Visit https://www.biopleo.com/products/erad-plus%E2%84%A2-pre-d-tablet to find out more about how misfolded proinsulin and the ER stress kills your pancreatic beta cells, and how enhanced ERAD can restore beta cell mass.
Просмотров: 173 BioPleo Inc.
This brief animation shows how a new drug screening technology developed at the Harvard T.H. Chan School of Public Health has identified a new potential anti-diabetes compound -- and a powerful way to test whether other molecules can have a positive effect on a critical molecular pathway in the endoplasmic reticulum that is believed to be the underlying cause of type 2 diabetes. Read more: http://www.hsph.harvard.edu/news/press-releases/new-tool-identifies-novel-compound-targeting-causes-of-type-2-diabetes/
Просмотров: 1201 Harvard T.H. Chan School of Public Health
FULL VIDEO - go to the site in the end of this video!
Просмотров: 3 Tyler Simone
Studies: Glycemic control in diabetes is restored by therapeutic manipulation of cytokines that regulate beta cell stress http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3705.html Involvement of il-22 in the expression of pancreatic beta cell regenerative Reg genes http://www.cellregenerationjournal.com/content/pdf/2045-9769-2-2.pdf Therapeutic opportunities of the IL-22–IL-22R1 system http://www.nature.com/nrd/journal/v13/n1/full/nrd4176.html One of the original articles on the topic: http://medicalxpress.com/news/2014-11-discovery-revolutionise-diabetes-treatment.html#ajTabs
Просмотров: 344 Trevor Johnson
Did you know that a single biological process is related to diseases as diverse as Parkinson's, diabetes and cancer? The process is called the unfolded protein response, and it helps cells deal with problematic proteins. Learn more about the award-winning discovery by UCSF's Peter Walter that helped scientists understand that regulating this process could lead to treatments - and even cures - for many diseases: http://www.ucsf.edu/news/2014/09/116931/peter-walter-wins-2014-lasker-award Animation by Mark Wooding
Просмотров: 39700 UC San Francisco (UCSF)
Dropping by New York I took the opportunity to have another enjoyable chat with Dr. Brookler. Since our last meeting, he has been focussing in on the clinical effects of low-carb, high-fat diets. He is seeing some impressive outcomes from the approach ! He has also been researching insulin's effects on endoplasmic reticulum stress, particularly that in the beta cells of the pancreas. It speaks to the mechanisms by which hyperinsulinemia wreaks havoc, leading to the chronic diseases of the insulin resistant state. Enjoy, and subscribe for free to: www.thefatemperor.com/subscribe ..this will deliver future content (always free). In fact, very shortly we'll have another great conversation with Professor Richard Feinman - on the key details of his cancer research with Professor Eugene Fine...!
Просмотров: 5531 Ivor Cummins
What is cystic fibrosis? Cystic fibrosis is an autosomal recessive disorder involving the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which causes complications in the lungs, pancreas, and other organs. Find more videos at http://osms.it/more. Hundreds of thousands of current & future clinicians learn by Osmosis. We have unparalleled tools and materials to prepare you to succeed in school, on board exams, and as a future clinician. Sign up for a free trial at http://osms.it/more. Subscribe to our Youtube channel at http://osms.it/subscribe. Get early access to our upcoming video releases, practice questions, giveaways, and more when you follow us on social media: Facebook: http://osms.it/facebook Twitter: http://osms.it/twitter Instagram: http://osms.it/instagram Our Vision: Everyone who cares for someone will learn by Osmosis. Our Mission: To empower the world’s clinicians and caregivers with the best learning experience possible. Learn more here: http://osms.it/mission Medical disclaimer: Knowledge Diffusion Inc (DBA Osmosis) does not provide medical advice. Osmosis and the content available on Osmosis's properties (Osmosis.org, YouTube, and other channels) do not provide a diagnosis or other recommendation for treatment and are not a substitute for the professional judgment of a healthcare professional in diagnosis and treatment of any person or animal. The determination of the need for medical services and the types of healthcare to be provided to a patient are decisions that should be made only by a physician or other licensed health care provider. Always seek the advice of a physician or other qualified healthcare provider with any questions you have regarding a medical condition.
Просмотров: 437751 Osmosis
https://www.ibiology.org/cell-biology/unfolded-protein-response/ Proteins that are secreted from the cell or inserted into the plasma membrane, transit through the endoplasmic reticulum where they are properly folded and assembled and may undergo post-translational modification. Walter tells the story of the exciting discovery made in his lab of the "unfolded protein response", a feedback pathway that ensures that the cell makes enough ER to properly modify all the secreted proteins in the cell.
Просмотров: 20301 iBiology Science Stories
Visit https://www.biopleo.com/products/erad-plus%E2%84%A2-pre-d-tablet to find out more about how ERAD Plus promotes healthy oxidative and ER stress levels. Also, the linkage between ER stress and the progression of Diabetes is included.
Просмотров: 2598 BioPleo Inc.
Handwritten Video Lectures on the pathophysiology, pathology, symptoms and treatment of Diabetes Mellitus Type 1 for USMLE Step 1 and Step 2. PHYSIOLOGY OF DIABETES MELLITUS TYPE 1 Islet cells have beta cells in the central which secrete insulin and beta cells which secrete glucagon. The beta cells has the GLUT2 transporter which transports glucose inside the cell. It is then acted upon by glucokinase which increases the level of ATP. ATP then deactivates KATP channels. Afterwards Calcium inlux activates vesicles of insulin to fuse with the membrane and release the insulin. Insulin is synthesized in the Rough Endoplasmic reticulum as the preproinsulin. After removla of the pre and the post Peptides to form proinsulin. After the golgi aparatus the c peptide bends over and is removed after a bond is formed between the a and b peptide. The c-peptide is a measure of endogenous insulin production. PATHOPHYSIOLOGY OF DIABETES MELLITUS TYPE 1 Destruction of the Islet Cells of Langerhan leads to hypglycemia. The genetic component of Diabetes Mellitus Type 1 involves HLA-DR3 and HLA-DR4. Autoimmune is also invovled in Diabetes Mellitus Type 1. Islet cell autoantibodies target insulin or Anti GAD65. Also Diabetes Mellitus is associated with other autoimmune disease. Viruses such as cocksackie virus also is known to cause Diabetes Mellitus. DIAGNOSIS OF DIABETES MELLITUS TYPE 1 HbA1c level greater then 6.5 percent 2 hour fasting glucose greater than 126 mgdL Oral Glucose Tolerance Test (OGTT) greater than 200 Random Plasma Glucose greater than 200 and symptomatic Anyone 1 of the previous is a diagnosis of Diabetes Mellitus SIGN AND SYMPTOMS OF DIABETES MELLITUS TYPE 1 Primary symptoms are polyuria polydypsia and weight loss occurs in approximately 90 percent of patients. Other symptoms include hyperphagia, perianal candidiasis. Diabetic Ketoacidosis also has polyuria, polydipsia, fruity death and neurological symptoms COMPLICATION OF DIABETES MELLITUS Diabetic patients who do no manage their glucose well may get diabetic neuropathy, diabetic nephropathy, diabetic retinopathy, necrobiosis lipoidica and increase risk of atherosclerosis MANAGEMENT OF DIABETES MELLITUS Insulin therapy with a goal of keeping HbA1c below 7 percent. Fast Acting Insulin includes Aspart, Lispro and Glulysine Intermediate Acting Insulin such as regular insulin and NPH Long acting insulin includes Glargine which has no peak, Determir which binds to albumin may all be using in different combination to manage glucose levels in Diabetic patients.
Просмотров: 10515 the study spot
Просмотров: 142 David Ellis
Visit https://www.biopleo.com/products/erad-plus%E2%84%A2-pre-d-tablet to find out more about a new strategy to reversing Type 2 Diabetes. You will see how reducing the Endoplasmic Reticulum (ER) Stress and Oxidative Stress in your pancreatic beta cells will benefit you.
Просмотров: 67 BioPleo Inc.
Please comment if you notice any errors or have any questions at all. Thanks for watching! @11:40 Note - I lost my train of thought ;) @37:10 Note - Interferometry (not inferometry) - detects interference patterns in electromagnetic waves caused by protein/protein interactions. - https://www.fortebio.com/interactions/Spring_2012/page5.html Amin-Wetzel, N., Saunders, R. A., Kamphuis, M. J., Rato, C., Preissler, S., Harding, H. P., & Ron, D. (2017). A J-Protein Co-chaperone Recruits BiP to Monomerize IRE1 and Repress the Unfolded Protein Response. Cell, 171(7). doi:10.1016/j.cell.2017.10.040
Просмотров: 856 AJ Keefe
This animation shows the regulation of insulin secretion in a beta cell. Glucose is transported via the glucose transporter GLUT2 into the cell. The enzyme glucokinase converts the glucose to glucose-6-phosphate. During glycolysis glucose-6-phosphate is metabolized and ATP as well as pyruvate are generated. The pyruvate is transported into the mitochondria where it is converted to acetyl CoA so it can enter the citric acid cycle. During the citric acid cycle more ATP is generated. The ATP-sensitive potassium channel regulates the transport of potassium ions. The elevated concentration of ATP in the cell leads to the closing of the potassium channel, thereby inducing membrane depolarization. The depolarization triggers the opening of the voltage-gated calcium channel. The influx of Ca2+ ions as well as their triggered release from the endoplasmic reticulum leads to the fusion of the insulin vesicles with the cell membrane, thereby releasing the insulin.
Просмотров: 1160 WJ R
This is a introduction video that explains the role of endoplasmic reticulum (ER) in atherosclerosis. We have simplified the biological process in this video so it is a great video for anyone who just wants to know a little about the role of ER in human diseases. Please like & comment about the video and subscribe to our channel Demystifying Medicine. This video was prepared by Babak Nouhi, Jim Zhou, Pavan Patel, Thinesan Thevarajah, Warren Viegas. © 2015. McMaster University. All rights reserved
Просмотров: 1125 Demystifying Medicine
Hi , Welcome to our YOUTUBE channel. Here we are going to tell you what causes the Diabetes. In this video we will tell you about the main causes of diabetes. The population of islet cells is established and not plastic in man after about age 20 years. Post mortem studies show that the B cell number at diagnosis of type 2 diabetes is around 50% and decreases to around 20 % after many years. A chronic increase in plasma FFA levels is harmful as shown by the important effects of these dietary components in pancreatic bet6a cell lipotoxicity. Fatty acid derivative can interfere with function of these cells and ultimately lead to their death through lipoapoptosis. Saturated fat is very harmful as compared to unsaturated fats. Saturated fats are harmful to beta cells which help in the production of insulin. The endocytosis of LDL can cause beta cell death as a result of ROS formation. Western diets rich in saturated fats cause obesity and insulin resistance and increase levels of circulating NEFAs . In addition they contribute to b cells failure in generally predisposed individuals. NEFAs cause beta cell apoptosis and may thus contribute to progressive Beat cell loss in type 2 diabetes. Type 2 diabetes is characterized by defects in both insulin secretion and insulin action but saturated fat effects the both. SFA ingestion reduced insulin sensitivity. Pancreas should increase insulin production but insulin secretion failed to compensate for insulin resistance in subjects who ingested SFA. Failure of insulin secretion to compensate for insulin resistance implies impaired beta cell function in the SFA study. Increased consumption of SFAs has a powerful short and long term effect on insulin action. Saturated fats are harmful to beta cells. Environmental factors such as diets rich in saturated fats contribute to dysfunction and death of pancreatic beta cells in diabetes, Endoplasmic reticulum stress is elicited in beta cells by saturated fatty acids.
Просмотров: 7 Diabetes Treatment
Worldwide, type 2 diabetes is at epidemic proportions, with over 300 million already having the condition with an estimated rise to 600 million diagnosed cases by the year 2030. Information regarding reduced risk of type 2 diabetes is fairly common. However, finding information regarding treatment and management for an individual who already has type 2 diabetes can be somewhat more difficult. Therefore, this article is designed as a mini literature review of sorts, pointing to some of the recent research around olive oil and its potential benefits for use as a dietary intervention in type 2 diabetes treatment. Endoplasmic reticulum stress (ER) is a central mediator for pancreatic beta-cell dysfunction in type 2 diabetes. An in vitro study published in Biochemical and Biophysical Research Communications, 2016, investigated if tyrosol, an antioxidant polyphenolic compound found in olive oil, could protect against beta-cell dysfunction. Researchers found that tyrosol did in fact protect against beta-cell ER stress-induced cell death, suggesting that it should be explored as a therapeutic agent for improving insulin resistance and diabetes. Insulin resistance (IR) is one of the major contributors to difficulties in maintaining blood glucose control. A study published in Diabetologia, 2015, randomized 642 patients to either an olive oil enriched Mediterranean diet (MedDiet) (35 percent fat; 22 percent from monounsaturated fat) or a low-fat diet (less than 28 percent fat) to determine whether dietary intervention effects tissue-specific IR and beta-cell function. The study found that both diets improved IR, however, liver IR is improved more through a low-fat diet, while muscle IR and muscle+liver IR could benefit more from the olive oil enriched MedDiet. At this point there are no clinical trials evaluating the role of dietary patterns on the incidence of microvascular complications such as retinopathy and nephropathy in type 2 diabetes. A post hoc analysis of a cohort of type 2 diabetic participants, published in Diabetes Care, 2015, shows that a MedDiet supplemented with EVOO may protect against diabetic retinopathy, a complication leading to blindness, but not nephropathy. According to a detailed review of 2824 studies, published in the British Medical Journal, 2015, consuming a MedDiet is associated with better glycaemic control and cardiovascular risk factors, even compared to a lower fat diet. Clinical conditions associated with obesity, such as type 2 diabetes, show improvements with daily intake of conjugated linoleic acid (CLA) or extra virgin olive oil (EVOO). A study on mice published in The Journal of Nutritional Biochemistry, 2015, investigated whether dietary supplementation of CLA or EVOO could change body metabolism associated with mitochondrial energetics. The study found that while EVOO alone did not change any metabolic parameter, combined with CLA it protects against IR and liver enlargement, while the CLA improves mitochondrial action and body metabolism. According to research published in Biochimia et Biophysica Acta, 2014, oleic acid, a major biological component in olive oil, is a primary component of membrane lipids and helps to regulate membrane structures by having the ability to incorporate into phospholipids, which has various advantages to cell composition. It is also thought that membranes rich in oleic acid have increased flexibility to promote GLUT4 glucose transport into cells and help reverse saturated fatty acid-induced IR.
Просмотров: 130 Videos Kingdom
Hi, Welcome to our YOUTUBE channel. Here we are going to tell you about various causes of diabetes. In this video we will tell you all the causes related to diabetes. After the age of 20, the population of islet cells is established and not plastic in man after age of 20 years. Post mortem studies show that beta cell number at diagnosis of type 2 diabetes is around 50 percent and decreases to around after many years. Exposure of human islet to fatty acid causes an increase in intra islet fat storage and marker of apoptosis. Saturated cells contributed more in death of beta cells. Saturated lipids are harmful to beta cells. The endocytosis of LDL can cause beta cell death as a result of ROS formation. Similarly, prolonged elevation of circulating NEFAs by lipid infusion impairs pancreatic beta cell function in vivo, particularly in individuals with a genetic predisposition to type2 diabetes. Western diets rich in saturated fats cause obesity and insulin resistance and increase levels of circulating NEFAs . In addition they contribute to beta cells failure in genetically predisposed individuals. NEFAs cause beta cell apoptosis and may thus contribute to progressive beta cell loss in type 2 diabetes. Type 2 diabetes is characterized by defects in both insulin secretion and insulin action. SFA ingestion reduced insulin sensitivity. Insulin secretion failed to compensate for insulin resistance in subjects who ingested SFA. Failure of insulin secretion to compensate for insulin resistance implies impaired beta cell function in the SFA. Increased consumption of SFAs has a powerful short and long term effect on insulin action. Saturated fats are harmful to insulin. Environmental factors such as diets rich in saturated fats contribute to dysfunction and death of pancreatic cells in diabetes. Endoplasmic reticulum stress is elicited in beta cells by saturated fatty acids.
Просмотров: 2 Diabetes Types
This type 2 diabetes webcast is one in a three-part series by Dr. Adi Mehta. It reviews the pathophysiology of insulin resistance and T2DM, as well as the medications available for management. Visit http://www.ccfcme.org/MastersCMEvideos to claim CME credit or learn more about the Masters in Medicine series. Take the opportunity to also learn from Dr. Mehta in Understanding Type 2 Diabetes: Linking Pathophysiology to Therapeutic Targets and Can Exogenous Insulin Mimic Endogenous Insulin Action? Interested in related CME education? Visit http://bit.ly/17iiXhR Like us on Facebook: https://www.facebook.com/CMEClevelandClinic Follow us on Twitter: https://twitter.com/cleveclinic_cme The video was produced by the Cleveland Clinic Foundation Center for Continuing Education.
Просмотров: 2826 ClevelandClinicCME
ADD YOUR SUCCESS STORY: https://www.drberg.com/add-client-success-story Take Dr. Berg's Free Keto Mini-Course: http://pxlme.me/-i717vtY or go here: https://www.drberg.com/how-to-do-ketosis Dr. Berg talks about whats inside your cells. There are many structures with specific functions. Dr. Berg explains these structures and breaks down the complexities. 1. Nucleus: DNA 2. RNA 3. Mitochondria 4. Endoplasmic Reticulum 5. Ribosomes 6. Glogi Apparatus 7. Lysosome 8. Peroxisome 9. Membranes Hey guys, I wanted to create a little video on your cells because it can be very complicated, I am gonna try to simplify it. There’s various parts of the cell, it is like a universe there are all sorts of things that’s happening. You have the center part which is called the nucleus and in the nucleus, you have what it’s called the DNA. The DNA is basically gonna give a program to tell what the rest of the cell should do as far as what the body tissue to make and what actions to perform. Then we have what’s called the RNA, there’s three different kinds but just to simplify it, you look at the RNA as the copy of the DNA. You have the copy machine of your cells. So it makes the copy of the code and then it paste it to the certain transport units that send it out to the rest of the cells. So just like the computer programmer that would write his certain code and maybe cut and paste it to the different thing to make a website, your body has an RNA to do that as well. Now it is even more amazing is the DNA and RNA could have over 10,000 errors every single day from things like radiation, chemicals, to things that oxidizes the cells, free radical damage, etc. But we have an entire repair unit in the cell that could go in there like a proofreader read the code translate the code and look for errors. Then it will cut out the section of errors replace it with new one or fuse it together. And there’s another proofreader unit that comes behind the initial proofreader to make sure they didn’t make any errors to look and read the code to make sure it is exact and they also have the capacity to cut out the bad code, put in the new code and replace it to the point that you can reduce the errors to 1 in a billion. This is incredible because when the errors are there, you have this mutation which are alterations of the code and that can lead to cancer and a lot of other diseases. Next thing we are going to talk about is the mitochondria. The mitochondria is the energy factory of the cell. It takes your foods, mixes the oxygen and it produces energy. In the body, the energy is called ATP. It is kind of the energy currency. And then you have something called the Endoplasmic Reticulum which is the part of the cell that either makes protein if its the rough part of makes lipids or steroid if its the smooth part. Because a lot of your body tissue is composed of fat and protein Hair, Nails, Brain, Nerve, etc. So this is one part of the assembly aligned in the manufacturing of the body tissue and then we have this little things called ribosomes which are basically protein making machines on steroid so they actually help in making different protein structures not just for body parts but for body chemicals like hormones, neurotransmitters, blood cells, you name it. Then we have something called the Golgi Apparatus. Dr. Eric Berg DC Bio: Dr. Berg, 52 years of age is a chiropractor who specializes in Healthy Ketosis & Intermittent Fasting. He is the author of The New Body Type Guide and other books published by KB Publishing. He has taught students nutrition as an adjunct professor at Howard University. DR. BERG'S SHOP: http://shop.drberg.com/ Follow us on FACEBOOK: fb.me/DrEricBerg Send a Message to his team: m.me/DrEricBerg ABOUT DR. BERG: https://www.drberg.com/dr-eric-berg/bio Disclaimer: Dr. Eric Berg received his Doctor of Chiropractic degree from Palmer College of Chiropractic in 1988. His use of “doctor” or “Dr.” in relation to himself solely refers to that degree. Dr. Berg is a licensed chiropractor in Virginia, California, and Louisiana, but he no longer practices chiropractic in any state and does not see patients. This video is for general informational purposes only. It should not be used to self-diagnose and it is not a substitute for a medical exam, cure, treatment, diagnosis, and prescription or recommendation. It does not create a doctor-patient relationship between Dr. Berg and you. You should not make any change in your health regimen or diet before first consulting a physician and obtaining a medical exam, diagnosis, and recommendation. Always seek the advice of a physician or other qualified health provider with any questions you may have regarding a medical condition. The Health & Wellness, Dr. Berg Nutritionals and Dr. Eric Berg, D.C. are not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this video or site.
Просмотров: 15638 Dr. Eric Berg DC
For more information, see the paper by Lee et al., Neuron 91(1), http://www.cell.com/neuron/fulltext/S0896-6273(16)30200-8. HIPK2 (homeodomain interacting protein kinase 2) is an essential link that promotes ER stress-induced neuronal cell death. Accumulation of misfolded SOD1 and TDP-43 proteins activates HIPK2, whereas deletion or pharmacological inhibition of HIPK2 mitigates neurodegeneration.
Просмотров: 1823 Cell Press
Gerardo Lederkremer Department of Cell Research and Immunology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, ISRAEL speaks on "Endoplasmic reticulum stress in the pathogenesis of Huntington’s disease". This seminar has been recorded by ICGEB Trieste
Просмотров: 450 Icgeb
Instagram: https://www.instagram.com/drnicosoto/ Facebook: https://www.facebook.com/dr.nicosoto Web: https://www.drnicosoto.com CC for english subtitles MUSIC Cash Out (Instrumental) - Calvin Harris https://goo.gl/8NKCjz Heatstroke (Instrumental) - Calvin Harris https://goo.gl/Yi8aky Focus (Instrumental) - Ashanti https://goo.gl/wmZePs Unfold - Moods https://goo.gl/okmiUt REFERENCIAS CIENTÍFICAS ANDERSEN, IR. et al. 2017. Increased VLDL-TG Fatty Acid Storage in Skeletal Muscle in Men With Type 2 Diabetes. - The Journal of Clinical Endocrinology & Metabolism https://goo.gl/52rVCu HONG, B. et al. 2016. Ectopic Fat Deposition on Insulin Sensitivity: Correlation of Hepatocellular Lipid Content and MValue. - Journal of Diabetes Research https://goo.gl/rxQMSK LOHER, H. et al. 2017. The Flexibility of Ectopic Lipids. - International Journal of Molecular Sciences https://goo.gl/ryZYUn KITESSA, S. et al. 2016. Lipid-Induced Insulin Resistance in Skeletal Muscle: The Chase for the Culprit Goes from Total Intramuscular Fat to Lipid Intermediates, and Finally to Species of Lipid Intermediates. - Nutrients https://goo.gl/kH2da3 LAURENS, C. et al. 2016. Intramyocellular fat storage in metabolic diseases. - Hormone Molecular Biology and Clinical Investigation https://goo.gl/FmAqJX BRONS, C. et al. 2017. Review. Mechanisms in Endocrinology: Skeletal muscle lipotoxicity in insulin resistance and type 2 diabetes: a causal mechanism or an innocent bystander? - Journal of European Society of Endocrinology https://goo.gl/DWacUN CHEE, C. et al. 2016. The relative contribution of intramyocellular lipid to whole body fat oxidation is reduced with age, but subsarcolemmal lipid accumulation and insulin resistance are only associated with overweight individuals. - Diabetes https://goo.gl/c2mvnp RACHEK, L. et al. 2014. Free fatty acids and skeletal muscle insulin resistance. - Progress in Molecular Biology and Translational Science https://goo.gl/cxYg4X EVANS, W. et al. 2013. Oxygen-Carrying Proteins in Meat and Risk of Diabetes Mellitus. - JAMA Internal Medicine https://goo.gl/LS12Yp TAYLOR, R. et al. 2013. Banting Memorial Lecture 2012 Reversing the twin cycles of Type 2 diabetes. - Diabetic Medicine https://goo.gl/xH4USp ESTADELLA, D. et al. 2013. Lipotoxicity: Effects of Dietary Saturated and Transfatty Acids. - Mediators of Inflammation https://goo.gl/YXYsfr CUNHDA, D. et al. 2012. Death protein 5 and p53-upregulated modulator of apoptosis mediate the endoplasmic reticulum stress-mitochondrial dialog triggering lipotoxic rodent and human β-cell apoptosis. - Diabetes https://goo.gl/BmE5sm MARTINS, A. et al. 2012. Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function. - Lipids in Health and Disease https://goo.gl/A4KMgp NOLAN, C. et al. 2009. Lipotoxicity: Why do saturated fatty acids cause and monounsaturates protect against it?. - Journal of Gastroenterology and Hepatology https://goo.gl/BuCCyk KRSSAK, M. et al. 1999. Intramyocellular lipid concentrations are correlated with insulin sensitivity in humans: a 1H NMR spectroscopy study. - Diabetologia https://goo.gl/ZBbYVP RODEN, M. et al. 1996. Mechanism of free fatty acid-induced insulin resistance in humans. - The Journal of Clinical Investigation https://goo.gl/j3yBqU
Просмотров: 6742 Dr. Nico Soto
Why Do Woman Outlive Men? Too much iron and/or ferritin indicates health disaster and might lead to death if not treated...fortunately, there are ways beyond phlebotomy. Please also refer to our article on Iron found at longevitypost.com. Keywords Tauroursodeoxycholic acid, TUDCA, endoplasmic reticulum, endoplasmic reticulum stress, ER stress, C282Y, C282Y mutation, Hereditary Hemochromatosis, hepcidin, ursodeoxycholic acid, UDCA, homozygous C282Y, phlebotomy, ferritin, iron overload, liver, hoarding iron, blood donation, benefits of blood donation, diabetes, chronic fatigue, memory loss, joint pain, abdominal pain, liver disease, cirrhosis, liver cancer, irregular heart rhythm, heart attack or heart failure, skin color changes, green tea inhibit iron, coffee inhibit iron, neurological disease iron, Black death, Bubonic plaque, Hereditary hemochromatosis, autosomal recessive disease, bacteria Yersinia pestis.. References . Ageing Res Rev. 2004 Jul;3(3):303-18 . Circulation, Vol 86, 803-811 . Circulation. 1997;96:3300-3307 . JAMA. 2007;297(6):603-610 . J. Nutr. 140: 812–816, 2010. . J Vasc Surg. 2010 Jun;51(6):1498-503 . Diabetes 51:1000-1004, 2002 . Metabolism 43:614-620, 1994 . Am J Clin Nutr 2010;91(suppl):1461S–7S . Br Med J 1997; 314: 793-794 . Redox Rep. 2008;13(1):2-10. . Hepatology. 2008 Jul;48(1):344-5. . Biochemistry Research International Volume 2011 (2011), Article ID 896474, 10 pages
Просмотров: 26267 longevitypost.com
In this video I have explained about the enzyme which helps in maintaining blood glucose under fasting condition by breaking glycogen and by participating in gluconeogenesis. Hepatocytes (liver cells) and renal tubular cells express glucose 6 phosphatase which helps in converting glucose 6 phosphate into glucose. You Can Subscribe to my Channel for REGULAR UPDATES by clicking on SUBSCRIBE button above or by following the link below www.youtube.com/PMUNGLI You can follow me on my BLOG by clicking the link below http://drmungli.blogspot.com/ You can follow my Facebook page Biochemistry Made Easy by Dr Prakash Mungli, MD by clicking the link below. Here I post USMLE step-1 style MCQs and you can participate in discussion. https://www.facebook.com/drmungli/ Key words: glucose 6 phosphate glucose 6 phosphatase endoplasmic reticulum blood glucose glucagon epinephrine hepatocytes liver liver cells renal tubular cells kidney fasting starvation glycogen gluconeogenesis usmle step1 Mungli
Просмотров: 639 Dr.Mungli
Dr. Rhonda Patrick speaks with Dr. Satchidananda Panda, a professor at the Salk Institute for Biological Studies in La Jolla, California. Satchin's work deals specifically with the timing of food and it's relationship with our biological clocks governed by circadian rhythm and also the circadian rhythm in general. ▶︎ Get the show notes! https://www.foundmyfitness.com/episodes/satchin-panda In this video we discuss... •The fascinating history of experimentation that ultimately elucidated the location for the region of the brain necessary for a properly timed sleep-wake cycles. • The relationship between our body's "master clock" and it's many peripheral clocks. • Why infants sleep so intermittently, instead of resting for a longer, sustained duration like healthy young adults... and why this sustained rest also goes haywire in the elderly. • The fascinating work Dr. Panda took part in that lead to the discovery of a specialized light receptor in the eye that sets circadian rhythms and is known as melanopsin. • The important relationship between the relatively light insensitive melanopsin, which requires around 1,000 lux of light to be fully activated, and its control of the circadian clock by means of activation of the suprachiasmatic nucleus and suppression of melatonin. • The effects light exposure seems to have on next-day cortisol, a glucocorticoid hormone that regulates around 10-20% of the human protein-encoding genome. • The clever experimental design by which Dr. Panda and his colleagues discovered that certain circadian rhythms, especially of the liver, are entrained by when we eat, instead of how much light we get. This underlines the fact that, when managing are circadian rhythm, both elements are important! • One of the more surprising effects of time-restricted feeding in mice eating a so-called healthy diet: increases in muscle mass and even endurance in some cases. You can try out time-restricted feeding and contribute to human research! Commit to 14 weeks and download Dr. Panda's mobile app to get started. Learn more: http://mycircadianclock.org/participant ▶︎ Visit Satchin Panda's Website: http://www.mycircadianclock.org/ ▶︎ Satchin Panda on Twitter: https://twitter.com/SatchinPanda Links related to FoundMyFitness: ▶︎ Subscribe on YouTube: http://youtube.com/user/FoundMyFitness?sub_confirmation=1 ▶︎ Join my weekly email newsletter: http://www.foundmyfitness.com/?sendme=lifestyle-heuristic ▶︎ Crowdfund more videos: http://www.patreon.com/foundmyfitness ▶︎ Subscribe to the podcast: http://itunes.apple.com/us/podcast/foundmyfitness/id818198322 ▶︎ Twitter: http://twitter.com/foundmyfitness ▶︎ Facebook: http://www.facebook.com/foundmyfitness ▶︎ Instagram: http://www.instagram.com/foundmyfitness
Просмотров: 468943 FoundMyFitness
Watch this Webinar on Labroots at http://www.labroots.com/virtual-event/genetics-genomics-2016 Wolframin is a major protein of the endoplasmic reticulum, it is expressed in most tissues and clinical data demonstrate its significant connection to diabetes mellitus. Loss of function mutations of the WFS1 gene result in the monogenic Wolfram-syndrome, characterized by optic atrophy, diabetes insipidus, early onset diabetes mellitus and deafness. Accordingly, polymorphic variants of the gene, which cause only minor alterations in protein function, are putative risk factors of diabetes. This presentation focuses on the association and molecular analysis of two SNPs (rs1046322 and rs9457) in the 3’ UTR region of the WFS1 gene, which are supposed to alter the binding of miRNA-668 and miRNA-185, respectively, based on in-silico data. Association analysis of the polymorphic loci and diabetes mellitus was carried out on 617 patients and 1147 health controls in the study. Genotype analysis was carried out using PCR and single base extension (SBE) reaction using the GenomeLab GeXP™ Genetic Analyzer. Functional analysis of miRNA binding was investigated by luciferase reporter system. The results suggested that rs9457 SNP “C” allele was significantly more frequent among patients with type 2 diabetes mellitus (p = 0.0008), whereas the rs1046322 variant showed a significant association with the type 1 form of the disease. Haplotype analysis confirmed the roles of the polymorphic variants in the genetic background of diabetes. In addition, the luciferase reporter experiments confirmed the data of the sequence analysis in where the rs1046322 and the rs9457 SNPs altered the binding of miRNA-668 and miRNA-185, respectively. Earlier studies indicated an association between a third variant of the 3’ UTR (rs1046320) and diabetes; however no biological function of the SNP could be observed. This is probably due to the strong linkage disequilibrium between rs9457 and rs1046322, thus the latter polymorphism could be a potential genetic marker of rs9457 miRNA-SNP.
Просмотров: 106 LabRoots
http://www.stomponstep1.com/usmle-biochemistry-high-yield-rating-biochem-for-step-1/ Biochem Material Listed By High Yield Rating: 8 – Kartagners Syndrome 7 – Tay-Sachs) 5 – I Cell Disease 4 – Osteogenesis Imperfecta 3 – Methanol Poisoning 3 – PKU 3 – Cytoskeleton Basics 3 – Marfan Synrome 3 – Collagen and Elastin Basics 2 – Alcohol Metabolism 2 – Fructose Disorder 2 – Galactose Disorder 2 – Chediak Higashi 2 – Ehlers Danlos 2 – Gaucher 2 – Von Gierkes 2 – McCardles 1 – Nieman-Pick 1 – Sorbitol 1 – OTC Deficiency 1 – Hurler 1 – Fabry 1 – Maple Syrup Urine Disease “No Yield” (HYR of 0): • The Biochemical Structures of Almost Anything • Ammonia Transport • Specifics about Lipid Transport • Hartnup Disease • Cori Disease • Pompe Disease • Cystinuria • Protein structure • Specific functions of most organelles • Specifics about cilia structure • Types of intermediate filaments & associated immunohistochemical stains • Cellular trafficking signals other than Mannose-6-Phosphate • Peroxisome & Proteasome • Smooth vs. rough endoplasmic reticulum • Cytoskeleton assembly and disassembly • Henderson Hasselbalch Eqn • Chemical Bonds • Thermodynamics • Michaelis-Menton Eqn • Specifics about most Laboratory Techniques
Просмотров: 28176 Stomp On Step 1
Date: 21 December 2014 Speaker: Prof.DR.dr. A Boedisantoso R. SpPD-KEMD Location: Shangri-La Hotel, Jakarta Event: Jakarta Diabetes Meeting
Просмотров: 43 Meetmed
http://www.peertechz.com/Vaccines-Immunology/pdf/JVI-1-107.pdf Expression of MHC I at the cell surface is essential for presenting peptides to circulating cytotoxic T cells. Interference with a number of components of the antigen processing machinery is an immune evasion mechanism that has been highlighted in a number of malignancies.
Просмотров: 13 immunology immunology
Poster winner Ankita Burman, MS shares her findings in how crucial alveolar epithelium is in IPF pathogenesis. Full Presentation Title: ER Stress Effector CHOP Augments AEC Apoptosis and Worsens Lung Fibrosis during the Disease Mechanisms I session of the PFF Summit 2017. Learn more about causes and symptoms of pulmonary fibrosis at http://www.pulmonaryfibrosis.org/life-with-pf/about-pf. This activity is jointly provided by Postgraduate Institute for Medicine and the Pulmonary Fibrosis Foundation, in collaboration with Global Academy for Medical Education. Please note that any information contained in this presentation is for informational and/or educational purposes only. This is not an endorsement of any specific service or medication. It is not intended to be a substitute for professional medical advice. Always consult your personal physician or health care provider with any questions you may have regarding your specific medical condition. If you desire or need advice or referral information, please consult your health care provider or contact the PFF Patient Communication Center (PCC). (Toll Free) 844-Talk-PFF or firstname.lastname@example.org. Opening Music: www.bensound.com
Просмотров: 224 Pulmonary Fibrosis Foundation
1. Contact me at email@example.com / Friend me on Facebook (kevin.g.ahern) 2. Download my free biochemistry book at http://www.davincipress.com/freeforall.html 3. Take my free iTunes U course at https://itunes.apple.com/us/course/biochemistry/id556410409 4. Lecturio videos for medical students - https://www.lecturio.com/medical-courses/biochemistry.course 5. Course video channel at http://www.youtube.com/user/oharow/videos?view=1 6. Check out all of my free workshops at http://oregonstate.edu/dept/biochem/ahern/123.html 7. Check out my Metabolic Melodies at http://www.davincipress.com/ 8. My courses can be taken for credit (wherever you live) via OSU's ecampus. For details, see http://ecampus.oregonstate.edu/soc/ecatalog/ecourselist.htm?termcode=all&subject=BB 9. Course materials at http://davincipress.com/bb450.html Highlights - Fatty Acid Oxidation 1. Fats are broken down to fatty acids and glycerol by enzymes known as lipases. Hormone sensitive triacylglycerol lipase is the only regulated enzyme of fat or fatty acid breakdown. 2. Triacylglycerol lipase action cleaves the first fatty acid off of a fat and this step is necessary before the other lipase can act to remove the other fatty acids from a fat. 3. Fatty acid oxidation occurs in the matrix of the mitochondrion. In the cell, fatty acids are attached to CoA and then at the mitochondrion, the CoA is replaced by carnitine. Inside the mitochondrial matrix, the carnitine is replace by CoA again. 4. Steps in fatty acid oxidation include dehydrogenation, hydration, oxidation, and thiolytic cleavage. The dehydrogenation and oxidation reactions yield reduced electron carriers. Thiolytic cleavage is catalyzed by the enzyme called thiolase. 5. The first reaction of fatty acid oxidation involves acyl dehydrogenases. These are specific for fatty acids with long, medium, or short chains. The medium chain acyl dehydrogenase has been implicated in some instances of sudden infant death syndrome. 6. The long chain acyl dehydrogenases are found in peroxisomes and this is where oxidation of long chain fatty acids (longer than 16 carbons) begins. Oxidation involves transfer of electrons to oxygen to make hydrogen peroxide, instead of FADH2. 7. The first step of oxidation generates a trans-intermediate plus FADH2. The second step involves addition of water across the trans double bond to create an intermediate in with an OH on carbon 3 in the L configuration. The third step involves oxidation of the hydroxyl intermediate to a ketone on carbon 3. The last step involves cleaving off of an acetyl-CoA and production of a fatty acyl-CoA with two fewer carbons. 8. Oxidation of biologically occurring fatty acids with cis double bonds requires two additional enzymes compared to oxidation of saturated fatty acids. These enzymes are enoyl-CoA-isomerase and 2,4-dienoyl-CoA-reductase. 9. Enoyl-CoA-isomerase converts cis or trans bonds between carbons 3 and 4 to trans bonds between carbons 2 and 3. 10. 2,4-dienoyl-CoA reductase acts on intermediates that have double bonds between carbons 2-3 and 4-5. It uses NADPH to reduce the two double bonds to one double bond and the resulting double bond is placed in a cis configuration between carbons 3-4. 11. Oxidation of fatty acids with odd numbers of carbons yields a final product of propionyl-CoA, not acetyl-CoA. 12. Conversion of propionyl-CoA to succinyl-CoA requires three steps. The first is addition of a carboxyl-group to the middle carbon in the molecule. 13. Ketone bodies are produced by the body when glucose precursors are not available to make glucose. Examples of ketone bodies include acetoacetate and hydroxybutyrate. Diabetics have problems with glucose metabolism and may produce ketone bodies to provide energy to keep the brain alive. One can detect this by the smell of acetone on their breath. Fatty Acid Biosynthesis 1. The process occurs similarly to beta-oxidation, though in reverse. Important distinctions are noted below in a-f. a. Fatty acid synthesis up to palmitate occurs in the cytoplasm. b. Fatty acids are built using an acyl carrier protein (ACP),. c. NADPH is used to donate electrons in synthesis. d. A three carbon molecule, malonyl-ACP donates two carbons to the growing fatty acid chain - a carbon dioxide is lost in the process. e. Synthesis of fatty acids longer than 16 carbons occurs in endoplasmic reticulum or mitochondrion. f. In fatty acid biosynthesis, a D-hydroxyl intermediate is formed at carbon #3. 2. Acetyl-CoA carboxylase catalyzes the addition of a carboxyl group to acetyl-CoA to form malonyl-CoA. 3. The enzymes of fatty acid synthesis apart from acetyl-CoA carboxylase are contained in a complex known as fatty acid synthase. 4. Fatty acid synthase produces the saturated 16 carbon fatty acid known as palmitate.
Просмотров: 34251 Kevin Ahern
This video describes how a common fungal infection, prenatal trauma, and the endoplasmic reticulum inside cells interact to cause the experience of 'voices'. Surprisingly, almost the entire human population has this problem, but most people can suppress the volume of their 'voices' adequately. Two approaches for treatment are discussed: a quick, one voice at a time treatment; or one that eliminates all voices simultaneously by using a psychoneuroimmunology technique that makes the client immune to the fungus. The video was created by Piotr Kawecki and narrated by Dr. McFetridge from the Institute for the Study of Peak States.
Просмотров: 2361 InstitutePeakStates
Hi, I am Dr. Dweipayan Goswami, Welcome to my YouTube channel "Learn at ease" I will be uploading animated videos related to biochemistry for the Under Graduates and Graduates purely based on the information form the traditional text books such as 'Lehninger’s Principles of Biochemistry, 5th Edition. Nelson and Cox', Biochemistry, 5th Edition. Garrett and Grisham'. etc. In almost the same order to that of the chapters in the book. I will also upload videos in the subjects of Microbiology, Biotechnology, Immunology etc. With your request, I will be uploading videos under this playlist with audio. If you like the concept, please subscribe to my channel 'LEARN AT EASE' Insulin (Part 1) Overview of Insulin Production & Signalling: https://www.youtube.com/watch?v=wixDPv0Ltkk Insulin (Part 2) Synthesis of Insulin by β Cells: https://www.youtube.com/watch?v=BmAPpHA081M Background music: Bay Breeze by FortyThr33 https://soundcloud.com/fortythr33-43 Creative Commons — Attribution 3.0 Unported— CC BY 3.0 http://creativecommons.org/licenses/b... Music provided by Audio Library https://youtu.be/XER8Zg0ExKU
Просмотров: 627 Learn-at-ease
Presented By: Jeffrey James Rodvold, PhD - Postdoctoral Researcher, UCSD Speaker Biography: Jeffrey is an expert in tumor microenvironment biology. Currently a postdoctoral researcher, he completed his PhD in Biomedical Sciences at UC San Diego focused on the unfolded protein response (UPR) within the tumor microenvironment. His research involved elucidating how the tumor microenvironment becomes dysregulated within both the cancer cell and immune infiltrate compartments through the production of signaling molecules cancers cells producing during the UPR. He earned his BS in Bioengineering : (Biotechnology) from UC San Diego in 2010 where he performed research in the fields of biomaterials and stem cell mechanotransduction. Webinar: Cancer Cells Send Signals Boosting Survival and Drug Resistance in Other Cancer Cells Webinar Abstract: Successful tumor outgrowth requires the coordination of a variety of cell intrinsic and cell extrinsic signaling events. These events include those establishing a tumor microenvironment (TME) that both enables tumor cell survival and disables anti-tumor immunity. Recent reports demonstrate that these events require molecules produced by resident tumor cells. Tumor-borne signals within the tumor microenvironment propagate tumor cell fitness and immune hijacking. The endoplasmic reticulum (ER) stress is an adaptive response to a variety of TME insults, including hypoxia and nutrient deprivation, raising the possibility that ER stress could serve as a potential source of tumor cell fitness and immune dysregulation. To that end, we induced cancer cells of various origin to undergo ER stress and harvested the resulting conditioned medium (CM) to explore its effects on both recipient cancer cells and immune cells. Cell culture medium became an invaluable tool to our studies as it allowed us to recreate stimuli existent within the tumor microenvironment under controlled conditions. Our results revealed that the CM of cancer cells undergoing ER stress transmits ER stress to recipient cells. On the one hand, myeloid cells (macrophages and dendritic cells) treated with the CM of ER stressed cancer cells acquire a mixed pro-inflammatory and immune suppressive phenotype, which restrained T cell anti-tumor immunity and facilitated tumor growth in vivo. On the other hand, cancer cells treated with the CM of ER stressed cancer cells acquire cellular fitness to a variety of challenges including nutrient deprivation and chemotherapies. When implanted into immune competent hosts, ER stress experienced cancer cells grew at markedly faster rates than inexperienced ones. These findings support the existence of a novel mechanism used by tumor cells to restrain anti-tumor immunity while enhancing cellular fitness with the TME. Sponsored By: Thermo Fisher Scientific/Gibco Earn PACE Credits: 1. Make sure you’re a registered member of LabRoots (https://www.labroots.com/ms/webinar/webinar-cancer-cells-send-signals-boosting-survival-drug-resistance-cancer-cells) 2. Watch the webinar on YouTube or on the LabRoots Website (https://www.labroots.com/ms/webinar/webinar-cancer-cells-send-signals-boosting-survival-drug-resistance-cancer-cells) 3. Click Here to get your PACE credits (Expiration date – November 14, 2019 10:00 AM): https://www.labroots.com/credit/pace-credits/2459/third-party LabRoots on Social: Facebook: https://www.facebook.com/LabRootsInc Twitter: https://twitter.com/LabRoots LinkedIn: https://www.linkedin.com/company/labroots Instagram: https://www.instagram.com/labrootsinc Pinterest: https://www.pinterest.com/labroots/ SnapChat: labroots_inc
Просмотров: 68 LabRoots
This day-in-the-life video serves to demystify aspects of the Ask Lab at McMaster University by following a student's typical day in the lab! The Ask Lab explores protein misfolding events, which have contributed to the development of various diseases such as cystic fibrosis, diabetes, and cancer. This lab is mainly interested in the events in the endoplasmic reticulum (ER) which occur when proteins do not fold correctly. The Unfolded Protein Response (UPR) is discussed, which may play a role in the development and further progression of chronic lung diseases. In addition, the video covers what fibrosis is and how we can test that in the lab, as well as the clinical implications. This video features a talk from a PhD student Ehab Ayaub, a Masters candidate Sohail Mahmood, and principal investigator Dr. Kjetil Ask. This video was created by Health Science 4DM3 students: Mawleshan Pathmajarah, Hassan Alsaleh, Dana Abu-Jazar, Aunima Bhuiya, and Hina Abdulla. © 2015. McMaster University. All rights reserved. Please find more information about the Ask-lab here: http://fhs.mcmaster.ca/ask-lab/index.html
Просмотров: 912 Demystifying Medicine
Faculty Of Medicine Tanta University Pharmacology Department By Student: Rabea Alomar ___________________________________ Thyroglobulin synthesized by endoplasmic reticulum Iˉ is transported actively from the blood to the follicular cell Thyroglobulin is transported to the lumen of thyroid follicle by exocytosis Iˉ is transported to the lumen of thyroid follicle by Pendrin which is sodium independent iodide transporter Iˉ oxidized to I by thyroid peroxidase enzyme Organification of I by peroxidase (MIT , DIT) Coupling of MIT and DIT by peroxidase Endocytosis occurs to get this complex inside the follicular cell Lysis of thyroglobulin by lysosomes Thyroid hormones released in the blood stream Some of T4 converted to the more active T3 K Perchlorate Thiocyanate B Blockers Corticosteroids Thioamides Amiodarone - Inhibit peripheral conversion of T4 into T3 - Used in thyroid crisis Thioamides Inhibit peroxidase enzyme: - No Oxidation - No Organification - No Coupling
Просмотров: 16679 Rabe3al3mr
Obesity is associated with insulin resistance, type 2 diabetes, cardiovascular disease, cancer and many other devastating diseases. Obesity is also a state of chronic inflammation and, as such, the cells in our immune system become overactive. Professor Mirela Delibegovic is studying proteins crucial in the on/off switches in our immune cells, called tyrosine phosphatases. Using the latest DNA sequencing technology, this research will improve our understanding of the immune system and allow development of specific therapies for different diseases.
Просмотров: 468 School of Medicine, Medical Sciences and Nutrition
Tommer Ravid - How misfolded substrates are marked for ERAD?
Просмотров: 48 Israel Institute for Advanced Studies
Defesa Doutorado Unicamp: ESTUDO DA VARIAÇÃO CIRCADIANA DA UPR NO HIPOTÁLAMO E SUAS IMPLICAÇÕES NA INGESTÃO ALIMENTAR. O dobramento das proteínas pode ser afetado ainda por processos fisiológicos, tais como o acúmulo de grandes quantidades de proteínas imaturas no RE ocasionado por um excesso de nutrientes que estimulam a produção da insulina. Quando há excesso de proteínas localizadas no reticulo ocorre sobrecarga da capacidade de dobramento, condições essas que alteram a homeostase do RE e comprometem seu adequado funcionamento, gerando um estado conhecido como estresse do reticulo endoplasmático, que em resposta celular ao estresse, ativa um denominado mecanismo adaptativo a proteínas desdobradas chamada de Unfolded Protein Response, a UPR.
Просмотров: 102 Dra. Caroline Mesquita
This video animation gives a brief overview of the unfolded protein response
Просмотров: 381 TrainERS network
Dr. Robert Melamede has a Ph.D. in Molecular Biology and Biochemistry from the City University of New York. Dr. Melamede retired as Chairman of the Biology Department at University of Colorado, Colorado Springs in 2005, where he continues to teach and research cannabinoids, cancer, and DNA repair. Dr. Melamede is recognized as a leading authority on the therapeutic uses of cannabis, and has authored or co-authored dozens of papers on a wide variety of scientific subjects. Dr. Melamede also serves on the Editorial Board of The Journal of the International Association for Cannabis as Medicine, the Scientific Advisory Board of Americans for Safe Access, Sensible Colorado, Scientific Advisor for Cannabis Therapeutics as well as a variety other of state dispensaries and marijuana patient advocacy groups. Dr. Melamede, is currently the President & CEO of Cannabis Science Inc., a pioneering U.S. biotech company that is focused on developing pharmaceutical cannabis products. Check out his channel at: https://www.youtube.com/user/doctorbobcannabuzz "The evidence is piling up in mice infested labs that the endocannabinoid system when stimulated by cannabinoids has an antitumor affect and can instruct cancer cells to commit suicide" Watch full version of "What If Cannabis Cured Cancer" https://www.youtube.com/watch?v=lK2pxyo3R8Y Still have doubts after watching this video? Well than here's lots more proof below :-) Pot Shrinks Tumors; Government Knew in '74 Published by: Raymond Cushing May 30, 2000 http://www.alternet.org/story/9257/pot_shrinks_tumors%3B_government_knew_in_'74 Lung Cancer (Lewis Lung Adenocarcinoma) Antineoplastic activity of cannabinoids First Published: December 26, 1974 http://www.ukcia.org/research/AntineoplasticActivityOfCannabinoids/index.php Prostate Cancer Δ9-Tetrahydrocannabinol Induces Apoptosis in Human Prostate PC-3 cells Via a Receptor-independent Mechanism First Published: September 1999 http://onlinelibrary.wiley.com/doi/10.1016/S0014-5793(99)01073-X/full Skin Cancer Published: January 2003 Inhibition of Skin Tumor Growth and Angiogenesis in Vivo by Activation of Cannabinoid Receptors http://www.jci.org/articles/view/16116 Glimoa Brain Cancer Cannabinoids Down-regulate PI3K/Akt and Erk Signalling Pathways and Activate Proapoptotic Function of Bad Protein Published: January 2004 http://www.medicinalgenomics.com/wp-content/uploads/2011/12/Cannabinoids-down-regulate-PI3K.pdf Prostate Cancer 2-Arachidonoylglycerol, A Novel Inhibitor of Androgen-Independent Prostate Cancer Cell Invasion Published: December 2004 http://cancerres.aacrjournals.org/content/64/24/8826.full Lymphoma Immune System Cannabinoid receptor ligands mediate growth inhibition and cell death in mantle cell lymphoma Published: November 2005 http://onlinelibrary.wiley.com/doi/10.1016/j.febslet.2005.11.020/full Breast Cancer Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma Published: September 2006 http://jpet.aspetjournals.org/content/318/3/1375.full Pancreatic Cancer Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum Stress–Related Genes Published: July 2006 http://cancerres.aacrjournals.org/content/66/13/6748.full Pancreatic Cancer Cannabinoid Derivatives Induce Cell Death in Pancreatic MIA PaCa-2 Cells Via a Receptor-independent Mechanism Published: March 2006 http://www.sciencedirect.com/science/article/pii/S0014579306002110 Skin Cancer Cannabinoid Receptors As Novel Targets for the Treatment of Melanoma Published: December 2006 http://bbml.ucm.es/cannabis/archivos/publicaciones/FASEB_J06_20_2633_2635.pdf Bone Cancer Potentiation of the Antitumor Activity of Adriamycin Against Osteosarcoma by Cannabinoid WIN-55,212-2 Published October 2015 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4580018/
Просмотров: 1331 Cannabis Saves Lives!