Podcasts about rbcs

In this podcast, I discuss RBCs from many different angles that are tested on the USMLEs. This podcast will help you answer many questions correctly on your exam. I make lots of integrations as I discuss the concepts. Audio Download

See all the Healthcasts at https://www.biobalancehealth.com/healthcast-blog Almost every week I hear from my male patients that their PCP doctor has scared them by telling them to stop taking testosterone pellets because their Hematocrit is too high.  Alternatively, their doctor recommended a lower dose of T. These two recommendations are those doctors who don't understand all the good that the testosterone is doing for these men. My male patients come to me for Testosterone pellets to treat their ED, lack of libido, loss of muscle, inability to think, weight gain, lack of motivation, anxiety attacks, poor stamina, arthritis, loss of balance, and basically everything that makes a man a man!  The most amazing thing is that I can treat them with ONE hormone, Testosterone in pellet form, and cure all these problems! If a man stops taking Testosterone, they get these symptoms again and have to take a multitude of drugs to feel just a fraction better! The treatment for a high H/H is simple…it is a routine removal of blood, either a blood donation or a phlebotomy (removal of 500 cc of blood) in the office, every 2-6 months to keep their H/H under control. The advice their doctors give them is going to cause them great pain and actually shorten their lives and there is little risk if any to removing blood every few months! In the event that a man demands that I lower their dose…..and I do it…the next inevitable phone call is to complain that their symptoms are coming back!  They literally blame me for the advice of their PCP! I would like to tell these men that the same doctors who could not help them with their low T are the same ones who are giving them the advice to lower or stop their testosterone therapy with T pellets.  It is human nature and especially that of doctors to try to criticize the advice of the doctor who got better results with a patient than they did! So, if you develop a condition called erythrocytosis secondary to your testosterone replacement, then you can keep your T therapy, if you are compliant and follow your testosterone doctor's directions and get your blood removed when it is scheduled.  This should prevent any severe reaction from your doctor. This is a typical response to my patient who has concerns.  However, I have given my patients many sources of written and video information about every aspect of testosterone replacement, the risks and benefits including erythrocytosis.  These include my book, Got Testosterone? was given to them on the first visit.  We also have over 650 informational blogs and videos on You Tube, FAQs and a very extensive handout given to each of them on the first visit. They just have to read! I have read your concern about erythrocytosis and testosterone replacement that was brought up by your PCP.  It is true that T replacement increases the H/H in both sexes.  It is useful if you are anemic, but if you have a genetic response to testosterone that elevates your H/H above what is considered normal, then we advise blood donation or phlebotomy every 2-6 months. It is true that the dose of T can affect the H/H, but men often need a high dose of T to feel normal. The removal of blood is low risk and effective. I am a Specialist in   Hormone Replacement Medical care with a 38-year history of replacing bioidentical hormones and 23 years of experience replacing bioidentical hormones with T and E2 pellets.  You came to me because your doctors were not helping you with the symptoms of testosterone deficiency and because I have the most experience in the Midwest. #1.    The first issue that we must always consider while we treat anyone is the primary goals for treatment, the relief of low testosterone which is why you came to me. You made an appointment with me because you had un-addressed issues that your PCP (Primary Care Doctor) didn't treat satisfactorily Your symptoms were treated with testosterone pellets successfully at a dose that is individual to you. Your health as you get older is also dependent on your blood level of free Testosterone (the total T is not significant) by delaying the diseases of aging. The level that is required to treat your symptoms is the young healthy Free T blood level of a young and healthy man. Most labs give a reference range for older men which reflects the fact that free testosterone levels drop with age. Old men don't feel well BECAUSE they have low free T.  The low free T level is why you don't feel well. Our practice has found that everyone has an ideal free T level that we try to maintain, and these are young-healthy level but not old-man level.  That is what we have been trying to achieve for our patients. #2. The second issue is a side-effect that you, as an individual, have experienced with pellets and will experience with any T replacement that you receive that is a high enough dose to treat your symptoms.  Erythrocytosis is a side effect that some men experience on any form of testosterone, however its occurrence doesn't mean you are on too much testosterone, it means you have a side effect of having a normal free T level.  Erythrocytosis is genetic, and your free T blood level stimulates the production of too many red blood cells.  We don't stop the treatment that is making you better, to treat the side effects of it.  We treat the side effects. We treat this side effect with phlebotomies to keep your H/H within the safe range.  Did your medical doctor/cardiologist tell you why this is important?  We tell you: too many red blood cells can increase the work of the heart, however the Hematologists that we consult with give us the HCT% number we should stay below is 58%.  We like to keep your HCT% below 52% but that requires you to be compliant with your regular blood donated or phlebotomized in our office (that takes an appointment). You must be compliant to keep your H/H normal. These 2 issues are at odds with one another. I cannot give a man enough testosterone to treat his symptoms, without stimulating some production of RBCs.  I have no other low T treatment that doesn't stimulate your bone marrow to make red cells BUT I do have a simple treatment to remove your extra blood cells routinely to keep you from having too many blood cells circulating. Only you can make the decision to choose health with T pellets and do phlebotomies regularly as recommended, or to stop T and allow your blood count to decrease., and your symptoms will come back. I want you to read your post-pellet instructions, locate my book Got Testosterone? and read it especially the section on Erythrocytosis, and look at FAQs (frequently asked questions) on the www.biobalanacehealth website, read related episodes of my 677 blogs and or listen to my health casts for your answers.  You can imagine how I feel when my patients don't read what I provide to them in multiple forms to answer their questions. In the future you should read the information I have given you or come in for an appointment to discuss these matters.

Controversy: RBCs in MI by TRANSFUSION's Monthly Podcast

In this episode of the RWS Clinician's Corner, we're diving into the fascinating world of mitochondrial health and longevity with our special guest, Jennifer Scheinman. Jennifer, a seasoned registered dietitian and senior manager at Timeline Nutrition, brings her expertise in integrative and functional nutrition to our discussion, where we explore the groundbreaking benefits of the postbiotic urolithin A. Jennifer sheds light on the critical roles mitochondria play beyond just cellular energy production, including their impact on calcium homeostasis, melatonin production, inflammation, and even cellular signaling. We discuss how aging affects mitochondrial function and how Urolithin A can support mitochondrial health, promoting cellular longevity and overall vitality.   We discuss: Specific benefits of Urolithin A, particularly for those over 40 Mitochondrial functions (beyond energy) and how longevity & aging impact mitochondria A study on Olympic endurance athletes (with exercise-induced inflammation) & the impact of Urolithin A. Safety and efficacy of Urolithin A, as well as practical applications and dosage Urolithin A for immune system health as well as skin and joint health Existing Urolithin A products and quality concerns The Clinician's Corner is brought to you by Restorative Wellness Solutions.  Follow us: https://www.instagram.com/restorativewellnesssolutions/ Timestamps:  00:00 Jen educates on cellular health and aging. 06:14 Most cells have dynamic mitochondria, except RBCs. 07:43 Understanding Urolithin A: postbiotic molecule from gut microbiome. 10:31 Focus on postbiotic function, not production origin. 15:39 Joined Timeline for rare research on supplements. 19:12 15 years of research showed improved mitochondrial function. 22:09 Robust improvements in muscle strength and inflammation. 23:26 Interest in Urolithin A's impact on aging brains. 28:34 Sponsored podcast teaches advanced gastrointestinal healing. 31:37 Mitophagy rejuvenates skin, boosts collagen, reduces sun damage. 35:04 Research-backed label criteria aid urolithin choices. 39:12 Tailor treatment based on the patient's condition. 42:00 Optimum dose vital for complex illnesses management. 44:09 Mitochondrial health supplements: biogenesis, compare CoQ10. 47:47 Safe supplement; no significant side effects reported. 49:58 People notice more energy from the nighttime dose. 56:06 Link to product, coupon, and affiliate program. 59:04 Join, follow, share Clinician's Corner podcast episode. Speaker bio:  Jennifer is an accomplished registered dietitian nutritionist with over two decades of expertise in nutrition and wellness. During her career, she has worked at some of the nation's leading health and wellness institutions, showcasing her depth of experience in the field.   Jen's master's degree in Integrative and Functional Nutrition, coupled with advanced training in bioenergetics and hormone health, provide her with a profound understanding of the complex interplay between nutrition, cellular health, and longevity. This specialized education has equipped Jen with a unique skill set, enabling her to delve into the nuances of how dietary and lifestyle factors influence the body's energy production and biological processes of aging.   Jen is currently the Senior Manager of Timeline Nutrition, where she plays a pivotal role in educating both healthcare professionals and consumers about the significance of cellular health and Urolithin A in the context of aging and longevity. Beyond her responsibilities at Timeline, she is a renowned speaker, writer, and media figure. Jennifer also continues to practice as a nutrition coach, dedicating herself to assisting clients in optimizing their nutrition for enhanced vitality and a longer healthspan.   Connect with Jennifer Scheinman / Timeline: Website: www.timeline.com/RWS Coupon Code: RWS Instagram: https://www.instagram.com/timeline_longevity/ and https://www.instagram.com/jenscheinman_nutrition/ Test to determine if you are a UA producer: https://challenge.timeline.com/ Our studies: https://www.timeline.com/studies Sign up for affiliate program: https://www.timeline.com/promotions/affiliate-program   Keywords:  Margaret Floyd Barry, Jennifer Scheinman, Restorative Wellness Clinicians Corner, Urolithin A, postbiotic, mitochondrial health, functional health professionals, cellular energy production, longevity, chronic illness treatment, bioenergetics, hormone health, Timeline Nutrition, mitochondria, mitophagy, muscle health, inflammation, chronic fatigue, immune system health, integrative and functional nutrition, dietary supplements, chronic Lyme, long COVID, muscle strength, oxidative stress, antioxidant, skin health, cognitive benefits, gut microbiome, aging, polyphenols Disclaimer: The views expressed in the RWS Clinician's Corner series are those of the individual speakers and interviewees, and do not necessarily reflect the views of Restorative Wellness Solutions, LLC. Restorative Wellness Solutions, LLC does not specifically endorse or approve of any of the information or opinions expressed in the RWS Clinician's Corner series. The information and opinions expressed in the RWS Clinician's Corner series are for educational purposes only and should not be construed as medical advice. If you have any medical concerns, please consult with a qualified healthcare professional. Restorative Wellness Solutions, LLC is not liable for any damages or injuries that may result from the use of the information or opinions expressed in the RWS Clinician's Corner series. By viewing or listening to this information, you agree to hold Restorative Wellness Solutions, LLC harmless from any and all claims, demands, and causes of action arising out of or in connection with your participation. Thank you for your understanding.  

Are you finding that your HbA1c levels are elevated despite being on a low-carb, ketogenic, or even carnivore diet? Recently, my HbA1c test came back at 5.7 (just under the prediabetic range), and I knew something was off; after all, I've been following a relatively low-carb lifestyle for years, so there's no way my blood sugar should be high enough to suggest prediabetes.  In consulting with carnivore diet expert and medical doctor Shawn Baker, I learned that healthy red blood cells that live longer than average can actually skew HbA1c readings, making it appear as though you have higher blood glucose than you do. This happens because the longer your red blood cells live, the more glucose has time to attach to hemoglobin, artificially inflating your HbA1c levels. (Conversely, shorter-lived red blood cells can lead to lower readings, even in those with high blood sugar.) In this episode, I break down the science of the HbA1c test and explain how factors like red blood cell lifespan, iron deficiency, anemia, and other health conditions can all affect your hemoglobin A1c results.  Even if you have healthy blood sugar and no signs of diabetes, your HbA1c might still be higher due to these factors. In my case, despite my elevated HbA1c, my continuous glucose monitor (CGM) showed average blood glucose levels between 85 and 89 mg/dL — well within the normal range. In this episode: 00:00:00 - Intro & elevated HBA1C discovery 00:01:15 - Investigating the cause of high HBA1C 00:02:54 - Understanding HBA1C and red blood cells 00:04:19 - Dr. Shawn Baker's explanation: longer lifespan of RBCs 00:06:28 - Conclusion & next episode sneak peek Learn more: Continuous Glucose Monitoring Explained: https://michaelkummer.com/continuous-glucose-monitoring/ Levels vs. Nutrisense: CGM Comparison: https://michaelkummer.com/levels-vs-nutrisense/ Why You Should Wear a Continuous Glucose Monitor (CGM): https://www.primalshiftpodcast.com/44-why-you-should-wear-a-continuous-glucose-monitor-cgm/ How Exercise Influences Your Blood Glucose Response [Coke Challenge]: https://www.youtube.com/watch?v=iIiuRoKtq1s Use the code YOUTUBE10 to get 10% off your order of Grass-Fed Beef Liver supplements at https://shop.michaelkummer.com Affordable At-Home Blood Testing with SiPhox Health: https://www.youtube.com/watch?v=R7qRLzBcp94 Get 20% off your SiPhox Health purchase with the code MICHAELKUMMER at: https://michaelkummer.com/go/siphoxhealth   Ultrahuman vs Oura Ring: What's the BEST Fitness and Sleep Tracker?: https://www.youtube.com/watch?v=E-vAgCh22zk Thank you to this episode's sponsor, OneSkin! OneSkin's lineup of topical skin health products leverage the power of the company's proprietary OS-01 peptide to remove dead skin cells, improve collagen production, increase skin hydration and more. Check out my before and after photos in my OneSkin review and visit OneSkin here. Get 15% off with my discount code MKUMMER: https://michaelkummer.com/go/oneskinshop  Find me on social media for more health and wellness content: Website: https://michaelkummer.com/ YouTube: https://www.youtube.com/@MichaelKummer Instagram: https://www.instagram.com/primalshiftpodcast/ Reddit: https://www.reddit.com/r/michaelkummer/ Pinterest: https://www.pinterest.com/michaelkummer/ Twitter/X: https://twitter.com/mkummer82 Facebook: https://www.facebook.com/realmichaelkummer/ [Medical Disclaimer] The information shared on this video is for educational purposes only, is not a substitute for the advice of medical doctors or registered dietitians (which I am not) and should not be used to prevent, diagnose, or treat any condition. Consult with a physician before starting a fitness regimen, adding supplements to your diet, or making other changes that may affect your medications, treatment plan, or overall health. [Affiliate Disclaimer] I earn affiliate commissions from some of the brands and products I review on this channel. While that doesn't change my editorial integrity, it helps make this channel happen. If you'd like to support me, please use my affiliate links or discount code. #PrimalShift #OptimalHealth #AncestralLiving #Biohacking #HBA1C   

In this part 2 episode, we dive into the pathology and symptoms of Babesiosis, exploring how the Babesia parasite infects red blood cells and evades the immune system. We discuss various labs and biomarkers to look out for. We then address various treatment protocols featuring anti-malarials including herbal supplements such as artemisinin and cryptolepis, and proteolytic enzymes like lumbrokinase and nattokinase. Additionally, we cover the use of methylene blue and its impact on Babesia parasites. Topics: 1. Introduction - Brief overview of Babesiosis and previous discussion - Overview of Babesia infection and its impact on red blood cells (RBCs) 2. Pathology of Babesiosis - Infection and multiplication within RBCs - Mechanisms of immune evasion - Expression of specific proteins on RBC surface - Adherence to capillary endothelial cells - Avoidance of spleen clearance - Antigenic variation and immune system evasion 3. Symptoms of Babesiosis - Air hunger - High fever - Severe fatigue - Muscle and joint pain - Persistent headaches - Jaundice - Dark urine - Organ failure (in severe cases) 4. Labs and Markers for Babesiosis - Hematological markers - Hemolytic anemia - Thrombocytopenia - Leukopenia - Hemoglobinuria - Hyperbilirubinemia - Elevated LDH levels - Reticulocytosis - Other markers - High C4a levels - Low CD57 count 5. Protocols - Importance of medical supervision and potential Herxheimer reaction - Overview of treatment approaches 6. Anti-Malarial Protocols for Babesiosis - Prescription Medications - Mepron (Atovaquone), Mechanism of action: inhibition of mitochondrial electron transport chain. - Azithromycin, Mechanism of action: blocking protein synthesis. - Herbal Approaches for Babesiosis - Artemisinin: Derived from sweet wormwood plant. Mechanism of action: production of reactive oxygen species (ROS). - Cryptolepis: Bioactive compound is Cryptolepine, Mechanism of action: disruption of DNA synthesis. 7. Proteolytic Enzymes - Lumbrokinase - Nattokinase 8. Methylene Blue - Synthetic dye - Mechanism of action: disrupting mitochondrial function and generating ROS within Babesia - Administration methods and effects 9. Conclusion - Recap of supplements and treatments discussed - Emphasis on individualized treatment plans, bioindividuality, and working with a medical physician Thank you to our episode sponsor: ⁠Liver Medic⁠ Use code Chloe20 to save 20% on ⁠⁠"Leaky Gut Repair"⁠⁠ ⁠⁠Brendan's YouTube Channel⁠⁠ ⁠⁠https://x.com/livermedic⁠⁠ Thanks for tuning in! Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" If you liked this episode, please leave a rating and review or share it to your stories over on Instagram. If you tag @synthesisofwellness, Chloe would love to personally thank you for listening! Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok @chloe_c_porter Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to purchase products, subscribe to our mailing list, and more! Or visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠linktr.ee/synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to see all of Chloe's links, schedule a BioPhotonic Scanner consult with Chloe, or support the show! --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

In this episode, we explore the intricacies of Babesia and Babesiosis, exploring how this protozoan parasite infects red blood cells and evades the immune system. We discuss the various pathological effects of the infection, including impaired blood flow, tissue ischemia, and multi-organ dysfunction syndrome. Additionally, we cover common symptoms, relevant bloodwork indicators, and an overview of anti-malarial herbs/supplements and other strategies often employed in cases of Babesia. Topics: Introduction Recap of previous discussions on Lyme disease and mold Overview of chronic inflammatory response syndrome (CIRS) or biotoxin illness protocols Introduction to the current topic: Babesia and Babesiosis Overview of Babesiosis Definition and cause of Babesiosis Explanation of protozoan parasites Transmission method: tick bites Broad overview of Babesia infection process Babesia Infection Process Entry into the bloodstream via tick bite Infection and multiplication in red blood cells (RBCs) Hemolytic event: rupture of RBCs and hemolytic anemia Babesia's Evasion Mechanisms Avoidance of immune detection and spleen clearance Expression of parasite-encoded proteins on infected RBCs (iRBCs) Adherence to capillary endothelial cells in internal organs Capillary blockage and tissue damage Antigenic variation: changing surface proteins to evade antibodies Pathological Effects of Babesia Impaired blood flow and tissue ischemia Local inflammatory responses Multi-organ dysfunction syndrome Symptoms of Babesiosis Air hunger and low oxygen levels Common symptoms: fever, fatigue, muscle and joint pain, headaches, jaundice, dark urine, nausea, abdominal pain Severe symptoms: organ failure, acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), splenomegaly, low blood pressure and shock Bloodwork Indicators for Babesiosis Diagnostic tests: FISH test Hematological markers: hemolytic anemia, thrombocytopenia, leukopenia, hemoglobinuria, hyperbilirubinemia, elevated LDH, reticulocytosis Complement protein C4A and CD57 count Strategies for Babesiosis Importance of working with licensed medical professionals Mention of standard herbs and treatments Anti-malarials (mepron, artemisinin, cryptolepis), antibiotics (azithromycin), methylene blue, lumbrokinase Thank you to our episode sponsor: Liver Medic Use code Chloe20 to save 20% on ⁠"Leaky Gut Repair"⁠ ⁠Brendan's YouTube Channel⁠ ⁠https://x.com/livermedic⁠ Thanks for tuning in! Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" If you liked this episode, please leave a rating and review or share it to your stories over on Instagram. If you tag @synthesisofwellness, Chloe would love to personally thank you for listening! Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok @chloe_c_porter Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to purchase products, subscribe to our mailing list, and more! Or visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠linktr.ee/synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to see all of Chloe's links, schedule a BioPhotonic Scanner consult with Chloe, or support the show! --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

In this week's episode we'll discuss extended follow-up from the ZUMA-5 trial of axicabtagene ciloleucel, or axi-cel. Then we'll learn about the role of platelets in binding and clearing senescent red blood cells. Finally, we'll hear about a new risk stratification strategy for lymphomas of the central nervous system, or CNS. 

In this episode we discuss: Studies showing that omega-3 consumption decreases lifespan and increases disease processes  The potentially harmful effects of omega-3 usage during pregnancy on offspring  The impact of omega-3s on inflammation, endotoxin, and mitochondrial respiration  The data in native cultures showing that omega-3 intake doesn't improve cardiovascular disease or mortality  Extremely healthy populations that consume high-carb and high-saturated fat diets with almost no omega-3s      Check out the Energy Balance Solution program here: https://www.jayfeldmanwellness.com/solution/     Download the Free Energy Balance Food Guide here: https://www.jayfeldmanwellness.com/guide/     Click here to check out the show notes: https:/jayfeldmanwellness.com/ep-107-omega-3s-decrease-lifespan-and-increase-disease   Timestamps: 0:00 – intro 1:30 – studies showing that omega-3 consumption decreases lifespan and increases disease processes in animals 13:55 – studies on animals showing the harmful effects of omega-3 consumption during pregnancy on offspring 17:37 – studies showing that omega-3 consumption contributes to disease processes, increases inflammation, causes oxidative stress, increases endotoxin, and interferes with mitochondrial respiration 28:19 – whether we should be concerned about saturated fats increasing endotoxin absorption 29:33 – how omega-3 consumption leaves us more susceptible to damage when we're under stress 32:53 – whether we should be consuming fatty fish 35:01 – the lack of benefit of omega-3 consumption in native populations consuming large amounts of fatty fish and seafood 38:40 – low incidence of cardiovascular disease in native populations consuming very little omega-3s 59:30 – concluding thoughts on whether we should consume omega-3s based on the data on omega-3s in RBCs and phospholipids and mortality

Red blood cells is also known as Erythrocytes. In the human body, erythrocytes (RBCs) are the most prevalent cell type. It performs the task of carrying oxygen from the lungs to the body's tissues. Haemoglobin, which is present in large amounts in RBCs, mediates oxygen transfer. 

Anemic? Tired all the time? Bruising? Spontaneous nose bleeds? Can't heal? Iron causing constipation or hemorrhoids? Is iron healthy? Red blood cells are likes trucks on the freeway. RBCs carry oxygen and nutrients to the tissues and remove waste products. Too little RBCs and it feel horrible. Too many RBC's and it feels awful. It's life! If red blood cells are healthy, then people are healthy. Too many, and traffic jams occur. Too little and exhaustion occurs. THE WORST THING IS TAKING IRON without knowing what the iron levels are. Iron is so important but also can be SOOOOO toxic. The wrong kind of iron is so bad for health. Free master class on red blood cells, iron toxicity and the breakthrough of refined plant blood infusions - a natural, safe and effective way to build the red blood cells in the body based upon 106 years of clinical experience. Here's is the link to our website if you need more information: https://www.westcliniconline.com/

Normal 96-108 mEq/L Indications Identify Acid-Base Imbalance Description Chloride (Cl-), an anion found in the blood, works together with sodium to help maintain oncotic pressure and water balance in the body. Chloride is inversely related to bicarbonate levels in the blood. Chloride is also part of hydrochloric acid (HCL) which is utilized in the stomach to breakdown food. When red blood cells (RBCs) take up CO2 they take up chloride as well. The negative ion bicarbonate then leaves the red blood cell so that the electrical charge is maintained. Extra chloride is excreted into the urine by the kidneys. What would cause increased levels? Dehydration Acute Renal Failure Cushing Disease Metabolic Acidosis Respiratory Alkalosis. What would cause decreased levels? Congestive Heart Failure (CHF) Water intoxication Burns Metabolic Alkalosis Respiratory Acidosis Addison Disease Salt-losing Nephritis Excessive sweating Diarrhea Vomiting

Platelet-rich plasma (PRP) has been used extensively in clinical practice to treat patients with symptomatic knee osteoarthritis (OA). Leukocyte-poor PRP (LP-PRP) has been clinically preferred over leukocyte-rich PRP (LR-PRP); however, it is unclear which cytokine mediators of pain and inflammation are present in LR-PRP and LP-PRP from patients with mild to moderate knee OA in order to rationalize a specific formulation.   In conclusion, although numerous studies have demonstrated the excellent safety profile of PRP in treating patients with knee OA symptoms, a specific formulation has yet to be determined. Although challenging to conduct, clinical trials are needed that incorporate a mechanistic approach in all study arms in order to assess the effect of all components in PRP formulations (growth factor profile, leukocytes, RBCs, platelet dose) that not only are responsible for improving symptoms but also could contribute to disease-modifying effects. Our results expand on the current literature and demonstrate novel findings in that LR-PRP that was neutrophil-rich was predominantly anti-inflammatory compared with LP-PRP with reduced neutrophil concentration in patients with knee OA.   To read the article, click here.

Objective: Determine the significance and clinical use of Erythrocyte Sedimentation Rate in clinical practice   Lab Test Name: Erythrocyte Sedimentation Rate- ESR   Description: The Erythrocyte Sedimentation Rate (ESR) test measures sedimentation of Red Blood Cells (RBCs).  In normal conditions, RBCs settle or sediment very little.  Inflammation affects proteins in the blood causing RBCs to stick and settle together out of the liquid portion of the blood.   Indications: Identifies inflammation which assists in diagnosing: Cancer Infection Autoimmune diseases   Normal Therapeutic Values: Normal – 0-20 mm/hr   What would cause increased levels? Increased Conditions: Anemia Chronic Renal Failure Systemic Lupus Erythematosus (SLE) Infection Tuberculosis Pregnancy Polymyalgia Rheumatica Multiple myeloma Medications: Oral contraceptives Theophylline Vitamin A   What would cause decreased levels? Decreased Conditions: Sickle cell anemia Polycythemia Vera Leukocytosis Congestive Heart Failure (CHF) Medications: Aspirin Cortisone Quinine

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Get a free nursing lab values cheat sheet at NURSING.com/63labs   What is the Lab Name for Red Blood Cell (RBC) Lab Values? Red Blood Cell   What is the Lab Abbreviation for Red Blood Cell? RBC   What is Red Blood Cell in terms of Nursing Labs? Red Blood Cells (RBCs) contain hemoglobin which is responsible for oxygen transport throughout the body. RBCs are primarily produced in the bone marrow, they have a life span of 120 days and are destroyed in the spleen and liver. RBC production is regulated by erythropoietin (EPO) which is produced and released from the kidneys.   What is the Normal Range for Red Blood Cell? Male: 4.5 – 5.5 x106/cells/mm3 Female: 4.0 – 4.9 x106/cells/mm3   What are the Indications for Red Blood Cell? Identify: Anemia Blood loss   What would cause Increased Levels of Red Blood Cell? Dehydration Polycythemia Vera Chronic Obstructive Pulmonary Disease (COPD) High altitude Congenital heart disease CorPulmonale Pulmonary fibrosis Thalassemia trait   What would cause Decreased Levels of Red Blood Cell? Chemotherapy Anemia Hemorrhage Hemolysis Hemoglobinopathy Advanced cancer Leukemia Lymphoma Pernicious anemia Rheumatoid disease Organ failure Bone marrow failure Hypervolemia Pregnancy

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.02.526657v1?rss=1 Authors: May, A., Ventura, T., Fidanza, A., Volmer, H., Taylor, H. A., Romano, N., D'Souza, S. L., Bieker, J. J., Forrester, L. M. Abstract: Congenital dyserythropoietic anaemia (CDA) type IV has been associated with an amino acid substitution, Glu325Lys (E325K), in the transcription factor KLF1. These patients present with a range of symptoms, including the persistence of nucleated red blood cells (RBCs) in the peripheral blood which reflects the known role for KLF1 within the erythroid cell lineage. The final stages of RBCs maturation and enucleation take place within the erythroblastic island (EBI) niche in close association with EBI macrophages. It is not known whether the detrimental effects of the E325K mutation in KLF1 are restricted to the erythroid lineage or whether deficiencies in macrophages associated with their niche also contribute to the disease pathology. To address this question, we generated an in vitro model of the human EBI niche using induced pluripotent stem cells (iPSCs) derived from a CDA type IV patient as well as iPSCs genetically modified to express an KLF1-E325K-ERT2 protein that could be activated with 4OH-tamoxifen. CDA patient-derived iPSCs and iPSCs expressing the activated KLF1-E325K-ERT2 protein showed significant deficiencies in the production of erythroid cells with associated disruption of some known KLF1 target genes. Macrophages could be generated from all iPSC lines but when the E325K-ERT2 fusion protein was activated, we noted the generation of a slightly less mature macrophage population marked by CD93. A subtle reduction in their ability to support RBC maturation was also associated with macrophages carrying the E325K-ERT2 transgene. Taken together these data support the notion that the clinically significant effects of the KLF1-E325K mutation are primarily associated with deficiencies in the erythroid lineage but that deficiencies in the niche might have the potential to exacerbate the condition. The strategy we describe provides a powerful approach to assess the effects of other mutations in KLF1 as well as other factors associated with the EBI niche. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this super HY podcast, I discuss a host of commonly tested adverse drug reactions around the blood elements (RBCs, WBCs, platelets). These things show up on almost every USMLE exam. It is a continuation of Episode 387 on the website. If you’re interested in helping with the transcription of my Step 1 podcasts, reach … Continue reading Divine Intervention Episode 433: Adverse Drug Reactions for The USMLE exams Part 2 (Step 1-3)

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.13.519447v1?rss=1 Authors: Bergaglio, T., Bhattacharya, S., Thompson, D., Nirmalraj, P. N. Abstract: Understanding the dose-dependent effect of over-the-counter drugs on red blood cells (RBCs) is crucial for hematology and digital pathology. Yet, it is challenging to continuously record the real-time, drug-induced nanoscopic shape changes of RBCs in a label-free manner. Here, we demonstrate digital holotomography (DHTM) enabled real-time, label-free concentration-dependent and time-dependent monitoring of ibuprofen on RBCs from a healthy donor. The RBCs are segmented based on 3D and 4D refractive index tomograms and their morphological and chemical parameters are retrieved with their shapes classified using machine learning. We directly observed the formation and motion of spicules on the RBC membranes when aqueous solutions of ibuprofen were drop cast on wet blood, creating rough-membraned echinocyte forms. At low concentrations of 0.25-0.50 mM, the ibuprofen-induced morphological change was transient but at high concentrations (1.5-3 mM) the spiculated RBC remained over a period of up to 1.5 hours. Molecular simulations confirmed that aggregates of ibuprofen molecules at high concentrations significantly disrupted the RBC membrane structural integrity and lipid order, but produced negligible effect at low ibuprofen concentrations. Control experiments on the effect of urea, hydrogen peroxide and aqueous solutions on RBCs showed zero spicule formation. Our work elucidates the dose-dependent chemical effects on RBCs using label-free microscopes that can be deployed for the rapid detection of overdosage of over-the-counter and prescribed drugs. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Get a free nursing lab values cheat sheet at NURSING.com/63labs   What is the Lab Name for Hemoglobin (Hbg) Lab Values? Hemoglobin   What is the Lab Abbreviation for Hemoglobin? Hbg   What is Hemoglobin in terms of Nursing Labs? Hemoglobin (Hbg), an iron containing compound, is the main protein in Red Blood Cells (RBCs). It enables oxygen and carbon dioxide (CO2) to bind to RBCs for transport throughout the body.   What is the Normal Range for Hemoglobin? Male: 13.5 – 16.5 g/dL | Female: 12.0 – 15.0 g/dL   What are the Indications for Hemoglobin? Identify: Bleeding disorders Anemia Blood loss     What would cause Increased Levels of Hemoglobin? Erythrocytosis Polycythemia Vera Shock Dehydration Severe burns Chronic Obstructive Pulmonary Disease (COPD) Congenital Heart Disease   What would cause Decreased Levels of Hemoglobin? Anemia Blood Loss Bone Marrow Disorders: Leukemia Lymphoma Multiple myeloma Aplastic anemia Severe burns Hyperthyroidism Renal disease Systemic Lupus Erythematosus (SLE)

Short Answer: If it can't be explained by the dose of salt, it may be that the salt is not being absorbed orally. Glucose, starch, or simply a meal consumed alongside the salted water may help with this. This is a clip from a live Q&A session open to CMJ Masterpass members. In addition to this episode, you can access two other free samples using this link:   https://chrismasterjohnphd.substack.com/p/questions-on-protein-and-longevity-1a2 In that batch of free episodes you will also find the answers to these questions: Protein and Longevity How to Increase or Decrease SHBG? If you want to become a Masterpass member so you can participate in the next live Q&A, or so you can have access to the complete recording and transcript of each Q&A session, you can save 10% off the subscription price for as long as you remain a member by using this link to sign up: https://chrismasterjohnphd.substack.com/qanda Learn more about the Masterpass here: https://chrismasterjohnphd.substack.com/about This snippet is from the August 15, 2022 AMA. The full recording and transcript is reserved for Masterpass members. Here is a preview of what's included: Does which food you eat matter when everything is digested anyway? How to know if your nitric oxide is dilating your blood vessels properly? How big of a problem are transient glucose spikes above 140 mg/dL? Can I take too much collagen? What is the maximum dose of cod liver oil safe to use long-term? How much A is safe to take when I need so much to resolve my symptoms? Generalizing from cell studies of green tea catechins to cups of green tea per day. What to do about lumbar discs bulging? Why would vitamin K2 cause a nosebleed? How to balance A with D when I react poorly to D and need so much A? Why would COVID decrease HRV long-term? How to raise secretory IgA? Rapid-fire answers to pre-submitted questions that didn't win the contest: alternatives to bone meal powder, herbal tea and nutrient absorption, retinol-binding protein, improving fat digestion, metal provocation tests, fatty liver, high-dose B vitamins, eyebrow thinning, itchy bumps after exercise, brain fog and rifaximin, low cholesterol, tolerating chlorine pools, cycling nutrients, copper toxicity, stopping supplements before blood tests, COVID vaccines causing post-nasal drip, natural vs synthetic vitamins, absorbing iron through baths, elevated EPA and DHA in RBCs, COVID affecting the vagus nerve, supplements for athletic performance, when water doesn't hydrate, tics and Tourette's, recalcitrant homocysteine, fraud and corruption in scienctific research. Here's a link to the full AMA: https://chrismasterjohnphd.substack.com/p/recording-and-transcript-of-the-august Access the show notes, transcript, and comments here.

Short Answer: SHBG is increased by adiponectin (vitamin K2, insulin sensitivity), thyroid hormone, fasting physiology (AMPK, fat oxidation), and estrogen (especially estrone), while it is decreased by insulin resistance, obesity, the fed state and carbohydrate-dominant physiology, androgens, and polyunsaturated fat. This is a clip from a live Q&A session open to CMJ Masterpass members. In addition to this episode, you can access two other free samples using this link:   https://chrismasterjohnphd.substack.com/p/questions-on-protein-and-longevity-1a2 In that batch of free episodes you will also find the answers to these questions: Protein and Longevity  Why is an IV more hydrating than salted water? If you want to become a Masterpass member so you can participate in the next live Q&A, or so you can have access to the complete recording and transcript of each Q&A session, you can save 10% off the subscription price for as long as you remain a member by using this link to sign up: https://chrismasterjohnphd.substack.com/qanda Learn more about the Masterpass here: https://chrismasterjohnphd.substack.com/about This snippet is from the August 15, 2022 AMA. The full recording and transcript is reserved for Masterpass members. Here is a preview of what's included: Does which food you eat matter when everything is digested anyway? How to know if your nitric oxide is dilating your blood vessels properly? How big of a problem are transient glucose spikes above 140 mg/dL? Can I take too much collagen? What is the maximum dose of cod liver oil safe to use long-term? How much A is safe to take when I need so much to resolve my symptoms? Generalizing from cell studies of green tea catechins to cups of green tea per day. What to do about lumbar discs bulging? Why would vitamin K2 cause a nosebleed? How to balance A with D when I react poorly to D and need so much A? Why would COVID decrease HRV long-term? How to raise secretory IgA? Rapid-fire answers to pre-submitted questions that didn't win the contest: alternatives to bone meal powder, herbal tea and nutrient absorption, retinol-binding protein, improving fat digestion, metal provocation tests, fatty liver, high-dose B vitamins, eyebrow thinning, itchy bumps after exercise, brain fog and rifaximin, low cholesterol, tolerating chlorine pools, cycling nutrients, copper toxicity, stopping supplements before blood tests, COVID vaccines causing post-nasal drip, natural vs synthetic vitamins, absorbing iron through baths, elevated EPA and DHA in RBCs, COVID affecting the vagus nerve, supplements for athletic performance, when water doesn't hydrate, tics and Tourette's, recalcitrant homocysteine, fraud and corruption in scienctific research. Here's a link to the full AMA: https://chrismasterjohnphd.substack.com/p/recording-and-transcript-of-the-august Access the show notes, transcript, and comments here.

Perhaps you, like many software testers and test managers, are enjoying the benefits of incorporating a lightweight analytical risk-based testing strategy such as RBCS' Pragmatic Risk Analysis and Management (PRAM) technique into your test approach. What if your organization is adopting an agile methodology? Can you still use PRAM and other similar analytical risk-based testing strategies? Absolutely. In this webinar, Rex will explain the process for integrating quality risk identification and assessment into the release and iteration planning processes, and for integrating quality risk mitigation into each iteration. You'll return to work with a proven method for injecting risk-based testing into your agile processes.

Short Answer: While protein restriction may have value in people with established cancer or kidney disease, cycling robustly between fasting and feeding states is likely to provide all the value that restriction of protein or calories might otherwise provide, and a high protein intake supports bone mass, muscle mass, and the detoxification of carcinogens, all of which are important to longevity. This is a clip from a live Q&A session open to CMJ Masterpass members. In addition to this episode, you can access two other free samples using this link:   https://chrismasterjohnphd.substack.com/p/questions-on-protein-and-longevity-1a2 In that batch of free episodes you will also find the answers to these questions: How to Increase or Decrease SHBG?  Why is an IV more hydrating than salted water? If you want to become a Masterpass member so you can participate in the next live Q&A, or so you can have access to the complete recording and transcript of each Q&A session, you can save 10% off the subscription price for as long as you remain a member by using this link to sign up: https://chrismasterjohnphd.substack.com/qanda Learn more about the Masterpass here: https://chrismasterjohnphd.substack.com/about This snippet is from the August 15, 2022 AMA. The full recording and transcript is reserved for Masterpass members. Here is a preview of what's included: Does which food you eat matter when everything is digested anyway? How to know if your nitric oxide is dilating your blood vessels properly? How big of a problem are transient glucose spikes above 140 mg/dL? Can I take too much collagen? What is the maximum dose of cod liver oil safe to use long-term? How much A is safe to take when I need so much to resolve my symptoms? Generalizing from cell studies of green tea catechins to cups of green tea per day. What to do about lumbar discs bulging? Why would vitamin K2 cause a nosebleed? How to balance A with D when I react poorly to D and need so much A? Why would COVID decrease HRV long-term? How to raise secretory IgA? Rapid-fire answers to pre-submitted questions that didn't win the contest: alternatives to bone meal powder, herbal tea and nutrient absorption, retinol-binding protein, improving fat digestion, metal provocation tests, fatty liver, high-dose B vitamins, eyebrow thinning, itchy bumps after exercise, brain fog and rifaximin, low cholesterol, tolerating chlorine pools, cycling nutrients, copper toxicity, stopping supplements before blood tests, COVID vaccines causing post-nasal drip, natural vs synthetic vitamins, absorbing iron through baths, elevated EPA and DHA in RBCs, COVID affecting the vagus nerve, supplements for athletic performance, when water doesn't hydrate, tics and Tourette's, recalcitrant homocysteine, fraud and corruption in scienctific research. Here's a link to the full AMA: https://chrismasterjohnphd.substack.com/p/recording-and-transcript-of-the-august

Get a free nursing lab values cheat sheet at NURSING.com/63labs   Objective: Determine the significance and clinical use of Erythrocyte Sedimentation Rate in clinical practice   Lab Test Name: Erythrocyte Sedimentation Rate- ESR   Description: The Erythrocyte Sedimentation Rate (ESR) test measures sedimentation of Red Blood Cells (RBCs).  In normal conditions, RBCs settle or sediment very little.  Inflammation affects proteins in the blood causing RBCs to stick and settle together out of the liquid portion of the blood.   Indications: Identifies inflammation which assists in diagnosing: Cancer Infection Autoimmune diseases   Normal Therapeutic Values: Normal – 0-20 mm/hr   What would cause increased levels? Increased Conditions: Anemia Chronic Renal Failure Systemic Lupus Erythematosus (SLE) Infection Tuberculosis Pregnancy Polymyalgia Rheumatica Multiple myeloma Medications: Oral contraceptives Theophylline Vitamin A   What would cause decreased levels? Decreased Conditions: Sickle cell anemia Polycythemia Vera Leukocytosis Congestive Heart Failure (CHF) Medications: Aspirin Cortisone Quinine

In this week's episode we'll learn more about the prognostic impact of NPM1 and FLT3 mutations in AML, discuss the progression and survival of monoclonal B-cell lymphocytosis, and learn more about the use of red blood cells derived from pluripotent stem cells in transfusion medicine.

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. Welcome to our Episode a 16-year-old who is coughing up blood. Here's the case: A 16-year-old female with h/o SLE was transferred to the PICU due to hypoxia requiring increasing FIO2. A few hours prior to admission to the PICU patient also started coughing up blood and had difficulty breathing. The patient was admitted to the general pediatric floor 2 days earlier for pneumonia requiring an IV antibiotic and O2 via NC. Once transferred to the PICU, she had a rapid deterioration with progressive hematemesis, worsening respiratory distress, and saturations in the low 70s requiring escalating FIO2. The patient was emergently intubated using ketamine + fentanyl and rocuronium. Chest radiograph showed: Worsening bibasilar alveolar and interstitial airspace disease concerning pulmonary hemorrhage. The patient was initially placed on HFOV Paw 26, FIO2 70%, Hz 8, Dp 70, and later transitioned to airway pressure release ventilation or APRV. The patient was also started on inhaled tranexamic acid or TXA and high-dose pulse steroids. The patient initially continued to have some blood coming out from the ETT with suctioning but secretions became clear in ~24 hours. The mother reported that the patient has never had hematemesis/hemoptysis before, or bleeding from any site in the past. Denied history of frequent respiratory infections or recent URI symptoms. The patient has been vaccinated/boosted x3 vs covid. Her COVID PCR is negative. The mother states that she does not engage in tobacco products or alcohol. A physical exam revealed a well-developed teenage girl laying supine in bed deeply sedated and mechanically ventilated. There was decreased AE at lung bases and coarse breath sounds throughout. There was no hepatosplenomegaly and exams of the heart, abdomen and other systems were normal. There was no skin rash and extremities were well perfused with no clubbing in the fingers. The pulmonary team was consulted and a workup was started for pulmonary hemorrhage. To summarize key elements from this case, this patient has: Autoimmune disease: Systemic lupus erythematosus Respiratory Failure warranting MV 2/2 Pulmonary hemorrhage Her presentation and deterioration bring up a concern for diffuse alveolar hemorrhage our topic of discussion for today. This episode will be organized… Definition Etiology Pathophysiology Diagnosis Management Rahul: How do we define pulmonary hemorrhage (PH): PH is defined as the extravasation of blood into airways and/or lung parenchyma. Blood in the airways produces a diffusion barrier resulting in hypoxemia. Due to the reduction of airway diameter from accumulated blood, there is increased airway resistance and even airway obstruction. Subsequently, ventilation can be impaired leading to increased WOB as well as myocardial work required for O2 delivery. Repeated episodes of PH can result in interstitial fibrosis thus changing lung compliance. Hemoptysis by definition is any bleeding from below the vocal cords. PH can be classified as focal or diffuse. Diffuse is further classified as diffuse immune or diffuse nonimmune. Loss of 10% of a patient's circulating blood volume into the lungs, regardless of age, causes a significant alteration in cardiorespiratory function and should be considered massive. In adults, massive pulmonary hemorrhage is defined as blood loss of 600mL or more in 24 hours. In infants, the involvement of at least two pulmonary lobes by confluent foci of extravasated RBCs constitutes as massive PH. “Enough bleeding to make one nervous is probably massive.” Let's pivot and talk about etiologies. Pradip, What are some of the causes of pulmonary hemorrhage in the PICU? Non-immune diffuse PH is usually seen in patients with congenital heart disease (TAPVR, pulmonary atresia, mitral stenosis, hypoplastic left heart syndrome to name a few) neonates (secondary to sepsis, HIE, BW < 1500...

Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our second hematologic emergency: disseminated intravascular coagulation (DIC) with an added bonus of an intro to thrombotic microangiopathic anemias (TMAs).Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!Disseminated intravascular coagulation (DIC):Workup: CBCCMPPT, PTT, INRFibrinogenPeripheral smear - concern for schistocytes. Example of these cells from ASH image bank: https://imagebank.hematology.org/image/60306/schistocytes?type=upload#:~:text=A%20schistocyte%20is%20present%20in,angles%20and%2For%20straight%20borders.Basic mechanism of DIC is consumption of clotting factors leading to coagulopathy Need to be weary of thrombotic microangiopathy: Small blood clots forming in the small vessels leading to endothelial damage, which cause shear stress on the RBCs, which then break down into a schistocyte (AKA triangulocyte or helmet cell) Examples: thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)Management (our opinion!): - Repeat coags q4-6 hours initially (but base interval based on patient) NOTE: INR Is NOT a good assessment of “clotting status” in these situations- Repeat fibrinogen q4-6 hours initially (but base interval based on patient); keep fibrinogen >100 with cryoprecipitate in more stable patients; consider higher thresholds for more acutely ill patients (such as >150) - Repeat CBC q6-8 hours initially; can provide platelets if low, especially if they are bleeding - Workup and treatment for trigger of DIC (infection, trauma, medications, etc.)How does cirrhosis affect data interpretation?- Use clinical context to determine if labs are acutely abnormal or if they have signs/symptoms to suggest underlying liver dysfunction- In the acute setting, always just replace what is missing! How can you tell the difference between nutritional deficiencies vs. consumption (as in with DIC?)- Factor activity levels! Consider checking: Factor 8 (made in endothelium), Factor 5 (Vit K independent), Factor 7 (vitamin K dependent) - If all down, then consider DIC- If Vit K-dependent low, then nutritional deficiency Reference:https://ashpublications.org/blood/article/131/8/845/104418/How-I-treat-disseminated-intravascular-coagulation - Great How I Treat article from Blood Please visit our website (TheFellowOnCall.com) for more information Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

#020 - Welcome back to the Reading Blues Podcast, the place to find out more about the school and to connect with staff, pupils and parents at a deeper level. Each week we'll be interviewing people within the school community, asking them questions and spending time understanding more about them and more about the school.In this episode we speak with Nina and Tytus, two new heads of school. We learn what the Heads of School actually mean, how you apply to get the position , how relationships have changed between teachers and students and what they are planing to do after Blue Coat.So come with me now as we jump into this conversation with Heads of School Tytus and NinaReading Blue Coat School onlineWebsite: www.rbcs.org.ukFacebook: www.facebook.com/ReadingBlueCoatlTwitter: @ReadingBluesInstagram: ReadingBlueCoatSchool

#019 - Welcome back to the Reading Blues Podcast, the place to find out more about the school and to connect with staff, pupils and parents at a deeper level. Each week we'll be interviewing people within the school community, asking them questions and spending time understanding more about them and more about the school. In this episode we're outdoors into some pretty harsh conditions as we find out about something called the Ten Tors event, a 45 mile hike across Dartmoor. Director of Adventure Education, Stephen Lamacraft is joined by Year 12 students Nina, Sergio, Chris, Sophie and also Eloise who's dialling in from home. Together they explain what the Ten Tors event is, how you prepare for something like this, what it's actually like to endure this and what it feels like to cross the finish line. But we also hear about teamwork, something that's at the heart of Reading Blue Coat School. So let's get boots out, laced up and step outdoors for this episode right now. Reading Blue Coat School onlineWebsite: www.rbcs.org.ukFacebook: www.facebook.com/ReadingBlueCoatlTwitter: @ReadingBluesInstagram: ReadingBlueCoatSchool Additional resources:Ten Tors: www.tentors.org.ukMr Lamacraft's email: sla@rbcs.org.uk

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat I'm Rahul Damania, a third-year PICU fellow. I'm Kate Phelps, a second-year PICU fellow and we are all coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine, joining Pradip and Rahul today. Welcome to our episode, where will be discussing gastrointestinal bleeding. Kate: Let's start with a case: A 4-year-old, previously healthy male presents to the emergency room after a large, bloody stool at home. He notably had an episode of dark emesis and an episode of blood-tinged emesis on the day prior. In triage, he is altered and unable to answer questions coherently. Initial vital signs are temperature 36.1 C, RR 24, HR 146, BP 110/54. Point-of-care labs show hemoglobin to be 5.1 with hematocrit 15. His venous blood gas is reassuring against respiratory disease, and he is in no respiratory distress. Further labs are sent and a massive transfusion protocol is initiated before transfer to the PICU. Before arrival in the PICU, he receives two aliquots of RBCs, 1 aliquot of FFP, and 1 aliquot of platelets. Additional labs are sent from the PICU, post-transfusion. His post-transfusion hemoglobin is 8.8. Other labs are notable for normal MCV, elevated total bilirubin to 4.1 (with direct component 3.4), and elevated AST and ALT to 309 and 495 respectively. Rahul: To summarize key elements from this case, this patient has: An undifferentiated gastrointestinal bleed with both hematemesis and hematochezia. He has symptomatic anemia, as evidenced by tachycardia Altered mental status. He is initially stabilized via transfusion of several blood products and liver function labs are shown to be very abnormal — which we will get more into later! PK: Let's get into important parts of the history and physical. Kate, can you tell me what some key history items in this patient are — and what are some areas to make sure to touch on when a patient has a GI bleed? Kate: Yeah! I'd love to. First - in our patient, some important elements are his rather acute onset. His parents mention he has had one day of bleeding symptoms - first with emesis yesterday, with components of old, partially digested blood, as well as some fresh blood. Second, he has a frankly bloody stool at home. Given his clinical instability, history taking was probably limited at first, so it's important to ask follow-up questions and really dig into the case after stabilization! I like to put my questions about gastrointestinal bleeding into buckets based on the questions I need to answer. I need to answer: is this active bleeding or old blood? Is this slow, insidious bleeding or fast, life-threatening bleeding? Is this an upper GI bleed or a lower GI bleed? Bright red blood in emesis tells us that bleeding is active, whereas coffee-ground or dark emesis tells us that, while recent, the blood has been partially digested in the stomach and may not be ongoing. Similarly, melena (dark, tarry stool), tells us blood has come through the colon. While coffee-ground emesis and melena don't rule out an active bleed, they do tell us the bleeding may be slower, as large volume, active bleedy is irritating to the stomach and gastrointestinal tracks and moves through the system quickly. The next question I want to answer is: what is the cause of this bleed? Easy bruising, petechiae and mucosal bleeding may point to a coagulation disorder. Abdominal cramping, frequent stooling, and weight loss may point to inflammatory bowel disease. Past medical history, family history, and a thorough review of systems are key here. Rahul: Yeah, that's great! Let's talk about your question of upper GI vs lower GI bleed. First, a definition: an upper GI bleed is bleeding that occurs above the ligament of Treitz — which is ligamentous tissue that supports the end of the duodenum and beginning of the jejunum at their junction. While not 100% specific, some...

See all the Healthcasts at https://www.biobalancehealth.com/healthcast-blog/ 50% of men who receive Testosterone replacement therapy (TRT) have elevated Red Blood cell counts, and high Hemoglobin and Hematocrits. The numbers that are considered normal are usually normal for men at sea level, and an elevated H/H doesn't necessarily mean that a man will have any negative effects If you have lung problems, or disease: For those men who have COPD, Chronic Bronchitis, or asthma, high counts are an adaptation that help you live with a compromised ability to oxygenate your blood. You should not get your blood dumped because the high counts are keeping you alive!  If you live at high altitude or if you spend a large amount of time at high altitudes, then you don't necessarily need your blood phlebotomized because you need higher counts to live or vacation there. Men who live at high altitude have adapted to a lower oxygen level making more RBCs. If you are an extreme athlete, or you train excessively you may have high red blood counts to help you collect and distribute oxygen during your exercise. You won't have to remove blood unless this level remains a year after you stop excessive exercise. Why are doctors telling us to get phlebotomies (blood dumped) all the time? The problem with having a diagnosis of Erythrocytosis from TRT is that it is almost always confused with the disease called Polycythemia Vera (PCV).  PCV does carry with it a high risk of blood clots, strokes and heart attacks.  The two conditions are completely different, but ER doctors and surgeons only know that a high H/H is a sign of PCV, and PVC causes blood clotting…but they don't know that elevated H/H from TRT or adaptation to a disease doesn't cause the same medical problems as Polycythemia vera.. One of the ways we can separate the disease of PVC from the condition of Erythrocytosis: The CBC will show us the difference.  PVC his elevated RBCs, H/H, Platelets and WBCs…all of them are elevated.  Erythrocytosis only has an elevated RBC, and H/H. If your doctor gets excited about your elevated blood count, please tell him we have evaluated you for PVC and you don't have that, so you are not in danger for clotting or CVDx. Here are the differences between PCV and Erythrocytosis from TFT:   Polycythemia Vera Erythrocytosis Blood test: high RBC, High H/H and High platelets, High WBC Blood test: only high H/H and RBC Abnormal Platelets, increase clotting Normal Platelets, no increase clotting Genetics: + Jak 2 mutation Genetics: no mutation Cause is genetic requires blood dumping to lower all counts or hydroxyurea meds Causes: High Altitude, TRT, COPD, Familial cause Treatment: requires blood dumping to lower all counts or hydroxyurea meds Treatment not necessary to keep it below HCT of 50.  Some people do better with higher counts especially COPD, High Altitude Living, exercise at high altitude. A lot of Research that supports the theory that these patients are at risk for blood clots and coronary artery disease. No research paper that says high H/H from T causes CVDX, Stroke, or Blood clots. Abnormal platelet number and function cause the vascular diseases and clotting TFT is associated with normal platelet counts and functions. Jak 2 increases clotting factors and platelet production, and erythropoietin from the kidneys  and increases clotting. Way it works:  T directly stimulated the bone marrow to make more RBCs. No other blood products are elevated Remember: It is not T that causes high H/H to require blood dumping, it is the confused medical community that goes crazy when they see high H/H and cry malpractice!  In many cases we are dumping blood to appease the primary care doctors.  We ideally would like to keep a man's H/H below 20/55.   Other reasons for elevated H/H: Do you have COPD, Asthma or chronic bronchitis? Don't get your blood dumped. The high counts are helping you. Do you have, or have you had elevated platelet count with your elevated red blood cell count? If you have, please tell your primary or your BioBalance Health Nurse Practitioner you will be evaluated for PCV with a genetic test. Do you live for part of the year at high elevation? If yes, then it is not necessary to phlebotomize you to get your counts down because you need those RBCs. Do you eat high iron foods (liver, braunsweiger, pate, bone marrow, Deep green leafy veggies) ? If so of if you are taking iron, you can stop because you shouldn't need it while taking T, because the bone marrow is stimulated to make more red cells with T. Do men in your family die of CVDX before age 50? Then you might have PCV! Get an iron panel + a Jak 2 genetic test. Blood Phlebotomies: Men over 70, should only have 250 cc removed at one time and told not to exercise for a few days. Blood pressure and blood volume take longer to equilibrate after the age of 70. Make sure these patients have a lot of water and that they drink it and eat something after the phlebotomy.  Remember you just removed blood sugar, dropped their blood pressure, and dehydrated them by removing blood. They may be dizzy, but they have to sit until they are stable.   Blood tests for erythrocytosis/ PCV: CBC Iron panel Ferritin Jak-2 mutation Hereditary hemochromatosis

In this podcast, Dr. Kim Thielen, a nephrologist/kidney specialist with Minnesota Kidney Specialists joins us today to continue part 2 of our discussion on acute kidney injury, as we wade further "into the weeds"  discuss intrinsic renal disease. This episode will break down hallmark urinary findings and further subdivide intrinsic concerns into bland, nephrotic and nephritic, various causes, and treatment. Enjoy the podcast! Objectives:   Upon completion of this podcast, participants should be able to: State the 3 types of urinary analysis findings related to instrinic acute kidney injury. Describe etiology of presentation of each type of intrinsic acute kidney injury. CME credit is only offered to Ridgeview Providers & Allied Health Staff for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks. You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org. To receive continuing education credit for this activity - click the link below, to complete the activity's evaluation. CME Evaluation (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.)  DISCLOSURE ANNOUNCEMENT  The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview Medical Center & Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws.  It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker's outside interest may reflect a possible bias, either the exposition or the conclusions presented. Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event. Thank-you for listening to the podcast. SHOW NOTES: *See the attachment for additional show information.  Intrinsic Kidney Injuries: Urinary analysis findings- Bland Urine: no protein - Nephrotic: protein - Nephritic: protein and blood Hallmark Urinary Findings: Casts - Tamm Horsfall Protein : Mucoprotein made by tubular epithelial cells that precipitate out and congeal    to form casts on whatever is in the cells at the time.  (i.e. RBCs, WBCs, tubular debris) Bland Urine States- Crystalline Induced Renal Injury: obstruction and infllamatory response       - Uric Acid Neuropathy (Most common)              - Cancers, lymphomas, etc.              - Drugs: acyclovir, methotrexate, protease inhibitors, etc.              - Toxins: Ethylene glycol - Bland Urine Disease states: results from injury to tubules, instertim or pre glomerular blodd vessels, not    the filters of the kidney       - Interstital Nephritis              - Hallmark: pyuria and WBC casts                      - Biopsy: inflammatory infiltrate              - Causes:  viral, PPIs, Adenover, mizalamin, etc., Checkpoint inhibitors       - Acute Tubular Necrosis              - Hallmark: tubular epithelial cell cast                      - Granular: (course or fine) diagnostic of ATN              - Biopsy: denuded dilated tubular cells              - Causes: #1: Ischemia;  toxins, drugs, contrast dye;  pigment injury. myoglobin              - What about contrast dye?                      - Categorized under ATN                      - Per Dr. Thielen, plays a role, but injury is not solely dependent on dye alone.       - Hepatorenal Syndrome: ischemic injury to the kidney due to unopposed vasocontstriction               - Ace inhibitors cause unopposed efferent vasoconstriction + nonsteroidals cause                 unposed afferent vasoconstriction = no glomerular perfusion pressure       - Multiple Myeloma              - Hallmark: Light chain cast nephropathy or myeloma kidney                      - Light chains precipitate  out causing obstruction, inflammatory response and causes                        tubular damage              - Presentation: older possibly with anemia, bone pain and elevated creatinine with a bland urine.              - Protein to creatinine ratio: + for protein (non albumin)              - Dipstick: (which measures for albumin and not light chains) will be negative for protein aka                 bland urine       - Hypertensive Nephrosclerosis              - Small vessel vascular disease                     - Blood vessels prematurely atherosclerosis causing glomerular drop out and scarring of the                        interstim       - Scleroderma                - Limited cutaneous systemic sclerosis                - Diffuse cutaneous systemic sclerosis: 60-80% have renal injury from disease state itself                           - FANA positive                           - Concern for Scleroderma Renal Crisis = medical emergency                                   - AKI, moderate to severe HTN and bland urine                                   - Uncontrolled accumulation of collage, thickens vascular walls, narrowing and renal                                       ischemia                          - Occurs in 10-15% of those with Diffuse Cutaneous Systemic sclerosis and happens early                              in disease                                     - Left untreated: renal failure in 1-2 months and death in 1 year                          - Treatment: ACE Inhibitor Nephrotic Urine States - Urine protein: albumin excretion greater than 3.5g in 24 hours - Nephrotic Syndrome:      - Present with 3 things (nephrotic range protein, hypoalbuminemia, peripheral edema)       - Hyperlipidemia: due to increased hepatic lipogenesis                - Increased risk of renal disease and arthroscleratic       - Venous thrombotic disease:                 - Loose proteins other than albumin and develop a hypercoagulale state                 - Renal and peripheral venous thrombosis      - Lipiduria (forms fatty casts,  looks like a latese cross under microscope)  -Pathophysiology or nephrotic syndrome    - Glomerular capillary wall           - 3 layers that work as a glomerular filtration and responsible in the filtration between blood and             urine                  - Fenestrated Capillary Enothelial cells (fenestrations allow plasma through to the basement                     membrane)                 - Glomerular Basement Membrane (maintains glomerular filtration barrier; negatively charged,                     repels albumin)                 - Epithelium: Podocytes (Have highly specialized foot processes that connect and form slit                     diaphragms; Slit diaphragm important for the efficient flow of small solute and water)          - Anything that messes with any of these layers: nephrotic proteinuria - Nephrotic Disease States:     - Biopsy: anyone with nephrotic proteinuria (besides diabetics)          1) Light microscopy: high overview          2) Immunofluorescens: looks for nephritic component and identif immunce complexes          3) Electron microscopy: (EM) helps look at the ultrastructure and better identify immune deposits    - Diabetic nephropathy           - Leading cause of kidney disease in U.S. and western society           - Responsible for 30-40% of all ESRD causes           - Hyperglycemia: produces inflammatory responses, oxidative stress, and injures the podocytes and             deposits that charge and affect the ability of the kidney to filter.     - Amyoidosis            - Organize into betapleted sheets and produce spikes of the capillary uniion and poke through the               GF membrane            - Easily identified by apple green birefringence on congo red            - Terminal illness            - Present with HTN, cardiac effects and elevated creatine  - Nephrotic Disease states based of histologic appearance      - Diagnosed by histologic appearance but does not determine the etiology      - Minimal Change Disease              - Fairly common              - Minimal change under light microscope              - EM: podocytes are abnormal, fused, no unique cell-cell junction              - Primary: Immune generated circulating facture;  alters the cytoskeleton of the podocytes       - Secondary               - Nonsteriodal - most common cause of secondary minimal change disease               - Gama interferon               - Hodgkin's lymphoma               - Allergy: 30% of minimal change have associate allergy (mechanism unknown)       - Presentation               - Sudden onset (days to weeks)               - Marked edema and hypoablbuminemia               - 60% have normal blood pressure,    82% have normal creatinine - Focal Segmental Glomerulosclerosis (FSGS) - primary and secondary         - Most common cause idopathic nephrotic syndrome in adults        - Primary glomerulonephritis in the US that causes ESRD        - Widespread podocyte injury     - Primary: circulating factor that messes with regulation of foot process and adhesion to the         glomerular basement membrane (afffect all podocytes)          - Present with nephrotic syndrome and rapid progression          - HTN and elevated creatinine    - Secondary: the visceral epithelial cells don't replicate          - Nephron loss or obesity or direct foot process injury          - Cannot replicate (podocytes), leads to decreased to podo denisty at specific areas (focal injury)          - 2/3 of all cases FSGS          - Present: with slowly increasing proteinuria and kidney impairment over time          - Causes: interferon, bisphosphonates, talc, anabolic steroids    - Genetics: gene mutations that encode for the slit diaphragms of the podocytes (affect all podocytes)            - Present in Childhood: full blown nephrotic and progress rapidly to ESRD Membranous Nephropathy - Most common cause of nephrotic syndrome in caucasion adults - 80% present with nephrotic but develops more slowly to ESRD - Primary: Major antigen identified      - antibody to trans-membrane receptor that is highly expressed on the glomerular podocyte - Secondary: Cancers (lung, breast, GI), Lupus, Thyroiditis, Hep B, Syphilis, Nonsteroidals, Monoclonal    Antibodies Nephritic Syndrome - Hematuria and proteinuria    - Hematuria: blood from kidney or outside the kidney             - Outside the kidney: look the same             - Inside the kidney: dysmorphic red cells    - Present:             - Renal impairment for days to weeks             - Edmatous, HTN and look critically ill              - Vasculitis, sinusitis, oral ulcers             - Pulmonary renal syndrome: short of breath or hemoptysis             - Skin changes: bruising , bleeding, purpura             - Myalgias and arthritis     - Urine:             - Hallmark: red blood cell casts (polymorphic red cells)             - dipstick + for blood             - elevated proteinuria    - Biopsy: nephritic and + urine Nephritic Disease States (based on immunofluorescence staining) - Pauci Immune Disease         - Ankle vasculitis, common         - A paucity (little amount) of immune complexes         - See black on imaging         - Lab work: check on ANCA and peripheral eosinophils - Anti-GBM Disease         - Renal limited, or classic pulmonary renal: Good Pasture's          - linear staining of the glomerular basement with anti IGG (looks like a ribbon on a package)          - Treat with cytotoxic agents - Immune Complex          - Starry sky pattern          - Glomerulus looks dotted with stars                - Stars = immune complex definition          - Diseases:  Lupus (FANA), Post Infectious GN, Membranous Proliferative GN  - IGA Nephropathy           - Most common cause of glomerulonephritis in the world          - Presentation:                 - Peak incidence is the 2nd and 3rd decades of life                - 40-50% gross hematuria with upper respiratory and GI illness          - Risk Factors for Progression:                - younger age or hypertension at time of presentation                - > 1g proteinuria                - Elevated creatinine at time of presentation Thanks for listening.

Mansi Zaveri, Founder of Kidsstoppress chatted with Ayurveda Health Coach Dimple Jangda about what parents can do to support their child's post covid recovery. They talked about Food that should be eaten to boost the RBCs in the body What food to completely avoid if you are recovering from Covid A few home remedies that can help the recovery process and more If you want to know how you can help your child recover from this illness faster, you should watch the interview. Listen her podcast on virudh ahaar - https://open.spotify.com/episode/6EKCE6CMt5eher2cxQajgQ?si=9f3581f5e0cd4f8f --- Send in a voice message: https://anchor.fm/kidsstoppress/message

Welcome to our new podcast! We are starting this new frontier with a topic that affects every single cattle operation — calf health. It doesn't matter if you're a seedstock or a commercial operator, you need to have live, healthy calves. We know it's not all rainbows and sunshine after a calf is born. Kasey sat down with veterinarian Halden Clark to talk about blind spots in calf health, and what we can do to set them up for a successful, healthy life.

Replacement heifers are an incredibly important, yet expensive part of our operations. Wouldn't it be great if we could program fertility in our replacement heifers? Shelby Rosasco from the University of Wyoming tells us that nutritional management of weaned heifers can help program puberty attainment, fertility, and the ovarian reserve. 

Kasey chats with SDSU meat scientists and ranchers Amanda Blair and Christina Bakker about the intricacies of direct marketing beef well. There are plenty of things to think about before starting a direct marketing venture — genetics, nutrition, facilities, marketing and more. 

#018 - Welcome back to the Reading Blues Podcast, the place to find out more about the school and to connect with staff, pupils and parents at a deeper level. Each week we'll be interviewing people within the school community, asking them questions and spending time understanding more about them and more about the school. In this episode we're speaking to Scott Yates, Director of Middle School, and Robert Tidbury, Deputy Head Academic. They'll be walking us through the process of choosing GCSEs at Reading Blue Coat, the kind of systems in place to ensure students pick the right GCSEs for them and what advice they'd offer to students in Year 9. So come with me now as we jump into this conversation with host Tracey and Reading Blue Coat staff Scott Yates and Robert Tidbury. Reading Blue Coat School onlineWebsite: www.rbcs.org.ukFacebook: www.facebook.com/ReadingBlueCoatlTwitter: @ReadingBluesInstagram: ReadingBlueCoatSchool 

#017 - Welcome back to the Reading Blues Podcast, the place to find out more about the school and to connect with staff, pupils and parents at a deeper level. Each week we'll be interviewing people within the school community, asking them questions and spending time understanding more about them and more about the school. In this episode we're going to be talking to Sarah Langdon, member of the Sixth Form pastoral team, who's joined by some students from the school, Archie, EJ and Ben. Sarah will tell us all about Rainbow Flag Award, what it is, why it is that Reading Blue Coat has applied and what it means to Sarah. But we'll also get to hear from some of the students, how they have been involved with the Rainbow Flag Award application and what is like being part of the LGBT+ community. This episode is great, the students and Sarah are very passionate about the Rainbow Flag Award and the LGBT+ community within the school, they open up about the challenges faced, the focus on inclusion and diversity and how things are changing. So enough from me, let me take you into this episode right now as we speak to Sarah and some of the Sixth Form students. Reading Blue Coat School onlineWebsite: www.rbcs.org.ukFacebook: www.facebook.com/ReadingBlueCoatlTwitter: @ReadingBluesInstagram: ReadingBlueCoatSchool 

In this episode, we are going to talk about Blood. Specifically what it is made up of, different types, how to administer it, and what to watch out for.   When people think of blood they usually think of something red that comes out of their body when they get a cut or injury. But blood is more than just that, blood has 3 different components. 1. Red Blood Cells: 44% 2. White Blood Cells and Platelets: 1% 3. Plasma: 55%   Join us as we discuss more the different blood types, anemia, and blood transfusion. Cup of Nurses: https://fanlink.to/CONsite Frontline Warriors: https://fanlink.to/FWsite Youtube https://fanlink.to/CONYT Apple https://fanlink.to/Applepodcast Spotify https://fanlink.to/Spotifypodcast Cup of Nurses Store https://fanlink.to/CONshop Frontline Warriors store https://fanlink.to/FWshop Interested in Travel Nursing? https://fanlink.to/TravelNurseNow Free Travel Nursing Guide  https://fanlink.to/Travelnursingchecklist Nclex Guide https://fanlink.to/NCLEXguide Cup of Nurses FB Group https://www.facebook.com/groups/cupofnurses Frontline Warriors FB group https://fanlink.to/FWFBgroup 0:00 Introduction 3:16 Episode Introduction 5:12 Red Blood Cells 6:21 2 Crucial functions of RBCs 11:20 Common Types of Anemia 19:50 Blood Types 26:45 Types of White Blood Cells 36:24 Platelets 47:00 Plasma 53:01 Blood Product Administration

#016 - Welcome back to the Reading Blues Podcast, the place to find out more about the school and to connect with staff, pupils and parents at a deeper level. Each week we'll be interviewing people within the school community, asking them questions and spending time understanding more about them and more about the school.  In this episode we're going online and finding out about the future of education with the Head of Physics at the school, Benjamin Schuler. Now, fun fact, Reading Blue Coat was one of the schools that was already looking at online learning before the pandemic arrived which means they were naturally in a good place to make that rapid switch back in 2020. Not that it came without its issues though, something that Benjamin talks about in this episode. So we get to hear what challenges they faced, how it all worked at school (especially in the Physics department) and what the opportunities were that came as a result of this. So enough chit chat from me, let me take you into this episode right now as we speak to Head of Physics, Benjamin Schuler. Reading Blue Coat School onlineWebsite: www.rbcs.org.ukFacebook: www.facebook.com/ReadingBlueCoatlTwitter: @ReadingBluesInstagram: ReadingBlueCoatSchool 

Today we end the RBCS with a gratitude letter.

Release what ails and add gratitude

Had a bad day? Let's reimagine it for our good!

On today's episode we are going to be tapping with Afformations and askfirmations!

Tapping Meditation to release negative feelings. We will be tapping on the meridian points! Eyebrow, side of the eye, under the eye, under the nose, under the mouth, collarbone, under arm, and top of the head!

Follow along as we use The Law of Assumption to manifest!

Manish Jain joins us and shares information on RBCs new Silent Listener Chat Bot: "We are building a silent listener chat bot, which will listen to the conversation when an agent and a client are having those discussions. While those discussions are happening, the chat bot or the silent listener is going to understand the intent of the conversation, what the client is talking about, getting the client, IDs. In the meanwhile while the discussion is happening in goes in the background, brings in all policies and procedures, client, all information ready on the agent's screen. Agent without putting the client on hold is having a continuous discussion"

History Sudden and maximal in onset Compared to previous headaches Family history of aneurysm Associated Symptoms Photophobia Visual Changes Neck Stiffness Exam Full neuro examination Cranial nerves Visual fields Speech Cerebellar (finger-nose) Motor Sensation Gait Testing Plan Non-contrast head CT Excellent sensitivity 100 RBCs in tube 4 Can be […]

The effect of platelet-rich plasma (PRP) on chondrocytes has been studied in cell and tissue culture, but considerably less attention has been given to the effect of PRP on synoviocytes. Fibroblast-like synoviocytes (FLS) compose 80% of the normal human synovium and produce cytokines and matrix metalloproteinases that can mediate cartilage catabolism. Treatment of synovial cells with LR-PRP and RBCs resulted in significant cell death and proinflammatory mediator production.   Click here to read the article.