Podcasts about cardiovascular sciences

On tonight's show, I'll have Sean Coady, Deputy Branch Chief in the Epidemiology Branch of the Division of Cardiovascular Sciences, at the National Heart, Lung, and Blood Institute to talk about heart health in rural areas and Lance Taylor with CEI Bookstore / Truth Publications to share about their progress after a tornado destroyed their business location in Athens.

On this MADM, I have Sean Coady, Deputy Branch Chief in the Epidemiology Branch of the Division of Cardiovascular Sciences, at the National Heart, Lung, and Blood Institute to talk about heart health in rural areas. Sponsor: Green's Dependable Hardware Russellville, AL

For this episode of the Global Kidney Care Podcast, Jonathan Barratt, MD, MSc, PhD is Professor of Renal Medicine, Department of Cardiovascular Sciences at the University of Leicester and Richard Lafayette, MD, FACP is a Nephrologist and Professor of Medicine at the Division of Nephrology Department of Medicine, Stanford University discuss the changing landscape in IgAN and disease modification approaches. This podcast is sponsored by Vera Therapeutics 

JMCC Social Media Editor Kate Weeks speaks with Andrew Gibb, Instructor, Cardiovascular Research Center, Department of Cardiovascular Sciences at Temple University on his research and scientific career. 

This podcast takes audience for a journey through time with Dr. C N Manjunath as Director of Sri Jayadeva Institute of Cardiovascular Sciences and Research in the city of Bangalore and provides an insight to evolution of treatment and result oriented leadership. #TheRightDoctors #TRD #Cardiology

Welcome back to our intercalation series! Join Afrida as she talks to Marsioleda about what it's like to study cardiovascular sciences at Imperial as an external student and learn more about the application process intercalating at Imperial as an external student. Find out more about lab-based research and what it's like learning to work in a non-clinical environment. Marsioleda discusses her experience working in a lab as well as her top tips for group projects, dissertations and starting at a new university.

00:00 Show Open / U.S. Senator Sherrod Brown (D-Ohio) 08:30 Dr. Charlotte Pratt, Deputy Branch Chief of the Division of Cardiovascular Sciences at the National Heart, Lung, and Blood Institute. 18:00 Courtesy of our sister station, WBNS 10-TV, Tracy Townsend presents information on a number of topics, including Ohio's infrastructure problems; a local mother on a mission to have portable defibrillators available to young athletes; sports betting; and distracted driving. 43:30 Stephanie Hightower, President and CEO of the Columbus Urban League.

Cocoa may enhance skeletal muscle function University of California at San Diego, May 3, 2022 A small clinical trial led by researchers at UC San Diego School of Medicine and VA San Diego Healthcare System (VASDHS) found that patients with advanced heart failure and type 2 diabetes showed improved mitochondrial structure after three months of treatment with epicatechin-enriched cocoa. Epicatechin is a flavonoid found in dark chocolate. The study published by the journal Clinical and Translational Science looked at profoundly ill patients with major damage to skeletal muscle mitochondria. The trial participants consumed dark chocolate bars and a beverage with a total epicatechin content of approximately 100 mg per day for three months. Biopsies of skeletal muscle were conducted before and after treatment. After the three-month treatment, the researchers looked at changes in mitochondria volume and the abundance of cristae, which are internal compartments of mitochondria that are necessary for efficient function of the mitochondria, and measurable by electron microscopy. After three months, we saw recovery – cristae numbers back toward normal levels, and increases in several molecular indicators involved in new mitochondria production.” Healthy habits may improve longevity, prevent Alzheimer's disease Rush University Medical Center, May 14, 2022 Everyday habits that serve as the backbone of a healthy lifestyle may keep your brain sharp and help you live longer, according to new research from aging experts at RUSH. A study recently published in the British Medical Journal found that people ages 65 and older who had a healthy lifestyle lived longer—3.1 years longer for women, 5.7 years longer for men—than their peers who didn't have the same healthy lifestyle. They also spent more of their remaining years without Alzheimer's disease. What constitutes a healthy lifestyle?Eating the Mediterranean-DASH Intervention for Neurogenerative Delay (MIND) diet Staying engaged in cognitive activities like reading and puzzles Being physically active for at least 150 minutes a week Not smoking Limiting alcohol use (no more than one drink a day for women and two drinks a day for men) This latest study builds on ongoing research from RUSH showing that lifestyle factors can potentially reduce the risk for Alzheimer's disease and dementia by up to 60%, says Kumar Rajan, Ph.D., professor of epidemiology and director of the Rush Institute for Healthy Aging. Ozone treated water v. lethal microbial material   University of Alberta,  May 9, 2022 A University of Alberta research team has discovered that technology commonly used to decontaminate food industry equipment can also rid meat processing plants of lethal microbial material responsible for the human version of the ailment Mad Cow disease. U of A microbiology professors Mike Belosevic and Norm Neumann and engineering professor Mohamed Gamal El-Din demonstrated that infectious proteins found in the brain matter of cattle can be eradicated from water treated with ozone. The discovery could have applications in decontaminating wastewater in settings such as slaughterhouse effluents where infected neural material known as prions may be present. The ozone decontamination procedure can potentially be used to sterilize instruments used for neurosurgery, and prevent the transfer of infectious prions during surgical procedures. Prions are able to destroy and can still be infectious after being incinerated at heats of 850o C. In the wild, soil contaminated by a carcass of a deer that died of Chronic Wasting Disease can remain a source of infection for many years. The U of A research team's technique of using water treated with ozone to destroy prions is an improvement on current prion decontamination methods. Tai Chi Benefits Patients With Parkinson's Oregon Research Institute, May 13, 2022 Tai chi, an ancient martial art characterized by slow, flowing movement and meditation, helps improve balance and movement control for people with Parkinson's disease. The finding, published in The New England Journal of Medicine, is the latest study to show the benefits of tai chi for people with chronic health problems. Past studies have shown that tai chi reduces falls and depression among the elderly, and lessens pain for patients with arthritis and fibromyalgia. In the latest research, 195 people with movement and balance problems caused by Parkinson's disease were recruited from four Oregon cities. The patients were divided into three exercise classes that met for an hour a day, twice a week. One group took part in an extensive stretching class, another was taught resistance training, and the third group performed tai chi. After six months, patients in the tai chi group performed better on a number of measures related to strength, movement control, balance, stride length and reach. Resistance training also offered some benefits, and both the tai chi and resistance training groups had fewer falls than the stretching group. Vitamin B12 shows promise against ALS Tokushima University (Japan), May 13 2022.  An article appearing on May 9, 2022 in JAMA Neurology described a randomized trial in which men and women with the progressive neurologic disease amyotrophic lateral sclerosis (ALS) exhibited improvement in their condition after receiving a high dose of a form of vitamin B12 known as methylcobalamin.  Among the 126 patients who completed the trial, Amyotrophic Lateral Sclerosis Functional Rating Scale  scores declined by an average of 2.66 points for those who received the vitamin and by 4.63 in the placebo group—a difference of 43%. (Lower scores indicate increased severity of symptoms.)  This randomized clinical trial demonstrated that use of ultrahigh-dose methylcobalamin resulted in a 43% reduction in clinical deterioration as evaluated with the ALSFRS-R total score throughout the 16-week treatment period in the patients with early-stage ALS, Diabetes risk from sitting around University of Leicester (UK), May 12, 2022 A new study has found that women who stay seated for long periods of time every day are more prone to developing type 2 diabetes, but that a similar link wasn't found in men. Researchers from the University of Leicester Departments of Health Sciences and Cardiovascular Sciences revealed that women who are sedentary for most of the day were at a greater risk from exhibiting the early metabolic defects that act as a precursor to developing type 2 diabetes than people who tend to sit less. The team assessed over 500 men and women of the age of 40 or more about the amount of time spent sitting over the course of a week. It was found that the women who spent the longest time sitting had higher levels of insulin, as well as higher amounts of C-reactive protein and chemicals released by fatty tissue in the abdomen, leptin, and interleukin6, and which indicate problematic inflammation. This study provides important new evidence that higher levels of sitting time have a deleterious impact on insulin resistance and chronic low-grade inflammation in women but not men and that this effect is seen regardless of how much exercise is undertaken. This suggests that women who meet the national recommendations of 30 minutes of exercise a day may still be compromising their health if they are seated for the rest of the day. Videos: 1. Fauci Clip Surfaces, As Incoherent In 1985 As He Is Now: Spreads Diabolical Lie That “HIV” Could Spread To Children Via Casual Contact In Household (0:35) 2. Margaret Heckler & Robert Gallo – 1984 Press Conference (0:38) 3. Melissa Ciummei Clip  (9:52) 4. A terrifying prediction for 2030 (the Great Reset) (start @ 1:12) 5. New Rule: American Carnage | Real Time with Bill Maher (HBO) (7:48)

00:00 Show Open / Doctor David Goff, Director of the Division of Cardiovascular Sciences at the National Heart, Lung & Blood Institute, discusses heart health. 13:00 Courtesy of our sister station, WBNS 10-TV, Clay Gordon presents information about the ongoing redistricting issues in Ohio; an interview with the National Teacher of the Year - from Oberlin; and the growing problem of guns being stolen from cars in Columbus. 41:00 Duane Casares, CEO of Directions for Youth & Families, discusses proper boundaries in the workplace and between therapists and clients.

00:00 Show Open / Doctor David Goff, Director of the Division of Cardiovascular Sciences at the National Heart, Lung & Blood Institute, discusses heart health. 10:45 Courtesy of our sister station, WBNS 10-TV, Tracy Townsend presents topics that include Intel's recent announcement to build a $20 Billion computer chip-making operation in New Albany, the ongoing fight over the redrawing of legislative districts in Ohio, and Hilliard's move toward equipping police officers with body cameras. 36:00 Chris Orestis, President of Retirement Genius, presents tips and advice for seniors.

In this week's podcast, Mark and Brian talk to Professor Noel Caplice. Noel Caplice is the Professor of Cardiovascular Sciences in the Department of Medicine and is the Director of the Centre for Research in Vascular Biology at University College Cork. He is also a consultant cardiologist in Cork University Hospital. He previously held professional positions in pharmacology and medicine at the Mayo Clinic, Rochester, Minnesota, USA, where he was an interventional cardiologist and directed the Vascular Stem Cell Laboratory. Prof Caplice discusses his research and clinical practice and speaks on how his research informs his clinical practice. He also talks about the idea of mentorship and critical thinking. In addition, the importance of lifelong learning was a central part to our discussion. Prof Caplice offers advice for upcoming scientists and doctors who may be interested in combining research and clinical practice. Hosts: Mark Vesey, Brian Curtin

Scientists in Sweden analyzed health records in over 279,000 subjects who had prior documented fitness and body fat screenings. They found strong, independent associations with low fitness levels and higher belly fat with increased odds of severe disease. Support Healthy Hydration and Exercise Performance with the new Electrolyte Stix by MYOXCIENCE Nutrition: https://bit.ly/3uAWrV6 **Pre-Sale Discount Ends October, 31st 2021** Link to studies, images and video: https://bit.ly/30UiScO Time Stamps: 0:00 intro 0:16 Fitness, Belly Fat and Poor Outcomes 0:17 Media has ignored these studies 1:15 Science on healthy living matters, too 1:43 New Swedish study in 279,455 adults REF: Ekblom-Bak, E., et al. (2021). Cardiorespiratory fitness and lifestyle on severe COVID-19 risk in 279,455 adults: a case control study. International Journal of Behavioral Nutrition and Physical Activity, 1–16. 2:10 UK study showing exercise is protective 3:23 Kaiser Permanente Study on Exercise and C*19 REF: Sallis, R. et al. Physical inactivity is associated with a higher risk for severe COVID-19 outcomes: a study in 48 440 adult patients. Br. J. Sports Med. https://doi.org/10.1136/bjsports-2021-104080 (2021). 4:32 Belly Fat, not overall body fat is the issue 5:15 Belly Fat and C*19 outcomes Pranata, R., et al. (2021). Visceral adiposity, subcutaneous adiposity, and severe coronavirus disease-2019 (COVID-19): Systematic review and meta-analysis. Clinical Nutrition ESPEN, 43, 163–168. http://doi.org/10.1016/j.clnesp.2021.04.001 6:21 Closing gyms is bad policy REF: The Big Mistake of not Considering Physical Activity an Essential Element of Care During the Covid-19 Pandemic. (2021). International Journal of Cardiovascular Sciences. 7:02 Mechanisms as to how exercise is protective 7:18 Everyone's risk is the same is a lie 10:00 Electrolyte promotion ends soon 11:09 Swedish study: low fitness is a problem 12:16 Death rate in Sweden (this data set) 13:01 Low fitness, large waist circumference and poor outcomes 13:26 Study summary: LISTEN TO THIS 14:14 Underlying health conditions were a major driver 15:45 Why isn't exercise, healthy living being promoted?

In your evening news brief, West Bengal Chief Minister Mamata Banerjee says at least one crore people were affected by Cyclone Yaas; Delhi High Court has awarded Rs 6 lakh interim compensation to a six-year-old victim of sexual assault, JEE (Advanced) postposed due to the pandemic and freedom fighter and centenarian H S Doreswamy is no more. Hi, this is Ahmed Shariff and you are listening to, From The Newsroom— your daily evening news catch-up show from Deccan Herald. Here is the top news of May 25, 2021: At least one crore people were affected and three lakh houses damaged in West Bengal due to the rough weather conditions arising out of cyclone 'Yaas', Chief Minister Mamata Banerjee said on Wednesday. Cautioning people that high tide in seas, caused by the storm surge, would persist, Banerjee claimed that Bengal happens to be the "most-affected state". Cyclone 'Yaas' made its landfall on Wednesday morning near Dhamra port in Odisha, at 130-140 kmph, gusting to 155 kmph, according to Doppler radar data. The Delhi High Court has awarded Rs 6 lakh interim compensation to a six-year-old victim of sexual assault, observing that though the system cannot undo the offence it can provide psychological security or empowerment with monetary help besides prosecuting the offender. The high court, which set aside the trial court's order awarding Rs 50,000 interim compensation to the boy-child, enhanced the amount to Rs 6 lakh saying the previous sum was low, to say the least. Justice Anup Jairam Bhambhani said that while attempting to quantify the compensation payable to the victim even at the interim stage, the court's effort should be to offer monetary recompense, to the extent possible, for atonement of the crime. The JEE (Advanced) 2021, which was scheduled to be held on July 03, 2021, has been postponed due to the Covid-19 pandemic. The revised date of examination will be announced later. Noted freedom fighter and centenarian H S Doreswamy passed away on Wednesday afternoon due to cardiac arrest. The 104-year-old Gandhian was admitted to Sri Jayadeva Institute of Cardiovascular Sciences and Research a few days ago due to old age-related sickness including hypertension and bronchitis. In the first week of May, Doreswamy had tested positive for Covid-19. He had successfully fought the Covid-19 virus and was discharged on May 12 from the Jayadeva Hospital. Several prominent personalities including Chief Minister B S Yediyurappa have expressed condolences over the demise of freedom fighter. Source: DHNS/PTI

Dr. Kalra is an interventional cardiologist and medical director of clinical research for regional cardiovascular medicine at the Cleveland Clinic, section head of cardiovascular research at Cleveland Clinic Akron General, a university professor at the Cleveland Clinic Lerner College of Medicine (Associate Professor) and NEOMED (Adjunct Associate Professor), and founder of the non-profit startup, makeadent.org. He is director of Barry J. Maron Hypertrophic Cardiomyopathy Center in New Delhi, India. He is also the host of the cardiology podcast show, Parallax. He has presented late-breaking science at national and international scientific cardiovascular meetings, and has published over 200 scientific manuscripts in various peer-reviewed journals. Educated at Indira Gandhi Medical College (Shimla, India), he completed medical and cardiology training at the All India Institute of Medical Sciences (New Delhi, India), Cooper University Hospital (Camden, NJ), and Hennepin County Medical Center and Minneapolis Heart Institute (Minneapolis, MN). He served as a clinical and research fellow in interventional cardiology at Beth Israel Deaconess Medical Center, and a clinical fellow in medicine at Harvard Medical School (Boston, MA). He then completed a year of advanced interventional and structural cardiology fellowship at Houston Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital (Houston, TX). Dr. Kalra is board-certified in Internal Medicine, Cardiovascular Disease and Interventional Cardiology from the American Board of Internal Medicine, and a Diplomate in Adult Comprehensive Echocardiography from the National Board of Echocardiography. He is also certified in patient safety, healthcare quality, health informatics and leadership from Harvard Medical School's 1-year Safety, Quality, Informatics and Leadership certification program. He is currently pursuing a Master of Science program in Health Economics, Outcomes and Management in Cardiovascular Sciences at the London School of Economics & Political Science in London, United Kingdom. He is also the author of the poetry book, "Ibadah" that was released on Amazon and Barnes & Noble, and launched in collaboration with Cleveland Clinic Arts and Medicine Institute on Valentine's Day, 2020. EHJ paper: https://academic.oup.com/eurheartj/article/38/23/1789/3867739 Non-profit startup, makeadent.org, and the poetry book, ibadahthebook.com

Welcome to season two of What on Earth?!In this episode, we are celebrating LGBTQ+ History month with Dr. Izzy Jayasinghe! We talk to Izzy about what happens during a heartbeat, the challenges of climbing the academic ladder, and the importance of visible LGBT+ and science role models in school. Dr. Izzy Jayasinghe majored in Cardiovascular Sciences and pursued a Ph.D. in Physiology at the University of Auckland. Since then, she's worked on several projects related to cell signaling and super-resolution microscopy in New Zealand, Australia and the UK. Currently, she is a UKRI Future Leader Fellow and developing optical microscopes to "study the physics underpinning life" at Sheffield University. If you'd like to contact Izzy for more information about her work or anything on the podcast, you can contact her on:Twitter: [at]i_jayasContent warning: This episode contains mention of death and suicide. This occurs between 1hr 10mins 15 seconds and 1hr 11mins 45 seconds. If you are not in a position to listen to this at the moment, we encourage you to skip this section and listen to the later part of the podcast. Thank you.

To watch the discussion follow the link below:How Does COVID-19 Cause Cardiovascular Disease?Speakers on today's episode:John P. Cooke, MD, PhDJoseph C. “Rusty” Walter and Carole Walter Looke Presidential Distinguished Chair in Cardiovascular Disease Research, Department of Cardiovascular SciencesProfessor of Cardiovascular Sciences, Academic InstituteHouston Methodist Leslie T. Cooper, Jr., MDProfessor of Medicine and Chair of Cardiovascular DepartmentMayo Clinic, Florida Martha Gulati, MD, MS, FACC, FAHA, FASPCDivision Chief of Cardiology and Professor of MedicineUniversity of Arizona College of Medicine Geoffrey Barnes, MD, MScAssistant Professor of Internal MedicineInstitute for Healthcare Policy and Innovation, University of Michigan

  This month on the Discover CircRes podcast, host Cindy St. Hilaire highlights three featured articles from recent issues of Circulation Research and talks with Denisa Wagner and Nicoletta Sorvillo about their article on how PAD4 in blood promotes VWF strings and thrombosis. Article highlights: Goodyer et al: ScRNA-seq of the Cardiac Conduction System   Xiong et al: Chemotaxis Mediated Second Heart Field Deployment   Ranchoux et al: Pulmonary Hypertension and Metabolic Syndrome   Rühl et al. Thrombin/APC Response in FVL and FII 20210G>A   Mahmoud et al. LncRNA SMILR’s Mechanism and Therapeutic Potential   Transcript   Cindy St. H:                         Hi, welcome to Discover CircRes, the monthly podcast of the American Heart Association's Journal, Circulation Research. I'm your host, Cindy St. Hilaire, and I'm an assistant professor at the University of Pittsburgh. My goal as host of this podcast is to share with you some highlights from the recent articles published in the August 2nd and August 16th issues of Circulation Research. Cindy St. H:                         After I discuss some highlights, we'll also have an in-depth conversation with Drs. Denisa Wagner and Nicoletta Sorvillo, from Boston Children's Hospital and Harvard Medical School, who are the lead authors of one of the exciting discoveries from the August 16th issue. Cindy St. H:                         The first article I want to share with you today is titled Transcriptomic Profiling of the Developing Cardiac Conduction System at Single-Cell Resolution. The first author is William R. Goodyer, and the corresponding author is Sean Wu. They are both located at the Cardiovascular Institute and the Department of Pediatrics at Stanford University. Cindy St. H:                         Have you ever wondered how your heart beats, and why there's always this glub-glub pattern, and where did it come from? How is the heart able to initiate that pattern, from cells that don't contract to cells that contract? Well, the beating of the heart is regulated by what's called the cardiac conduction system, and this is an area in the heart of specialized cells, and these cells establish the rhythmic beating by coordinating the contraction of the chambers of the heart. Cindy St. H:                         There's several components to the CSS. The sinoatrial node acts as the pacemaker in the right atrium. The arterial ventricle node is the electrical relay that slows down the pulse from the SA node. A His bundle helps to transmit those impulses, and the Purkinjie fibers are the terminus of the electrical signal. Between all of these different components are a heterogeneous population of what are called transitional cells. There are several studies that have linked these somewhat amorphous or heterogeneous transitional cells to different arrhythmic disorders. Cindy St. H:                         For the normal function of the heart, all of these parts must come together, and when they don't, there's severe clinical manifestations such as arrhythmias, like I said, but also you can get decreased cardiac output and even sudden cardiac death. While important, the cells of the CSS are rather elusive, and that's because they're in a relatively small number compared to the rest of the cells in the heart, and there also aren't very clear markers to identify the cells in the CSS. Cindy St. H:                         To address this, Goodyer and colleagues harvested cells from embryonic mouse hearts and performed single-cell RNA sequencing on 22,000 individually barcoded cells. What they were looking for is learning what type of cells they are, but more importantly, they had the goal of identifying what these elusive transitional cells are, and can we find a marker for these cells to study them? And in some, yes. Together, the sequencing and spatial data provided gene expression atlas of the mouse CSS. Hopefully, this atlas will guide future studies into the essential electrical system that regulates the heartbeat. Cindy St. H:                         The next article I'd like to highlight is titled Single-Cell Transcriptomics Reveals Chemotaxis-Mediated Intra-Organ Crosstalk During Cardiogenesis. We're really going to hit you over the head with some single-cell transcriptomics in this month's podcast. The first authors of this article are Halqing Xiong, Yingjie Lou, Yanzhu Yue, Jiejie Zhang and the corresponding author is Aibin He and they're all from the Institute of Molecular Medicine, Beijing Key Laboratory of Cardiometabolic Molecular Medicine and the Peking-Tsinghua Center for Life Sciences, all at Peking University in Beijing, China. Cindy St. H:                         During development, the mammalian heart originates from two distinct areas in the early embryo and they're called the first heart field and the second heart field. Progenitor cells from these regions give rise to very different structures. From the first heart field comes the atria and the left ventricle, and the second heart field forms the right ventricle and the outflow tract. While we know the outcomes of these different developmental layers, a full understanding of how the first and second heart fields are regulated and how they actually interact with one another is actually lacking a lot of detail and we're not exactly sure how those structures can influence one another. Cindy St. H:                         So to learn more, Xiong and colleagues utilized two different murine models that were engineered to label cells coming from either the first or second heart fields red, and by labeling these cells red, it allows for their very pure isolation and then downstream studying at the single-cell level. So from each of these two models, they collected about 600 red-labeled cells and they collected these cells at four different time points, that were essentially at 12 hour intervals, and they did this starting at embryonic day 7.5, and that's because that's the time point in the mouse where these second and first heart fields are starting to develop. Cindy St. H:                         What they found, by using single-cell RNA sequencing, is that the first heart field cells differentiated into cardiomyocytes, in what they called a gradual, wave-like manner, while the second heart field cells differentiated in what they referred to as a more stepwise, defined pattern. The team also found high expression of migration factor MIF in first heart field cells and they found MIF's receptor CXCR2 in the second heart field progenitor cells. This suggests that perhaps the first heart field cells could regulate the migration of the second heart field cells. Sure enough, blocking MIF- CXCR2 interaction in cultured mouse embryos prevented second heart field cell migration and also prevented normal development of the right ventricular outflow tract structures. So together these results provide insight into both normal heart development and also suggest what might go awry in certain congenital heart malformations. Cindy St. H:                         The next paper I want to highlight is titled Metabolic Syndrome Exacerbates Pulmonary Hypertension due to Left Heart Disease. The first author is Benoit Ranchoux and the corresponding author is Francois Potus, and they are from the Pulmonary Hypertension Research Group at Laval University in Quebec City in Quebec, Canada. The disease pulmonary hypertension can arise from a number of causes, but one of the main drivers of what's called group two pulmonary hypertension is left heart disease. Left heart disease itself is caused by several conditions, such as diastolic dysfunction, aortic stenosis, which is a disease that I study, or mitral valve disease. All of these pathologies result in the left heart not beating efficiently or exerting too much energy. Cindy St. H:                         More than half of all group 2 PH patients also have metabolic syndrome, and metabolic syndrome is a condition that is ever increasing in the modern age, especially in America, and it's characterized by obesity coupled with pathology such as dyslipidemia, type 2 diabetes and high blood pressure. Metabolic syndrome is also marked by elevated levels of the inflammatory cytokine IL6. Rat studies have shown that IL6 can induce proliferation of the pulmonary artery smooth muscle cells and consequently, pulmonary hypertension. Cindy St. H:                         In this study Ranchoux and colleagues pulled together all these different pieces in a rat model and essentially want to test left heart disease coupled with metabolic syndrome coupled with does pulmonary hypertension happen or get worse? What they found was really interesting. Left heart disease was induced in a rat model using super coronary aortic banding and then metabolic syndrome was induced with a high fat diet feeding, or with treatment with Olanzapine, which is a second generation anti-psychotic agent, and it's known to induce metabolic syndrome not only in rats, but also in humans. The data from this paper show that inducing metabolic syndrome in rats coupled with left heart disease resulted in elevated IL6 levels and also greatly exacerbated pulmonary hypertension. Cindy St. H:                         Digging into this mechanism, they found that inhibition of IL6, using either an anti-IL6 antibody or by reducing IL6 secretion from macrophages, using the diabetes drug Metformin, ameliorated the pulmonary hypertension in the rats. They then went on and looked at human samples and they found that IL6 was higher in the lungs of pulmonary hypertension patients and that this IL6 could induce proliferation of human pulmonary artery smooth muscle cells. So together these data suggest that the observation in rats holds true for humans, but further goes on to suggest that perhaps Metformin, which is a well-known, well-used diabetic drug, could perhaps be used for the potential treatment of Group 2 pulmonary hypertension patients.   Cindy St. H:                           In the August 16th issue, we have an article titled Increased Activated Protein C Response Rates Reduce the Thrombotic Risk of Factor V Leiden Carriers but not of Prothrombin 20210G>A Carriers. That is some title. The first authors are Heiko Rühl, and Christina Berens, and Dr Rühl is also the corresponding author, and they are at the Institute of Experimental Hematology and Transfusion Medicine, University Hospital Bonn, in Bonn, Germany. Genetic studies have found two mutations that convey particularly increased risk for venous thrombo-embolism, and VTE is also more commonly referred to as deep vein thrombosis. These mutations are called factor five Leiden mutations, or FVL, and the prothrombin 20210G>A mutation we're just going to call F2. Interestingly, the penetrance of these mutations, or how likely they are to exhibit a phenotype, is variable. Some individuals with mutations never experience deep vein thrombosis, while others experience multiple episodes. Cindy St. H:                         As a group, the FVL carriers produce a higher than normal level of an anticoagulation factor called APC, or activated protein c. They also produce high levels of the pro-coagulation factor thrombin, and the authors of this study wondered if it was the balance, or rather perhaps an imbalance, of these factors that could explain the phenotypic variations in the patients that harbor the same mutation. To test this, they collected 58 patients. 30 were FVL and 28 were F2 carriers, and they injected these patients with clotting factors and examined their response rates. In both of the groups, about half of the individuals had no history of deep vein thrombosis, while the other half had had at least one episode. Cindy St. H:                         The team found that while both types of mutations were associated with increased APC and thrombin levels after coagulant injection compared with a control group, in the FVL group lower APC levels correlated with a much higher risk of deep vein thrombosis. In other words, the FVL carriers who had never experienced deep vein thrombosis produced higher levels of APC. Translating this to the clinic, perhaps APC testing could help identify individuals who are carriers of the FVL mutation and determine which of them are at higher risk due to lower levels of APC. Cindy St. H:                         The last paper we're going to highlight before switching to our interview is titled The Human- and Smooth Muscle Cell Enriched lncRNA, SMILR, Promotes Proliferation by Regulating Mitotic CENPF mRNA and Drives Cell Cycle Progression Which Can Be Targeted to Limit Vascular Remodeling. Now that is a crazy title! We’ve got to limit these names here this is difficult. The first authors are Amira Mahmoud and Margaret Ballantyne and the corresponding author is Andrew Baker, and they're all from Queens Medical Research Institute, BHF Center for Cardiovascular Sciences at University of Edinburgh in Edinburgh, UK. Cindy St. H:                         Before we dive into this article, I think it's important that we give a quick explanation of what is a lncRNA? lncRNA, or L-N-C RNA, stands for long non-coding RNA, and these are described as being transcripts which are made into RNA that are in lengths exceeding 200 nucleotides. So that differs them from micro RNAs or peewee RNAs or snRNAs, and they are classically or, I guess originally, considered not to be translated into protein. However, I think now more and more studies are finding that perhaps they are made into peptide sequences. However it's not fully clear what the function of those sequences are. Similar to micro RNAs, they also harbor regulatory functions that can control cellular functions by helping to fine tune the regulation of gene transcription and translation. Cindy St. H:                         Largely speaking, vascular smooth muscle cells are quiescent, but they can be stimulated to proliferate and migrate following injury to the vessel wall. While such activation of smooth muscle cells is essential for wound healing, these same processes are operative in vascular disease or after a cardiovascular procedure. Often what happens is an excess of proliferation of the smooth muscle cell wall can lead to dangerous occlusion of the blood vessel. The long non-coding RNA, SMILR, was recently identified as a promoter of smooth muscle cell proliferation and now in this article, Mahmoud and colleagues have defined its mechanism of action. Through transcriptome analysis of human smooth muscle cells, in which the levels of SMILR were either modulated to be increased or suppressed, the team found that lncRNA regulated expression of several genes involved in mitosis, or cell division. Furthermore, RNA interaction experiments revealed that the messenger RNA encoding the mitotic centromere protein, CENPF, was a direct interaction partner of SMILR. So just like the suppression of SMILR, the inhibition of CENPF resulted in reduced mitosis of the smooth muscle cells. Cindy St. H:                         The team then went on to show the inhibition of SMILR via RNA interference could block the smooth muscle cell proliferation ex-vivo, and they did this using intact sections of human saphenous vein. These results suggest that targeting this lncRNA could be a potential clinical treatment in situations where vessel occlusion is at risk. Cindy St. H:                       Okay, so now we're going to switch and have our interview with Drs Denisa Wagner and Nicoletta Sorvillo, and we're going to discuss their paper entitled Plasma Peptidylarginine Deiminase IV Promotes VWF-Platelet String Formation and Accelerates Thrombosis after Vessel Injury. Thank you Drs. Wagner and Sorvillo for joining us today. I think a funny thing is that between Nicoletta in Switzerland, me and you on the East coast and my producer on the West coast, I think we're spanning about nine hours of time zones here. Thank you all for taking the time, whatever time of day it is, wherever you are. Dr Wagner:                         Thank you. Cindy St. H:                         I was wondering, Denisa, if you could please introduce yourself and tell us a little bit about your background. Dr Wagner:                         I am a vascular biologist. I was always interested in platelets, endothelial cells, and leukocyte. I started with a background of von Willebrand factor research. Von Willebrand factor is the most important adhesion molecule for platelets and it is stored in endothelial cells as we have found very early on, in an organelle called Weibel-Palade bodies. So my work on this paper is actually related to the first observation I ever made scientifically of showing that von Willebrand factor is released from endothelium. Cindy St. H:                         Wow, that's wonderful. And Nicoletta, could you please introduce yourself and tell us a little bit about your background? Nicoletta:                            I'm Italian, I studied in Italy and I did my PhD in the Netherlands, and I've always worked on inflammation and thrombosis during my PhD. One of the major proteins I was working on is ADAMTS13. That is again a protagonist of our paper. Then I moved to Boston, where I had the pleasure to be able to work in Denisa Wagner's lab, and there I continued working on inflammation and ADAMTS13 and now currently I moved here to Bern and I'm bringing my expertise here, but I moved a little bit towards ischemia and reperfusion injury and transplantation. Cindy St. H:                         Interesting. Wow. Denisa, I want to circle back to this factor being one of the first findings that you worked on. How does it feel to still be working on it? Is it still exciting? Dr Wagner:                         It is nice and it's refreshing to come back to it. I did a lot of stuff in between. We did a lot of adhesion molecule work, leukocyte rolling. We made the early knockouts like b-selectin, p-selectin, and von Willebrand factor knockout as well. So it's fun. And by the way, since Nicoletta said that she was Italian, I am originally Czech, from Prague. Cindy St. H:                         Interesting. I did not know that. And actually, Denisa, I don't know if you remember, but when I was a graduate student in Katya Ravid’s lab, we collaborated with you to use some of this intravital imaging on one of our JCI papers. Dr Wagner:                         Oh right, right. I was wondering where I knew your name from. That's funny. Cindy St. H:                         Yes. Yeah, yeah. So it's wonderful to speak to you again. Really I wanted to interview you because I loved this paper, not only because it was a really interesting mechanism that actually I wasn't very well aware of, this citrullination and also because of the beautiful intravital imaging you could do and then link it to patient disease states. Maybe you can start by telling me what's the clinical unmet need or the question that your paper was trying to address? Nicoletta:                            So Denisa Wagner's lab always has worked on neutrophils and NETs and it has been shown that these NETs are involved in thrombosis. So we were curious what happens when even the enzyme that is important to make these NETs, this extracellular DNA, does when it's in the circulation. And this enzyme is of course PAD4 and it is known that it can modify our [inaudible] residues on protein through this process of citrullination. So we went to see if it could modify plasma proteins and as Denisa already said, an important molecule that initiates thrombotic processes is vWF that can be released during inflammation or when there's a damage to the endothelium .  So we went to see what happens if the enzyme that is involved in removing this vWF that is ADAMTS13 happens if it gets modified by this enzyme path. So our question was more like what happens if you have the release of an enzyme that is normally intracellular? What would happen if it gets outside of the cell? Cindy St. H:                         Interesting. So before we get too deep in the weeds, what is citrullinization and why is it important? What do these modifications do? Nicoletta:                            It changes the charge of a protein. It goes and modifies arginine, and it transforms it into citrulline. It changes the charge of a protein and therefore you can imagine if you change a charge of protein it can change even the structure of a protein and if you change the structure then you can change the function. So this is what this modification can do. Cindy St. H:                         And that's what it's doing on the ADAMTS13? It's essentially altering or inhibiting its function? Nicoletta:                            Yes. What we saw is that we can find these citrullinated residues on ADAMTS13 and we identify them by mass spectrometry and then we saw that if it is modified by citrullination, it loses its activity so it doesn't function anymore. Cindy St. H:                         Interesting. Very neat. Could you talk a little bit about the process of where this is happening naturally and where it goes wrong in a diseased state such as either sepsis or aging or just general clotting? Dr Wagner:                         These neutrophil extracellular traps are generated often more during a disease state when there is either an infection or exacerbated inflammation that would be like in sepsis or for example, in a metabolic disorder like diabetes. So there is a lot more of them being generated. Also, for example, in diabetes, PAD4 is elevated inside the neutrophil four-fold. If it's released from diabetic neutrophils , then there would be really a lot more of it. And in aging also, then a NETosis becomes much more prominent. We have done this only with mice, but I believe that it will be also, unfortunately, the case with humans that old mice make a lot more NETs than young mice. Therefore this is relevant to look. Since thrombosis increases both with aging, the incidence of thrombosis, thrombosis increases with a disease like diabetes or in sepsis, you will have micro thrombosis. We thought it would be interesting to study those processes as well, then. Cindy St. H:                         That's really neat. One of the techniques that you utilize heavily in this paper and several of your papers that I'm familiar with is this intravital imaging or intravital microscopy. Just so people can get a sense of what it is you're actually doing, could you maybe describe what that experiment is? Maybe Nicoletta, you could describe that for us? Nicoletta:                            During intravital microscopy, we are able to image in vivo, a vessel in a live mouse. And in this case we use mice and we can label leukocytes and platelets and then look at them in the vessel in vivo and you can then look for a thrombus forming or you can look at the [inaudible 00:23:43] already had leukocyte rolling and you can see what is happening inside the vessel during a proper blood flow and you can damage the vessel in some cases. In our case, in our paper, we do a ferric chloride injury where we damaged the vessel with ferric chloride and therefor you initiate a thrombus development and you can visualize it in vivo and real time. Cindy St. H:                         Excellent. Yes. And hopefully our listeners will look and see the beautiful pictures because those are some serious clots you get forming in the vessels. Yeah. Yeah. And so the other thing that you did was confirming the modification on ADAMTS13, you use mass spectrometry. How difficult was it to confirm that what you thought was happening was happening using that technique? Nicoletta:                            It was very difficult and challenging, I have to say. Dr Wagner:                         See, I would love to hear more about it because you often read, Oh, then we did mass spec and we got this beautiful whatever. Could you tell us a little bit about the struggles? Nicoletta:                            It was quite a struggle. I mean I think trying to identify such a modification that is very, first of all, novel and it changes the math only of one thousandth it's very difficult. To identify you can confuse it with a deiminasion again because of the increase of mass is the same. And another problem was that ADAMTS13, our plasma protein, is low abundance in plasma compared to other plasma proteins like Fibrinogen, that is very, very much abundant. It was a challenge for this reason. So trying to pinpoint out a small, tiny modification already in a protein that is not so abundant in plasma and therefore we have to use this probe, this Biosyn PG program. And we did this in collaboration with Paul Thompson's lab and we were able to then fish out what was modified by the citrullination, but it was very challenging. We tried several different types of techniques that were different types of approaches before being able to show that in vivo. So in human samples we can find this modification. Dr Wagner:                         Nicoletta grew a lot of gray hair during that period. (laughs) Dr Wagner:                         It took us about a year to figure out how we could detect it in vivo because also some antibodies to ADAMTS13 don't work so well. It's a minor protein, but she figured it out. Cindy St. H:                         Wow. That's amazing. Well, congratulations on that. That's excellent. I guess what I'm wondering now is what are the next steps and what might your findings mean in terms of future potential therapeutic options or treatment strategies for different detrimental thrombotic events? Dr Wagner:                         I think what we have really verified that the PAD4 remains active when it circulates in circulation, when the release, and there are several diseases in which PAD4 levels were found to be elevated, like rheumatoid arthritis and what it means in general. That is PAD4 is actually causing havoc. It is citrullinating probably quite indiscriminately. Several proteins may be finding the exposed parts. Maybe it could have some binding sites, but I think it just affects proteins in general and for some of them like, ADAMTS13, this had a very detrimental effect. So in diseases where there is a lot of PAD4, one has to worry about the consequences of citrullinating things and perhaps spot for inhibitors should be used. What do you think, Nicolleta? Nicoletta:                            I totally agree with you. Yes, I totally agree. I mean PAD4 outside the cell could be dangerous, of course. However, we never know if there's something good that it can do that protects by citrullinating proteins so there's so much more to discover about extracellular PAD4 and its effect on the environment. Dr Wagner:                         However, Nicoletta when she wrote a paper at the end she decided to talk about ADAMTS13 as a therapeutic because both she and I, we are convinced that ADAMTS13 it's a possible future therapeutic and it's already given to patients who are lucky in ADAMTS13 and may be given to patients who have thrombotic events in the future, like stroke or myocardial infarction. And these situations are highly pro-inflammatory. Therefore, we would anticipate that in these situations, NETs, and we know NETs are released and therefore, what Nicolleta suggests at the end, is that introducing together with ADAMTS13 an inhibitor of citrullination would be a good thing so that the protein, the ADAMTS13, remains active in circulation. Cindy St. H:                         Wow. So a two-hit strategy. I mean I can think of a handful of potential diseases this would be good for. You know, patients with sickle cell, there's a lot of NETs released then thrombotic events or even stroke. I mean, do you see that this is a potential mechanism that's common to all thrombotic disease or just kind of specific subsets? Nicoletta:                            All is a big word I think, but I think that there are many disorders where together with a thrombotic event, you can find also low levels or low activity of ADAMTS13 and in many of these disorders, nobody knew really why you have a reduction of ADAMTS13 activity, what is happening? Why do you lose this ADAMTS13? What we believe, but of course further studies are needed, is that maybe in these disorders, what is causing the loss of ADAMTS13 is this release of PAD4 because in stroke or in some DIC sepsis, you can find patients or many patients who do have low levels of ADAMTS13 activity and we believe that it's due to maybe citrullination by PAD4. So in that case, I agree with you maybe then that this therapy can be used in different thrombotic events as you suggested. Cindy St. H:                         So what does PAD4 normally do when it's intracellular? What is its, I guess healthy role, in a cell, if it has one? Nicoletta:                            So what is known now is that it really regulates transcription. So that's very important because it citrullinates transcription factors to facilitate transcription. And what Denisa Wagner's lab has identified is that it's extremely important to form these NETs because it citrullinates histone and allows the unraveling of the chromatin and then the NET release. However, it's extremely interesting. We are very interested to understand what else does it do within the cell. Cindy St. H:                         Interesting. That is so neat. I love this story. Dr Sorvillo and Dr Wagner, thank you so much for joining us and congratulations again on a wonderful paper. Dr Wagner:                         Thank you. Nicoletta:                            Thank you for having us and inviting us. Thank you. Cindy St. H:                         So that's it for the highlights from our August issues of Circulation Research. Thank you for listening. This podcast is produced by Rebecca McTavish and edited by Melissa Stoner and supported by the editorial team of Circulation Research. Copy text for the highlighted articles is provided by Ruth Williams. I'm your host, Cindy St Hilaire and this is Discover CircRes, your source for the most up-to-date and exciting discoveries in basic cardiovascular research.  

It’s February — the month of love. People everywhere are rushing through Hallmark stores and florists to get their significant others heartfelt cards, flowers and heart-shaped boxes of chocolates. Although showing your loved ones that you care every day is important — not just on Valentine’s day — perhaps more important is making sure that your own heart is healthy. February is American Heart Month, and we’re proud to partner with the National Heart, Lung and Blood Institute’s (NHLBI) The Heart Truth® program, encouraging people to get more physically active and pledge to #MoveWithHeart. Heart disease is the leading cause of death in the United States, yet it is largely preventable by taking certain steps. On today’s episode, we’re joined by Dr. Jerome Fleg, a medical officer with NHLBI’s Division of Cardiovascular Sciences, discussing simple things you can do during the month of February, and throughout the year, to ensure your heart is healthy. After all, in order to live your best life and love those around you, you have to have a healthy heart. Learn more and find out what you can do to make the pledge to #MoveWithHeart.

John Cooke, chair of the Department of Cardiovascular Sciences at the Houston Methodist Research Institute and the director of the Center for Cardiovascular Regeneration in the Houston Methodist DeBakey Heart and Vascular Center in Houston, Texas is working to use science to rejuvenate aging cells.  More here: http://nationalpost.com/health/scientists-discover-method-to-rejuvenate-aging-human-cells/wcm/14c95c54-7c26-4c3a-8815-d1d8030fe901

Go to audibletrial.com/TUMS for a free 30-day trial membership and free audiobook! Show notes! Dr. Richard Josephson Dr. Josephson is the Medical Director of the Cardiac Intensive Care Unit at University Hospitals Cleveland Medical Center, as well as a Professor of Medicine at Case Western Reserve University School of Medicine in Cleveland, OH. Dr. Josephson received his undergraduate degree from The University of Rochester in 1977; his medial degree from the New York University School of Medicine (where he was also a part of the Medical Scientist Training Program, receiving a master’s of science in Pharmacology); completed his residency in Internal Medicine in 1985 and a fellowship in Cardiology 1988 both at Johns Hopkins Medical Institutions, where he was also a research fellow in the Laboratory of Cardiovascular Sciences at the National Institute on Aging. After his formal training, Dr. Josephson began his career in Akron, Ohio in private practice cardiology and grew what was initially a 4-physician group into a practice encompassing over 30 cardiologists. Over the next two decades, he worked at various Akron City Hospitals, where he assumed roles as varied as Director of Cardiopulmonary Rehabilitation, Director of Non-Invasive Cardiology, and Director of Cardiology Research and Education. He joined the faculty at Case Western and University Hospitals in 2007 where he remains today. Dr. Josephson is heavily involved in cardiovascular research and has been supported by NIH funding for over 30 years. Lastly, Dr. Josephson has received numerous awards, most notable among them having been voted Best Doctors in America every year since 2004. Please enjoy with Dr. Richard Josephson!

Mario Garcia, M.D., introduces keynote speaker Michael Lauer, M.D., director of the Division of Cardiovascular Sciences at NHLBI. Dr. Lauer presents “Science for Policy (or Policy for Science): Comparative Effectiveness Research in the Era of Health Care Reform” at the 2010 “Translating Clinical Research Into Better Health” symposium hosted by the Einstein-Montefiore Institute for Clinical and Translational Research (ICTR). Dr. Garcia is the Pauline Levitt Endowed Chair in Medicine and chief of the division of cardiology, department of medicine and co-director of the Montefiore-Einstein Heart Center. (November 12, 2010)

Mario Garcia, M.D., introduces keynote speaker Michael Lauer, M.D., director of the Division of Cardiovascular Sciences at NHLBI. Dr. Lauer presents “Science for Policy (or Policy for Science): Comparative Effectiveness Research in the Era of Health Care Reform” at the 2010 “Translating Clinical Research Into Better Health” symposium hosted by the Einstein-Montefiore Institute for Clinical and Translational Research (ICTR). Dr. Garcia is the Pauline Levitt Endowed Chair in Medicine and chief of the division of cardiology, department of medicine and co-director of the Montefiore-Einstein Heart Center. (November 12, 2010)