Podcasts about leukocyte

Play Episode Listen Later Nov 13, 2022 3:29

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Gross Week Morning Story (11-13-2022)

Play Episode Listen Later Nov 13, 2022 3:19

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers. Learn more about your ad choices. Visit podcastchoices.com/adchoices

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Stories Week Walter Part 1 Night (9-19-2022)

Play Episode Listen Later Sep 19, 2022 3:33

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Stories Week Walter Part 1 Morning (9-19-2022)

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Play Episode Listen Later Sep 19, 2022 3:23

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers. Learn more about your ad choices. Visit podcastchoices.com/adchoices

stories story chompers leukocyte can walter

Membrane Biochemistry XXXV. Lipocortin-1 induces cortisol thus suppressing phospholipase A2, blocking eicosanoid and leukocyte inflammatory events. DJGPhD.16.8.22. Authentic Biochemistry

Authentic Biochemistry

Play Episode Listen Later Aug 16, 2022 29:49

References Dr Guerra's notes Curr Neuropharmacol. 2013 Mar; 11(2): 141–159 Advances in Neurobiology, 01 Jan 2014, 11:13-30 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message

Role of PIEZO1 in leukocyte extravasation, CD8+ T-cell activation in macrophage activation syndrome, and ABO O blood group as a novel risk factor for HIT

Blood Podcast

Play Episode Listen Later Jul 21, 2022 21:10

In this week's episode we first review new work revealing the critical role of the tension-sensitive cation channel PIEZO1 in the transendothelial migration of leukocytes. We'll also review new research suggesting that CD8+ T-cells dimly expressing the CD4 antigen are increased in patients with various forms of secondary HLH, a finding that may have diagnostic, prognostic, and therapeutic significance. Finally, we'll review a large, genome-wide association study identifying the ABO O blood group as a novel risk factor for heparin-induced thrombocytopenia—a finding that could have implications for prediction of this syndrome and for the management of related conditions.

medical syndrome activation oncology risk factors medical research hematology cd4 macrophages cd8 t hlh leukocyte blood group extravasation

Toward Clinical Application of Leukocyte Counts Based on Targeted DNA Methylation Analysis

Clinical Chemistry Podcast

Play Episode Listen Later May 12, 2022 11:46

application clinical counts targeted dna methylation leukocyte

Pathology | Leukocyte Extravasation

The Medbullets Step 1 Podcast

Play Episode Listen Later Apr 30, 2022 8:11

In this episode, we review the high-yield topic of Leukocyte Extravasation from the Pathology section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficialx Twitter: www.twitter.com/medbulletsIn this episode --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

pathologies leukocyte extravasation

Diversity matters in Digital Scholarly Technology - A Conversation with Mark Hahnel

Access 2 Perspectives – Conversations. All about Open Science Communication

Play Episode Listen Later Apr 21, 2022 51:28

Mark Hahnel is the CEO and founder of Figshare, which he created whilst completing his PhD in stem cell biology at Imperial College London. Figshare currently provides research data infrastructure for institutions, publishers and funders globally. He is passionate about open science and the potential it has to revolutionize the research community. For the last eight years, Mark has been leading the development of research data infrastructure, with the core aim of reusable and interoperable academic data. Mark sits on the board of DataCite and the advisory board for the Directory of Open Access Journals (DOAJ). He was on the judging panel for the National Institutes of Health (NIH), Wellcome Trust Open Science prize and acted as an advisor for the Springer Nature master classes. ORCID iD: 0000-0003-4741-0309 Website: figshare.com Linkedin: /mark-hahnel Twitter: @MarkHahnel Which researcher – dead or alive – do you find inspiring? My old PI Sara Rankin, just for the sheer range of her interests and achievements. She is a Professor of Leukocyte and Stem Cell Biology Imperial College London, a science/art collaborator, and a more recent leader in the UK neurodiversity movement. --- Send in a voice message: https://anchor.fm/access2perspectives/message

ceo conversations uk technology phd professor digital national institutes imperial college london directories health nih scholarly diversity matters springer nature leukocyte figshare mark hahnel

Episode 89 - Gonorrhea Basics

Rio Bravo qWeek

Play Episode Listen Later Apr 8, 2022 31:18

Episode 89: Gonorrhea Basics. Written by Robert BensacenezRobert, Dr. Schlaerth, and Dr. Arreaza discuss the basics of gonorrhea, including presentation, treatment, and even a potential gonococcal vaccine.Introduction: Gonorrhea is commonly known as “the clap” or “the drip”. This ancient disease, described as “the perilous infirmity of burning” in a book called The History of Prostitution, has been treated with many remedies throughout history, including mercury, sulfur, silver, multiple plants, and even gold. Today we will discuss the clinical features, diagnosis, and current therapy of gonorrhea. By the way, did you know that gonorrhea in Spanish is used as an insult in Colombia? Well, now you know it. Definition: Gonorrhea is a sexually transmitted disease caused by the bacterium Neisseria gonorrhoeae (common name gonococcus), which is a gram-negative, intracellular, aerobic, diplococci. This disease leads to genitourinary tract infections such as urethritis, cervicitis, pelvic inflammatory disease (PID), and epididymitis. This is Rio Bravo qWeek, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California. Our program is affiliated with UCLA, and it's sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. ___________________________Gonorrhea. Written by Robert Besancenez, MS4, Ross University School of Medicine. Moderated and edited by Hector Arreaza, MD. Discussion participation by Katherine Schlaerth, MD. Epidemiology: The disease primarily affects individuals between 15–24 years of age (half of the STI patients in the US). CDC estimates that approximately 1.6 million new gonococcal infections occurred in 2018. Incidence rates are highest among African Americans, American Indians, and Hispanic populations.Transmission is sexual (oral, genital, or anal) or perinatal (causing gonococcal conjunctivitis in neonates). Risk factors include unsafe sexual behaviors (lack of barrier protection, multiple partners, men who have sex with men (MSM), and asplenia, complement deficiencies. Individuals with low socioeconomic status are at the highest risk: poor access to medical treatment and screening, poor education, substance use, and sex work. Presentation: The incubation period is ~ 2–7 days, and sometimes patients do not develop any symptoms. Urogenital infection: Gonorrhea is commonly asymptomatic, especially in women, which increases the chance of further spreading and complications. When symptoms are present, typical symptoms include purulent vaginal or urethral discharge (purulent, yellow-green, possibly blood-tinged). Discharge is less common in female patients. Urinary symptoms include dysuria, urinary frequency, and urgency. Male: - Typical presentation is urethritis. - Penile shaft edema without other signs of inflammation.- Epididymitis: unilateral scrotal fullness sensation, scrotal swelling, redness, tenderness, relief of pain with elevation of scrotum —Prehn Sign— and positive cremasteric reflex.- Robert: Prostatitis: fever, chills, general malaise, pelvic or perineal pain, cloudy urine, prostate tenderness (examine prostate gently). Female: - Cervicitis: Friable cervix and discharge (purulent, yellow, malodorous), - PID: pelvic or lower abdominal pain, dyspareunia, fever, cervical discharge, cervical motion tenderness but also uterine or adnexal tenderness, abnormal intermenstrual bleeding. PID can be subclinical and diagnosed retroactively when tubal occlusion is discovered as part of a workup for infertility. PID can cause Fitz-Hugh-Curtis syndrome (perihepatitis with RUQ pain).- Bartholinitis presents with introitus pain, edema, and discharge from the labia. - Vulvovaginitis may occur but is rare (due to the tissue preference of gonococci)Extragenital infection: Proctitis: Rectal purulent discharge, possible anorectal bleeding and pain, rectal mucosa inflammation, or rectal abscess (less common).Pharyngitis: sore throat, pharyngeal exudate, cervical lymphadenitis. Disseminated gonococcal infection (DGI): Triad of arthritis, pustular skin lesions, and tenosynovitis. As mentioned in Episode 46, on December 23, 2020, the California Department of Public Health (CDPH) sent a “Dear Colleague” letter to warn the medical community about the increased cases of DGI in California and Michigan. Increased cases may be caused by decreased STD testing and treatment because of the COVID-19 pandemic, and not necessarily because of a more virulent strain of gonorrhea. Later, treatment of gonorrhea was updated because of resistance.  Epidemiology: ∼ 2% of cases. Most common in individuals younger than 40 years old, the female to male ratio is 4:1. A history of recent symptomatic genital infection is uncommon. Asymptomatic infections increase the risk of dissemination due to delayed diagnosis and treatment. Clinical features: Two distinct clinical presentations are possible. Arthritis-dermatitis syndrome:Polyarthralgias: migratory, asymmetric arthritis that may become purulent.Tenosynovitis: simultaneous inflammation of several tendons (e.g. fingers, toes, wrist, ankle).Dermatitis: vesicular, pustular, or maculopapular lesions, possibly with a necrotic or hemorrhagic center.  Most commonly distributed on the trunk, extremities (sometimes involving the palms and soles). Typically, < 10 lesions with a transient course (subside in 3–4 days). Additional manifestations: fever and chills (especially in the acute phase). Purulent gonococcal arthritis: Abrupt inflammation in up to 4 joints (commonly knees, ankles, and wrists). No skin manifestations, rarely tenosynovitis. Genitourinary manifestations in only 25% of affected individuals. Not to be confused with reactive arthritis. Health care providers living in California: Order Nucleic acid amplification test (NAAT) and culture specimens from urogenital, extragenital mucosal sites (e.g., pharyngeal and rectal), and from disseminated sites (e.g., skin, synovial fluid, blood, and cerebrospinal fluid) before initiating empiric antimicrobial treatment for patients with suspected DGI. Report within 24 hours of diagnosis to the California Department of Public Health. Complications of DGI: sepsis with endocarditis, meningitis, osteomyelitis, or pneumonia. Diagnosis of gonorrhea: The test of choice is Nucleic acid amplification testing (NAAT) of first-catch urine or swabs of urethra, endocervix and pharynx, and synovial fluid in disseminated infection. Other possible tests: gram stains and bacterial cultures (Thayer-Martin agar, useful for antibiotic resistance, results may take 48 hours, sensitivity is lower than NAAT.)Synovial fluid analysis: Appearance of fluid can be clear or cloudy (purulent), high Leukocyte count (up to 50,000 cells/mm3): especially segmented neutrophils, gram stain positive in < 25% of cases. Treatment: Ceftriaxone and doxycycline for uncomplicated cases, but may require different approaches in case of allergies or intolerance to these antibiotics, or in severe cases. Uncomplicated gonorrhea (affecting cervix, urethra, rectum, pharynx)First-line treatment: single-dose ceftriaxone 500 mg IM (1 G for patients >150 Kg) PLUS doxycycline 100 mg PO twice a day for 7 days If a chlamydial infection has not been excluded.During pregnancy: Ceftriaxone PLUS single-dose azithromycin 1 gram PO(doxy is contraindicated – teratogen) Complicated gonorrhea (salpingitis, adnexitis, PID/ epididymitis, orchitis)Single-dose ceftriaxone IM PLUS doxycycline PO for 10–14 days  (women may require additional administration of Metronidazole PO for 14 days). DGICeftriaxone IV every 24 hours for 7 days In case Chlamydia infection has not been ruled out: PLUS doxycycline PO twice a day for 7 daysDrainage of purulent joint(s) Sequelae: Without treatment, a prolonged infection may lead to complications, such as hymenal and tubal synechiae that lead to infertility in women. Prevention:-Screening for gonorrhea (USPSTF recommendations, September 2021, Grade B): Annual NAAT screening of gonorrhea AND chlamydia for sexually active women ≤ 24 years (including pregnant persons) or > 25 years with risk factors (e.g. new or multiple sex partners, sex partner with an STI, etc.). Evaluate for other STIs if positive (e.g. chlamydia, syphilis, and HIV). There is insufficient evidence to recommend for or against screening gonorrhea in asymptomatic males (Grade I).In all patients: Evaluate and treat the patient's sexual partners from the past 60 days. Provide expedited partner therapy if the timely evaluation of sexual partners is not feasible. Single-dose cefixime PO (if chlamydia has been excluded in the patient) OR Single-dose cefixime PO PLUS doxycycline PO for 7 days. Sexual partners must be treated simultaneously to avoid reinfections. A possible gonococcal vaccine: A gonococcal vaccine is theoretically possible, let's remember that the meningococcal vaccine exists. Meningococcus is closely related to gonococcus. A study published in 2017 showed that MeNZB® (a vaccine used in New Zealand until 2011 to fight against a meningitis epidemic) provided partial protection against gonorrhea. Food for thought for you guys. Conclusion: Let's remember to screen asymptomatic women for gonorrhea, identify symptomatic patients and start treatment promptly, and prevent serious complications, and more importantly, let's promote safe sex practices to prevent this disease.Now we conclude our episode number 89 “Gonorrhea Basics”. Gonorrhea affects mainly the urogenital area, but it can spread to the pharynx, rectum, skin, and even joints. When you see septic arthritis in patients with high risk for gonorrhea, suspect disseminated gonococcal infection and start treatment promptly. Even without trying, every night you go to bed being a little wiser.Thanks for listening to Rio Bravo qWeek. If you have any feedback about this podcast, contact us by email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. This podcast was created for educational purposes only. Visit your primary care physician for additional medical advice. This week we thank Hector Arreaza, Robert Besancenez, and Katherine Schlaerth. Audio edition: Suraj Amrutia. See you next week! _____________________References:Seña, Arlene C, MD, MPH; and Myron S Cohen, MD. Treatment of uncomplicated Neisseria gonorrhoeae infections, UpToDate, updated on Jan 27, 2022. Accessed on April 5, 2022. https://www.uptodate.com/contents/treatment-of-uncomplicated-neisseria-gonorrhoeae-infections Ghanem, Khalil G, MD, PhD. Clinical manifestations and diagnosis of Neisseria gonorrhoeae infection in adults and adolescents, UpToDate, updated on Sep 17, 2021, accessed on April 5, 2022. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-neisseria-gonorrhoeae-infection-in-adults-and-adolescents Klausner, Jeffrey D, MD, MPH. Disseminated gonococcal infection, UpToDate, updated on March 3, 2022. Accessed on April 5, 2022. https://www.uptodate.com/contents/disseminated-gonococcal-infection Petousis-Harris H, Paynter J, Morgan J, et al. Effectiveness of a group B OMV meningococcal vaccine on gonorrhea in New Zealand – a case control study. Abstract presented at: 20th International Pathogenic Neisseria Conference. Manchester, UK; 2016.

March 2022 Discover CircRes

Discover CircRes

Play Episode Listen Later Mar 17, 2022 31:20

This month on Episode 34 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the March 4 and March 18th issues of Circulation Research. This episode also features a conversation with Dr Mireille Ouimet and Sabrina Robichaud from the University of Ottawa Heart Institute to discuss their study, Autophagy is Differentially Regulated in Leukocyte and Non-Leukocyte Foam Cells During Atherosclerosis. Article highlights: Pauza, et al. GLP1R in CB Suppress Chemoreflex-Mediated SNA Lim, et al. IL11 in Marfan Syndrome Hohl, et al. Renal Denervation Prevents Atrial Remodeling in CKD Liu, et al. Smooth Muscle Cell YAP Promotes Arterial Stiffness Cindy St. Hilaire: Hi and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today I'm going to be highlighting articles from our March issues of Circulation Research. I'm also going to speak with Dr Mireille Ouimet and Sabrina Robichaud from the University of Ottawa Heart Institute, and they're with me to discuss their study, Autophagy is Differentially Regulated in Leukocyte and Non-Leukocyte Foam Cells During Atherosclerosis. The first article I want to share is titled GLP1R Attenuates Sympathetic Response to High Glucose via Carotid Body Inhibition. The first author is Audrys Pauza, and the corresponding authors are Julian Paton and David Murphy at the University of Bristol. Cindy St. Hilaire: Hypertension and diabetes are risk factors for cardiovascular disease. And yet, for many patients with these two conditions, lowering blood pressure and blood sugar is insufficient for eliminating the risk. The carotid body is a cluster of sensory cells in the carotid artery, and it regulates sympathetic nerve activity. Because hypertension and diabetes are linked to increased sympathetic nerve activation, this group investigated the role of the carotid body in these disease states. They performed a transcriptome analysis of crowded body tissue, from rats with and without spontaneous hypertension. And they found among many differentially-expressed genes that the transcript encoding glucagon-like peptide-1 receptor or GLP1R, was considerably less abundant in hypertensive animals. Cindy St. Hilaire: This was of particular interest because the gut hormone GLP-1 promotes insulin secretion and tends to be suppressed in Type 2 diabetes. Moreover, GLP1R agonists are already used as diabetic treatments. This group showed that treating rat carotid body with GLP1R agonist suppresses sympathetic nerve activation and arterial blood pressure, suggesting that these drugs may provide benefits in more than one way. Perhaps the carotid body could be a novel target for lowering cardiovascular disease risk in metabolic syndrome. Cindy St. Hilaire: The second article I want to share is titled Inhibition of IL11 Signaling Reduces Aortic Pathology in Murine Marfan syndrome. The first author is Wei-Wen Lim, and the corresponding author is Stuart Cook and they're from the National Heart Center in Singapore. People with the genetic connective tissue disorder Marfan syndrome, are typically tall and thin with long limbs and are prone to skeletal, eye and cardiovascular problems, including a life-threatening weakening of the aorta. While Marfan syndrome patients commonly take blood pressure-lowering treatments to minimize risk of aortic aneurysm and dissection, there's currently no cure for Marfan syndrome or targeted therapy. Cindy St. Hilaire: The cytokine IL11 is strongly induced in vascular smooth muscle cells upon treatment with the growth factor TGF-beta, which is over activated in Marfan syndrome patients. And TGF-beta is also considered a key feature of the syndrome's molecular pathology. This study found that IL11 is strongly upregulated in the aortas of Marfan syndrome model mouse, and that genetically eliminating IL11 in these animals protected them against aortic dilation, fibrosis, inflammation, elastin degradation and loss of smooth muscle cells. Treating Marfan syndrome mice with anti-IL11 neutralizing antibodies exhibited the same beneficial effects. These results suggest that perhaps inhibiting IL11's activity could be a novel approach for protecting the aortas of Marfan syndrome patients. Cindy St. Hilaire: The next article I want to mention is titled Renal Denervation Prevents Atrial Arrhythmogenic Substrate Development in Chronic Kidney Disease. The first authors are, Mathias Hohl, Simina-Ramona Selejan and Jan Wintrich, and the corresponding authors also Mathias Hohl, and they're from Saarland University. People with chronic kidney disease have a two to three fold higher risk than the general population of developing atrial fibrillation, which is a common form of arrhythmia that can be life-threatening. Chronic kidney disease is associated with activation of the sympathetic nervous system, which can be damaging to the heart. Thus, this group examined myocardial tissues from atrial fibrillation patients with and without chronic kidney disease to see how they differ. They found that atrial fibrosis was more pronounced in patients with both conditions than in patients with atrial fibrillation alone, suggesting that chronic kidney disease perhaps exacerbates or even drives arterial remodeling. Cindy St. Hilaire: Sure enough, induction of chronic kidney disease in rats led to greater atrial fibrosis and incidence of atrial fibrillation than seen in the control animals. Renal denervation is a treatment in which the sympathetic nerves are ablated, and it's a medical procedure that's used for treating uncontrolled hypertension, and it has also been shown in animals to reduce atrial fibrillation. Performing renal denervation in the rats with chronic kidney disease reduced atrial fibrosis and atrial fibrillation susceptibility. This study not only shows that chronic kidney disease induces atrial fibrosis and in turn atrial fibrillation, but also suggests that renal denervation may be used in chronic kidney disease patients to break this pathological link and prevent potentially deadly arrhythmias. Cindy St. Hilaire: The last article I want to highlight is titled YAP Targets the TGFβ Pathway to Mediate High-Fat/High-Sucrose Diet-Induced Arterial Stiffness. First author is Yanan Liu and the corresponding author is Ding Ai from Tianjin Medical University. Metabolic syndrome is characterized as a collection of conditions that increase the risk of cardiovascular diseases, such as obesity, hypertension and diabetes. Among the tissue pathologies associated with metabolic syndrome is arterial stiffness, which itself is a predictor of cardiovascular disease incidence and mortality. To specifically investigate how arterial stiffness develops in metabolic syndrome, this group fed mice a high-fat, high-sugar diet, which is known to induce metabolic syndrome and concomitant arterial stiffness. Cindy St. Hilaire: After two weeks on the diet, the animals' aorta has exhibited significant upregulation of TGF-beta signaling, which is a pathway known for its role in tissue fibrosis, and the aorta has also exhibited increased levels of yes-associated protein, or YAP, which has previously been implicated in vascular remodeling, collagen deposition and inflammation. YAP gain and loss of function experiments in transgenic mice revealed that while knockdown of protein in the animals' smooth muscle cells attenuated arterial stiffness, increased expression exacerbated the condition. Cindy St. Hilaire: The team went on to show that YAP interacted with and prevented the activation of PPM-1 B, which is a phosphatase that normally inhibits TGF-beta signaling and thus fibrosis. Together the results suggest that targeting the YAP, PPM-1 B pathway, could be a strategy for reducing arterial stiffness and associated cardiovascular disease risk in metabolic syndrome. Cindy St. Hilaire: Today, Sabrina Robichaud and Dr Mireille Ouimet from University of Ottawa Heart Institute are with me to discuss their study Autophagy is Differentially Regulated in Leukocyte and Non-Leukocyte Foam Cells During Atherosclerosis, which is in our March 18 issue of Circulation Research. So thank you both for joining me today. Sabrina Robichaud: Thank you so much for having us. It's a pleasure. Mireille Ouimet: Thank you for having us. Cindy St. Hilaire: Yeah, and congrats on the study. So we know that LDL particles contain cholesterol and fats, and these are the initiating factors in atherosclerosis. And it's also really now appreciated that inflammation in the vessel wall is a secondary consequence to this lipid accumulation. Macrophages are an immune cell that, in the context of the plaque, gobble up this cholesterol to the point that they become laden with lipids and exhibit this foamy appearance, which we now call foam cells. And these foam cells can exhibit atheroprotective properties, one of them called reverse cholesterol transport, and that's really one of the focuses of your paper. So before we dig into what your paper is all about, could you give us a little bit of background about what reverse cholesterol transport is in the context of the atherosclerotic plaque? And maybe introduce how it links to this cellular recycling program, autophagy, which is also a big feature of your study. Mireille Ouimet: Yes, so the reverse cholesterol transport pathway is a pathway that's very highly anti-atherogenic. It's linked to HDL function and the HDL protective effects, in that HDL can serve as a cholesterol acceptor for any excess cholesterol from arterial cells or other cells of the body and return this excess cholesterol to the liver for excretion into the feces. There is also trans-intestinal cholesterol efflux that can help eliminate any excess bodily cholesterol. Mireille Ouimet: So reverse cholesterol transport is a way that we can eliminate excess cholesterol from foam cells in the vascular wall, and that's why we're really interested in the process. But the rate-limiting step of cholesterol efflux out of foam cells in plaques is actually, they have to be mobilized in the form of free cholesterol to be pumped out of the cells through the action of the ATP-binding cassette transporters. And so the rate-limiting step of the process is the hydrolysis of the cholesterol esters and the lipid droplets, because that's where the excess cholesterol is stored in foam cells. Mireille Ouimet: And so for years, people investigated the actions of cytosol like lipases in mobilizing free cholesterol from lipid droplets, although the identity of those lipases are not well-known and in macrophage themselves, but our recent work showed a role for autophagy in the catabolism of lipid droplets. And in fact, in macrophage foam cells, 50% of lipid droplet hydrolysis is attributable to autophagy while the other half is mediated by neutral lipases, which makes it really important to investigate the mechanisms of autophagy-mediated lipid droplet catabolism. Cindy St. Hilaire: That is so interesting. I guess I didn't realize it was that significant a component in that kind of rate-limiting step. That's so cool. So really, a lot of the cholesterol efflux studies, and maybe this is just limited to my knowledge of a lot of these cholesterol efflux studies, but to my knowledge, it's been really focused on the foam cell itself, the macrophage foam cell. However, there's been a lot of recent work that has now implicated vascular smooth muscle cells in this process. So could you share some of the research specific to smooth muscle cells and smooth muscle-derived foam cells that led you to want to investigate the contributions of smooth muscle cell-derived foam cells in cholesterol efflux? Mireille Ouimet: Yeah, so you're right in the sense that macrophages have always been the culprit foam cells in the atherosclerotic plaques but pioneering work from several groups, including Edward Fisher and Gordon Francis, they've shown that the smooth muscle cells can actually acquire a macrophage-like phenotype becoming lipid-loaded and foamy. And there's been work specifically looking at the ABC transporters, and their ability to efflux cholesterol from these vascular smooth muscle cell-derived foam cells, because as they trans-differentiate into macrophage-like cells, they acquire the expression of ABCA1, but this is to a lower extent, as compared to their macrophage counterparts. Mireille Ouimet: And the efflux is defective because there's an impairment in liposomal cholesterol processing of the lipoproteins that's really important to activate a like cell, and the expression of the ABC transporters, so vascular smooth muscle cell-derived foam cells are very poor effluxes. Sabrina Robichaud: There's very few studies that look at the vascular smooth muscle cell foam cells, and the very few that did look at it mostly focused on the ABCA1 transporters, and did show that they were poor effluxes. And as we all know, ABC1 is not the only cholesterol transporters that can transport cholesterol out of cells, there's also ABCG1 which is also one of our major findings in our paper. Cindy St. Hilaire: Can you tell us a little bit about the models you chose in the study and why you picked them? And also maybe a step back in terms of, what are the pros and cons of using mouse models in atherosclerotic studies? Sabrina Robichaud: So we chose to use the GFP-LC3 reporter mouse model because it allows us to track in lifestyle the movement of LC3, which is the main component of the autophagosome which is involved in pathology. So by using this reporter model, we could infer whether or not the cells had high autophagy or low autophagy. And to induce atherosclerosis in these mice, instead of backcrossing them to either an LDLR knockout or an ApoE knockout, we chose to do the adeno-associated virus that encode the gain of function PCSK9 instead to kind of minimize the time for breeding. It did have the effect that we needed in terms of raising plasma cholesterol to induce the atherosclerosis. So that was one of the models that we used in our paper. Mireille Ouimet: There's not very many good mouse models to study autophagy flux in vivo and GFP-LC3 is kind of the main one currently. We're working on developing some other tools to track lipophagy in vivo, but these things take time to put in place. So in the future, we hope to have some better tools to track lipophagy in real-time in vivo. Cindy St. Hilaire: How difficult is it to measure autophagy flux in vivo? I know there's certain part like LC3 or P62, a lot of people use a western blot and it's like, oh, it's high, it must be active, but it's a flux. So it's a little bit more... There's more subtleties to that, dynamic than that. So how difficult is it to really measure this flux in in vivo tissues? Mireille Ouimet: Yes, so now there are more recent mouse models that have been developed more recently to replace kind of the GFP-LC3 is the Rosella LC3. So it has both a red and a green tag, and so two LC3, so when autophagosomes are fused to lysosomes and are degraded, then there's preferential quenching of the GFP first, and then you have the red appearance that predominates so we know that then it's kind of like it a live flux measurements. Because we use the GFP-LC3 mouse, Sabrina treated her cells ex vivo. When we dissected out the aortic arches, digested the cells then we divided those into two components and added bafilomycin so that we can inhibit lysosome acidification to see the changes in the flux. And that's really to get the differences in untreated versus bafilomycin-treated. Mireille Ouimet: When we inhibit the lysosome, then we're sure that it is a functional flux or not. But it's kind of an indirect way of measuring it, and it reads very complex when we're talking about P62 and LC3 degradation with or without lysosome inhibition, but you really need that lysosomal inhibition, to show that if you block the degradation of the autophagosomes that fuse in with a lysosome, then you get an increase in the LC3 and the P62, and that's when you know that the flux is you intact. Mireille Ouimet: Because you could get an increase in LC3, that's just related to a defect in the breakdown of the autophagosome. But in our study, we've used phosphorylated ATG16L1, which is a now better marker of active autophagy. And I would recommend researchers to begin to use that rather than the combination of P62 and LC3 together with or without a lysosome inhibitors such as- Cindy St. Hilaire: Oh, interesting. So let's repeat that, phosphorylated ATG- Mireille Ouimet: 16L1, yes. So there's been an antibody that was developed by a colleague at the University of Ottawa, Dr Ryan Russell, and it's commercially available through cell signaling now, and it really has been a great tool to track active autophagy. Cindy St. Hilaire: That's great. I remember my lab was looking at that at one point, and I was trying to explain the flux as... I don't know if people are going to remember this, but there's this amazing, I Love Lucy skit, where her and Ethel are working on a chocolate factory conveyor belt, and it picks up speed. And because she can't get it all done quick, she starts stuffing them in her mouth. And it's like, if you just took a snapshot of that, you would not know whether it's going too fast, or not functioning properly. And so I equate the flux experiments to that. Which are probably aging myself a lot on so. Cindy St. Hilaire: All right, so sticking to kind of the autophagy angle, what were the differences you found in autophagy in early and late atherosclerotic plaques? Because I know you looked at those two time points, but also, importantly, between the macrophage foam cells and the smooth muscle cell-derived foam cells? Sabrina Robichaud: So surprisingly, there weren't that big of a difference between each time point when we were looking at the individual cell type by themselves. Surprisingly, we did find that the macrophages did have a functional autophagy flux, even at the later stages of atherosclerosis, which was kind of interesting in itself. But when we looked at the vascular smooth muscle cell foam cells, though, that was a whole other story, and we found that these were actually defective at a very early stage and stayed defective up until the very late stage of atherosclerosis. Cindy St. Hilaire: And what is the very early stage like? What's that definition with the smooth muscle cell? Sabrina Robichaud: So we did a six-week time points in terms of our atherosclerosis study, and then a 25-week time point. So there are far apart, which shows like the very early, early stage and what would be considered the most effective autophagy at that point with the necrotic core and everything. So surprisingly, the two phenotype were quite similar at early and both late stages for both cell types, but were functional in the macrophages but dysfunctional in the smooth muscle cells. Cindy St. Hilaire: So you mentioned at one point in the discussion that you observed inconsistent lipid loading of the smooth muscle cells, and you mentioned that a lipase, which is excreted from the foam cells can then be internalized by, I assume kind of neighboring or in the vicinity, smooth muscle cells. And so the question I had it's kind of one of those chicken-and-egg question, and it's, is the smooth muscle cell-derived foam cell an independent process? Does it happen alone or de novo as a function of a smooth muscle-mediated process? Or is it really dependent first on this macrophage foam cell providing this lipid that is efflux that is then internalized by a smooth muscle cell that kind of goes on to become a foam cells. It's kind of a question of like the continuum of an atherosclerotic plaque and what do you think is happening, either based on your data or just kind of a hunch? Mireille Ouimet: That's an excellent question. And there's no doubt that macrophages really drive the initiating events of atherosclerosis. So I don't think that without the macrophage there would ever be a vascular smooth muscle cell, or there would be minimal vascular smooth muscle cell-derived foam cells. Definitely the inconsistencies that we observed in our study, were if we added like aggregated LDL on its own to a primary mouse vascular smooth muscle cell, we would get poor lipid loading and a very low percentage of those cells that would become foamy, relative to treating them with cyclodextrin complex cholesterol, for instance. Mireille Ouimet: So free cholesterol, that's cell permeable, will go into the vascular smooth muscle cell, no problem, and generate the foaminess and then allow that cell to acquire the macrophage-like phenotype. But aggregated LDL on its own in our hands, just gave very poor loading. And when we treated the vascular smooth muscle cells with aggregated LDL along with macrophage-derived condition media, we got some improvements, but it was still kind of inconsistent. But then we thought if we treat the vascular smooth muscle cells with aggregated LDL in the presence of conditioned media from macrophage foam cells that were preloaded with the aggregated LDL, would that promote their foaminess to a greater extent? And it did. Mireille Ouimet: So, there have been studies from Gordon Francis's lab that showed that adding recombinant lysosomal acid lipase to vascular smooth muscle cells that contained aggregated LDL, promoted the lysosomal hydrolysis of the aggregated LDL and to generate the foamy macrophages and allow the lysosomal processing. So we know that that vascular smooth muscle cells take up lysosomal acid lipase, and we know that macrophages undergo lysosome exocytosis and they can secrete lysosome acid lipase and acidify the extracellular milieu. Mireille Ouimet: So work from Fred Maxfield group has shown the presence of these cell surface connected compartments that are acidified, containing macrophage-derived lysosomal acid lipase, that even hydrolyze extra cellularly-aggregated LDL for macrophages. So we're not sure whether there's probably a local production of free cholesterol in the plaque by macrophages, this free cholesterol could be taken up by the vascular smooth muscle cell. And also the vascular smooth muscle cells do express some scavenger receptors, whether the expression of these scavenger receptors like LRP or CD36 even goes up when they've taken up a little bit of the free cholesterol. And then that allows the aggregated LDL to come in and then there would be some lysosomal acid lipase secreted by the macrophage foam cells that would promote the lysosomal processing of this aggregated LDL. All of those are very complex questions that will require some addressing in vivo models. Cindy St. Hilaire: You also mentioned in the paper that studies... There's a handful of them now. Studies have shown that between 30% and 70% of the cells that are staining positively for macrophage markers, meaning they're foam cells, are of the smooth muscle cell lineage. And so I believe people have seen that in mouse plaques with lineage tracing, but they've also used newer techniques to really see this also in human atherosclerotic plaques. So we know it's not just from a mouse, we know that smooth muscle cells can turn into a macrophage-like foam cell, and it's 30% to 70%, which is a huge range. Cindy St. Hilaire: So do we know the factors that dictate whether a specific plaque is going to have more or less smooth muscle cell derived foam cells? And I guess more important to what you found in your paper is, how important would it be to know whether a plaque is on the 30% end or on the 70% end in terms of therapeutic strategies? Sabrina Robichaud: Yeah, most of these studies, the range can be attributed to the different time points at which these studies have been collected early on will be a little bit more macrophage understanding would be at a later time point. Now of course in terms of therapeutics, as we saw in our paper, metformin actually will positively increase cholesterol efflux in the vascular smooth muscle cell foam cells, but not in the macrophages. So obviously, being able to know at which point there's a majority of macrophages versus vascular smooth muscle cells, definitely going to determine which therapeutic we're going to be able to use. Sabrina Robichaud: Ideally, we would be able to find a therapeutic that would work in both foam cell, but from what we've seen, the mechanistic behind the autophagy dysfunction between both cell types are so different, that I'm not entirely sure that that would be possible, we would need some sort of combination therapy. But again, we need to be a little bit more targeted depending on the percentage of the foam cells that are comprising the plaque at that particular moment in time. Cindy St. Hilaire: Yeah, so you mentioned there's a function of time there. If you look earlier, there's more macrophage, if you look later, the percent of smooth muscle cell-derived foam cell increases. Is there a point in a very advanced atherosclerotic plaque where it's just mostly smooth muscle cells? Or do those macrophage foam cells stay, and it's just the increasing number of smooth muscle cell-derived foam cells? Do we know? Mireille Ouimet: This is an excellent question, and I was going to bring up the topic of clonal expansion of the vascular smooth muscle cells. So it's a very heterogeneous population and understanding that might be some of the differences that we see in different studies. It could be the model has one type of a smooth muscle cell that's expanding more than another, what are the factors that govern that? Does one clone take over at the later stages versus the earlier stages? We don't know. Mireille Ouimet: But we were surprised in our studies to see that the macrophages that are present at least on the lumen of the plaques were very active in autophagy. They had the highest staining for the phospho-ATG16L1 in that late stage. So we're not sure if it's newly-recruited macrophages that come in, that are more active and in autophagy, and then have good lysosomal capacity that keeps degrading the lipid present in the plaque and tries to ingest it, but also as a consequence keeps releasing some of the degraded cholesterol into the milieu where the smooth muscle cells that are proliferating are internalizing it and becoming more foamy. So these are really great open questions that need to be addressed in the field. Cindy St. Hilaire: So drug-eluting stents are coated with rapamycin or the various chemical compositions that are derived from rapamycin. And rapamycin itself induces autophagy. So while the thought behind using this coating on stents was to prevent smooth muscle cell proliferation, and thus restenosis or ingrowing of the stent, your study suggests that this could also help to promote autophagy in the cells underlying the stent. So has anyone gone in and looked at plaques that have been stented and either failed or not, and investigated the foam cell content or markers for autophagy activity? Mireille Ouimet: Not to my knowledge, and this has been something we've definitely... We think that this is what's happening. Some of the protective effects of these drug-eluting stents that have everolimus or sirolimus or the rapamycin or rapamycin analogs, we do believe that some of their protective effect can be attributed to autophagy activation, but this remains to be demonstrated. We think that autophagy activation locally would promote reverse cholesterol transport and would be one of the processes that prevents restenosis because we can promote the efflux of cholesterol out. Cindy St. Hilaire: Great. So I guess stemming from my question on the stents, what are the other translational implications of the findings of your study? And what would you like to see come out of this? Mireille Ouimet: So one of the things is, as Sabrina mentioned, would be to target both foam cell populations because it seems as though the vascular smooth muscle cell foam cells are very much defective in their autophagy capacity, and they're very poor effluxes, but we could potentially restore autophagy in the cell population to promote reverse cholesterol transport. And looking at prevention of atherosclerosis is a bit different than looking at regression, because regression is at a later stage where the plaques are more advanced. And if they're mostly vascular smooth muscle cell-derived, maybe then those drugs that we're considering that protect against the development of atherosclerosis are effective on the macrophage themselves early on, but might not be mimicking what we would see in the clinic where the patients that present are older. Cindy St. Hilaire: Yeah, it's kind of really reminiscent of like the CANTOS trial and like, where do we want to target the therapy? It's going to be very different if it's an early smaller plaque, versus a late-stage possibly pro close to rupturing type of plaque. Well, Sabrina Robichaud and Dr Ouimet, thank you so much for joining me today. Congratulations again on a wonderful study, and I'm really looking forward to hearing more about this from your group. Sabrina Robichaud: Thank you. Mireille Ouimet: Thank you very much. And we also want to thank all the co-authors on the study, specifically also Adil Rasheed, who is co-first author on the work and Katey Rayner's group for all the support and involvement in this study. Cindy St. Hilaire: That's it for the highlights from the March issues of Circulation Research. Thank you for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @circres and #DiscoverCircRes. Thank you to our guests, Sabrina Robichaud and Dr Mireille Ouimet Sabrina. This podcast is produced by Ashara Ratnayaka, edited by Melissa Stoner and supported by the editorial team of Circulation Research. Some of the copy text for highlighted articles was provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire and this is Discover CircRes, you're on-the-go source for the most up-to-date and exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022, The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, visit ahajournals.org.

Module 3 Foundation Lecture: Immune System and Leukocyte Function

FNU PC705 Advanced Pathophysiology

Play Episode Listen Later Jan 4, 2022 47:00

Module 3 Foundation Lecture

foundation function lecture immune system module leukocyte

Fast Facts: Perio Edition “Periodontitis as a Manifestation of Systemic Disease - Leukocyte Adhesion Deficiency Syndrome”

A Tale of Two Hygienists Podcast

Play Episode Listen Later Dec 20, 2021 6:41

On this week's episode of Fast Facts - Perio Edition, Katrina Sanders, we are continuing the conversation that we started last week in discussing periodontitis as a manifestation of systemic disease highlighting patients that present with Leukocyte Adhesion Deficiency Syndrome. Quotes: “When we talk about patients who have Leukocyte Adhesion Deficiency Syndrome, there's a problem with the way these white blood cells actually adhere to that endothelium.” “So if you see patients who are experiencing recurrent infection of periodontal disease, delayed wound healing, and sores in the area, it would behoove this patient to get testing done to identify if they've experienced any type of a genetic component or change in gene expression associated with Leukocyte Adhesion Deficiency Syndrome.” Resources: DentistRX: https://www.dentistrx.com More Fast Facts: https://www.ataleoftwohygienists.com/fast-facts/ Katrina Sanders Website: https://www.katrinasanders.com Katrina Sanders Instagram: https://www.instagram.com/thedentalwinegenist/ Sources: Papapanou, P. N., Sanz, M., Buduneli, N., Dietrich, T., Feres, M., Fine, D. H., ... & Tonetti, M. S. (2018). Jepsen S, Caton JG, Albandar JM, Bissada NF, Bouchard P, Cortellini P, Demirel K, de Sanctis M, Ercoli C, Fan J, Geurs NC, Hughes FJ, Jin L, Kantarci A, Lalla E, Madianos PN, Matthews D, McGuire MK, Mills MP, Preshaw PM, Reynolds MA, Sculean A, Susin C, West NX, Yamazaki K. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018 Jun;89 Suppl 1:S237-S248. doi: 10.1002/JPER.17-0733. PMID: 29926943.

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Fast Facts: Perio Edition “Periodontitis as a Manifestation of Systemic Disease - Leukocyte Adhesion Deficiency Syndrome”

A Tale of Two Hygienists Podcast

Play Episode Listen Later Dec 20, 2021 6:41

On this week's episode of Fast Facts - Perio Edition, Katrina Sanders, we are continuing the conversation that we started last week in discussing periodontitis as a manifestation of systemic disease highlighting patients that present with Leukocyte Adhesion Deficiency Syndrome. Quotes: “When we talk about patients who have Leukocyte Adhesion Deficiency Syndrome, there's a problem with the way these white blood cells actually adhere to that endothelium.” “So if you see patients who are experiencing recurrent infection of periodontal disease, delayed wound healing, and sores in the area, it would behoove this patient to get testing done to identify if they've experienced any type of a genetic component or change in gene expression associated with Leukocyte Adhesion Deficiency Syndrome.” Resources: DentistRX: https://www.dentistrx.com More Fast Facts: https://www.ataleoftwohygienists.com/fast-facts/ Katrina Sanders Website: https://www.katrinasanders.com Katrina Sanders Instagram: https://www.instagram.com/thedentalwinegenist/ Sources: Papapanou, P. N., Sanz, M., Buduneli, N., Dietrich, T., Feres, M., Fine, D. H., ... & Tonetti, M. S. (2018). Jepsen S, Caton JG, Albandar JM, Bissada NF, Bouchard P, Cortellini P, Demirel K, de Sanctis M, Ercoli C, Fan J, Geurs NC, Hughes FJ, Jin L, Kantarci A, Lalla E, Madianos PN, Matthews D, McGuire MK, Mills MP, Preshaw PM, Reynolds MA, Sculean A, Susin C, West NX, Yamazaki K. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018 Jun;89 Suppl 1:S237-S248. doi: 10.1002/JPER.17-0733. PMID: 29926943.

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Immunology | Leukocyte Adhesion Deficiency Type I

The Medbullets Step 1 Podcast

Play Episode Listen Later Dec 15, 2021 12:54

In this episode, we review the high-yield topic of Leukocyte Adhesion Deficiency Type I from the Immunology 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://anchor.fm/medbulletsstep1/message

immunology deficiency adhesion leukocyte

Gross Week Morning Story (11-14-2021)

Play Episode Listen Later Nov 14, 2021 3:19

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers. Learn more about your ad choices. Visit podcastchoices.com/adchoices

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Gross Week Night Story (11-14-2021)

Play Episode Listen Later Nov 14, 2021 3:29

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Pure PRP vs. Leukocyte Rich PRP for the Intervertebral Disc

The PainExam podcast

Play Episode Listen Later Nov 11, 2021 11:28

Pure PRP vs. Leukocyte Rich PRP for the Intervertebral Disc Regenerative Pain Medicine Journal Club... In this podcast Dr. Rosenblum reviews an article on comparing in vitro preparations of Platelet Rich Plasma on intervertebral disc stem cells... New 2 in 1 Charging Station for Clarius HD Wireless Ultrasound System- Click on the following link and you can enter your credit card info, billing and shipping and your code (DARO) for 20% off! https://store.clarius.com/collections/accessories/products/package-2-in-1-charging-station-hd Events: Plymouth Medical Dec. 2nd and NRAP Tampa Ultrasound Workshop Jan.29, 2022! NRAP Tampa- Jan. 29th, 2022 This 1 day intensive workshop has been developed for both novices and advanced pain physicians providers who would like to either learn the basics or further advance their skills in ultrasound guided pain procedures. Participants will have up to 5 hours of hands on ultrasound scanning on live models of different body habitus to learn and identify different sono‐anatomy. Get Your Tickets Advanced Ultrasound Training Workshop! Register Now! Breast Relief- A Systematic Approach to Post-Mastecomy Pain Monday November 15, 2021 4PM: Register Now! https://bit.ly/3hww1hX Plymouth Medical Upcoming Orthobiologics Education Webinar! December 2nd, 2021 8PM: Join PLYMOUTH MEDICAL's Orthobiologics Education Webinar with David Rosenblum, M.D., AABP on December 2 at 8:00PM ET to discuss the most effective Orthobiologics solutions and learn how to optimize treatments in your clinic from patient selection to marketing. Register Now! Podcast Resources: Wang, Sz., Fan, Wm., Jia, J. et al. Is exclusion of leukocytes from platelet-rich plasma (PRP) a better choice for early intervertebral disc regeneration?. Stem Cell Res Ther 9, 199 (2018). https://doi.org/10.1186/s13287-018-0937-7 https://www.hindawi.com/journals/omcl/2020/8893819/ New Updates- New 1 on 1 Training Service! New Hospital and Medical Network Group Training Program! Exclusive Dr/Medical Professional affiliate program! Leverage Your Social Network! PainExam "Complete" Complete CME Course now available! Subscribe to PainExam's Mailing List * indicates required Email Address * Download the PainExam Official Apps for Android and IOS Devices! https://play.google.com/store/apps/details?id=com.painexam.android.painexam&hl=en_US https://apps.apple.com/us/app/the-pain-management-review/id997396714 Follow PainExam- https://painexam.com/blog/ https://www.facebook.com/PainExam/ https://twitter.com/painexams https://www.instagram.com/painexam/ https://www.linkedin.com/company/painexam https://www.pinterest.com/painexam https://www.youtube.com/user/DocRosenblum/videos

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Pure PRP vs. Leukocyte Rich PRP for the Intervertebral Disc

The PMRExam Podcast

Play Episode Listen Later Nov 11, 2021 11:28

Pure PRP vs. Leukocyte Rich PRP for the Intervertebral Disc Regenerative Pain Medicine Journal Club... In this podcast Dr. Rosenblum reviews an article on comparing in vitro preparations of Platelet Rich Plasma on intervertebral disc stem cells... New 2 in 1 Charging Station for Clarius HD Wireless Ultrasound System- Click on the following link and you can enter your credit card info, billing and shipping and your code (DARO) for 20% off! https://store.clarius.com/collections/accessories/products/package-2-in-1-charging-station-hd Events: Plymouth Medical Dec. 2nd and NRAP Tampa Ultrasound Workshop Jan.29, 2022! NRAP Tampa- Jan. 29th, 2022 This 1 day intensive workshop has been developed for both novices and advanced pain physicians providers who would like to either learn the basics or further advance their skills in ultrasound guided pain procedures. Participants will have up to 5 hours of hands on ultrasound scanning on live models of different body habitus to learn and identify different sono‐anatomy. Get Your Tickets Advanced Ultrasound Training Workshop! Register Now! Breast Relief- A Systematic Approach to Post-Mastecomy Pain Monday November 15, 2021 4PM: Register Now! https://bit.ly/3hww1hX Plymouth Medical Upcoming Orthobiologics Education Webinar! December 2nd, 2021 8PM: Join PLYMOUTH MEDICAL's Orthobiologics Education Webinar with David Rosenblum, M.D., AABP on December 2 at 8:00PM ET to discuss the most effective Orthobiologics solutions and learn how to optimize treatments in your clinic from patient selection to marketing. Register Now! Podcast Resources: Wang, Sz., Fan, Wm., Jia, J. et al. Is exclusion of leukocytes from platelet-rich plasma (PRP) a better choice for early intervertebral disc regeneration?. Stem Cell Res Ther 9, 199 (2018). https://doi.org/10.1186/s13287-018-0937-7 https://www.hindawi.com/journals/omcl/2020/8893819/ New Updates- New 1 on 1 Training Service! New Hospital and Medical Network Group Training Program! Exclusive Dr/Medical Professional affiliate program! Leverage Your Social Network! PainExam "Complete" Complete CME Course now available! Subscribe to the PMRExam mailing list for Free Board Prep Material & More! * indicates required Email Address * Email Format html text Download the PainExam Official Apps for Android and IOS Devices! https://play.google.com/store/apps/details?id=com.painexam.android.painexam&hl=en_US https://apps.apple.com/us/app/the-pain-management-review/id997396714 Follow PainExam- https://painexam.com/blog/ https://www.facebook.com/PainExam/ https://twitter.com/painexams https://www.instagram.com/painexam/ https://www.linkedin.com/company/painexam https://www.pinterest.com/painexam https://www.youtube.com/user/DocRosenblum/videos

pain doctors rich er md android pure disc wm ultrasounds sz cme prp msk jia pocus rosenblum charging stations pmr get your tickets daro platelet rich plasma ios devices anes leukocyte training service david rosenblum pmnr docrosenblum

Pure PRP vs. Leukocyte Rich PRP for the Intervertebral Disc

AnesthesiaExam Podcast

Play Episode Listen Later Nov 11, 2021 11:28

Pure PRP vs. Leukocyte Rich PRP for the Intervertebral Disc Regenerative Pain Medicine Journal Club... In this podcast Dr. Rosenblum reviews an article on comparing in vitro preparations of Platelet Rich Plasma on intervertebral disc stem cells... New 2 in 1 Charging Station for Clarius HD Wireless Ultrasound System- Click on the following link and you can enter your credit card info, billing and shipping and your code (DARO) for 20% off! https://store.clarius.com/collections/accessories/products/package-2-in-1-charging-station-hd Events: Plymouth Medical Dec. 2nd and NRAP Tampa Ultrasound Workshop Jan.29, 2022! NRAP Tampa- Jan. 29th, 2022 This 1 day intensive workshop has been developed for both novices and advanced pain physicians providers who would like to either learn the basics or further advance their skills in ultrasound guided pain procedures. Participants will have up to 5 hours of hands on ultrasound scanning on live models of different body habitus to learn and identify different sono‐anatomy. Get Your Tickets Advanced Ultrasound Training Workshop! Register Now! Breast Relief- A Systematic Approach to Post-Mastecomy Pain Monday November 15, 2021 4PM: Register Now! https://bit.ly/3hww1hX Plymouth Medical Upcoming Orthobiologics Education Webinar! December 2nd, 2021 8PM: Join PLYMOUTH MEDICAL's Orthobiologics Education Webinar with David Rosenblum, M.D., AABP on December 2 at 8:00PM ET to discuss the most effective Orthobiologics solutions and learn how to optimize treatments in your clinic from patient selection to marketing. Register Now! Podcast Resources: Wang, Sz., Fan, Wm., Jia, J. et al. Is exclusion of leukocytes from platelet-rich plasma (PRP) a better choice for early intervertebral disc regeneration?. Stem Cell Res Ther 9, 199 (2018). https://doi.org/10.1186/s13287-018-0937-7 https://www.hindawi.com/journals/omcl/2020/8893819/ New Updates- New 1 on 1 Training Service! New Hospital and Medical Network Group Training Program! Exclusive Dr/Medical Professional affiliate program! Leverage Your Social Network! PainExam "Complete" Complete CME Course now available! Subscribe to the AnesthesiaExam Mailing List! * indicates required Email Address * Download the PainExam Official Apps for Android and IOS Devices! https://play.google.com/store/apps/details?id=com.painexam.android.painexam&hl=en_US https://apps.apple.com/us/app/the-pain-management-review/id997396714 Follow PainExam- https://painexam.com/blog/ https://www.facebook.com/PainExam/ https://twitter.com/painexams https://www.instagram.com/painexam/ https://www.linkedin.com/company/painexam https://www.pinterest.com/painexam https://www.youtube.com/user/DocRosenblum/videos

pain doctors rich er md android pure disc wm ultrasounds sz cme prp msk jia pocus rosenblum charging stations pmr get your tickets daro platelet rich plasma ios devices anes leukocyte training service david rosenblum pmnr docrosenblum

Stories Week Walter Part 1 Night (9-20-2021)

Play Episode Listen Later Sep 20, 2021 3:33

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Stories Week Walter Part 1 Morning (9-20-2021)

outcomes formation reconstruction donor antibodies recurrent antigens occurs hla arthroscopic leukocyte allograft

Play Episode Listen Later Sep 20, 2021 3:23

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers. Learn more about your ad choices. Visit podcastchoices.com/adchoices

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AJSM April 2021 Podcast: Donor-Specific Human Leukocyte Antigen Antibody Formation After Allograft Glenoid Reconstruction Occurs But Does Not Impact Clinicoradiographic Outcomes

SAGE Orthopaedics

Play Episode Listen Later Mar 27, 2021 15:33

Recurrent shoulder instability is a prevalent condition, with glenoid bone loss as a common cause. Arthroscopic repair using distal tibial allografts provides long-lasting treatment by restoring glenoid surface area and presumably avoids risks of sensitization against donor human leukocyte antigen (HLA). Two case studies have challenged this assumption, suggesting that small bone allografts are able to induce host adaptive immune responses to donor HLA. The incidence of small bone allograft HLA sensitization and its effects on resorption and patient outcomes are unclear. In conclusion, sensitization against donor HLA after small bone graft allografting was not previously considered but has been brought to light as a possibility. Aside from potential complications for future organ transplants, HLA sensitization does not introduce a risk for adverse outcomes or higher grades of resorption compared with nonsensitized patients after small bone allografting for shoulder instability. Click here to read the article.

Alien Worlds - The Leukocyte Maneuver

Alien Worlds Radio Show

Play Episode Listen Later Feb 23, 2021 24:12

Alien Worlds was a science fiction/adventure omnibus—an anthology with the same characters set in the same universe, as opposed to an anthology of completely unrelated stories. The series was independently created, produced, and directed by Lee Hansen from 1979 to 1980. He produced 30 episodes covering 19 individual plotlines. Episodes were in standard 30-minute format, but story arcs were as long as 90 minutes. It's the mid-21st century and the International Space Authority (ISA) is the body which governs space exploration and development. Alien Worlds follows the adventures of ISA staff as they encounter strange cosmic mysteries. Some episodes take place aboard Starlab, an orbiting space station, while other episodes take place throughout the galaxy. All of the episodes are full of action. The series was written by Lee Hansen and Ron Thompson, with various co-writers, including Ken Ross, Jim Cook, Skip Press, Dudley Brown, Mike Hodel, and Babylon 5 writer J. Michael Stracynski. The full-symphonic soundtrack was written by Jim Kirk and performed by the London Symphony Orchestra.

TalkCast 468 – Leukocyte? I Never Touched That Antigen!

Sci-Fi Saturday Night

Play Episode Listen Later Jan 31, 2021

On tonight’s show we talk with comic creator Trevor Fernandes-Lenkiewicz, someone who by his own admission came into comic books late in life. This did not deter him from developing a deep love and respect for the craft of comics. He has created two websites, Dark Knight Nation and Pocket Watch Press. While in his […]

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Leukocyte Extravasation

First Past the Post

Play Episode Listen Later Dec 23, 2020 1:17

This episode covers leukocyte extravasation!

leukocyte extravasation

Human Leukocyte Antigen Subtypes

First Past the Post

Play Episode Listen Later Dec 22, 2020 1:35

This episode covers human leukocyte antigen subtypes!

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Gross Week Morning Story (11-15-2020)

Play Episode Listen Later Nov 15, 2020 3:19

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers.

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Gross Week Night Story (11-15-2020)

Play Episode Listen Later Nov 15, 2020 3:29

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story.

Stories Week Walter Part 1 Night (9-21-2020)

Play Episode Listen Later Sep 21, 2020 3:33

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story.

Stories Week Walter Part 1 Morning (9-21-2020)

Golden Classics Great OTR Shows

Play Episode Listen Later Sep 21, 2020 3:23

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers.

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Alien Worlds_xx-xx-xx_(28)_The Leukocyte Maneuver

Play Episode Listen Later Jun 6, 2020

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Alien Worlds_xx-xx-xx_(28)_The Leukocyte Maneuver

Alien Worlds

Play Episode Listen Later Jun 6, 2020 24:11

A new episode Support this podcast at — https://redcircle.com/alien-worlds/donations

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Episode 63 Intro | TAPP Radio Preview

The A&P Professor

Play Episode Listen Later Feb 20, 2020 14:55

A brief preview of the upcoming full episode, featuring upcoming topics—making mistakes, how stress grays hair, a new kind of immune cell—plus word dissections, a book club recommendation (Mary Roach's Gulp!), and more! 00:18 | Topics 01:19 | Sponsored by HAPI Online Graduate Program 01:49 | Word Dissection 10:30 | Sponsored by HAPS 10:51 | Book Club 13:28 | Survey Says... 13:57 | Sponsored by AAA 14:13 | Staying Connected If you cannot see or activate the audio player click here. Please take the anonymous survey: theAPprofessor.org/survey Questions & Feedback: 1-833-LION-DEN (1-833-546-6336) Follow The A&P Professor on Twitter, Facebook, Blogger, Nuzzel, Tumblr, or Instagram! Upcoming Topics 1 minute Making mistakes in teaching. In front of students! Stress causes hair to gray. But how, exactly? A surprising answer. Not a B-lymphocyte. Not a T-lymphocyte. An X-lymphocyte! Sponsored by HAPI Online Graduate Program 0.5 minute The Master of Science in Human Anatomy & Physiology Instruction—the MS-HAPI—is a graduate program for A&P teachers. A combination of science courses (enough to qualify you to teach at the college level) and courses in contemporary instructional practice, this program helps you power up your teaching. Kevin Patton is a faculty member in this program. Check it out! nycc.edu/hapi Word Dissection 8.5 minutes Imposter syndrome The Impostor Phenomenon in High Achieving Women: Dynamics and Therapeutic Intervention (the paper that started it all) my-ap.us/2HFVXVX Imposter syndrome usage via Ngram Viewer my-ap.us/2HJuJ0p Norepinephrine Noradrenaline Adrenergic Melanin Eumelanin Pheomelanin HLA Sponsored by HAPS 0.5 minute The Human Anatomy & Physiology Society (HAPS) is a sponsor of this podcast. You can help appreciate their support by clicking the link below and checking out the many resources and benefits found there. Don't forget the early-bird discount for the HAPS Annual Conference expires on February 21, 2020—the same deadline for submitting workshops and posters. Anatomy & Physiology Society theAPprofessor.org/haps Book Club 2.5 minutes Recommendation from Mike Pascoe Gulp: Adventures on the Alimentary Canal by Mary Roach amzn.to/2HE3KDO For the complete list (and more) go to theAPprofessor.org/BookClub Special opportunity Contribute YOUR book recommendation for A&P teachers! Be sure include your reasons for recommending it Any contribution used will receive a $25 gift certificate The best contribution is one that you have recorded in your own voice (or in a voicemail at 1-833-LION-DEN) For the complete list (and more) go to theAPprofessor.org/BookClub Survey Says... 0.5 minute Please take about 5 minutes to answer some questions—it will really help improve this podcast! theAPprofessor.org/survey Sponsored by AAA 0.5 minutes A searchable transcript for this episode, as well as the captioned audiogram of this episode, are sponsored by the American Association for Anatomy (AAA) at anatomy.org. Searchable transcript Captioned audiogram Don't forget—HAPS members get a deep discount on AAA membership! If the hyperlinks here are not active, go to TAPPradio.org to find the episode page. More details at the episode page. Transcript available in the transcript box. Listen to any episode on your Alexa device. Need help accessing resources locked behind a paywall? Check out this advice from Episode 32 to get what you need! https://youtu.be/JU_l76JGwVw?t=440 Tools & Resources Amazon TextExpander Rev.com Snagit & Camtasia The A&P Professor Logo Items Sponsors Transcript and captions for this episode are supported by the American Association for Anatomy. anatomy.org The Human Anatomy & Physiology Society aprovides marketing support for this podcast. theAPprofessor.org/haps Distribution of this episode is supported by NYCC's online graduate program in Human Anatomy & Physiology Instruction (HAPI) nycc.edu/hapi Clicking on sponsor links helps let them know you appreciate their support of this podcast! Follow The A&P Professor on Twitter, Facebook, Blogger, Nuzzel, Tumblr, or Instagram! The A&P Professor® and Lion Den® are registered trademarks of Lion Den Inc. (Kevin Patton)

learning master science stress teaching imposters anatomy recommendations preview bloggers book club distribution tumblr aaa american association physiology patton new york comic con terminology melanin survey says gulp antigens tapp mary roach hla haps searchable hapi nuzzel impostor phenomenon tools resources leukocyte therapeutic intervention alimentary canal captioned high achieving women dynamics ngram viewer

Gross Week Night Story (11-17-2019)

Play Episode Listen Later Nov 17, 2019 3:29

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story.

Gross Week Morning Story (11-17-2019)

Play Episode Listen Later Nov 17, 2019 3:19

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers.

story gross chompers leukocyte can walter

Stories Week Walter Part 1 Night (10-7-2019)

Play Episode Listen Later Oct 7, 2019 3:33

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story.

Stories Week Walter Part 1 Morning (10-7-2019)

rich medicine pure rehabilitation regenerative leukocyte

Play Episode Listen Later Oct 7, 2019 3:23

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers.

stories story chompers leukocyte can walter

A Closer Look at PRP- Leukocyte Rich vs. Prep PRP & More!

AnesthesiaExam Podcast

Play Episode Listen Later Sep 27, 2019 24:04

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rich prep pure closer look prp biologics leukocyte

PRP Revisited- Pure PRP vs. Leukocyte Rich PRP

The PMRExam Podcast

Play Episode Listen Later Sep 27, 2019 24:04

Subscribe to our mailing list for Free Board Prep Material & More! * indicates required Email Address * Email Format

1303: DIM Supplement, Candibactin AR, Best Degree, Leukocyte Disorders, Cyst Prevention, POIS Sex Symptoms (HouseCall)

The Cabral Concept

Play Episode Listen Later Aug 31, 2019 28:56

Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions: Janice: Would you please give the benefits of taking the dim supplement on one of your podcasts? Tyson: Hello, What do you know about Candibactin AR? I’m about 2/3 of the way through the CBO protocol in hopes of getting rid of acne on my face, chest and back. Up to this point I’ve had reduced acne on my face, but not as much progress with my chest or back. A family friend of mine just told me her daughter took Candibactin AR to help her with acne and she got great results - is this something I could start taking during my CBO protocol? Or should I wait till it’s done? Or should I skip trying this supplement all together? Thank you! Tyson Erica: Hey Dr. Cabral! I actually have a career question for you today. I am recently out of college, and just finished up your IHP level 1 and level 2 courses. They were fantastic. After seeing what you've done, I have to say I'd like to continue down a similar path. So I have a few questions about what your opinion is for different doctorate degrees. Financially speaking, an MD seems like a safer path, as I can always diverge back into a functional practice, but it seems to be longer - around 5-8 years. I would have to take out loans for this, so it seems like a "financially" safer way. But the thing is -- I am definitely most interested in helping / healing others in a natural way. And I'm not sure if it's worth it to commit that much time going down the MD path when I could keep my focus on what I want my true expertise to be. The thing about becoming an ND is though, the salary might be much lower out of school, it could be harder to pay off debt, and I've heard you mention before that ND school isn't the same as it has always been from an educational standpoint. So basically, my question is, if you had to do this all over again.. what path would you choose? Where do you think one could receive the BEST education for learning to heal others from a foundational standpoint? Does it involve leaving the US altogether? Which countries seem to be the most advanced in these methodologies? Being able to take insurance is another "safe" side of this, but I've also heard you mention that you choose not to be insured anyways so you can practice the way you'd like to practice. Thanks so so much in advance! Looking forward to hearing your response! Elizabeth: Hello Doc, I'm one of your IHP students and I feel beyond grateful to be part of your community. I have a client with Leukocyte Disorders, every 2-3 months he wakes up at night with fever above 103° and no other symptoms except for extreme fatigue. When that happens, his conventional Docs treat him with cortisone and Tylenol. He's doing the 21 days DCD protocol, eating healthy + meditation everyday. He is 25 y.o. He has also a history of Cytomegalovirus and Mononucleosis (looks like his immune system is quite weakened) I really would love to help him, besides Adrenal lab testing (that i've already recommended) do you have any suggestion? Thank you for your time and everything you do to empower people with knowledge. The world needs more Dr Cabral! :) Bernice: Hi Dr. Cabral, I recently had to have a 12 cm ovarian cyst removed surgically. The OBGYN was recommending to take birth control after the surgery to help prevent future cysts from growing. Are there any holistic/naturopathic remedies to help with preventing future cyst issues? Thank you! Steve: Hi Dr. Cabral,What can you tell me about POIS? Though I have a host of issues, one that is particularly concerning as of late is when my wife and I have sex, I experience fatigue, extreme back pain, racing heart, flu-like symptoms, and brain fog for up to a week afterwards. Could this be POIS or something else? I have already ordered your Big 5 lab tests, so I’m hoping some of the results can bring some clarity to my situation. Thanks Thank you for tuning into today's Cabral HouseCall and be sure to check back tomorrow where we answer more of our community’s questions! - - - Show Notes & Resources: http://StephenCabral.com/1303 - - - Get Your Question Answered: http://StephenCabral.com/askcabral - - - Dr. Cabral's New Book, The Rain Barrel Effect https://amzn.to/2H0W7Ge - - - Join the Community & Get Your Questions Answered: http://CabralSupportGroup.com - - - Dr. Cabral’s Most Popular Supplements: > “The Dr. Cabral Daily Protocol” (This is what Dr. Cabral does every day!) - - - > Dr. Cabral Detox (The fastest way to get well, lose weight, and feel great!) - - - > Daily Nutritional Support Shake (#1 “All-in-One recommendation in my practice) - - - > Daily Fruit & Vegetables Blend (22 organic fruit & vegetables “greens powder”) - - - > CBD Oil (Full-spectrum, 3rd part-tested & organically grown) - - - > Candida/Bacterial Overgrowth, Leaky Gut, Parasite & Speciality Supplement Packages - - - > See All Supplements: https://equilibriumnutrition.com/collections/supplements - - - Dr. Cabral’s Most Popular At-Home Lab Tests: > Hair Tissue Mineral Analysis (Test for mineral imbalances & heavy metal toxicity) - - - > Organic Acids Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Thyroid + Adrenal + Hormone Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Adrenal + Hormone Test (Run your adrenal & hormone levels) - - - > Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Omega-3 Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - > Stool Test (Use this test to uncover any bacterial, h. Pylori, or parasite overgrowth) - - - > Genetic Test (Use the #1 lab test to unlocking your DNA and what it means in terms of wellness, weight loss & anti-aging) - - - > Dr. Cabral’s “Big 5” Lab Tests (This package includes the 5 labs Dr. Cabral recommends all people run in his private practice) - - - > View all Functional Medicine lab tests (View all Functional Medicine lab tests you can do right at home for you and your family!)

SHR # 2287 :: RLRx: Connecting The Dots: Human Leukocyte Antigen B27, Autoimmunity and Vitamin C ::

Super Human Radio

Play Episode Listen Later Jan 10, 2019 91:02

SHR # 2287 :: RLRx: Connecting The Dots: Human Leukocyte Antigen B27, Autoimmunity and Vitamin C :: Adam Lamb - Human Leukocyte Antigen B27 (HLA-B27) is a genetic marker of autoimmunity that leads to horrific life-derailing disorders. Almost all effect a degrading of chondrocytes and soft tissue that causes immense pain and disability. A few of the disorders caused by HLA-B27 is ankylosing spondylitis, inflammation of the eyes, several forms of joint pain and arthritis, joint stiffness, skin lesions, and much more. The standard of care is biologics that weaken the immune system that carry a host of negative side effects. But what if a simple vitamin could actually eliminate the pain and symptoms better than dangerous biologics? Could it be that the medical orthodoxy doesn't know about this? Or are they just ignoring it? ::

vitamin c connecting the dots autoimmunity antigens shr leukocyte hla b27

SHR # 2287 :: RLRx: Connecting The Dots: Human Leukocyte Antigen B27, Autoimmunity and Vitamin C ::

Super Human Radio

Play Episode Listen Later Jan 9, 2019 91:02

SHR # 2287 :: RLRx: Connecting The Dots: Human Leukocyte Antigen B27, Autoimmunity and Vitamin C :: Adam Lamb - Human Leukocyte Antigen B27 (HLA-B27) is a genetic marker of autoimmunity that leads to horrific life-derailing disorders. Almost all effect a degrading of chondrocytes and soft tissue that causes immense pain and disability. A few of the disorders caused by HLA-B27 is ankylosing spondylitis, inflammation of the eyes, several forms of joint pain and arthritis, joint stiffness, skin lesions, and much more. The standard of care is biologics that weaken the immune system that carry a host of negative side effects. But what if a simple vitamin could actually eliminate the pain and symptoms better than dangerous biologics? Could it be that the medical orthodoxy doesn't know about this? Or are they just ignoring it? ::

vitamin c connecting the dots autoimmunity antigens shr leukocyte hla b27

Immune 15: Happy neu-trophil year

Immune

Play Episode Listen Later Dec 22, 2018 86:27

Stephanie takes the Immune team on a tour of neutrophils, the most abundant leukocytes in mammals, including tethers and slings, neutrophil rolling, and neutrophil nets. Hosts: Vincent Racaniello, Stephanie Langel, and Cynthia Leifer Subscribe (free): iTunes, Google Podcasts. RSS, email Become a patron of Immune! Links for this episode Slings enable neutrophil rolling (Nature) Sling video (La Jolla Inst Allergy Immunol) Neutrophil extracellular traps kill bacteria (Science) Neutrophil review (Sci Immunol) Image credit Time stamps by Jolene. Thanks! Weekly Science Picks Steph- Should reviewers remain anonymous? Cindy- Breast Cancer Research Foundation Vincent- Initiative to End Paywalls (The Scientist) Music by Steve Neal. Immune logo image by Blausen Medical. Send your immunology questions and comments to immune@microbe.tv

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Gross Week Morning Story

Play Episode Listen Later Jun 17, 2018 3:19

Can Walter the Leukocyte defeat the bad bacteria that has invaded the body? Find out in our STORY on today's Chompers.

story gross chompers leukocyte can walter

Gross Week Night Story

Play Episode Listen Later Jun 17, 2018 3:29

What happens when Walter the Leukocyte pushes the mysterious green button? Find out the dramatic conclusion on tonight's story.

Clean Eating for Women with Carrie Forrest, MPH in Nutrition

#12: Alcat Food Sensitivity Testing with Nutrition Expert Amy Pieczarka,RDN

Play Episode Listen Later Dec 18, 2017 38:20

Nutrition Expert Amy Pieczarka, RDN is here to talk about Alcat Food Sensitivity Testing. Welcome to Episode #12 of Clean Eating for Women. In this episode of the Clean Eating for Women podcast, we talk about: How food sensitivities can cause chronic effects including weight gain for no reason The difference between food allergies and food sensitivities How most people can benefit from the Alcat test and results Some highlights of this episode: How Amy discovered that testing for food sensitivities would be a great help for her clients and an important tool in finding root causes of problems. [03:44] Cell Science Systems is the laboratory that does the Alcat test and how they put the recommendations into practice. [04:15] How allergies are associated with antibodies and the reaction and symptoms often happen within minutes to an hour later. [06:10] Sensitivities involve the innate immune system and the symptoms are more delayed. They could come up hours or days later and aren't as profound but they can be chronic. [07:06] How food sensitivities cause inflammation which is a major contributing factor to chronic issues. [11:48] Testing is required to pinpoint symptoms that are being experienced on a daily basis. Food sensitivity is a piece of the puzzle, and the Alcat test takes the guesswork out of the process. [14:18] The Alcat test measures white blood cell response. Leukocyte activation is measured as they are introduced to the food extracts. This indicates an inflammatory response. [16:22] How consuming the same food everyday can cause food sensitivities. [22:56] The Alcat test includes colored coded results. Red is reactive and green is all the foods that you can have. To begin, focus on eating the green foods and follow the rotation plan on the second page to not bombard the immune system everyday. [25:36] Links mentioned in this episode (some affiliate links included): PreviMedica PreviMedica Facebook Page Wellio.co Amy Pieczarka LinkedIn @AMYPIECZARKA on Twitter Podcast #6: Discovering & Managing Food Sensitivities Cell Science Systems Alcat Test Institute for Functional Medicine

women food testing sensitivity functional medicine rdn clean eating nutrition experts food sensitivity testing leukocyte alcat

What is Human Leukocyte Antigen?

FX Medicine Podcast Central

Play Episode Listen Later Jun 28, 2017

Human leukocyte antigens (HLAs) can be found on the surface of most cells of the body. They are a method of categorising one's 'tissue type' and they play a role in determining a person's immune response to foreign substances. Most notably, they are used to establish donor matching for organ transplants. Today, Dr Mark Donohoe takes us through some of the emerging ways HLAs can reveal a person's predisposition to certain adverse health outcomes, such as mould toxicity, thyroiditis, type 1 diabetes, psoriasis and other autoimmune issues.*****DISCLAIMER: The information provided on FX Medicine is for educational and informational purposes only. The information provided is not, nor is it intended to be, a substitute for professional advice or care. Please seek the advice of a qualified health care professional in the event something you learn here raises questions or concerns regarding your health.*****

human antigens hlas leukocyte fx medicine

Leukocyte Rich Versus Leukocyte Poor Platelet Rich Plasma for Cartilage Repair: In Vitro Results

Sports Review Journal Podcast Radio

Play Episode Listen Later Oct 12, 2015 10:12

SRJ Episode 6, Volume 1(2) by Siddiqui and Ibrahim

poor repair vitro siddiqui cartilage platelet rich plasma leukocyte

TWiP 88: French foreign lesion

This Week in Parasitism

Play Episode Listen Later May 2, 2015 113:37

Vincent, Dickson, and Daniel discuss how a secreted protein from the protozoan parasite Theileria transforms its host cells via a cellular proto-oncogene. Hosts: Vincent Racaniello, Dickson Despommier, and Daniel Griffin Links for this episode: Leishmania (TWiP #14) Transformation by a prolyl isomerase (Nature) Theileria.org Prolyl isomerase (Wikipedia) Image from Transformation & Oncogenesis Letters read on TWiP 88 Contact Send your questions and comments (email or mp3 file) to twip@twiv.tv Subscribe Subscribe to TWiP (free) in iTunes, by the RSS feed or by email

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Leukocyte trafficking during infection with modified vaccinia virus Ankara

Tierärztliche Fakultät - Digitale Hochschulschriften der LMU - Teil 06/07

Play Episode Listen Later Feb 8, 2014

Sat, 8 Feb 2014 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/17373/ https://edoc.ub.uni-muenchen.de/17373/1/Price_Philip.pdf Price, Philip John Ritchie ddc:590, ddc:500, Tierärztliche Fak

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SCCM Pod-216 PCCM: Critical Pertussis Illness in Children

iCritical Care: Pediatric Critical Care Medicine

Play Episode Listen Later Jun 6, 2013 16:12

Margaret Parker, MD, FCCM, speaks with John T. Berger, MD, FCCM, Medical Director for Cardiac Critical Care at Childrens National Medical Center in Washington, DC, USA.

united states children washington dc md illness outcome medical director critical care medicine pulmonary hypertension pertussis sccm leukocyte

SCCM Pod-216 PCCM: Critical Pertussis Illness in Children

iCritical Care: All Audio

Play Episode Listen Later Jun 6, 2013 16:12

Margaret Parker, MD, FCCM, speaks with John T. Berger, MD, FCCM, Medical Director for Cardiac Critical Care at Childrens National Medical Center in Washington, DC, USA.

united states children washington washington dc md illness outcome medical director berger critical care medicine john t pulmonary hypertension pertussis sccm leukocyte

Science Signaling Podcast, 30 April 2013

Science Signaling Podcast

Play Episode Listen Later Apr 29, 2013 12:26

The chemokine scavenging activity of an atypical chemokine receptor requires signaling through β-arrestin.

science inflammation signaling immune response leukocyte gpcr chemotaxis

In vivo temporal and spatial profile of leukocyte adhesion and migration after experimental traumatic brain injury in mice

Medizin - Open Access LMU - Teil 21/22

Play Episode Listen Later Jan 1, 2013

Background: Leukocytes are believed to be involved in delayed cell death following traumatic brain injury (TBI). However, data demonstrating that blood-borne inflammatory cells are present in the injured brain prior to the onset of secondary brain damage have been inconclusive. We therefore investigated both the interaction between leukocytes and the cerebrovascular endothelium using in vivo imaging and the accumulation of leukocytes in the penumbra following experimentally induced TBI. Methods: Experimental TBI was induced in C57/Bl6 mice (n = 42) using the controlled cortical impact (CCI) injury model, and leukocyte-endothelium interactions (LEI) were quantified using both intravital fluorescence microscopy (IVM) of superficial vessels and 2-photon microscopy of cortical vessels for up to 14 h post-CCI. In a separate experimental group, leukocyte accumulation and secondary lesion expansion were analyzed in mice that were sacrificed 15 min, 2, 6, 12, 24, or 48 h after CCI (n = 48). Finally, leukocyte adhesion was blocked with anti-CD18 antibodies, and the effects on LEI and secondary lesion expansion were determined 16 (n = 12) and 24 h (n = 21), respectively, following TBI. Results: One hour after TBI leukocytes and leukocyte-platelet aggregates started to roll on the endothelium of pial venules, whereas no significant LEI were observed in pial arterioles or in sham-operated mice. With a delay of >4 h, leukocytes and aggregates did also firmly adhere to the venular endothelium. In deep cortical vessels (250 mu m) LEIs were much less pronounced. Transmigration of leukocytes into the brain parenchyma only became significant after the tissue became necrotic. Treatment with anti-CD18 antibodies reduced adhesion by 65%; however, this treatment had no effect on secondary lesion expansion. Conclusions: LEI occurred primarily in pial venules, whereas little or no LEI occurred in arterioles or deep cortical vessels. Inhibiting LEI did not affect secondary lesion expansion. Importantly, the majority of migrating leukocytes entered the injured brain parenchyma only after the tissue became necrotic. Our results therefore suggest that neither intravascular leukocyte adhesion nor the migration of leukocytes into cerebral tissue play a significant role in the development of secondary lesion expansion following TBI.

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The polyomaviruses WUPyV and KIPyV: a retrospective quantitative analysis in patients undergoing hematopoietic stem cell transplantation

Medizin - Open Access LMU - Teil 19/22

Play Episode Listen Later Jan 1, 2012

Background: The polyomaviruses WUPyV and KIPyV have been detected in various sample types including feces indicating pathogenicity in the gastrointestinal (GI) system. However, quantitative viral load data from other simultaneously collected sample types are missing. As a consequence, primary replication in the GI system cannot be differentiated from swallowed virus from the respiratory tract. Here we present a retrospective quantitative longitudinal analysis in simultaneously harvested specimens from different organ sites of patients undergoing hematopoietic stem cell transplantation (HSCT). This allows the definition of sample types where deoxyribonucleic acid (DNA) detection can be expected and, as a consequence, the identification of their primary replication site. Findings: Viral DNA loads from 37 patients undergoing HSCT were quantified in respiratory tract secretions (RTS), stool and urine samples as well as in leukocytes (n = 449). Leukocyte-associated virus could not be found. WUPyV was found in feces, RTS and urine samples of an infant, while KIPyV was repeatedly detected in RTS and stool samples of 4 adult patients. RTS and stool samples were matched to determine the viral load difference showing a mean difference of 2.3 log copies/ml (p < 0.001). Conclusions: The data collected in this study suggest that virus detection in the GI tract results from swallowed virus from the respiratory tract (RT). We conclude that shedding from the RT should be ruled out before viral DNA detection in the feces can be correlated to GI symptoms.

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Science Signaling Podcast, 6 September 2011

Science Signaling Podcast

Play Episode Listen Later Sep 5, 2011 16:03

Activating integrin signaling may be an effective strategy for developing therapeutics to reduce leukocyte recruitment during inflammation.

science injury migration inflammation activating signaling adhesion inflammatory disease leukocyte integrin

RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner

Medizin - Open Access LMU - Teil 18/22

Play Episode Listen Later Jan 1, 2011

Background: The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-kappa B but also due to its function as ligand for the beta(2)-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated beta(2)-integrin-dependent leukocyte adhesion in RAGE(-/-) and Icam1(-/-) mice in different cremaster muscle models of inflammation using intravital microscopy. Results: We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucylphenylalanine (fMLP)-induced leukocyte adhesion in TNF-alpha-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo. Conclusion: Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.

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Leukocyte 4 and Microcytic Anemia (01.14.10)

Play Episode Listen Later Jan 18, 2010 51:29

Leukocyte 4 and Microcytic Anemia (01.14.10)

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Leukocyte 1 (01.11.10)

byu hematology cls leukocyte

Play Episode Listen Later Jan 13, 2010 43:34

Leukocyte 1 (01.11.10)

Leukocyte 2 (01.12.10)

byu hematology cls leukocyte

Play Episode Listen Later Jan 13, 2010 46:30

Leukocyte 2 (01.12.10)

Leukocyte 3 (01.13.10)