rss=1 Authors: Saladin, L., Breton, V., Lequeu, T., Didier, P., Danglot, L., Collot, M. Abstract: Photomodulable fluorescent probes are drawing an increasing attention due to their applications in advanced bioimaging. Whereas photoconvertible probes can be advantageously used in tracking, photoswitchable probes constitute key tools for single molecule localization microscopy to perform super resolution imaging. Herein we shed light on a red and far-red BODIPY, namely BDP-576 and BDP-650 possessing both properties of conversion and switching. Our study demonstrates that theses pyrrolyl-BODIPYs respectively convert towards typical green- and red-emitting BODIPYs that are perfectly adapted to microscopy. We also showed that these pyrrolyl-BODIPYs undergo Directed Photooxidation Induced Conversion, a photoconversion mechanism that we recently introduced and where the pyrrole moiety plays a central role. These unique features were used to develop targeted photoconvertible probes towards different organelles or subcellular units (plasma membrane, mitochondria, nucleus, actin, Golgi apparatus, etc.) using chemical targeting moieties and Halo tag. We notably showed that BDP-650 could be used to track intracellular vesicles over more than 20 minutes in two color imaging with laser scanning confocal microscopy demonstrating its robustness. The switching properties of these photoconverters were studied at the single molecule level and were then successfully used in live Single Molecule Localization Microscopy in epithelial cells and neurons. Both membrane and mitochondria targeted probes could be used to decipher membrane 3D architecture and mitochondria dynamics at the nanoscale. This study builds a bridge between the photoconversion and photoswitching properties of probes undergoing directed photooxidation and shows the versatility and efficacy of this mechanism in live advanced imaging. 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/2023.07.25.550497v1?rss=1 Authors: Avila-Gutierrez, K., Slaoui, L., Alvear, R., Kozlowski, E., Oudart, M. F., Augustin, E., Mailly, P., Monnet, H., Mignon, V., Saubamea, B., Boulay, A.-C., Cohen-Salmon, M. Abstract: Astrocytes (the main glial cells in the brain) are highly ramified and send out perivascular processes (PvAPs) that entirely sheathe the brain s blood vessels. PvAPs are equipped with an enriched molecular repertoire that sustains astrocytic regulatory functions at the vascular interface. In the mouse, PvAP development starts after birth and is essentially complete by postnatal day (P) 15. Progressive molecular maturation also occurs over this period, with the acquisition of proteins enriched in PvAPs. The mechanisms controlling the development and molecular maturation of PvAPs have not been extensively characterized. We reported previously that mRNAs are distributed unequally in mature PvAPs and are locally translated. Since dynamic mRNA distribution and local translation influence the cell s polarity, we hypothesized that they might sustain the postnatal maturation of PvAPs. Here, we used a combination of molecular biology and imaging approaches to demonstrate that the development of PvAPs is accompanied by the transport of mRNA and polysomal mRNA into PvAPs, the development of a rough endoplasmic reticulum (RER) network and Golgi cisternae, and local translation. By focusing on genes and proteins that are selectively or specifically expressed in astrocytes, we characterized the developmental profile of mRNAs, polysomal mRNAs and proteins in PvAPs from P5 to P60. Furthermore, we found that distribution of mRNAs in PvAPs is perturbed in a mouse model of megalencephalic leukoencephalopathy with subcortical cysts. Lastly, we found that some polysomal mRNAs polarized progressively towards the PvAPs. Our results indicate that dynamic mRNA distribution and local translation influence the postnatal maturation of PvAPs. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

"You just need to stretch more" If you have been in a gym, physical therapist, or doctor's office, you probably heard this.In this episode of the Pain and Performance Podcast, our guest, Dr. Claude Tremblay, discusses the topic of stretching and flexibility. We will learn about the complexities of stretching and its various components, from structural flexibility to the neurological feedback loop involved in the process. We learn about the importance of neural adaptations and training the spindles and Golgi's (proprioceptive feedback mechanisms) to improve functional range of motion. We discuss different types of stretches and the significance of training the body to adapt to new ranges of motion for improved flexibility.Links from today's show:spartascience.comwww.acadianapain.com/resetwww.derrickhines.comFollow me on social at:https://www.tiktok.com/@drderrickhttps://www.instagram.com/derrickbhines 

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.23.550229v1?rss=1 Authors: Manzer, K. M., Fromme, J. C. Abstract: Arf GTPases are central regulators of the Golgi complex, which serves as the nexus of membrane trafficking pathways in eukaryotic cells. Arf proteins recruit dozens of effectors to modify membranes, sort cargos, and create and tether transport vesicles, and are therefore essential for orchestrating Golgi trafficking. The regulation of Arf activity is controlled by the action of Arf-GEFs, which activate via nucleotide exchange, and Arf-GAPs, which inactivate via nucleotide hydrolysis. The localization dynamics of Arf GTPases and their Arf-GAPs during Golgi maturation have not been reported. Here we use the budding yeast model to examine the temporal localization of the Golgi Arf-GAPs. We also determine the mechanisms used by the Arf-GAP Age2 to localize to the Golgi. We find that the catalytic activity of Age2 and a conserved sequence in the unstructured C-terminal domain of Age2 are both required for Golgi localization. This sequence is predicted to form an amphipathic helix and mediates direct binding of Age2 to membranes in vitro. We also report the development of a probe for sensing active Arf1 in living cells and use this probe to characterize the temporal dynamics of Arf1 during Golgi maturation. 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/2023.07.24.550375v1?rss=1 Authors: Willet, A. H., Turner, L. A., Park, J. S., Ren, L., Snider, C. E., Gould, K. L. Abstract: Phosphatidylinositol (PI)-4-phosphate (PI4P) is a lipid found at the plasma membrane (PM) and Golgi in cells from yeast to humans. PI4P is generated from PI by PI4-kinases and can be converted to PI-4,5-bisphosphate [PI(4,5)P2]. Schizosaccharomyces pombe have 2 essential PI4-kinases: Stt4 and Pik1. Stt4 localizes to the PM and its loss from the PM results in a decrease of PM PI4P and PI(4,5)P2. As a result, cells divide non-medially due to disrupted cytokinetic ring-PM anchoring. However, the localization and function of S. pombe Pik1 has not been thoroughly examined. Here, we found that Pik1 localizes exclusively to the trans-Golgi and is required for Golgi PI4P production. We determined that Ncs1 regulates Pik1, but unlike in other organisms, it is not required for Pik1 Golgi localization. When Pik1 function was disrupted, PM PI4P but not PI(4,5)P2 levels were reduced, a major difference with Stt4. We conclude that Stt4 is the chief enzyme responsible for producing the PI4P that generates PI(4,5)P2. Also, that cells with disrupted Pik1 do not divide asymmetrically highlights the specific importance of PM PI(4,5)P2 for cytokinetic ring-PM anchoring. 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/2023.07.21.550021v1?rss=1 Authors: Georgiou, X., Dimou, S., Diallinas, G., Samiotaki, M. Abstract: Neosynthesized plasma membrane (PM) proteins co-translationally translocate to the ER, concentrate at regions called ER-exit sites (ERes) and pack into COPII secretory vesicles which are sorted to the early-Golgi through membrane fusion. Following Golgi maturation, membrane cargoes reach the late-Golgi, from where they exit in clathrin-coated vesicles destined to the PM, directly or through endosomes. Post-Golgi membrane cargo trafficking also involves the cytoskeleton and the exocyst. The Golgi-dependent secretory pathway is thought to be responsible for the trafficking of all major membrane proteins. However, our recent findings in Aspergillus nidulans showed that several plasma membrane cargoes, such as transporters and receptors, follow a sorting route that seems to bypass Golgi functioning. To gain insight on membrane trafficking and specifically Golgi-bypass, here we used proximity dependent biotinylation (PDB) coupled with data-independent acquisition mass spectrometry (DIA-MS) for identifying transient interactors of the UapA transporter. Our assays, which included proteomes of wild-type and mutant strains affecting ER-exit or endocytosis, identified both expected and novel interactions that might be physiologically relevant to UapA trafficking. Among those, we validated, using reverse genetics and fluorescence microscopy, that COPI coatomer is essential for ER-exit and anterograde trafficking of UapA and other membrane cargoes. We also showed that ArfAArf1 GTPase activating protein (GAP) Glo3 contributes to UapA trafficking at increased temperature. This is the first report addressing the identification of transient interactions during membrane cargo biogenesis using PDB and proteomics coupled with fungal genetics. Our work provides a basis for dissecting dynamic membrane cargo trafficking via PDB assays. 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/2023.07.20.549860v1?rss=1 Authors: Link, F., Borges, A., Karo, O., Jungblut, M., Mueller, T., Meyer-Natus, E., Krueger, T., Sachs, S., Jones, N. G., Morphew, M., Sauer, M., Stigloher, C., McIntosh, J. R., Engstler, M. Abstract: Endocytosis is a common process observed in all eukaryotic cells, although its complexity varies among different organisms. In Trypanosoma brucei, the endocytic machinery is under special selective pressure because rapid membrane recycling is essential for immune escape. This unicellular parasite effectively removes host antibodies from its cell surface through hydrodynamic drag and fast endocytic internalization. The entire process of membrane recycling occurs exclusively through the flagellar pocket, an extracellular organelle situated at the posterior pole of the spindle-shaped cell. The high-speed dynamics of membrane flux in trypanosomes do not seem compatible with the conventional concept of distinct compartments for early, late and recycling endosomes. To investigate the underlying structural basis for the remarkably efficient membrane traffic in trypanosomes, we employed advanced techniques in light and electron microscopy to examine the three-dimensional architecture of the endosomal system. Our findings reveal that the endosomal system in trypanosomes exhibits a remarkably intricate structure. Instead of being compartmentalized, it constitutes a continuous membrane system, with specific functions of the endosome segregated into membrane subdomains enriched with classical markers for early, late, and recycling endosomes. These membrane subdomains can partly overlap or are interspersed with areas that are negative for endosomal markers. This continuous endosome allows fast membrane flux by facilitated diffusion that is not slowed by multiple fission and fusion events. Our study further suggests that in trypanosomes, the endosome has taken over the role of the trans-Golgi network as the master regulator of membrane trafficking. 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/2023.07.16.549189v1?rss=1 Authors: Morella, M. L., Moors, T. E., Bertran-Cobo, C., Geut, H., Udayar, V., Timmermans-Huisman, E., Ingrassia, A. M., Breve, J. J., Bol, J. G., Bonifati, V., Jagasia, R., van de Berg, W. D. Abstract: Transcription factor EB is a master regulator of genes involved in the maintenance of autophagic and lysosomal homeostasis, processes which have been implicated in the pathogenesis of GBA-related and sporadic Parkinson's disease (PD) and dementia with Lewy bodies (DLB). TFEB activation at the lysosomal level results in its translocation from the cytosol to the nucleus. Here, we aimed at investigating whether TFEB subcellular localization is altered in post-mortem human brain of aged individuals with either prodromal PD/DLB (incidental Lewy body disease, iLBD, N=3), GBA-related PD/DLB (N=9) or sPD/DLB (N=9), compared to control subjects (N=12). We scanned nigral dopaminergic neurons using high-resolution confocal and stimulated emission depletion (STED) microscopy and semi-quantitatively scored the observed TFEB subcellular localization patterns. In line with previous studies, we observed reduced nuclear TFEB immunoreactivity in PD/DLB patients compared to controls, both sporadic and GBA-related cases, as well as in iLBD cases. Nuclear depletion of TFEB was more pronounced in neurons with Ser129-phosphorylated (pSer129) aSyn cytopathology and in cases carrying pathogenic GBA variants. Interestingly, we further observed previously unidentified TFEB-immunopositive somatic clusters in human brain dopaminergic neurons and in human embryonic stem cell (hESC)-derived neurons, which localized at the Golgi apparatus. The TFEB clustering was more frequently observed and more severe in iLBD, sPD/DLB and GBA-PD/DLB compared to controls, particularly in pSer129 aSyn-positive neurons but also in neurons without apparent cytopathology. Notably, increased frequency of cytoplasmic TFEB clusters in aSyn-negative cells correlated with reduced total GBA enzymatic activity and higher Braak LB stage. In the studied patient population, altered TFEB distribution was accompanied by a reduction in overall mRNA expression levels of selected CLEAR genes, indicating a possible early dysfunction of lysosomal regulation. Overall, these findings suggest the early cytoplasmic TFEB retention and accumulation at the Golgi prior pSer129 aSyn accumulation in incidental, GBA-related and sporadic PD/DLB and indicate TFEB as potential as early therapeutic target for synucleinopathies. 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/2023.07.18.549521v1?rss=1 Authors: Wallace, N. S., Gadbery, J. E., Cohen, C. I., Kendall, A. K., Jackson, L. P. Abstract: Tepsin is an established accessory protein found in Adaptor Protein 4 (AP-4) coated vesicles, but the biological role of tepsin remains unknown. AP-4 vesicles originate at the trans-Golgi network (TGN) and target the delivery of ATG9A, a scramblase required for autophagosome biogenesis, to the cell periphery. Using in silico methods, we identified a putative LC3-Interacting Region (LIR) motif in tepsin. Biochemical experiments using purified recombinant proteins indicate tepsin directly binds LC3B, but not other members, of the mammalian ATG8 family. Calorimetry and structural modeling data indicate this interaction occurs with micromolar affinity using the established LC3B LIR docking site. Loss of tepsin in cultured cells dysregulates ATG9A export from the TGN as well as ATG9A distribution at the cell periphery. Tepsin depletion in a mRFP-GFP-LC3B HeLa reporter cell line using siRNA knockdown increases autophagosome volume and number, but does not appear to affect flux through the autophagic pathway. Re-introduction of wild-type tepsin partially rescues ATG9A cargo trafficking defects. In contrast, re-introducing tepsin with a mutated LIR motif or missing N-terminus does not fully rescue altered ATG9A subcellular distribution. Together, these data suggest roles for tepsin in cargo export from the TGN; delivery of ATG9A-positive vesicles at the cell periphery; and in overall maintenance of autophagosome structure. 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/2023.07.15.549172v1?rss=1 Authors: Zheng, J.-X., Du, T.-Y., Shao, G.-C., Ma, Z.-H., Jiang, Z.-D., Hu, W., Suo, F., He, W., Dong, M.-Q., Du, L.-L. Abstract: Killer meiotic drivers (KMDs) skew allele transmission in their favor by killing meiotic progeny not inheriting the driver allele. Despite their widespread presence in eukaryotes, the molecular mechanisms behind their selfish behavior are poorly understood. Here we investigate how the poison and antidote products of a fission yeast wtf-family KMD gene can act antagonistically. Both the poison and the antidote are multi-transmembrane proteins, differing only in their N-terminal cytosolic tails. We find that the antidote employs N-terminal PY motifs to bind Rsp5/NEDD4 family ubiquitin ligases, which ubiquitinate the antidote. Mutating PY motifs or attaching a deubiquitinating enzyme transforms the antidote into a toxic protein. Ubiquitination promotes the transport of the antidote from the trans-Golgi network to the endosome, thereby neutralizing its toxicity and that of the bound poison. We propose that post-translational modification-mediated protein localization and/or activity changes may be a common mechanism governing the antagonistic duality of single-gene KMDs. 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/2023.07.13.548868v1?rss=1 Authors: de Caestecker, C., Macara, I. Abstract: Apical sorting of epithelial membrane proteins is an essential process but remains incompletely understood. Apical cytoplasmic domains are significantly smaller than those of basolateral proteins; however, the reason for this attribute is unknown. We asked if a diffusion barrier at the trans-Golgi network might impede apical sorting of proteins with large cytoplasmic tails. We used Crumbs3 and Ace2 as example apical transmembrane proteins with short cytoplasmic tails. FKBP was attached to the C-termini for inducible dimerization to FRB-tagged proteins. A streptavidin-binding peptide on the extracellular domain traps the proteins in the endoplasmic reticulum (ER). Biotin addition triggers release to the Golgi, then departure in vesicles to the apical cortex. Increasing cytoplasmic bulk by dimerization to FRB-SNAPtag moieties significantly delayed departure. Crb3 binds through its cytoplasmic tail to the Pals1 protein, and although Crb3 and Pals1 are associated at the ER and Golgi, Pals1 disassociates before Crb3 departure. A non-dissociable mutant Pals1 impedes Crb3 exit. We conclude that small cytoplasmic domains facilitate apical sorting. Reducing cytoplasmic domain size by timely Pals1 release is essential for normal kinetics of Crb3 sorting. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This podcast and video is the second in the treating Plantar Fasciitis. Many patients ask about this, and there are solutions for the home and the office. Take a listen, watch the video, and ask questions at questions@chalmerswellness.com. I answer all questions. Dr. Matt Chalmers [00:00:04] Okay, So the way I treat Plantar Fasciitis in the office is I always start off with my version of the Charette Protocol to adjust the ankle. And so we adjusted, just kind of reset the joint, make sure it's where it's supposed to be.Dr. Matt Chalmers [00:00:23] So now that the joints have moved around with activity, the joint thing where it is, where you compress the Achilles tendon all the way up into the active neurosis and into the calf muscle itself.Dr. Matt Chalmers [00:00:34] And the reason is that I want to add the muscle spindle fibers, the Golgi-tuned organs, and the entire function of the neuro receptors in the whole lower extremity.Dr. Matt Chalmers [00:00:42] So as we do that, we're going to have her point her toes over and over, pull it back as far as you can. Range emotions are very important in this so if they start to fatigue, make sure you get them to pull that toe back and point out as much as they can.Dr Matt Chalmers [00:00:55] And we don't want to stop we want to continue as they move and when we compress the ankle, just understand it's not the most comfortable thing in the world. So if they complain or you notice, it hurts, it's okay you want to be really uncomfortable you don't want to hurt. So we're just gonna compress it and point and pull, point and pull about this speed is what we're going to do.Dr. Matt Chalmers [00:01:16] Now, what I'll usually do is, as I compress this, I'll feel the tendon if there are little nodules in here I'll work those nodules until I feel them break up but you can stand up and down like I said so we get a lot of the Golgi tendon organs in the Achilles.Dr. Matt Chalmers [00:01:30] And then as we kind of come up and down pointing to the aponeurosis and we get a lot of those muscle spindle fibers and then we just keep coming up and down, move up just slide your hands up and down so I usually go up well do about five or six seven movements at each point you can come up and down.Dr. Matt Chalmers [00:01:52] You can kind of figure out how your patient is kind of doing with it but as you kind of come up and down, you kind of notice that they squirm a little bit more or they just fatigue out and they can't do it so the first couple times to watch that but as they go along, they're going to get obviously better and better at this as the tone equalizes. So just let them do this like I said, I usually do this three times a week for about 3 to 4 weeks, and it works really well.Dr. Matt Chalmers [00:02:17] Now, the big thing to understand is that if they're running, if they're walking if they're standing a lot while we're doing this, it's going to make it take longer. The more activation we get to the calf, the higher the tone stays.Dr. Matt Chalmers [00:02:30] And so the whole point of this is to give a reason for the body to think, oh, no, this is too tight we're going to tear. Sends a message to the brain, the brain sends a message back down to the calleb and tells it to reduce its tone.Dr. Matt Chalmers [00:02:40] As we're activating the Plantar Fasciitis this tone starts to come up and it starts to balance again and so that's the whole purpose of doing this.Dr. Matt Chalmers [00:02:47] So as we go through it, if they're running a whole lot, they're trying to activate the calf more and tone of the cattle to more so it'll still work it just takes a little longer.Dr. Matt Chalmers [00:02:56] That's my NFL guys we have to do this with and we have to do it all throughout the season because they're training so much that people who are training for marathons start to feel this come on, and they'll come in and we have to do this entirely until they're done with their training.Dr. Matt Chalmers [00:03:08] So just remember that if you're activating the calf a lot, it's going to take longer. But like I said, most people have three weeks, about three times a week so that's the compression that's how we treat Plantar Fasciitis.Check out Chalmers Pillarsofwellness.com for Wellness updates! And ask me any questions you have at questions@chalmerswellness.com. I answer all of them and look forward to hearing from you.The Chalmers Wellness Stubstack just launched. Comment, Like, and Interact with other people on their wellness journey. Communities can make a difference. DrChalmers.substack.comDr. Matt ChalmersDisclaimer: This content is for informational purposes only. Before taking any action based on this information you should first consult with your physician or health care provider. This information is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health providers with any questions regarding a medical condition, your health, or wellness.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.10.548399v1?rss=1 Authors: Suda, Y., Tachikawa, H., Suda, T., Kurokawa, K., Nakano, A., Irie, K. Abstract: Gametogenesis in budding yeast involves large-scale rearrangement of membrane traffic to allow de novo formation of a membrane, called the prospore membrane (PSM). However, the mechanism underlying this event is not fully elucidated. Here, we show that the number of endoplasmic reticulum exit sites (ERES) per cell fluctuates and switches from decreasing to increasing upon the onset of PSM formation. Reduction in ERES number is accompanied by a transient stall in membrane traffic, resulting in loss of the preexisting Golgi apparatus from the cell, as well as local ERES regeneration, leading to Golgi reassembly in nascent spores. We have revealed that protein phosphatase-1 (PP-1) and its development-specific subunit, Gip1, promote ERES regeneration through Sec16 foci formation. Furthermore, a mutant with impaired ERES formation showed defects in PSM growth and spore formation. Thus, ERES regeneration in nascent spores facilitates the segregation of membrane traffic organelles, leading to PSM growth. 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/2023.07.07.548115v1?rss=1 Authors: Listian, S. A., Kol, M., Ufelmann, E., Eising, S., Froehlich, F., Walter, S., Holthuis, J. C. M., Barisch, C. Abstract: Dictyostelium discoideum is a professional phagocyte frequently used as experimental model to study cellular processes underlying the recognition, engulfment and infection course of microbial pathogens. Sphingolipids are abundant components of the plasma membrane that bind cholesterol, control vital membrane properties, participate in signal transmission and serve as adhesion molecules in recognition processes relevant to immunity and infection. While the pathway of sphingolipid biosynthesis has been well characterized in plants, animals and fungi, the identity of sphingolipids produced in D. discoideum, an organism at the crossroads between uni- and multicellular life, is not known. Combining lipidomics with a bioinformatics-based cloning strategy for key sphingolipid biosynthetic enzymes, we show here that D. discoideum produces phosphoinositol-containing sphingolipids with predominantly phytoceramide backbones. Cell-free expression of candidate inositol-phosphorylceramide (IPC) synthases from D. discoideum in defined lipid environments enabled identification of an enzyme that selectively catalyses the transfer of phosphoinositol from phosphatidylinositol onto ceramide. The corresponding IPC synthase, DdIPCS1, is non-homologous to but shares multiple sequence motifs with yeast IPC and human sphingomyelin synthases and localizes to the Golgi apparatus as well as the contractile vacuole of D. discoideum. Collectively, these findings open up important opportunities for exploring a role of sphingolipids in phagocytosis and infection across major evolutionary boundaries. 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/2023.07.06.547837v1?rss=1 Authors: Bagley, D. C., Morham, S. G., Kaplan, J., Ward, D. M. Abstract: Mon1a has been shown to function in the endolysosomal pathway and the secretory pathway, interact with dynein and affecting ER to Golgi traffic. Here we show that Mon1a is also required for maintenance of the Golgi apparatus. We identified the F-BAR protein FCHO2 as a Mon1a-interacting protein by both yeast two-hybrid analysis and co-immunoprecipitation. siRNA-dependent reductions in Mon1a or FCHO2 resulted in Golgi fragmentation. Membrane trafficking through the secretory apparatus in FCHO2-depleted cells was unaltered, however, reduction of FCHO2 affected the uniform distribution of Golgi enzymes necessary for carbohydrate modification. Fluorescence recovery after photobleaching analysis showed that the Golgi ministacks in Mon1a- or FCHO2-silenced cells did not exchange resident membrane proteins. The effect of FCHO2 silencing on Golgi structure was partially cell cycle-dependent and required mitosis-dependent Golgi fragmentation, whereas the effect of Mon1a-silencing on Golgi disruption was not cell cycle-dependent. mCherry-FCHO2 transiently colocalized on Golgi structures independent of Mon1a. These findings suggest that Mon1a has functions throughout the secretory pathway including interacting with dynein at the ER-Golgi interface in vesicle formation and then interacting with FCHO2 at the Golgi to generate lateral links between ministacks, thus creating Golgi ribbons. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

We often talk about how this country has a massive Mental Health problem. It does and there's no argument. This is one of the few things that, you know, Republicans and Democrats and rich and poor and everybody can be like, yeah, we got some Mental Health issues in this country. The real question is what are some of the solutions and who is going to pay for them? Are there ways of using alternative medicine and regular lifestyle changes to make a significant difference? Well, I believe there are and would change people's lives for the better. Dr. Matt Chalmers [00:00:17] The problem is, is that while it's great that we can point it out, I mean, identifying the problem is obviously the very first thing we got to do before we can start solving it well, we don't say anything about it I don't know why that is. Dr. Matt Chalmers [00:00:29] So here are the top two things you can do to eradicate depression and mental illness in your life. Exercise and testosterone, exercise actually increases testosterone so that's why it's the number one. Dr. Matt Chalmers [00:00:44] When you exercise, what actually happens is all the little joint mechanoreceptors, all the neurology from your body that's connected to your brain, your muscle spindle, fibers, Golgi, tendon organs, all those things send tremendous amounts of information up through the joints into the spine, from the spine to spinal cord, spinal cord to the brain but it hits the cerebellum. And so all that information that to the cerebellum has to be processed. So it sends it from the cerebellum to the frontal lobe to be an actual process and function, and we make sure everything's going right. Dr. Matt Chalmers [00:01:12] Here's the cool thing everybody talks about you only use 10% of your brain that's not necessarily accurate. What is accurate is the body can only focus energy in one spot or the other for a very long. As you increase function in the frontal lobe, you actually decrease function in the temporal lobe, the temporal lobe houses, the amygdala, the amygdala is your fear, hate, anger, terror, and all the bad stuff so you actually shut that part down. Dr. Matt Chalmers [00:01:39] As you shut that down, the only thing that's left is a dopaminergic function, which is reward happy, Great all those things. You also get something that shifts what's called the sympathetic parasympathetic shunt back and forth. Dr. Matt Chalmers [00:01:55] So what ends up happening is you shift out of sympathetic, which is fight-flight, and into parasympathetic, which is resting digesting. This allows the gut to start functioning at a higher level. Well, guess where all of your serotonin is made? It's made in the gut. So now all of a sudden we have high dopamine function because we're actually achieving goals that we set for ourselves and we start producing serotonin again, which helps us stay more awake and more alert and feel better so we have both of these things going for us. Dr. Matt Chalmers [00:02:23] Now. The other thing is that neurologic drive, your body understands the tissues being damaged, so it increases the delivery and production of testosterone. Now, testosterone is fantastic for the whole body, it's the healing hormone, we talk about this a lot, it's hypercritical to actual health. Dr. Matt Chalmers [00:02:39] However, what people don't understand is that the reason testosterone was first made in 1935 was to treat depression. That was it. Not for muscles, not for bones it was specifically to treat depression and it is spectacular at doing that. Dr. Matt Chalmers [00:02:56] So if you work out, you get more testosterone, if you recognize the need for testosterone, you supplement with testosterone, everything starts building back, back better. You start producing testosterone, start producing more muscle. Inside those muscles are ATP generators called mitochondria, that ATP keeps the brain functioning and moving. Everything starts building back together when you have testosterone and you actually exercise, all of these things start building themselves back up. Dr. Matt Chalmers [00:03:23] So if we really want to make a push to fix mental health in this country, we would institute exercise. We would take our kids who are we're decreasing recess, we're decreasing P.E. we're not making them exercise, we're letting them get fat and sit around and stare at screens all the time. If you would take those kids and get up and make them move and exercise a couple of times a day. What we would see in the teenage adolescent era is that anxiety, depression, the mental issues would start radically decreasing. Dr. Matt Chalmers [00:03:56] But that's not something we want to do for some unknown reason, it's as if we're actually trying to foster mental health issues. We need to start exercising more, we need to get out and move. You guys don't have to, you know, lift weights like I do, you guys don't have to run marathons just get out and move. Walking around outside is a fantastic option to start with now, the more you do this, the better things get. Dr. Matt Chalmers [00:04:20] There is a caveat to this COVID has really increased what ends up happening when we get sick for a long time, we see this with lives, we see this chronic fatigue from ALS or things like that. What ends up happening is what's called the point of diminishing returns gets a little screwed up. Dr Matt Chalmers [00:04:36] Now, the point of diminishing returns is where you exercise for three units you break yourself down three units, but your body can only heal two. So what ends up happening is you get more tired, more sore, and you feel worse for exercise. This is one of those things where you have to go back through clean up the got increased nutritional function oftentimes have to increase testosterone in the body, usually exogenously. Dr. Matt Chalmers [00:05:01] Then once the body heals a little bit, then it will have the ability with nutrition and testosterone and the ability to sleep again, to heal at a greater rate. So now you can break yourself down into three units in the gym and you can rebuild four or five units. Dr. Matt Chalmers [00:05:15] Now, that damage you're doing to the body, the body then has to increase your metabolism, which is the creation of new cells has to create those who cells and actually can. And once it can do that, now we can heal, regenerate and grow better instead of just breaking ourselves down without the ability to heal and we get past that point of diminishing returns we start getting healthier and better as we go along. Dr. Matt Chalmers [00:05:37] Again, that is nutrition and that is sleep and that is testosterone, proper hormone balance. So if we can get those things added to exercise, we really start to see a massive change in the way your psychological function happens. Dr. Matt Chalmers [00:05:51] So if we really want to take a chance and say we're going to make a positive change to radically push for positive health, health care, mental health care changes, we're going to have to start really focusing on physical motion and exercise, as well as testosterone and nutrition. But if we start moving, a lot of people are going to start getting better. So let's start exercising and start moving if we really do care about our mental health. Check out Chalmers Pillarsofwellness.com for Wellness updates! And ask me any questions you have at questions@chalmerswellness.com. I answer all of them and look forward to hearing from you.The Chalmers Wellness Stubstack just launched. Comment, Like, and Interact with other people on their wellness journey. Communities can make a difference. DrChalmers.substack.comDr. Matt ChalmersDisclaimer: This content is for informational purposes only. Before taking any action based on this information you should first consult with your physician or health care provider. This information is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health providers with any questions regarding a medical condition, your health, or wellness.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.25.546468v1?rss=1 Authors: Bracey, K., Noguchi, P., Edwards, C., Cario, A., Gu, G., Kaverina, I. Abstract: In pancreatic islet beta cells, molecular motors use cytoskeletal polymers microtubules as tracks for intracellular transport of insulin secretory granules. Beta-cell microtubule network has a complex architecture and is non-directional, which provide insulin granules at the cell periphery for rapid secretion response, yet to avoid over-secretion and subsequent hypoglycemia. We have previously characterized a peripheral sub-membrane microtubule array, which is critical for withdrawal of excessive insulin granules from the secretion sites. Microtubules in beta cells originate at the Golgi in the cell interior, and how the peripheral array is formed is unknown. Using real-time imaging and photo-kinetics approaches in clonal mouse pancreatic beta cells MIN6, we now demonstrate that kinesin KIF5B, a motor protein with a capacity to transport microtubules as cargos, slides existing microtubules to the cell periphery and aligns them to each other along the plasma membrane. Moreover, like many physiological beta-cell features, microtubule sliding is facilitated by a high glucose stimulus. These new data, together with our previous report that in high glucose sub-membrane MT array is destabilized to allow for robust secretion, indicate that MT sliding is another integral part of glucose-triggered microtubule remodeling, likely replacing destabilized peripheral microtubules to prevent their loss over time and beta-cell malfunction. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Dr. Matt Chalmers highlights the importance of exercise and testosterone in addressing mental health challenges. Exercise stimulates testosterone production, positively impacting mental well-being. Neurological signals from physical activity facilitate brain function, particularly in the frontal lobe responsible for emotions and cognition. Exercise also regulates the sympathetic and parasympathetic systems, promoting serotonin production and shifting the body into a state of rest and digestion.Testosterone, initially developed to treat depression, has proven effective in improving mood and combating depressive symptoms. Regular exercise not only boosts testosterone levels but also enhances muscle development and ATP production, benefiting brain function.Dr. Chalmers emphasizes the need to prioritize exercise to address the mental health crisis. Society's decline in physical activity, particularly among children and adolescents, has contributed to anxiety, depression, and other mental health issues. Incorporating physical movement into daily routines can significantly reduce these challenges.While navigating challenges like COVID-19, it's important to address factors that disrupt exercise recovery, such as illness or fatigue. Improving nutrition, optimizing hormone balance, and ensuring sufficient rest and sleep are necessary to restore the body's healing capacity.In conclusion, prioritizing physical activity and exercise is crucial for addressing mental health issues. By combining exercise with proper nutrition, sleep, and hormone balance, individuals can experience positive changes in psychological function. It's time to recognize the transformative potential of exercise and embrace it for the betterment of mental health.Dr Matt Chalmers [00:00:02] We often talk about how this country has a massive Mental Health problem and it does there's there's no argument. This is one of the few things that, you know, Republicans and Democrats and rich and poor and everybody can be like, yeah, we got some Mental Health issues in this country.Dr Matt Chalmers [00:00:17] The problem is, is that while it's great that we can point it out, I mean, identifying the problem is obviously the very first thing we got to do before we can start solving it well, we don't say anything about it I don't know why that is.Dr Matt Chalmers [00:00:29] So here are the top two things you can do to eradicate depression and mental illness in your life. Exercise and testosterone, exercise actually increases testosterone so that's why it's the number one.Dr Matt Chalmers [00:00:44] When you exercise, what actually happens is all the little joint mechanoreceptors, all the neurology from your body that's connected to your brain, your muscle spindle, fibers, Golgi, tendon organs, all those things send tremendous amounts of information up through the joints into the spine, from the spine to spinal cord, spinal cord to the brain but it hits the cerebellum. And so all that information that to the cerebellum has to be processed. So it sends it from the cerebellum to the frontal lobe to be an actual process and function, and we make sure everything's going right.Dr Matt Chalmers [00:01:12] Here's the cool thing everybody talks about you only use 10% of your brain that's not necessarily accurate. What is accurate is the body can only focus energy in one spot or the other for very long. As you increase function to the frontal lobe, you actually decrease function to the temporal lobe, the temporal lobe houses, the amygdala, the amygdala is your fear, hate, anger, terror, all the bad stuff so you actually shut that part down.Dr Matt Chalmers [00:01:39] As you shut that down, only thing that's left is dopaminergic function, which is reward happy, Great all those things. You also get something that shifts what's called the sympathetic parasympathetic shunt back and forth.Dr Matt Chalmers [00:01:55] So what ends up happening is you shift out of sympathetic, which is fight flight and into parasympathetic, which is resting digesting. This allows the gut to start functioning at a higher level. Well, guess where all of your serotonin is made? It's made in the gut. So now all of a sudden we have high dopamine function because you're actually achieving goals that you set for yourself and we start producing serotonin it again, which helps us stay more awake and more alert and feel better so we have both of these things going for us.Dr Matt Chalmers [00:02:23] Now. The other thing is that neurologic drive, your body understands the tissues being damaged, so it increases the delivery and production of testosterone. Now, testosterone is fantastic for the whole body, it's the healing hormone, we talk about this a lot, it's hypercritical to actual health.Dr Matt Chalmers [00:02:39] However, what people don't understand is that the reason testosterone was first made in 1935 was to treat depression. That was it. Not for muscles, not from bones it was specifically to treat depression and it is spectacular at doing that.Dr Matt Chalmers [00:02:56] So if you work out, you get more testosterone, if you if you recognize the need for testosterone, you supplement with testosterone, everything starts building back, back better. You start producing with testosterone, start producing more muscle. Inside those muscles are ATP generators called mitochondria, that ATP keeps the brain functioning and moving. Everything starts building back together when you have testosterone and you actually exercise, all of these things start building themselves back up.Dr Matt Chalmers [00:03:23] So if we really want to make a push to fix mental health in this country, we would institute exercise. We would take our kids who are we're decreasing recess, we're decreasing P.E. we're not making them exercise, we're letting them get fat and sit around and stare at screens all the time. If you would take those kids and get up and make them move and exercise a couple of times a day. What we would see in the teenage adolescent era is that the anxiety, the depression, the mental issues would start radically decreasing.Dr Matt Chalmers [00:03:56] But that's not something we want to do for some unknown reason, it's as if we're actually trying to foster mental health issues. We need to start exercising more, we need to get out and move. You guys don't have to, you know, lift weights like I do, you guys don't have to run marathons just get out and move. Walking around outside is a fantastic option to start with now, the more you do this, the better things get.Dr Matt Chalmers [00:04:20] There is a caveat to this COVID has really increased this what ends up happening when we get sick for a long time, we see this with lives, we see this chronic fatigue from ALS or things like that. What ends up happening is what's called the point of diminishing returns gets a little screwed up.Dr Matt Chalmers [00:04:36] Now, the point of diminishing returns is where you exercise for three units you break yourself down three units, but your body can only heal two. So what ends up happening is you get more tired, more sore, and you feel worse for exercise. This is one of those things where you have to go back through clean up the got increased nutritional function oftentimes have to increase testosterone in the body, usually exogenously.Dr Matt Chalmers [00:05:01] Then once the body heals a little bit, then it will have the ability with nutrition and testosterone and the ability to sleep again, to heal at a greater rate. So now you can break yourself down into three units in the gym and you can rebuild four or five units.Dr Matt Chalmers [00:05:15] Now, that damage you're doing to the body, the body then has to increase your metabolism, which is the creation of new cells has to create those who cells and actually can do that. And once it can do that, now we can heal, regenerate and grow better instead of just breaking ourselves down without the ability to heal and we get past that point of diminishing returns we start getting healthier and better as we go along.Dr Matt Chalmers [00:05:37] Again, that is nutrition and that is sleep and that is testosterone, proper hormone balance. So if we can get those things added exercise, we really start to see a massive change the way your psychological function happens.Dr Matt Chalmers [00:05:51] So if we really want to take a chance and say we're going to make a positive change to radically push for positive health, health care, mental health care changes, we're going to have to start really focusing on physical motion and exercise, as well as testosterone and nutrition. But if we start moving, a lot of people are going to start getting better. So let's start exercising and start moving if we really do care about our mental health.Check out Chalmers Pillarsofwellness.com for Wellness updates! And ask me any questions you have at questions@chalmerswellness.com. I answer all of them and look forward to hearing from you.The Chalmers Wellness Stubstack just launched. Comment, Like, Interact with other people on their wellness journey. Communities can make the difference. DrChalmers.substack.comDr. Matt ChalmersDisclaimer: This content is for informational purposes only. Before taking any action based on this information you should first consult with your physician or health care provider. This information is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health providers with any questions regarding a medical condition, your health, or wellness.

On compare un réflexe avec une Fuse, comment on ce rend là? Écoute l'épisode sur le réflexe myotatique inverse.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.26.538454v1?rss=1 Authors: Larriva-Sahd, J. A., Lozano-Flores, C., Martinez-Cabrera, G., Concha, L., Varela-Echavarria, A. Abstract: 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/2023.04.19.537613v1?rss=1 Authors: Gupta, A., Ruturaj,, Mishra, M., Saha, S., Maji, S., Rodriguez-Boulan, E., Schreiner, R. Abstract: We suggest a model of apico-basolateral sorting in polarized epithelia using homologous Cu-ATPases as membrane cargoes. In polarized epithelia, upon copper treatment, homologous copper-ATPases ATP7A and ATP7B traffic from trans-Golgi network (TGN) to basolateral and apical membranes respectively. We characterized sorting pathways of Cu-ATPases between TGN and plasma-membrane and identified the machinery involved. ATP7A and ATP7B reside on distinct domains of TGN and in high copper, ATP7A traffics directly to basolateral membrane, whereas ATP7B traverses common-recycling, apical-sorting and apical-recycling endosomes en-route to apical membrane. Mass-spectrometry identified regulatory partners of ATP7A and ATP7B that include Adaptor Protein-1 complex. Upon knocking-out pan-AP-1, sorting of both copper-ATPases are disrupted. ATP7A loses polarity and localizes on both apical and basolateral surfaces in high copper. Contrastingly, ATP7B loses TGN-retention but retains apical polarity that becomes copper-independent. Using isoform-specific knockouts, we found that AP-1A provides directionality and TGN-retention for both Cu-ATPases, whereas, AP-1B governs polarized trafficking of ATP7B solely. Trafficking phenotypes of Wilson disease-causing ATP7B mutants that disrupts putative ATP7B-AP1 interaction further substantiates the role of AP-1 in apical sorting of ATP7B. 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/2023.04.18.537395v1?rss=1 Authors: Castello-Serrano, I., Heberle, F. A., Diaz-Rohrer, B., Ippolito, R., Shurer, C. R., Lujan, P., Campelo, F., Levental, K. R., Levental, I. Abstract: The organelles of eukaryotic cells maintain distinct protein and lipid compositions required for their specific functions. The mechanisms by which many of these components are sorted to their specific locations remain unknown. While some motifs mediating subcellular protein localization have been identified, many membrane proteins and most membrane lipids lack known sorting determinants. A putative mechanism for sorting of membrane components is based on membrane domains known as lipid rafts, which are laterally segregated nanoscopic assemblies of specific lipids and proteins. To assess the role of such domains in the secretory pathway, we applied a robust tool for synchronized secretory protein traffic (RUSH, Retention Using Selective Hooks) to protein constructs with defined affinity for raft phases. These constructs consist solely of single-pass transmembrane domains (TMDs) and, lacking other sorting determinants, constitute probes for membrane domain-mediated trafficking. We find that while raft affinity can be sufficient for steady-state PM localization, it is not sufficient for rapid exit from the endoplasmic reticulum (ER), which is instead mediated by a short cytosolic peptide motif. In contrast, we find that Golgi exit kinetics are highly dependent on raft affinity, with raft preferring probes exiting Golgi ~2.5-fold faster than probes with minimal raft affinity. We rationalize these observations with a kinetic model of secretory trafficking, wherein Golgi export can be facilitated by protein association with raft domains. These observations support a role for raft-like membrane domains in the secretory pathway and establish an experimental paradigm for dissecting its underlying machinery. 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/2023.04.13.536018v1?rss=1 Authors: Stalder, D., Yakunin, I., Gershlick, D. C. Abstract: ACBD3 is a protein known to localise to the Golgi apparatus, and recruits various proteins to the Golgi, including PI4KIIIbeta, but the mechanism of its recruitment has remained unclear. This study demonstrates there are two mechanisms for ACBD3 recruitment to the Golgi. First, we identified that an MWT374-376 motif in the unique region upstream of the GOLD domain in ACBD3 is essential for Golgi localisation. Second, we use unbiased proteomics to demonstrate that ACBD3 interacts with SCFD1, a Sec1/Munc-18 (SM) protein, and a SNARE protein, SEC22B. CRISPR-KO of SCFD1 causes ACBD3 to become cytosolic. We also found that ACBD3 is redundantly recruited to the Golgi apparatus by two golgins, golgin-45 and giantin, which bind to ACBD3 through interaction with the MWT374-376 motif. Taken together, our results demonstrate that ACBD3 is recruited to the Golgi in a two-step sequential process, with the SCFD1-mediated interaction occurring upstream of the interaction with the golgins. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this episode, we review the high-yield topic of Muscle Spindles/Golgi Tendon ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠from the Neurology section. Follow ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets --- Send in a voice message: https://podcasters.spotify.com/pod/show/medbulletsstep1/message

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.07.536056v1?rss=1 Authors: Puig, S., Xue, X., Salisbury, R., Shelton, M. A., Kim, S.-M., Hildebrand, M. A., Glausier, J. R., Freyberg, Z., Tseng, G. C., Yocum, A. K., Lewis, D. A., Seney, M. L., MacDonald, M. L., Logan, R. W. Abstract: Opioid craving and the vulnerability to relapse is associated with severe and persistent disruptions to sleep and circadian rhythms. Investigations into the cellular and molecular pathways in the human brain underlying the relationship between circadian rhythms and OUD remain limited. In human subjects with OUD, previous transcriptomics work implicated a role for circadian regulation of synaptic processes in key cognitive- and reward-related brain regions, dorsolateral prefrontal cortex (DLPFC) and nucleus accumbens (NAc). To provide further insights into the synaptic alterations associated with OUD, we used mass-spectrometry based proteomics to deeply profile protein alterations in tissue homogenates and synaptosomes from both NAc and DLPFC of unaffected and OUD subjects. Between unaffected and OUD subjects, we identified 43 differentially expressed (DE) proteins in NAc homogenates and 55 DE proteins in DLPFC homogenates. In synaptosomes, we found 56 DE proteins in NAc of OUD subjects and 161 DE proteins in DLPFC. Examining synaptosome enrichment of specific proteins enabled us to identify brain region- and synapse-specific pathway alterations in NAc and DLPFC associated with OUD. Across both regions, we found OUD-associated protein alterations primarily in pathways involved in GABAergic and glutamatergic synaptic functions, as well as circadian rhythms. Using time-of-death (TOD) analyses, where the TOD of each subject is used as a time-point across a 24-hour cycle, we were able to map circadian-related changes in the synaptic proteomes in NAc and DLPFC associated with OUD. In OUD, TOD analysis revealed significant circadian changes in endoplasmic reticulum to Golgi vesicle-mediated transport and protein membrane trafficking in NAc synapses, accompanied by changes in platelet derived growth factor receptor beta signaling in DLPFC synapses. Together, our results lend further support for molecular disruption of circadian regulation of synaptic signaling in the human brain as a key factor in opioid addiction. 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/2023.04.06.535922v1?rss=1 Authors: Tang, V. T., Abbineni, P. S., da Veiga Leprevost, F., Basrur, V., Emmer, B. T., Nesvizhskii, A., Ginsburg, D. Abstract: Most proteins secreted into the extracellular space are first recruited from the endoplasmic reticulum into coat protein complex II (COPII)-coated vesicles or tubules that facilitate their transport to the Golgi apparatus. Although several secreted proteins have been shown to be actively recruited into COPII vesicles/tubules by the cargo receptors LMAN1 and SURF4, the full cargo repertoire of these receptors is unknown. We now report mass spectrometry analysis of conditioned media and cell lysates from HuH7 cells CRISPR targeted to inactivate the LMAN1 or SURF4 gene. We found that LMAN1 has limited clients in HuH7 cells whereas SURF4 traffics a broad range of cargoes. Analysis of putative SURF4 cargoes suggests that cargo recognition is governed by complex mechanisms rather than interaction with a universal binding motif. 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/2023.04.06.535716v1?rss=1 Authors: Montgomery, A. C., Mendoza, C. S., Garbouchian, A., Quinones, G. B., Bentley, M. Abstract: Neurons are polarized cells that require accurate membrane trafficking to maintain distinct protein complements at dendritic and axonal membranes. The Kinesin-3 family members KIF13A and KIF13B are thought to mediate dendrite-selective transport, but the mechanism by which they are recruited to polarized vesicles and the differences in the specific trafficking role of each KIF13 have not been defined. We performed live-cell imaging in cultured hippocampal neurons and found that KIF13A is a dedicated dendrite-selective kinesin. KIF13B confers two different transport modes, both dendrite- and axon-selective transport. Both KIF13s are maintained at the trans-Golgi network by interactions with the heterotetrameric adaptor protein complex AP-1. Interference with KIF13 binding to AP-1 resulted in disruptions to both dendrite- and axon- selective trafficking. We conclude that AP-1 is the molecular link between the sorting of polarized cargoes into vesicles and the recruitment of kinesins that confer polarized transport. 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/2023.04.03.535355v1?rss=1 Authors: Yi, S., Wang, L., Ho, M. S., Zhang, S. Abstract: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the motor deficits, selective loss of dopaminergic (DA) neurons, and the brain accumulation of [alpha]-synuclein ([alpha]-syn)-composed protein aggregates called Lewy bodies (LBs). Whereas dysfunction in the protein degradation pathway, like autophagy in neurons, has been demonstrated as a critical mechanism for eliminating protein aggregates in PD, how protein aggregates are eliminated in the other brain cell type, glia, is less well characterized. In the present study, we show that Atg9, the only transmembrane protein in the core autophagy pathway, is highly expressed in Drosophila adult brain glia. Results from immunostaining and live-cell imaging analysis reveal that a significant portion of Atg9 localizes to the trans-Golgi network (TGN), autophagosomes, and lysosomes in glia; Atg9 is persistently in contact with these organelles. Lacking glial atg9 reduces the number of omegasome and autophagosome and impairs autophagic substrate degradation, suggesting that glial Atg9 participates in the early steps of autophagy, hence the control of autophagic degradation. Importantly, loss of glial atg9 induces parkinsonian symptoms in Drosophila including progressive DA neuron loss and locomotion deficits. Our findings identify a functional role of Atg9 in glial autophagy and establish a potential link between glial autophagy and PD. These results provide new insights on the underlying mechanism of PD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Blog summary of an editorial perspective published in Oncotarget on entitled, “Leakage? or Secretion? unconventional protein secretion in cancer.” ________________________________________ Conventional protein secretion is fairly well understood in this day and age. Proteins that are secreted through the classical, secretory vesicle-related pathway contain a signal peptide that guides them to the endoplasmic reticulum (ER), where they are further processed and transported to the Golgi apparatus. From there, the Golgi apparatus modifies, sorts and packages proteins for transport to their final destinations within the cell or for secretion outside of the cell. However, in recent years, it has become clear that not all secreted proteins follow this conventional pathway. Instead, some proteins are secreted through unconventional pathways that do not require a signal peptide or the involvement of the ER or Golgi apparatus. In a recent editorial perspective published in Oncotarget on February 20, 2023, “Leakage? or Secretion? unconventional protein secretion in cancer,” researchers Kohji Yamada and Kiyotsugu Yoshida from The Jikei University School of Medicine in Tokyo, Japan, discuss unconventional protein secretion (UPS) and its significance in the progression of cancer. “In contrast, the secretion of proteins that do not code for signal peptides may occur via two or more mechanisms, often collectively referred to as unconventional protein secretion (UPS).” Full blog - https://www.oncotarget.org/2023/03/16/unconventional-protein-secretion-ups-in-cancer/ DOI - https://doi.org/10.18632/oncotarget.28368 (PDF Download) Correspondence to - Kohji Yamada - kyamada@jikei.ac.jp, and Kiyotsugu Yoshida - kyoshida@jikei.ac.jp Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28368 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - unconventional protein secretion, cancer, endoplasmic reticulum About Oncotarget Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ Twitter - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

Katherine Sherwood's work is an embodiment of her ideals as a feminist and reflect her personal experience with disability. In 1997, at the age of 44, she had a cerebral hemorrhage which paralyzed the right side of her body. Teaching herself how to paint again using her non-dominant hand was part of her healing process. Her recent Brain Flowers series of mixed media paintings on the reverse of antique art historical prints include collages of cerebral angiograms of her own brain. As part of her mission to bring attention to underrecognized women painters, Sherwood repaints vanitas paintings by 17th century Dutch and Baroque women artists, in which still lives with fading flowers suggest the brevity of life and the vanity of earthly achievements. Sherwood was born in New Orleans, Louisiana in 1952. She received a BA from the University of California, Davis, in 1975, and an MFA from the San Francisco Art Institute in 1979. She is Professor Emerita of Painting at the UC Berkeley Department of Art Practice, where she taught painting and drawing, developed two groundbreaking courses; Art, Medicine and Disability and Art and Meditation, and played an active role in the expansion of the Disability Studies program. She serveson the board of Creative Growth Art Center in Oakland, which serves artists with developmental disabilities by providing a supportive studio environment and gallery representation. Sherwood's work has been exhibited in the 2000 Whitney Museum Biennial, at Yerba Buena Center for the Arts in 2003 and 2009, and at the Smithsonian in 2010. Recent solo exhibitions include Anglim/Trimble in San Francisco, George Adams Gallery in New York, and Walter Maciel Gallery in Los Angeles. She had a retrospective exhibition at Worth Ryder Art Gallery at UC Berkeley in 2016. The relevance of her work to medicine and brain science has led to her participation in “Visionary Anatomies” at the National Academy of Science in Washington DC, “Inside Out Loud: Visualizing Women's Health in Contemporary Art” at the Kemper Museum in St. Louis, “Human Being” at the Chicago Cultural Center,and a solo exhibition “Golgi's Door” at the National Academy of Sciences in 2007. She co-curated the exhibition “Blind at the Museum” at the Berkeley Art Museum. Sherwood was the recipient of a 1989 National Endowment for the Arts Grant, 1999 Pollock Krasner Foundation Grant, 2005 Guggenheim Fellowship, 2006 Joan Mitchell Foundation Grant, and 2012 Newhouse Foundation Grant. Her work is in many major public collections including the Ford Foundation, New York; the San Francisco Museum of Modern Art, California; the National Academy of Sciences, Washington DC; and the University of Missouri, Columbia, among others. She published a chapter, “Out of the Blue: Art, Disability and Yelling,” in the book Contemporary Art and Disability Studies (Routledge Press, 2019). She is represented by George Adams Gallery in New York, Walter Maciel Gallery in Los Angeles, and Anglim/Trimble Gallery in San Francisco. She lives and works in the San Francisco Bay Area. Katherine Sherwood Pandemic Madonna (Lucas Cranach the Elder), 2022 Mixed media on found print 29 x 21 inches, © Katherine Sherwood, courtesy George Adams Gallery, New York. Photo: Dana Davis. Katherine Sherwood Venus After De Obidos, 2019-2022 Mixed media on found cotton duck 77 x 91 inches, © Katherine Sherwood, courtesy George Adams Gallery, New York. Photo: Dana Davis. Bread and Brains (After Josefa de Obidos), 2022 Mixed media on found cotton duck 25 1/2 x 60 inches, © Katherine Sherwood, courtesy George Adams Gallery, New York. Photo: Dana Davis.

Episode 127 is one of our winter shorts, where I replay interesting segments from previous episodes. In this one, you'll hear about the role of platelets in immunity, how the Golgi apparatus gets its weird shape, exactly how hot mitochondria get, and why we may want to consider marking assignments and tests with a green pen, rather than a red one. 00:00 | Introduction 01:07 | Mitochondria 02:29 | Platelets 07:15 | Sponsored by AAA, HAPI, and HAPS 08:49 | Golgi Apparatus 13:51 | Green Pens 16:20 | Staying Connected   ★ If you cannot see or activate the audio player, go to: theAPprofessor.org/podcast-episode-127.html

Join me on today's journey as I interview Fitness professional and personal trainer Jason Grant, born in the beautiful country of Guyana. (Linden Town). Jason loves the science of physiology - fast-twitch muscles, Golgi tendon organs, and motor skills. The simple fun of running was Jason's method of pushing his fitness in his formative years.  With athleticism coming naturally, it was important for Jason to challenge himself scholastically; knowing that he had the discipline and drive, Jason buckled down to obtain his license to become a personal trainer. Jason's journey started with his application to become certified by the National Academy Of Sports Medicine. After receiving his license in December 2009, Jason realized his journey was just beginning. He then moved on to obtain specialties in Weight Loss Management, Fitness Nutrition Specialist, Corrective Exercise Specialist, and numerous other certifications. Fitness, nutrition, and overall health and well-being is Jason's passion, and his drive is limitless.  For Jason to design the perfect plan for you, he will ask a lot of questions about you and your lifestyle, so it's only fitting that you learn a bit about him. Trust and communication will see you both to the finish line to accomplish your goals!  FITNESS GRANTED BY Jason If you would like to work with Jason you can connect with him at jason.grant3@gmail.com or (718)-916-2874.   Special Note: Garvin's Resistance bands: 12pcs / Set Rubber Latex Fitness Resistance Bands Exercise Elastic Pull String, Exercise Stretch Fitness Home Set, Workout Bands, Yoga Strap for Stretching with Exercise for Home.   This episode mentions Yoga and references our podcast on yoga which can be found here: https://www.wellnessod.com/podcast/episode/78bab0f4/garvin-reid-interviews-jamel-west-registered-yoga-teacher-on-how-to-get-started-with-yoga-on-the-wellness-on-demand-podcast. Also, check out our blog post on Yoga for Beginners this article can help you get started with yoga: wellnessod.com/post/yoga-for-beginners-how-yoga-can-help-inform-wellness.

Module 2 Jake and Hunt talk about the difference between On-Off Bipolar Cells, Muscle Spindle Tension, Golgi, and the activity of Rho Kinase in Phasic-Tonic smooth muscle contractions.

My AP Biology Thoughts  Unit 2 Cell Structure and FunctionWelcome to My AP Biology Thoughts podcast, my name is Shriya and I am your host for episode #53 called Unit 2 Cell Structure and Function: Lysosomes and Vacuoles. Today we will be discussing the importance of each in regards to the cells and our bodies, and how they fit into the overarching topic of Cell Structure and Function.  Segment 1: Introduction to Lysosomes and VacuolesWe will begin by discussing what exactly lysosomes and vacuoles are and why they are so important for our cells to contain Both of these are essential organelles, and organelles are subcellular structures with specific jobs to perform in the cell, much like an organ does in the body  Lysosomes are membrane-bound sacs of enzymes which digest cellular macromolecules  They are made by proteins from the ER and enclosed in vesicles by the Golgi apparatus and are formed by budding from the Golgi apparatus  They break down excess cell parts, and can be used to destroy invading viruses and bacteria so if the cell is damaged beyond repair, lysosomes can help it self-destruct through a process called apoptosis  Lysosomes also play a role in phagocytosis which is when a cell engulfs a molecule to break it down which is known as “cell eating” White blood cells have more lysosomes than other cells because they destroy bacteria, dead cells, cancerous cells, and foreign matter through disgestion  Vacuoles are fluid-filled enclosed structures separated from the cytoplasm by a single membrane which are found mostly in plant cells and fungi  They have a less prominent role in some protists, animal cells, and bacteria and in animal cells they function to sequester waste products; in plant cells, they help maintain water balance Overall, they function to provide nutrient storage, detoxification, and as waste exportation  Vacuoles are also known as “specialized lysosomes” because both function to get rid of waste products, but when that product is water, the vacuole activates its function to balance water inside and outside a cell Segment 2: More About Structure/Function of Lysosomes and Vacuoles Above is a picture of the structure of lysosomes which are generally known to be very acidic meaning it has to be protected from the rest of the inside of the cell The membrane around it stores the digestive enzymes that require the acidic, low-pH environment, also known as hydrolytic enzymes  Hydrolytic enzymes break down large molecules into smaller ones such as large amino acids into smaller proteins and by doing so they provide necessary nutrients to the rest of the cell  Storing the large molecules is detrimental to your health and can cause disease  Another type of lysosome storage disease is where the small molecules that are produced from those large molecules can't get out of the lysosome They're stored there because the transporters for moving these small molecules out are missing genetically Above, is a picture of the vacuole which is similar to vesicles, another organelle, because both are membrane-bound sacs, but vacuoles are significantly larger than vesicles and are formed when multiple vesicles fuse together Filled tight with water, the vacuole pushes the cytoplasm into a thin strip adjacent to the membrane and pushes outwards like a water filled balloon; it is this turgor pressure that holds the cell firm and provides the characteristic shape of plant structures such as leaves. So when the plant has been without water for a long time, the central vacuoles lose water, the cells lose shape, and the whole leaf wilts Segment 3: Connection to the CourseLysosomes and vacuoles fit into the bigger picture of cell structure and function because they contribute to supporting the origin of eukaryotic cells, one of the big ideas of Unit 2 Eukaryotic cells arose through endosymbiotic events that which rise to the...

What do you know about prokaryote structure and the gram stain? Bacteria are members of a unique taxonomic kingdom consisting of prokaryotic unicellular organisms. Prokaryote is a term from ancient Greek meaning “before the kernel.” The kernel in this case is a nucleus, which prokaryotes lack. Prokaryotes also do not have any membrane-bound organelles. In fact, many of the organelles found in eukaryotes—like an endoplasmic reticulum, mitochondria, Golgi apparatus, lysosomes, and peroxisomes—are completely absent in prokaryotes. Bacteria first began to be identified by a “defective method.” Or so its Danish inventor, a recent medical school grad named Hans Christian Gram, deemed it in 1884. Gram was working with lung tissue from cadavers who had died of infections from Streptococcus pneumoniae and Klebsiella pneumoniae when he discovered that those organisms reacted differently to certain substances under the microscope, and—voilà—the Gram stain was born, to identify gram-positive bacteria. The defect he mentioned was overcome by German pathologist Carl Weigert, who added a final step to Gram's procedure and gave us the method to identify gram-negative bacteria. We're still using the same techniques more than 130 years later! After listening to this AudioBrick, you should be able to: Describe the structure of prokaryotic cells. Discuss the physiologic niche of bacteria and their growth characteristics. Describe the staining characteristics and classification and identification of bacteria. To learn more about prokaryote structure and the gram stain, check out the original brick on Gastrointestinal Regulatory Substances from our Gastrointestinal collection, which is available for free. Learn more about Rx Bricks by signing up for a free USMLE-Rx account: www.usmle-rx.com You will get 5 days of full access to our Rx360+ program, including nearly 800 Rx Bricks.  After the 5-day period, you will still be able to access over 150 free bricks, including the entire collections for General Microbiology and Cellular and Molecular Biology. *** If you enjoyed this episode, we'd love for you to leave a review on Apple Podcasts.  It helps with our visibility, and the more med students (or future med students) listen to the podcast, the more we can provide to the future physicians of the world. Follow USMLE-Rx at: Facebook: www.facebook.com/usmlerx Blog: www.firstaidteam.com Twitter: https://twitter.com/firstaidteam Instagram: https://www.instagram.com/firstaidteam/ YouTube: www.youtube.com/USMLERX Learn how you can access over 150 of our bricks for FREE: https://usmlerx.wpengine.com/free-bricks/

Corey and Steve are joined by Bobby Kausthuri, a Neuroscientist at Argonne National Laboratory and the University of Chicago. Bobby specializes in nanoscale mapping of brains using automated fine slicing followed by electron microscopy. Among the topics covered: Brain mapping, the nature of scientific progress (philosophy of science), Biology vs Physics, Is the brain too complex to be understood by our brains? AlphaGo, the Turing Test, and wiring diagrams, Are scientists underpaid? The future of Neuroscience.▶️ WATCH: Bobby Kausthuri & Brain Mapping — Episode #2Resources Bobby Kasthuri Bio The Physicist and the Neuroscientist: A Tale of Two Connectomes Computing Machinery and Intelligence by Alan M. Turing Transcript