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    Home > Biochemistry News > Biotechnology News > Life Sciences Breakthrough Award 2020: Progress in genetic research related to obesity and pain.

    Life Sciences Breakthrough Award 2020: Progress in genetic research related to obesity and pain.

    • Last Update: 2020-08-05
    • Source: Internet
    • Author: User
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    What is a truly "unfinished" career? It's not weight loss.
    weight loss bitter, weight loss tired, a do not pay attention to the white.
    science is the ultimate goal of solving human problems, scientists decrypt the mechanism of life may be "trickle" to achieve this cause. On September 5,
    , the Science Breakthrough Award, known as the Science Oscar, presented the science science award to Jeffrey Friedman, a Professor at Rockefeller University who discovered leptin mechanisms, and four other scientists whose research brings ground-breaking insights into the mechanisms of human activity and the most grounded explanations and solutions for a variety of diseases like the enigma.
    you "fail" I "overeat" with gene-positioning technology to find that the leptin gene that causes obesity for most people, open legs, shut down the mouth can effectively control weight, but for some people, they in the appetite "lost" the mind, eat, constantly hungry.
    life sciences, all symptoms are material-based.
    Friedman found the gene in mice that "don't know how to be full."
    he inherited the "clothes" of the theory's author, Glass Gorman, and used gene-positioning techniques to discover the first obesity gene, which was positioned on chromosome 6.
    this gene expression forms a secreted protein, which Friedman calls leptin.
    surprisingly, the gene is only active in adipose tissue.
    this is unexpected, and it was previously notknown that fat cells also produce important hormones.
    later, he and other researchers identified leptin receptors and found that leptin controls weight, requiring leptin and leptin receptors to exist at the same time, and that the absence of any one makes mice "snobs."
    this finding in mice, which has since been shown to exist in humans, and very few people ate surprisingly much, most likely because of their leptin gene mutation, which produces too little leptin, a patient who rapidly lost weight after receiving leptin replacement therapy.
    commented that weight-loss drugs, which are mainly used in leptin, are expected to emerge in the near future.
    but studies have shown that leptin doesn't make people thin for some common obese people.
    further, people are looking for the "key" to leptin gene regulation.
    leptin genes are regulated by adjacent DNA sequences and regulatory factors, which are activated in fat cells and control the amount of leptin produced, a process called long non-coding RNA regulation of leptin production, rather than the generic factor (a protein) that is not commonly thought.
    that is, in addition to increasing leptin itself, it can also regulate the production of leptin through other ways, once leptin has side effects on the human body, there are other ways of intervention.
    whether leptin diet pills appear or whether there are unbearable side effects, leptin findings have led scientists to find physiological and neuroscience mechanisms that regulate food intake and body weight, thus creating a new theoretical framework for understanding the pathogenesis of obesity.
    you "mistake" I "aging" molecular companion GroE let protein folding art feel like if the protein folding is a "ghost work" art treasures, then the molecular companion GroE is a skilled "artist."
    it grabs the loose proteins, and in its own unique "studio", it's able to access the energy generated by ATP (adenosine triphosphate), giving the unfolded polypeptide art a feel.
    franzel Ulrich Harter, a researcher at the Max Planck Institute for Biochemistry, and Arthur Horridge, a professor at Yale University, were among the artists who discovered the artist.
    , Hartleand and Horridge discovered the protein that was misfolded or defected early in the study, and they wanted to find the cause of the error in life.
    they confirmed the activity of a molecular companion called GroE in a test tube, and then, through detailed research, high-resolution structural analysis showed the precise atomic structure of its folding cavity.
    using structural biology, Horridge also intuitively "beats" the "continuous frame" of GroE's work, solving the atomic structure of the folding mechanism.
    , Hartle and Horridge show that GroE captures an unfolded peptide in a closed chamber that, under the action of ATP energy, can change its shape at different stages until the final release of a fully folded protein product.
    as we age, molecular partners may "mistake" protein aggregation, which is now thought to be linked to many geriatric diseases, including cancer, Alzheimer's disease (AD) and Parkinson's disease (PD).
    many studies are exploring ways to restore or maintain the folding mechanisms of these cells to keep the body functioning normally and healthily by preventing the false polymerization of proteins during aging.
    now, more and more research into protein folding has turned to the use of molecular companion GroE families. some scholars
    have successfully used molecular partners to assist protein recovery function in the body and in vitro.
    but molecular partners in the actual application of high cost and need to separate from complex proteins and other shortcomings, so the development of molecular companion reuse and stability is the key to achieve its application.
    you "discharge" I "pain" to find pain mechanism, identify and clone the relevant ion channel "pain, pain, pain", in the context of the brain, should be translated as "electric, electric, electricity." David Julius of the University of California, San Francisco, who
    the winner, spent more than a decade answering one question: Why do you find it hot and painful to apply to your skin with chili peppers?
    he eventually discovered the molecules, cells, and related mechanisms involved in pain.
    his team answered questions about how capsaicin makes the skin feel hot in a groundbreaking article published in 1997, and they identified and cloned the relevant ion channel TRPV1.
    TRPV1 is a unique ion channel located at the end of the sensory nerve.
    these channels can open and close, thus controlling the operation of charged atoms across the cell membrane.
    ion channels keep opening and closing, electrical signals continue to "run position", so that the nerve cell membrane produces rapid potential changes, electrical signals will be transmitted along the nerve cells to the brain.
    experiments have shown that TRPV1 can be activated not only by capsaicin, but also by temperatures above 43 degrees C.
    that's why the burning pain of burns and pepper spray is very similar.
    then, Julius successfully cloned and identified other sensory-related ion channels, such as TRPA1 channels, which conduct pain, irritating sensations and inflammation activated by mustard and other substances containing mustard oil;
    pain-related ion channels can warn the body to make their own actions, such as TRPA1 can also find the environment of irritating substances such as propylene aldehyde, and tear gas, car exhaust gas, etc. are acrylonitrile, these harmful chemicals, before humans have entered the chemical society, the body knows how to distinguish.
    it can be seen that different ion channels produce not exactly the same electrical signals, for the brain, different electrical signals from the pain channel represent a different crisis.
    later, Julius identified specific cell targets associated with chronic pain in diseases such as irritable bowel syndrome (IBS), arthritis, and cancer.
    his team has created a solid theoretical foundation for the development of a new generation of non-opioid precision painkillers.
    at present, a large number of research work focused on the TRP channel, hoping to target the development of new analgesic drugs to avoid opioid addiction, itching and other side effects.
    you "entangled" i "dementia" "tau protein hypothesis" rich neurodegenerative disease characterization molecular species before tau protein, people believe that beta-amyloid protein is the "cause" of AD, a number of large pharmaceutical companies with beta-amyloid as the "attack key point" to develop drugs to treat AD, and eventually are turned into clinical trials.
    , Ferginia Manyi Lee, a member of the American Academy of Medicine and a professor at the University of Pennsylvania, proposed the "tau protein hypothesis" in 1991, arguing that tau proteins appear in neurons in Patients with AD and form a theative network that inhibits normal discharge of neurons.
    she also found similar tangenty structures in the neurons of patients with PD and amyotrophic lateral sclerosis. Professor
    Li's research focused on AD, PD, frontal lobe dementia (FTD), amyotrophic lateral sclerosis (ALS) and related neurodegenerative diseases.
    her major achievements include the discovery of disease-related proteins such as tau, alpha-synaptic nucleoproteins and TDP-43 in these diseases, the elaboration of the role of these proteins in neurodegeneration, the discovery of TDP-43 protein polymers in FTD and ALS, and the discovery of different forms of alpha-synaptic nucleoproteins in different cell types that contribute to PD and multisystem atrophy. Professor
    Li's findings not only open a new path for the search for relevant drug targets, but also enrich the types of characterization molecules of neurodegenerative diseases, allowing people to explore their interrelationships and study the diversity of pathogenesis.
    beta-amyloid (A-beta) and tau proteins are iconic proteins of AD and have been extensively studied for their respective toxic forms.
    recently, the possible interactions and synergies between the two in AD have been gradually clarified.
    Source: Science Daily.
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