Podcasts about histones

“Now, what we found is that epigenetics is actually heritable and it's actually reversible. And we can now manipulate these principles with pharmacotherapy drugs,” Eric Zack, RN, OCN®, BMTCN®, clinical assistant professor at Loyola College Chicago Marcella Niehoff School of Nursing in Chicago, IL, and RN3 at Rush University Medical Center in Chicago, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about the epigenetics drug class.  Music Credit: “Fireflies and Stardust” by Kevin MacLeod  Licensed under Creative Commons by Attribution 3.0   Earn 0.75 contact hours (including 40 minutes of pharmacotherapeutic content) of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by February 28, 2027. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation.  Learning outcome: Learners will report an increase in knowledge related to the epigenetics drug class.  Episode Notes   Complete this evaluation for free NCPD.  ONS Podcast™ Pharmacology 101 series ONS Voice articles: Financial Navigation During Hematologic Cancer Saves Patients and Caregivers $2,500 Oncology Drug Reference Sheets What Is MCED Testing? ONS book: Clinical Guide to Antineoplastic Therapy: A Chemotherapy Handbook (Fourth Edition) ONS Biomarker Database ONS course: Genomic Foundations for Precision Oncology ONS Huddle Card: Financial Toxicity  ONS Learning Libraries: Genomics and Precision Oncology Oral Anticancer Medication American Cancer Society: Patient Programs and Services Centers for Disease Control and Prevention: Epigenetics, Health, and Disease Leukemia & Lymphoma Society: Financial Support National Institutes of Health: Epigenetics University of Pennsylvania: Epigenetics Institute University of Utah: Genetic Science Learning Center To discuss the information in this episode with other oncology nurses, visit the ONS Communities.   To find resources for creating an ONS Podcast Club in your chapter or nursing community, visit the ONS Podcast Library.  To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org.  Highlights From This Episode  “Epigenetics is influenced by several factors. Right now, there's about seven of them that we've identified, and we can only manipulate right now about two of those seven. So the first one is DNA methylation. When you methylate DNA, that's adding or subtracting a methyl group, which is CH3, chemically. The addition of methyl to DNA tightens the DNA around the chromatin, which then can block some genes from being expressed.” TS 7:21  “Histones basically package DNA into the chromatin, which is a mixture of DNA and proteins, and they spool around this structure like the DNA is coiled around that. And again, it has to do with how tight or loose that is coiled. That determines if the genes are expressed or not. And again, we found that histones also play a role in DNA repair as well as regulating the cell cycle.” TS 8:21  “When we're dealing with the azacitidine and decitabine, these drugs cause pancytopenia. Pancytopenia is neutropenia, thrombocytopenia, and anemia. So it affects the complete blood count. We see GI toxicity, nausea, vomiting, diarrhea, constipation, sometimes mouth sores, and urticaria—hives.” TS 15:34  “It's really, really important to take these drugs exactly as they are prescribed. They have to follow the doctor's orders carefully, which requires taking them properly, doing the proper follow up. There's a lot of blood tests and appointments that we have to do to make sure that everything is okay. And again, because we know when there is nonadherence, the disease progresses and becomes resistant, so that's a really, really important teaching point. We have to monitor the patient for expected side effects and unexpected side effects.” TS 23:58  “Now, we expect the landscape to change dramatically over the next few years. And again, it's just an explosion of science information. As we learn more about the science, it's going to translate into practice. We're always identifying new biomarkers. These biomarkers are essentially DNA mutations or variations. There's so many variants of unknown significance.” TS 30:02  “Every patient deserves biomarker testing. Very important, whether it's through IHC, polymerase chain reactions, or the most common next-gen sequencing. Again, there's several companies out there that have standard kits available.” TS 31:33  “This is a precision medicine. This is what we've always dreamed about—tailoring the treatment to the specific patient. We've gone away from treating standard diseases, like lung cancer and breast cancer, the way they're supposed to be treated to now looking at these biomarkers and using epigenetic drugs and other medications tailored to those variants that that patient is having, not necessarily based on their disease type.” TS 33:59   

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body, but how do these cells know what to do? Researchers at UC San Diego and Hebrew University of Jerusalem share an intercontinental effort working to determine just that. Alon Goren and Itamar Simon discuss some of the work they are doing to learn more about the human body beyond the cellular level. [Health and Medicine] [Science] [Show ID: 40516]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body, but how do these cells know what to do? Researchers at UC San Diego and Hebrew University of Jerusalem share an intercontinental effort working to determine just that. Alon Goren and Itamar Simon discuss some of the work they are doing to learn more about the human body beyond the cellular level. [Health and Medicine] [Science] [Show ID: 40516]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body, but how do these cells know what to do? Researchers at UC San Diego and Hebrew University of Jerusalem share an intercontinental effort working to determine just that. Alon Goren and Itamar Simon discuss some of the work they are doing to learn more about the human body beyond the cellular level. [Health and Medicine] [Science] [Show ID: 40516]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body, but how do these cells know what to do? Researchers at UC San Diego and Hebrew University of Jerusalem share an intercontinental effort working to determine just that. Alon Goren and Itamar Simon discuss some of the work they are doing to learn more about the human body beyond the cellular level. [Health and Medicine] [Science] [Show ID: 40516]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body, but how do these cells know what to do? Researchers at UC San Diego and Hebrew University of Jerusalem share an intercontinental effort working to determine just that. Alon Goren and Itamar Simon discuss some of the work they are doing to learn more about the human body beyond the cellular level. [Health and Medicine] [Science] [Show ID: 40516]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body, but how do these cells know what to do? Researchers at UC San Diego and Hebrew University of Jerusalem share an intercontinental effort working to determine just that. Alon Goren and Itamar Simon discuss some of the work they are doing to learn more about the human body beyond the cellular level. [Health and Medicine] [Science] [Show ID: 40516]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body, but how do these cells know what to do? Researchers at UC San Diego and Hebrew University of Jerusalem share an intercontinental effort working to determine just that. Alon Goren and Itamar Simon discuss some of the work they are doing to learn more about the human body beyond the cellular level. [Health and Medicine] [Science] [Show ID: 40516]

rWotD Episode 2770: HIST1H2AE Welcome to Random Wiki of the Day, your journey through Wikipedia’s vast and varied content, one random article at a time.The random article for Tuesday, 3 December 2024 is HIST1H2AE.Histone H2A type 1-B/E is a protein that in humans is encoded by the HIST1H2AE gene.Histones are basic nuclear proteins that are responsible for the nucleosome structure of the chromosomal fiber in eukaryotes. Nucleosomes consist of approximately 146 bp of DNA wrapped around a histone octamer composed of pairs of each of the four core histones (H2A, H2B, H3, and H4). The chromatin fiber is further compacted through the interaction of a linker histone, H1, with the DNA between the nucleosomes to form higher order chromatin structures. This gene is intronless and encodes a member of the histone H2A family. Transcripts from this gene lack polyA tails; instead, they contain a palindromic termination element. This gene is found in the large histone gene cluster on chromosome 6p22-p21.3.This recording reflects the Wikipedia text as of 00:57 UTC on Tuesday, 3 December 2024.For the full current version of the article, see HIST1H2AE on Wikipedia.This podcast uses content from Wikipedia under the Creative Commons Attribution-ShareAlike License.Visit our archives at wikioftheday.com and subscribe to stay updated on new episodes.Follow us on Mastodon at @wikioftheday@masto.ai.Also check out Curmudgeon's Corner, a current events podcast.Until next time, I'm neural Amy.

In this conversation, Stephen Thomas and Richard Smith discuss the concept of epigenetics, sharing his personal journey from obesity and health issues to becoming a professional bodybuilder. He explains the difference between genetics and epigenetics, emphasising how lifestyle and diet can influence gene expression. The discussion delves into the science of DNA, protein synthesis, and the role of histones and enzymes in gene expression. Richard also critiques common dietary recommendations, particularly focusing on cruciferous vegetables and their potential negative effects on health due to compounds like isothiocyanates and oxalates. He highlights the importance of understanding these concepts for better health management. In this conversation, they discuss the impact of various foods on health, particularly focusing on the dangers of certain commonly consumed items like fruits and vegetables that may contain harmful compounds. They emphasise the importance of understanding epigenetics and how nutrition can influence DNA expression. The discussion also covers the concept of weight set points, the role of a ketogenic and carnivore diet in health, and the implications of dietary choices on cancer treatment. Stephen advocates for a diet rich in animal products while cautioning against the long-term consumption of certain plant-based foods. Chapters 00:00 Introduction to Epigenetics 02:52 Personal Journey and Transformation 06:00 Understanding Genetics vs. Epigenetics 08:53 The Science of DNA and Protein Synthesis 11:46 The Role of Histones and Enzymes 15:05 Diet, Lifestyle, and Epigenetic Expression 17:56 The Dark Side of Cruciferous Vegetables 21:11 The Impact of Oxalates and Flavonoids 24:04 Cyanogenic Compounds and Their Risks 26:54 Conclusion and Final Thoughts 33:19 The Dangers of Common Foods 39:25 Understanding Epigenetics and DNA Expression 43:45 The Role of Nutrition in Health 45:03 Weight Set Points and Body Composition 54:01 Short-Term vs Long-Term Dietary Choices 01:00:57 Cancer Treatments and Dietary Implications

In this episode, Dr. Jess Steier and Dr. Sarah Scheinman explore the fascinating field of epigenetics, which examines how external factors influence gene expression and impact health outcomes. They discuss the interplay between nature and nurture, explaining how epigenetics involves information layered on top of DNA that affects gene operation. The scientists cover key mechanisms like DNA methylation and histone modifications, and how factors such as nutrition and stress can impact these processes. They highlight landmark studies, including research on agouti mice and the Dutch Famine Birth Cohort Study, which demonstrate the long-term effects of environmental factors on gene expression and disease risk. The conversation also touches on the implications of epigenetics for mental health and the potential for future advancements in personalized medicine. Throughout the episode, Dr. Steier and Dr. Scheinman emphasize the complex relationship between genetics and environment in shaping human development and health. All our sources from this episode are available at: https://www.unbiasedscipod.com/episodes/ (00:00) Introduction  (02:27) Understanding Genetics and the Human Genome (06:23) Epigenetics: Layered Information on Top of DNA (10:19) Explaining Methylation and Histones (16:20) External and Internal Regulation of Epigenetic Modifications (18:43) Transgenerational Epigenetic Inheritance (21:21) Landmark Studies in Epigenetics: Agouti Mice (23:35) Environmental Influence on Epigenetic Markers in Twins (26:07) Prenatal Exposure to Famine and DNA Methylation (28:36) The Effects of Space Travel on Epigenetic Markers (30:52) Epigenetics and Mental Health (36:25) Final Thoughts: Future Advancements in Manipulating Epigenetic Changes Interested in advertising with us? Please reach out to advertising@airwavemedia.com, with “Unbiased Science” in the subject line. PLEASE NOTE: The discussion and information provided in this podcast are for general educational, scientific, and informational purposes only and are not intended as, and should not be treated as, medical or other professional advice for any particular individual or individuals. Every person and medical issue is different, and diagnosis and treatment requires consideration of specific facts often unique to the individual. As such, the information contained in this podcast should not be used as a substitute for consultation with and/or treatment by a doctor or other medical professional. If you are experiencing any medical issue or have any medical concern, you should consult with a doctor or other medical professional. Further, due to the inherent limitations of a podcast such as this as well as ongoing scientific developments, we do not guarantee the completeness or accuracy of the information or analysis provided in this podcast, although, of course we always endeavor to provide comprehensive information and analysis. In no event may Unbiased Science or any of the participants in this podcast be held liable to the listener or anyone else for any decision allegedly made or action allegedly taken or not taken allegedly in reliance on the discussion or information in this podcast or for any damages allegedly resulting from such reliance. The information provided herein do not represent the views of our employers. Learn more about your ad choices. Visit megaphone.fm/adchoices

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body. From the skin to the brain, muscles to blood, and everything in between, these countless cells collaborate harmoniously to keep us alive and well, but how do these cells know what to do? When a cell divides, how does it know that it's exact counterpart should do the same thing as the original. Researchers at the Goren Lab at UC San Diego are working to determine just that. They discuss some of the work they are doing to learn more about the human body beyond the cellular level [Health and Medicine] [Science] [Show ID: 38259]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body. From the skin to the brain, muscles to blood, and everything in between, these countless cells collaborate harmoniously to keep us alive and well, but how do these cells know what to do? When a cell divides, how does it know that it's exact counterpart should do the same thing as the original. Researchers at the Goren Lab at UC San Diego are working to determine just that. They discuss some of the work they are doing to learn more about the human body beyond the cellular level [Health and Medicine] [Science] [Show ID: 38259]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body. From the skin to the brain, muscles to blood, and everything in between, these countless cells collaborate harmoniously to keep us alive and well, but how do these cells know what to do? When a cell divides, how does it know that it's exact counterpart should do the same thing as the original. Researchers at the Goren Lab at UC San Diego are working to determine just that. They discuss some of the work they are doing to learn more about the human body beyond the cellular level [Health and Medicine] [Science] [Show ID: 38259]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body. From the skin to the brain, muscles to blood, and everything in between, these countless cells collaborate harmoniously to keep us alive and well, but how do these cells know what to do? When a cell divides, how does it know that it's exact counterpart should do the same thing as the original. Researchers at the Goren Lab at UC San Diego are working to determine just that. They discuss some of the work they are doing to learn more about the human body beyond the cellular level [Health and Medicine] [Science] [Show ID: 38259]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body. From the skin to the brain, muscles to blood, and everything in between, these countless cells collaborate harmoniously to keep us alive and well, but how do these cells know what to do? When a cell divides, how does it know that it's exact counterpart should do the same thing as the original. Researchers at the Goren Lab at UC San Diego are working to determine just that. They discuss some of the work they are doing to learn more about the human body beyond the cellular level [Health and Medicine] [Science] [Show ID: 38259]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body. From the skin to the brain, muscles to blood, and everything in between, these countless cells collaborate harmoniously to keep us alive and well, but how do these cells know what to do? When a cell divides, how does it know that it's exact counterpart should do the same thing as the original. Researchers at the Goren Lab at UC San Diego are working to determine just that. They discuss some of the work they are doing to learn more about the human body beyond the cellular level [Health and Medicine] [Science] [Show ID: 38259]

The human body is made up of billions of cells. These cells are the basic building blocks of life, and they work together to form tissues, organs, and systems that enable our body to function and carry out various activities. Each cell has its own specific function and role in maintaining the overall health and functionality of the body. From the skin to the brain, muscles to blood, and everything in between, these countless cells collaborate harmoniously to keep us alive and well, but how do these cells know what to do? When a cell divides, how does it know that it's exact counterpart should do the same thing as the original. Researchers at the Goren Lab at UC San Diego are working to determine just that. They discuss some of the work they are doing to learn more about the human body beyond the cellular level [Health and Medicine] [Science] [Show ID: 38259]

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.02.547417v1?rss=1 Authors: Kato-Inui, T., Ono, T., Miyaoka, Y. Abstract: As a versatile genome editing tool, the CRISPR-Cas9 system induces DNA double-strand breaks at targeted sites to activate mainly two DNA repair pathways: HDR which allows precise editing via recombination with a homologous template DNA, and NHEJ which connects two ends of the broken DNA, which is often accompanied by random insertions and deletions. Therefore, how to enhance HDR while suppressing NHEJ is a key to successful applications that require precise genome editing. Histones are small proteins with a lot of basic amino acids that generate electrostatic affinity to DNA. Since H2A.X is involved in DNA repair processes, we fused H2A.X to Cas9 and found that this fusion protein could improve the HDR/NHEJ ratio. As various post-translational modifications of H2A.X play roles in the regulation of DNA repair, we also fused H2A.X mimicry variants to replicate these post-translational modifications including phosphorylation, methylation, and acetylation. However, none of them were effective to improve the HDR/NHEJ ratio. We further fused other histone variants to Cas9 and found that H2A.1 exhibited the improved HDR/NHEJ ratio better than H2A.X. Thus, the fusion of histone variants to Cas9 is a promising option to enhance precise genome editing. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Eukaryotic cells manage to pull off a number of remarkable feats. One is packing quite a long DNA molecule, with potentially billions of base pairs, into a tiny central nucleus. A key role is played by histones, proteins that provide scaffolding for DNA to wrap around. Histones also appear in archaea (one of the other domains of life), but until recently there wasn't evidence for them in bacteria (the final of the three domains). Todays guest, Tobias Warnecke, is an author on a recent paper that claims to provide such evidence. We discuss this new result, as well as background questions of how cells evolved and what their current structure can teach us about their histories.Support Mindscape on Patreon.Tobias Warnecke received his Ph.D. in biology from the University of Bath. He is currently a Programme Leader and MRC Investigator at the London Institute of Medical Sciences. He is a co-author on A. Hochner et al. (2023), "Histone-Organized Chromatin in Bacteria."Web pageLab web siteGoogle Scholar publicationsTwitterSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Episode 130: Epigenetics in childhood obesitySaakshi and Dr. Arreaza discuss some principles of epigenetics implicated in the development of obesity in children. Written by Saakshi Dulani, MS3, Western University College of Osteopathic Medicine of the Pacific. Edited by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.This topic is constantly expanding, and I'm excited to talk about it. It is a fact that epigenetic changes play a role in the development of certain diseases such as Prader-Willi syndrome, Fragile X syndrome, and various cancers. It has been demonstrated that certain foods can alter gene expression in animals, for example. What is epigenetics?Epigenetics is the regulation of gene expression without a change in the base sequence of DNA. Epigenetics means “on top of” the genes. Genes can be turned “on” or “off” as a response to external influences. Obesity and Epigenetics.The link between genetics and obesity is complex, but it is known that epigenetics plays a significant role in childhood obesity. Surprisingly, exposure to environmental factors starts in the uterus. Fetuses are exposed to intrauterine signals that increase their potential to develop obesity. Factors such as in-utero hyperglycemia, gestational diabetes mellitus, and early childhood diet and lifestyle practices can affect the development of the gut microbiome, modify gene expression through DNA methylation, and increase the risk of childhood obesity. These gene expression changes can be passed on to future generations. DNA methylation is the addition of a methyl group to part of the DNA molecule. That methyl group acts as a “chemical cap,” which prevents gene expression. Another example of epigenetics is histone modification. Histones are proteins that are used by DNA as spools to wrap around pieces of information that are “not needed”. The reason why a scalp cell and a neuron are different is that the expression of certain genes is suppressed while other genes are expressed.Factors that influence obesity.Some factors that increase the risk of childhood obesity through epigenetic changes include neonatal intestinal microbiome, C-section delivery, maternal insulin resistance, exposure to antibiotics and other environmental toxins, early introduction of complementary foods, parental diets high in carbohydrates and low in fruits and vegetables, and poor sleep. There are many other factors, but we will discuss only a few of them.Microbiome:The microbiome is a whole new world that is being explored by many investigators. The gut microbiome refers to the diverse community of organisms, including bacteria, fungi, and viruses, that reside in the human intestine. The neonatal intestinal microbiome is established during the first two years of life and may be influenced by factors such as the method of delivery, maternal obesity, and the maternal gut microbiome. Some bacteria worth mentioning are Bacteroides, Clostridium, and Staphylococcus. These gut bacteria are higher in pregnant women who have obesity, and they also have a low count of Bifidobacterium. Infants born to obese mothers have higher levels of bacteria associated with increased energy harvest compared to infants born to normal-weight mothers. The gut microbiome of infants delivered by C-section is different than infants delivered vaginally.Link to antibiotics:Early exposure to antibiotics is associated with the development of resistance in microorganisms. The intestinal microbiota exposed to antibiotics also shows reduced diversity. Antibiotics can decrease the number of mitochondria and impair their function, which is important in maintaining energy metabolism. Evidence suggests that some antibiotics can cause mutations in the mitochondrial genome, and they have a direct effect on the microbiome and influence metabolism. There is a strong association between early-life antibiotic exposure and childhood adiposity, with a strong dose-response relationship. A stronger association has been seen with exposure to broad-spectrum antibiotics and macrolides. Maternal insulin resistance (IR):Insulin resistance means that the mother needs levels of insulin that are higher than normal to stay normoglycemic. It means the insulin receptors are “exhausted” and do not respond to normal levels of insulin. Insulin does NOT cross the blood-placenta barrier, but glucose and other nutrients do. This causes the fetus to have an abundance of glucose that stimulates the secretion of high levels of insulin by the fetal pancreas to stay normoglycemic. The combination of insulin + glucose is the perfect combination for anabolism, adipocyte hyperplasia, and fetal growth. That explains why mothers with insulin resistance deliver larger babies (macrosomia). Maternal insulin resistance is a predictor of infant weight gain and body fat in the first year of life. This is not influenced by the mother's BMI before pregnancy. Maternal insulin resistance causes alterations in gene regulation for lipids, amino acids, and inflammation, leading to long-term health implications for both the mother and future pregnancies.C-section and obesity:C-section delivery is a saving procedure for many obstetrical emergencies. C-sections have improved the survival of larger infants and their mothers. C-sections are more frequent among populations with obesity and sedentary lifestyles. This method of delivery is also strongly associated with childhood obesity. Among many other reasons, whenever a vaginal delivery is feasible, a vaginal delivery is preferred over a c-section.   In summary, we discussed 4 factors that may influence childhood obesity: the newborn microbiome, exposure to antibiotics, maternal insulin resistance, and C-sections. There are many other factors that we did not talk about, but the more we know about genetics, epigenetics, and metabolism, the closer we get to a better understanding of obesity._____________________Conclusion: Now we conclude our episode number 130, “Epigenetics in childhood obesity.” Saakshi discussed with Dr. Arreaza that the in-utero environment can alter gene expression and increase the risk of obesity in children. Some factors, such as maternal insulin resistance and changes in gut microbiome, can be the cause of obesity in some children. This week we thank Hector Arreaza and Saakshi Dulani. Audio editing by Adrianne Silva.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________Sources:Burdge GC, Hoile SP, Uller T, Thomas NA, Gluckman PD, Hanson MA, Lillycrop KA. Progressive, transgenerational changes in offspring phenotype and epigenotype following nutritional transition. PLoS One. 2011;6(11):e28282. doi: 10.1371/journal.pone.0028282. Epub 2011 Nov 30. PMID: 22140567; PMCID: PMC3227644. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3227644/Rachael Rettner, Epigenetics: Definition & Examples, Live Science, published on June 24, 2013, available at: https://www.livescience.com/37703-epigenetics.htmlMulligan CM, Friedman JE. Maternal modifiers of the infant gut microbiota: metabolic consequences. J Endocrinol. 2017;235: R1-R12.Aghaali, M. and S. S. Hashemi-Nazari (2019). “Association between early antibiotic exposure and risk of childhood weight gain and obesity: a systematic review and meta-analysis.” J Pediatr Endocrinol Metab 32(5): 439-445.Yuan C, Gaskins AJ, Blaine AI, et al. Association between cesarean birth and risk of obesity in offspring in childhood, adolescence, and early adulthood. JAMA Pediatr. 2016;170(11):e162385. doi: 10.1001/jamapediatrics.2016.2385.Royalty-free music used for this episode: “Gushito - Burn Flow." Downloaded on October 13, 2022, from https://www.videvo.net/

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: What is epigenetics?, published by Metacelsus on November 6, 2022 on LessWrong. Among all areas of biology related to my research, epigenetics is the one that is most commonly misunderstood, not only by the general public but even by other scientists. After being irritated one too many times, I've decided to make a series of posts to explain what epigenetics really is, why it's important, and how it's misunderstood. I will also explain how epigenetics is important for my own research on making gametes from stem cells. This first post covers the definition of epigenetics, and the basic biology of epigenetic marks. What is genetics? Before defining epigenetics, let's start with a definition of genetics. Genetics is the study of genes, which are sequences of genetic material that encode functional products. Let's take the IGF2 gene as an example. Depicted above is a region of human chromosome 11 containing the IGF2 gene, which encodes the IGF2 protein, an important growth factor for fetal development. The boxes represent exons and lines represent introns. The darker green color is the protein-coding sequence, and non-coding (i.e. untranslated) regions are shown in lighter green. Arrows represent the direction of transcription. The bottom of this image shows the location of common genetic variants (present at >1% frequency). If you look closely, you might notice that none of them are in the protein-coding sequence (the dark green boxes). This is not a coincidence, because nothing is ever a coincidence most mutations to essential proteins (including IGF2) are harmful and thus selected out of the population. However, there are several common mutations in non-coding regions of this gene. To recap, genetics is the study of genes (such as IGF2) and the effects of genetic variation on their functions. What is epigenetics? Epigenetics is the study of epigenetic marks, which are changes to genetic material that alter gene expression, but do not change the genetic sequence. A decent analogy for epigenetic marks is CAPITALIZATION, bolding, or strikethroughs in text. DNA methylation and histone modifications are the two kinds of epigenetic marks. Some people also consider long noncoding RNAs (such as those involved in X-chromosome inactivation) to be epigenetic marks. Although these RNAs are undoubtedly important for regulating gene expression, I would not classify them as epigenetic marks since they are not direct modifications to genetic material. In vertebrate animals, the cytosine in CG sequences often has a methyl group attached, forming 5-methylcytosine. A CG sequence is also CG on the opposite strand, so the cytosines on both strands can be methylated. To make things confusing, methylation at CG sequences is termed CpG methylation, the lowercase p standing for phosphate. 5-methylcytosine will pair with guanine just like normal cytosine, but it is not equivalent to cytosine in its interactions with DNA-binding proteins. Generally, CpG methylation suppresses the expression of nearby genes. CpG sites often cluster together to form “CpG islands” in important regulatory regions. Other organisms (invertebrates, plants, fungi, bacteria) have different ways of methylating DNA. I won't get into them in this post series, but you should know that CpG methylation is not universal. Modifications to histones are another important set of epigenetic marks. Histones are DNA packaging proteins, which form complexes called nucleosomes. DNA winds around nucleosomes sort of like thread around spools. The overall assembly of DNA and histones is known as chromatin. Chemical modifications to histones are important epigenetic marks that can have drastic changes on gene expression. For example, trimethylation of lysine 4 on histone H3 (known as H3K4me3) marks promoters of actively transcribed genes. ...

Link to original articleWelcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: What is epigenetics?, published by Metacelsus on November 6, 2022 on LessWrong. Among all areas of biology related to my research, epigenetics is the one that is most commonly misunderstood, not only by the general public but even by other scientists. After being irritated one too many times, I've decided to make a series of posts to explain what epigenetics really is, why it's important, and how it's misunderstood. I will also explain how epigenetics is important for my own research on making gametes from stem cells. This first post covers the definition of epigenetics, and the basic biology of epigenetic marks. What is genetics? Before defining epigenetics, let's start with a definition of genetics. Genetics is the study of genes, which are sequences of genetic material that encode functional products. Let's take the IGF2 gene as an example. Depicted above is a region of human chromosome 11 containing the IGF2 gene, which encodes the IGF2 protein, an important growth factor for fetal development. The boxes represent exons and lines represent introns. The darker green color is the protein-coding sequence, and non-coding (i.e. untranslated) regions are shown in lighter green. Arrows represent the direction of transcription. The bottom of this image shows the location of common genetic variants (present at >1% frequency). If you look closely, you might notice that none of them are in the protein-coding sequence (the dark green boxes). This is not a coincidence, because nothing is ever a coincidence most mutations to essential proteins (including IGF2) are harmful and thus selected out of the population. However, there are several common mutations in non-coding regions of this gene. To recap, genetics is the study of genes (such as IGF2) and the effects of genetic variation on their functions. What is epigenetics? Epigenetics is the study of epigenetic marks, which are changes to genetic material that alter gene expression, but do not change the genetic sequence. A decent analogy for epigenetic marks is CAPITALIZATION, bolding, or strikethroughs in text. DNA methylation and histone modifications are the two kinds of epigenetic marks. Some people also consider long noncoding RNAs (such as those involved in X-chromosome inactivation) to be epigenetic marks. Although these RNAs are undoubtedly important for regulating gene expression, I would not classify them as epigenetic marks since they are not direct modifications to genetic material. In vertebrate animals, the cytosine in CG sequences often has a methyl group attached, forming 5-methylcytosine. A CG sequence is also CG on the opposite strand, so the cytosines on both strands can be methylated. To make things confusing, methylation at CG sequences is termed CpG methylation, the lowercase p standing for phosphate. 5-methylcytosine will pair with guanine just like normal cytosine, but it is not equivalent to cytosine in its interactions with DNA-binding proteins. Generally, CpG methylation suppresses the expression of nearby genes. CpG sites often cluster together to form “CpG islands” in important regulatory regions. Other organisms (invertebrates, plants, fungi, bacteria) have different ways of methylating DNA. I won't get into them in this post series, but you should know that CpG methylation is not universal. Modifications to histones are another important set of epigenetic marks. Histones are DNA packaging proteins, which form complexes called nucleosomes. DNA winds around nucleosomes sort of like thread around spools. The overall assembly of DNA and histones is known as chromatin. Chemical modifications to histones are important epigenetic marks that can have drastic changes on gene expression. For example, trimethylation of lysine 4 on histone H3 (known as H3K4me3) marks promoters of actively transcribed genes. ...

Listen to a blog summary of a recently published research paper in Volume 13 of Oncotarget, entitled, "HDAC inhibitors suppress protein poly(ADP-ribosyl)ation and DNA repair protein levels and phosphorylation status in hematologic cancer cells: implications for their use in combination with PARP inhibitors and chemotherapeutic drugs." _______________________________________ Chromatin constitutes chromosomes in eukaryotic cells and comprises DNA and proteins. Chromosomes produce proteins and enzymes that are essential for cellular function and maintenance, including DNA repair. A critical process for DNA repair is poly(ADP-ribosyl)ation, or PARylation. PARylation is triggered by poly(ADP ribose) polymerase (PARP) enzymes. When DNA becomes damaged, PARP enzymes bind to the damaged location in the cell. In cancer cells, however, this natural process can be counterproductive in respect to cancer treatment. PARylation can produce DNA repair mechanisms in cancer cells that can lead to the evasion of cell death, and even drug resistance. Inhibiting PARylation may be a viable therapeutic strategy for cancer treatment. Histones, the main proteins that constitute chromatin, undergo post-translational modifications that regulate gene expression. Histone acetylation is an important epigenetic process that affects gene expression by relaxing the chromatin structure, making chromatin remodeling more feasible. Histone deacetylases (HDACs) are enzymes that can have the opposite effect. Histone deacetylation makes the chromatin more compact and difficult to remodel. The overexpression of HDAC has also been associated with tumorigenesis. Histone deacetylase inhibitors (HDACi) are a class of therapeutics that have shown promise in the treatment of hematologic malignancies (blood cancer) and solid tumors. In a new study, researchers Benigno C. Valdez, Yago Nieto, Bin Yuan, David Murray, and Borje S. Andersson from the Department of Stem Cell Transplantation and Cellular Therapy at the University of Texas MD Anderson Cancer Center and the Cross Cancer Institute's Department of Experimental Oncology at the University of Alberta investigate the efficacy of HDACi in combination with PARP inhibitors (PARPi) and chemotherapeutic drugs to treat hematologic cancer. On October 14, 2022, their research paper was published in Volume 13 of Oncotarget, entitled, “HDAC inhibitors suppress protein poly(ADP-ribosyl)ation and DNA repair protein levels and phosphorylation status in hematologic cancer cells: implications for their use in combination with PARP inhibitors and chemotherapeutic drugs.” Full blog - https://www.oncotarget.org/2022/10/19/synergy-of-hdaci-parpi-and-chemotherapeutics-against-blood-cancer/ DOI - https://doi.org/10.18632/oncotarget.28278 Correspondence to - Benigno C. Valdez - bvaldez@mdanderson.org Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28278 Keywords - poly(ADP-ribosyl)ation, HDAC inhibitors, PARP inhibitors, chemotherapy, hematologic malignancy About Oncotarget Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ Twitter - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/OncotargetYouTube LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

In this episode of the Epigenetics Podcast, we caught up with Yael David from Memorial Sloan Kettering Cancer Center in New York to talk about her work on Effects of Non-Enzymatic Covalent Histone Modifications on Chromatin.  The David lab studies on non-enzymatic covalent modifications of Histones, including Histone glycation and citrullination. These modifications recognize metabolites that are produced in the cell and aid as a sensor for chromatin to quickly adapt to cellular changes. These unique modifications do not have a so-called erasing enzyme, which makes them terminal, rendering these sites inaccessible for further modifications such as methylation or acetylation.   A second area of research in the David lab is Histone H1. The lab has developed a new method to purify Histone H1, superior to the commonly used method of acid extraction which leads to degradation of Histone H1. This purification method enabled the lab to purify and characterize the functional properties of all Histone H1 variants.    References David, Y., Vila-Perelló, M., Verma, S., & Muir, T. W. (2015). Chemical tagging and customizing of cellular chromatin states using ultrafast trans -splicing inteins. Nature Chemistry, 7(5), 394–402. https://doi.org/10.1038/nchem.2224 David, Y., & Muir, T. W. (2017). Emerging Chemistry Strategies for Engineering Native Chromatin. Journal of the American Chemical Society, 139(27), 9090–9096. https://doi.org/10.1021/jacs.7b03430 Osunsade, A., Prescott, N. A., Hebert, J. M., Ray, D. M., Jmeian, Y., Lorenz, I. C., & David, Y. (2019). A Robust Method for the Purification and Characterization of Recombinant Human Histone H1 Variants. Biochemistry, 58(3), 171–176. https://doi.org/10.1021/acs.biochem.8b01060 Zheng, Q., Omans, N. D., Leicher, R., Osunsade, A., Agustinus, A. S., Finkin-Groner, E., D'Ambrosio, H., Liu, B., Chandarlapaty, S., Liu, S., & David, Y. (2019). Reversible histone glycation is associated with disease-related changes in chromatin architecture. Nature Communications, 10(1), 1289. https://doi.org/10.1038/s41467-019-09192-z Zheng, Q., Osunsade, A., & David, Y. (2020). Protein arginine deiminase 4 antagonizes methylglyoxal-induced histone glycation. Nature Communications, 11(1), 3241. https://doi.org/10.1038/s41467-020-17066-y   Related Episodes Synthetic Chromatin Epigenetics (Karmella Haynes) Variants of Core Histones: Modulators of Chromatin Structure and Function (Sandra Hake) Influence of Histone Variants on Chromatin Structure and Metabolism (Marcus Buschbeck)   Contact Active Motif on Twitter Epigenetics Podcast on Twitter Active Motif on LinkedIn Active Motif on Facebook Email: podcast@activemotif.com

In this episode of the Epigenetics Podcast, we caught up with Sandra Hake from the Justus Liebig University in Giessen to talk about her work on variants of core histones and their role as modulators of chromatin structure and function. The overarching goal of Sandra Hake's research group is to understand how changes in chromatin structure and composition can influence various DNA-based processes, such as gene expression, repair of DNA damage, cell cycle progression, and genome stability. Their work deals with the study of histone variants which, together with DNA, represent the building blocks of the smallest chromatin components, the nucleosomes. They also investigate whether mutations and/or post-translational histone modifications and the deregulation of histone variant networks influence the emergence of diseases, especially the emergence of tumors. In this episode we discuss how Sandra Hake approaches the characterization and identification of novel histone variants like H3.3, H3.X and H3.Y, what it's like to work in such a small field like histone variants, and what is coming up next for the Hake lab.   References Hake, S. B., Garcia, B. A., Duncan, E. M., Kauer, M., Dellaire, G., Shabanowitz, J., Bazett-Jones, D. P., Allis, C. D., & Hunt, D. F. (2006). Expression Patterns and Post-translational Modifications Associated with Mammalian Histone H3 Variants. Journal of Biological Chemistry, 281(1), 559–568. https://doi.org/10.1074/jbc.M509266200 Wiedemann, S. M., Mildner, S. N., Bönisch, C., Israel, L., Maiser, A., Matheisl, S., Straub, T., Merkl, R., Leonhardt, H., Kremmer, E., Schermelleh, L., & Hake, S. B. (2010). Identification and characterization of two novel primate-specific histone H3 variants, H3.X and H3.Y. Journal of Cell Biology, 190(5), 777–791. https://doi.org/10.1083/jcb.201002043 Bönisch, C., Schneider, K., Pünzeler, S., Wiedemann, S. M., Bielmeier, C., Bocola, M., Eberl, H. C., Kuegel, W., Neumann, J., Kremmer, E., Leonhardt, H., Mann, M., Michaelis, J., Schermelleh, L., & Hake, S. B. (2012). H2A.Z.2.2 is an alternatively spliced histone H2A.Z variant that causes severe nucleosome destabilization. Nucleic Acids Research, 40(13), 5951–5964. https://doi.org/10.1093/nar/gks267 Link, S., Spitzer, R. M. M., Sana, M., Torrado, M., Völker-Albert, M. C., Keilhauer, E. C., Burgold, T., Pünzeler, S., Low, J. K. K., Lindström, I., Nist, A., Regnard, C., Stiewe, T., Hendrich, B., Imhof, A., Mann, M., Mackay, J. P., Bartkuhn, M., & Hake, S. B. (2018). PWWP2A binds distinct chromatin moieties and interacts with an MTA1-specific core NuRD complex. Nature Communications, 9(1), 4300. https://doi.org/10.1038/s41467-018-06665-5   Related Episodes Regulation of Chromatin Organization by Histone Chaperones (Geneviève Almouzni) Influence of Histone Variants on Chromatin Structure and Metabolism (Marcus Buschbeck) Chromatin Analysis using Mass Spectrometry (Axel Imhof)   Contact Active Motif on Twitter Epigenetics Podcast on Twitter Active Motif on LinkedIn Active Motif on Facebook Email: podcast@activemotif.com

#therichsolution #epigenetics #empoweredhealthJoin Gwen Rich for another episode on mojo50.com @ 10:00am CT. As your health advocate she will speak on the topic of "Epigenetics: Can Your Decisions Affect Your Health, Your Families & Generations To Come?”. Epigenetics is an emerging field of science that, eventually, could have massive implications on how we address our health and that of future generations. Listen at 10:00am CT on:www.mojo50.comiHeart RadioiTunesAppleLive streaming via: YouTube and Facebook:https://www.facebook.com/Therichsolution/https://www.youtube.com/c/therichsolution

Princeton University Anthropology Professor Agustín Fuentes explains why race is a social construct — as in, biological race isn’t real. Then, learn how plants pass down “bad” memories to their offspring through epigenetics.  Additional resources from Agustín Fuentes:  Pick up "Why We Believe: Evolution and the Human Way of Being" from Amazon: https://amzn.to/361ug6j  Pick up "The Creative Spark: How Imagination Made Humans Exceptional" from Amazon: https://amzn.to/3qNgWdI  Agustín Fuentes's website: https://afuentes.com/  Agustín Fuentes on Twitter: https://twitter.com/Anthrofuentes  Plants pass down "bad" memories to their offspring, which can inhibit growth by Grant Currin Chemical memory in plants affects chances of offspring survival. (2020). Warwick.Ac.Uk. https://warwick.ac.uk/newsandevents/pressreleases/chemical_memory_in  Antunez-Sanchez, J., et. al. (2020, October 27). A new role for histone demethylases in the maintenance of plant genome integrity. ELife; eLife Sciences Publications, Ltd. https://elifesciences.org/articles/58533  Subscribe to Curiosity Daily to learn something new every day with Cody Gough and Ashley Hamer. You can also listen to our podcast as part of your Alexa Flash Briefing; Amazon smart speakers users, click/tap “enable” here: https://www.amazon.com/Curiosity-com-Curiosity-Daily-from/dp/B07CP17DJY See omnystudio.com/listener for privacy information.

This podcast is designed for Pre-medical students preparing to take their Medical College Admissions Test (MCAT). In this episode, Austin asks a question about how histones interact with DNA. This is a question you might see from the Biological and Biochemical Foundations of Living Systems or the Chemical and Physical Foundations of Biological Systems section of the MCAT. This episode is powered by Premed Consultants, an all-inclusive premed advising program. Whether you are starting out as a freshman or about to start prepping for the MCAT, the premed consultants will help you throughout your entire premed process until you get into medical school. Not only is there a full MCAT program utilizing the most effective study tactics, but they will also help you through the entire admissions process as well. If you're interested in one on one mentorship, go to thepremedconsultants.com and you can schedule a free 30 min strategy session to see if Premed Consultants is the right fit for you. If you have any suggestions, concerns, or question, feel free to e-mail us at mcatflashgo@gmail.com We wish you the best of luck on your educational journey!

The series starts off with my bread and butter, Biology. Contents: Introduction to Cells (1600s - the present day). The Four Tenets of Cell Theory/Eukaryotes, Prokaryotes, and Viruses RNA World Hypothesis/Why DNA is Preferred Today Organelles of the Cell/How Cell Integrity Against an Osmotic Gradient Exists DNA, Histones, Genes, Chromosomes Song for ending credits: ILY by Sea Mesa ft. Emilee --- Send in a voice message: https://anchor.fm/moleculardrugs/message Support this podcast: https://anchor.fm/moleculardrugs/support

  VIDEO WITH VISUAL AIDS ON YOUTUBE!!   How did you get so put together?  DNA is the blueprint, but it doesn't determine everything.  DNA gets turned into RNA, and then finally into proteins that help build your body and brain.  But there are SO many steps in that process that affect the final product- you.   The sum of these steps is a process called genetic regulation.  Genetic regulation makes sure that not all of our genes are expressed and turned into protein at the same time and same place- that would be a mess! This episode is all about genetic regulation by long, non-coding RNAs (lncRNAs, pronounced "link-R N A").  LncRNAs are long segments of RNA that serve non-traditional functions in the genome.  Although recently discovered, lncRNAs seem to be involved in everything from the genetic regulation of development to diseases like cancer.  LncRNAs could help rewrite the field of genetic regulation, and might be the biggest shift to understanding genetics since epigenetics became a hot topic. https://www.straightfromascientist.com/rachel-cherney/ Rachel is also highly involved in other forms of science communication!  Check out the Pipettepen and UNC SWAC for more info!  If you're at UNC, make sure to check TIBBS for career training and opportunities.    Specific visual references and their approximate timestamps are listed below.  Make sure to watch the Youtube Video for the full experience! 5:00: DNA vs RNA vs Protein - (image in video) 7:30: Alternative splicing - (image in video) 9:00: Jimena giudice lab at UNC  - http://giudicelab.web.unc.edu/ (Alternative splicing and intracellular trafficking in development and diseases) 9:30: It's estimated that >90% of proteins undergo alternative splicing 13:30: protein coding gene structure (image in video) 15:30: Additional note:  smaller ncRNAs have more defined structure than lncRNAs, their functions are better known 17:33: dosage compensation - calico cats (image in video) 20:50: An example of a motif that proteins recognize (http://www.rnajournal.org/cgi/pmidlookup?view=long&pmid=31097619, figure 3 ) 21:00: xist repeat structure (https://www.mdpi.com/2311-553X/4/4/28/htm, figure 2, human vs mouse xist) 23:00:in cis lncRNA function (https://dev.biologists.org/content/143/21/3882, figure 2 b and c) 25:05: Markers are placed on histones, rather than DNA. Histones are proteins that DNA wraps around to compact dna into cells (image in video) 25:30: A note: polycomb complexes are conserved to plants and even fungi.  lncRNAs can be found in plants* 28:15: immunoprecipitation pipeline (image in video) 31:30 -33:35: Examples of Single Nucleotide Polymorphisms (SNPs) (image in video) 35:00: Enhancer rnas (https://www.sciencedirect.com/science/article/pii/S1672022917300761 figure 1 38:30: single line RNA vs double line DNA, 3DRNA structure (image in video) 41:00: xist vs rsx  (http://www.rnajournal.org/cgi/pmidlookup?view=long&pmid=31097619, figure 6b ) 42:30: SWAC /pipettepen,com - link to swac article that prompted this podcast -http://www.thepipettepen.com/what-determines-our-complexity/ 44:30: TIBBS -https://tibbs.unc.edu/

In this week's podcast, we continue our conversation on therapeutic aspects of the ketogenic diet. More specifically, how the ketogenic diet affects the NADH/NAD ratio. What's that you might ask? Well, NAD stands for nicotinamide adenine dinucleotide. It's a cofactor found in every cell in our body and is a pivotal player in numerous reactions throughout our entire body. We focused on the role of NAD as it pertains to the proteins called sirtuins. Sirtuins are a group of proteins that control how old or young our cells are. When they're active, they're able to perform a process called deacetylation, which is very important within our cells. Removing acetyl groups from proteins allows them to be acted upon and puts them in their "active" form, meaning they're now able to do work. One of these proteins is histone. Histones are a group of proteins that our DNA wraps itself around for protection. When they have an acetyl group on them, our DNA is unwound and unprotected. However, in the presence of NAD, sirtuins are capable of removing that acetyl group, allowing our DNA to wrap back around the histones for protection. This is just one of the ways sirtuins keep our cells young. A high carb diet depletes the body of NAD, which limits the ability of sirtuins to do their job. A ketogenic diet regenerates NAD, giving sirtuins the tools they need to perform optimally. To learn more, listen to this week's podcast. Website: https://tntwellnessandnutrition.com Email: tntwellnessandnutrition@gmail.com Itunes: itunes.apple.com/us/podcast/tnt-w…d1428217037?mt=2 Google Play Music: https://play.google.com/music/listen#/ps/Ibnzgb5hwnwd2aymtaixp6lvee4 SoundCloud: @user-422365757-83307870 Stitcher: https://www.stitcher.com/s?fid=445098&refid=stpr Social Media Links Twitter:twitter.com/tnt_wellness Facebook:www.facebook.com/tntwellnessandnutrition/ Instagram:www.instagram.com/tntwellnessandnutrition/ YouTube:https://www.youtube.com/channel/UCXb2pCmzu6JxW27bunmFytQ?view_as=subscriber

This episode: Giant viruses produce DNA-packing proteins that seem to have branched off from eukaryotes far back in evolutionary history! Download Episode (6 MB, 6.5 minutes) Show notes: Microbe of the episode: Caulobacter maris News item Journal Paper: Erives AJ. 2017. Phylogenetic analysis of the core histone doublet and DNA topo II genes of Marseilleviridae: evidence of proto-eukaryotic provenance. Epigenetics & Chromatin 10:55. Other interesting stories: Swimming bacteria can affect liquid viscosity, to the point of superfluidity Tiny soil roundworms can sense and avoid pathogens by their gases Beetle bacterium makes defensive compound with genes taken from an ocean microbe   Email questions or comments to bacteriofiles at gmail dot com. Thanks for listening! Subscribe: Apple Podcasts, RSS, Google Play. Support the show at Patreon, or check out the show at Twitter or Facebook

"Gene" is a general word for a piece of DNA that creates proteins, but what exactly are genes? Why do they matter? ____________________ Sources: DNA can't explain all inherited biological traits, research shows https://www.sciencedaily.com/releases/2015/04/150402161751.htm "Characteristics passed between generations are not decided solely by DNA, but can be brought about by other material in cells, new research shows. Scientists studied proteins found in cells, known as histones, which are not part of the genetic code, but act as spools around which DNA is wound. Histones are known to control whether or not genes are switched on." Rosalind Franklin: Biography & Discovery of DNA Structure? https://www.livescience.com/39804-rosalind-franklin.html "Many people recall that the structure of the DNA molecule has the shape of a double helix." What Are Proteins And What Do They Do? https://ghr.nlm.nih.gov/primer#howgeneswork "Proteins are large, complex molecules that play many critical roles in the body. They do most of the work in cells and are required for the structure, function, and regulation of the body's tissues and organs." ____________________ Follow Trace on twitter: http://twitter.com/tracedominguez Follow Seeker on twitter: http://twitter.com/seeker And, subscribe on YouTube too: http://youtube.com/seeker Seeker inspires us to see the world through the lens of science and evokes a sense of curiosity, optimism and adventure. Visit the Seeker website for more science coverage https://www.seeker.com/  Learn more about your ad choices. Visit megaphone.fm/adchoices

"Gene" is a general word for a piece of DNA that creates proteins, but what exactly are genes? Why do they matter? ____________________ Sources: DNA can't explain all inherited biological traits, research shows https://www.sciencedaily.com/releases/2015/04/150402161751.htm "Characteristics passed between generations are not decided solely by DNA, but can be brought about by other material in cells, new research shows. Scientists studied proteins found in cells, known as histones, which are not part of the genetic code, but act as spools around which DNA is wound. Histones are known to control whether or not genes are switched on." Rosalind Franklin: Biography & Discovery of DNA Structure? https://www.livescience.com/39804-rosalind-franklin.html "Many people recall that the structure of the DNA molecule has the shape of a double helix." What Are Proteins And What Do They Do? https://ghr.nlm.nih.gov/primer#howgeneswork "Proteins are large, complex molecules that play many critical roles in the body. They do most of the work in cells and are required for the structure, function, and regulation of the body's tissues and organs." ____________________ Follow Trace on twitter: http://twitter.com/tracedominguez Follow Seeker on twitter: http://twitter.com/seeker And, subscribe on YouTube too: http://youtube.com/seeker Seeker inspires us to see the world through the lens of science and evokes a sense of curiosity, optimism and adventure. Visit the Seeker website for more science coverage https://www.seeker.com/  Learn more about your ad choices. Visit megaphone.fm/adchoices

Crescentic glomerulonephritis is characterized by glomerular necrosis. Dying cells release intracellular proteins that act as danger-associated molecular patterns to activate the innate immune system. Previously, we have demonstrated that dying tubular cells release histones, which can kill endothelial cells and activate the toll-like receptor 2/4 (TLR2/4). This drives tubulointerstitial inflammation in septic or post-ischemic acute kidney injury (AKI). Furthermore, other groups have also reported that extracellular histones cause organ damage during acute lung injury, stroke, peritonitis and retinal dysfunction, and that blocking extracellular histones represents a beneficial approach during the disease progression. In this thesis, we investigated whether extracellular histones can elicit similar pathogenic effects during necrotizing glomerulonephritis. To do so, we used an animal model based on the necrotizing type of severe glomerulonephritis. Necrotic glomerulonephritis was induced in mice by a single intravenous injection of 100µl sheep anti-GBM antiserum. The impact of histone neutralization was studied by using an antibody isolated from the BWA-3 clone, which had the capacity to neutralize released extracellular histones in-vivo and in-vitro. After 7 days, mice were sacrificed and kidneys were collected for further data analysis. Proteinuria was assessed in spot urine samples. Anti-GBM treated mice showed increased proteinuria (albumin/creatinine ratio), plasma creatinine and BUN levels. This was associated with a reduced number of podocytes, increased crescentic glomeruli and the infiltration of neutrophils and macrophages into the kidney. Interestingly, neutralization of extracellular histones significantly reduced proteinuria leading to less podocyte damage. This was linked to an improved renal function defined by lower plasma creatinine and BUN levels, and with a decrease in neutrophil and macrophage infiltration and activation in kidney. Histone blockade also significantly reduced renal mRNA expression of TNF-α and fibrinogen in the glomerular capillaries, which was associated with less glomerulosclerosis, crescents and tubular atrophy. In-vitro studies demonstrated that extracellular histones and NETs-related histones kill glomerular endothelial cells, podocytes and parietal epithelial cells in a dose-dependent manner. Histone-neutralizing agents such as anti-histone IgG, activated protein C or heparin prevented this cytotoxic effect. Stimulation of BMDCs with histones upregulated the expression of the activation marker including MHC-II, CD48, CD80 and CD86 significantly as well as increased the production of TNF-α and IL-6. It has been previously reported by others including us that in biopsies from patients with ANCA-associated vasculitis showed an over-expression of the TLR2/4 receptor compared to the healthy glomeruli. Histone toxicity on glomeruli ex-vivo was also dependent on the TLR2/4 receptor axis given that the lack of TLR2/4 attenuated histone-induced renal thrombotic microangiopathy and glomerular necrosis in mice. Anti-GBM glomerulonephritis involved NET formation and vascular necrosis, while blocking NET formation via PAD inhibitor or pre-emptive anti-histone IgG injection significantly reduced all parameters of glomerulonephritis including vascular necrosis, podocyte loss, albuminuria, cytokine induction, recruitment and activation of glomerular leukocytes, and glomerular crescent formation. Finally, to evaluate histones as a therapeutic target, mice with established glomerulonephritis were treated with three different histone-neutralizing agents such as anti-histone IgG, recombinant activated protein C and/or heparin. Interestingly, all agents were equally effective in abrogating severe glomerulonephritis, while combination therapy had no additive effect. In summary, the results of this thesis indicate that NET-related histones released during glomerulonephritis elicit cytotoxic and immunostimulatory effects and that neutralizing extracellular histones, therefore, represents a potential therapeutic approach when applied during already established glomerulonephritis.

Genes are the instructions that tell our cells what to do, but how do different types of cells know which genes to switch on or off at the right time? The solution lies in epigenetics - the molecular bells and whistles that act on top of our DNA to control gene activity. Plus, a new gene involved in severe obesity, and a mythical gene of the month. Like this podcast? Please help us by supporting the Naked Scientists

April 05, 2012 Host Dr. Tim Cripe welcomes back co-host Dr. Lionel Chow to discuss somatic mutations in pediatric brain tumors. After recapping the consensus paper on molecular subgroups in medulloblastoma discussed in TWiPO episode 22 (Brain Tumor Round Robin) Dr Chow highlights the significance of the driver mutations in histone H3.3 in pediatric glioblastoma. Results of whole exome sequencing have shown that significantly more somatic mutations are present in adult tumors compared to pediatric tumors. This difference might suggest a reason for better success rates in pediatric tumors and possibly more escape mechanisms in adult tumors. Dr. Chow also discusses a paper published by the Pediatric Cancer Genome Project (a St. Jude Children's Research Hospital–Washington University collaboration) on somatic histone H3 alterations in diffuse intrinsic pontine glioma (DIPG). The findings are significant in showing that this mutation is present in 36% of non-brain stem gliomas and in 78% of brain stem gliomas, but in none of the other pediatric tumor types. Please send comments and questions to twipo@solvingkidscancer.org Papers discussed: Taylor MD, Northcott PA, Korshunov A, et al. Molecular subgroups of medulloblastoma: the current consensus. Acta Neuropathol. 2012 Apr;123(4):465-72. Epub 2011 Dec 2.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3306779/ Schwartzentruber J, Korshunov A, Liu XY, Jones DT, et al. Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma. Nature. 2012 Jan 29;482(7384):226-31. doi: 10.1038/nature10833. http://www.ncbi.nlm.nih.gov/pubmed/22286061 Wu G, Broniscer A, McEachron TA, Lu C, Paugh BS, et al. Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas. Nat Genet. 2012 Jan 29;44(3):251-3. doi: 10.1038/ng.1102. St. Jude Children's Research Hospital–Washington University Pediatric Cancer Genome Project.http://www.ncbi.nlm.nih.gov/pubmed/22286216

Summary: Structure of the FACT chaperone domain in complex with histones H2A-H2B, and a model for FACT-mediated nucleosome reorganization Nucleosomes are the smalles unit of chromatin: two coils of DNA are wrapped around a histone octamer core, which neutralizes its charge and `packs' the lengthy molecule. Nucleosomes confer a barrier to processes that require access to the eukaryotic genome such as transcription, DNA replication and repair. A variety of nucleosome remodeling machines and histone chaperones facilitate nucleosome dynamics by depositing or evicting histones and unwrapping the DNA. The eukaryotic FACT complex (composed of the subunits Spt16 and Pob3) is an essential and highly conserved chaperone. It assists the progression of DNA and RNA polymerases, for example by facilitating transcriptional initiation and elongation. Further, it promotes the genome-wide integrity of chromatin structure, including the suppression of cryptic transcription. Genetic and biochemical assays have shown that FACT's chaperone activity is crucially mediated by a direct interaction with histones H2A-H2B. However, the structural basis for how H2A-H2B are recognized and how this integrates with FACT’s other functions, including the recognition of histones H3-H4 and of other nuclear factors, is unknown. In my PhD research project, I was able to reveal the structure of the yeast chaperone domain in complex with the H2A-H2B heterodimer and show that the Spt16M module in FACT’s Spt16 subunit establishes the evolutionarily conserved H2A-H2B binding and chaperoning function. The structure shows how an alpha-helical `U-turn' motif in Spt16M interacts with the alpha-1-helix of H2B. The U-turn motif scaffolds onto a tandem pleckstrin-homology-like (PHL) module, which is structurally and functionally related to the H3-H4 chaperone Rtt106 and the Pob3M domain of FACT. Biochemical and in vivo assays validate the crystal structure and dissect the contribution of histone tails and H3-H4 toward FACT binding. My results show that Spt16M makes multiple interactions with histones, which I suggest allow the module to gradually invade the nucleosome and ultimately block the strongest interaction surface of H2B with nucleosomal DNA by binding the H2B alpha-1-helix. Together, these multiple contact points establish an extended surface that could reorganize the first 30 base-pairs of nucleosomal histone–DNA contacts. Further, I report a brief biochemical analysis of FACT’s heterodimerization domain. Its PHL fold indicates shared evolutionary origin with the H3-H4-binding Spt16M, Pob3M and Rtt106 tandem PHL modules. However, the Spt16D–Pob3N heterodimer does not bind histones, rather it connects FACT to replicative DNA polymerases. The snapshots of FACT’s engagement with H2A-H2B and structure-function analysis of all its domains lay the foundation for the systematic analysis of FACT’s vital chaperoning functions and how the complex promotes the activity of enzymes that require nucleosome reorganization.

Almost every single cell of your body is packed with more than two metres of DNA, containing your genes. But not only does it have to be packed up to fit in there, it also has to be organised and read. Plus, how genetic variations are linked to cancer risk,analysing dinosaur DNA, and an adventurous gene of the month. Like this podcast? Please help us by supporting the Naked Scientists

Article discussion from January 15, 2013

The conditions that permit the interaction of immediate-early proteins of murine cytornegalovirus (MCMV) with DNA were studied. Chromatography of extracts from infected cells on MCMV DNA cellulose and calf thymus DNA cellulose showed that pp89, the regulatory major immediate-early protein, interacts with DNA and dissociates at salt concentrations between 0.3 and 0.6 M NaCl. pp76, a cleavage product of pp89, and additional minor ie1 proteins eluted already at low ionic strength. Cellular DNA-binding factors were required for association of pp89 with DNA. These factors were identified as core histones. Chromatography of IE proteins on histone-Sepharose in the absence of DNA revealed a high-binding affinity that was resistant to 2 M NaCl. These results suggest that pp89 has no direct DNA-binding activity. A role for an amino acid sequence homology in the N-terminal region of pp89 with histone H2B in the pp89-histone-DNA Interaction is discussed.