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  • Jo Bowyer
    replied
    Scientists find key proteins control risk of osteoarthritis during aging

    https://www.sciencedaily.com/release...0214181949.htm



    The study's findings suggest that FOXO proteins are responsible for the maintenance of healthy cells in the cartilage of our joints.

    "We discovered that FoxO transcription factors control the expression of genes that are essential for maintaining joint health," says Martin Lotz, MD, a TSRI professor and senior author of the study, published today in the journal Science Translational Medicine. "Drugs that boost the expression and activity of FoxO could be a strategy for preventing and treating osteoarthritis."

    Previous research from Lotz' lab showed that as joints age, levels of FoxO proteins in cartilage decrease. Lotz and his colleagues had also found that people with osteoarthritis have a lower expression of the genes needed for a process called autophagy. Autophagy ("auto" meaning "self" and "phagy" meaning "to eat") is a cell's way of removing and recycling its own damaged structures to stay healthy.

    For the new study, researchers used mouse models with FoxO deficiency in cartilage to see how the FoxO proteins affect maintenance of cartilage throughout adulthood.

    The researchers noticed a striking difference in the mice with "knockout" FoxO deficiency. Their cartilage degenerated at much younger age than in control mice. The FoxO-deficient mice also had more severe forms of post-traumatic osteoarthritis induced by meniscus damage (an injury to the knee), and these mice were more vulnerable to cartilage damage during treadmill running.

    The culprit? The FoxO-deficient mice had defects in autophagy and in mechanisms that protect cells from damage by molecules called oxidants. Specific to cartilage, FoxO-deficient mice did not produce enough lubricin, a lubricating protein that normally protects the cartilage from friction and wear. This lack of lubricin was associated with a loss of healthy cells in a cartilage layer of the knee joint called the superficial zone.

    These problems all came down to how FoxO proteins work as transcription factors to regulate gene expression. Without FoxO proteins running the show, expression of inflammation-related genes skyrockets, causing pain, while levels of autophagy-related genes plummet, leaving cells without a way to repair themselves.

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  • Jo Bowyer
    replied
    Timing is Everything, to Our Genes

    http://neurosciencenews.com/genetics-timing-8461/

    “This is the first time a reference map of daily gene expression has been established,” says Satchidananda Panda, a professor in Salk’s Regulatory Biology Laboratory and senior author on the paper. “It’s a framework to understand how circadian disruption causes diseases of the brain and body, such as depression, Crohn’s disease, IBD, heart disease or cancer. This will have huge impact on understanding the mechanisms or optimizing cures for at least 150 diseases.”

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  • Jo Bowyer
    replied
    Major mental illnesses unexpectedly share brain gene activity, raising hope for better diagnostics and therapies

    http://www.sciencemag.org/news/2018/...et_cid=1841749

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  • Jo Bowyer
    replied
    The Stress-Induced Transcription Factor NR4A1 Adjusts Mitochondrial Function and Synapse Number in Prefrontal Cortex

    http://www.jneurosci.org/content/38/6/1335?etoc=

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  • Jo Bowyer
    replied
    Gene Network That Regulates Motor Neuron Formation During Embryonic Development Identified

    http://neurosciencenews.com/motor-ne...elopment-8431/

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  • Jo Bowyer
    replied
    We are multitudes

    https://aeon.co/essays/microchimeris...4d912-69418129

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  • Jo Bowyer
    replied
    Reprogramming bacteria instead of killing them could be the answer to antibiotic resistance

    https://theconversation.com/reprogra...c%20resistance

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  • marcel
    replied
    This research may open a (new) window to finding therapies for disease with epigenetic components



    [QUOTE]The laboratory staff demonstrated that under conditions of extreme stress, such as starvation, a fascinating phenomenon occurs: offsprings whose parents had suffered starvation showed a much longer life expectancy than worms whose parents had been well-fed. This phenomenon lasts several generations - and then disappears.
    This mechanism can also be reset. If normal inheritance of small RNA molecules continues for a limited number of generations, renewed stress will cause the cycle to start again, and will prolong the epigenetic, or beyond the DNA, inheritance. Studies conducted on relatively simple animals are the research basis for understanding the operational mechanisms of inheritance processes that also apply to humans, including epigenetic mechanisms. The next step is to investigate whether small RNA inheritance may also affect the process of evolution.
    /QUOTE]

    from

    http://www.odedrechavilab.com

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  • Jo Bowyer
    replied
    Researchers have developed new single-cell sequencing methods that could be used to map the cell origins of various brain disorders, including Alzheimer’s, Parkinson’s, schizophrenia

    http://neurosciencenews.com/brain-ce...-disease-8157/

    Using the information from RNA sequencing and chromatin mapping methods, researchers were able to map which cell types in the brain were affected by common risk alleles–snippets in DNA that occur more often in people with common genetic diseases. Researchers could then rank which subtypes of neurons or glial cells are more genetically susceptible to different brain diseases. For example, they found that two subtypes of glial cells, microglia and oligodendrocytes, were the first and second most at risk, respectively, for Alzheimer’s disease. They also identified microglia as most at risk for bipolar disorder, and a subtype of excitatory neurons as most at risk for schizophrenia.

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  • Jo Bowyer
    replied
    Reading the genome like a history book

    http://science.sciencemag.org/conten...68/1265.2.full

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  • Jo Bowyer
    replied
    CLOCK Gene May Hold Answers to Human Brain Evolution

    http://neurosciencenews.com/clock-brain-evolution-8124/

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  • Jo Bowyer
    replied
    New Genes Associated With Cognitive Ability Identified

    http://neurosciencenews.com/genetics-cognition-8048/

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  • marcel
    replied
    Study uncovers mutation that supercharges tumor-suppressor

    http://med.stanford.edu/news/all-new...uppressor.html

    Stanford scientists have found an answer to one of cancer biology’s toughest and most important questions: How does the body suppress tumors? Cancer researchers have long hailed p53, a tumor-suppressor protein, for its ability to keep unruly cells from forming tumors. But for such a highly studied protein, p53 has hidden its tactics well.

    Now, researchers at the Stanford University School of Medicine have tapped into what makes p53 tick, delineating a clear pathway that shows how the protein mediates antitumor activity in pancreatic cancer. The team’s research also revealed something unexpected: A particular mutation in the p53 gene amplified the protein’s tumor-fighting capabilities, creating a “super tumor suppressor.”

    The protein functions a bit like a puppet master in the genome, guiding the activation or suppression of many cancer-relevant genes in the body. “But if you simply ask how cells with and without p53 are different, you’ll see that there are at least 1,000 genes whose expression is affected by p53 status,” said Laura Attardi, PhD, professor of radiation oncology and of genetics. “So, getting to the bottom of which of those many genes are critical to tumor suppression is not a trivial question.”

    A paper describing the work was published online Oct. 9 in Cancer Cell. Attardi is the senior author. Research associate Stephano Mello, PhD, is the lead author.

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  • Jo Bowyer
    replied
    An Internal Fountain of Youth: Why These Amish Live Longer and Healthier

    http://neurosciencenews.com/amish-genetics-aging-7961/

    Summary:
    Researchers have identified a genetic mutation in an extended Amish family that allow them to live 10 percent longer and have 10 percent longer telomeres than other Amish kindred members who do not have the mutation. People with this mutation also have a lower diabetes risk and lower vascular aging, researchers note.

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  • Jo Bowyer
    replied
    Communicating the promise, risks, and ethics of large-scale, open space microbiome and metagenome research

    https://microbiomejournal.biomedcent...A3B05EFCC6B4FE
    Abstract

    The public commonly associates microorganisms with pathogens. This suspicion of microorganisms is understandable, as historically microorganisms have killed more humans than any other agent while remaining largely unknown until the late seventeenth century with the works of van Leeuwenhoek and Kircher. Despite our improved understanding regarding microorganisms, the general public are apt to think of diseases rather than of the majority of harmless or beneficial species that inhabit our bodies and the built and natural environment. As long as microbiome research was confined to labs, the public’s exposure to microbiology was limited. The recent launch of global microbiome surveys, such as the Earth Microbiome Project and MetaSUB (Metagenomics and Metadesign of Subways and Urban Biomes) project, has raised ethical, financial, feasibility, and sustainability concerns as to the public’s level of understanding and potential reaction to the findings, which, done improperly, risk negative implications for ongoing and future investigations, but done correctly, can facilitate a new vision of “smart cities.” To facilitate improved future research, we describe here the major concerns that our discussions with ethics committees, community leaders, and government officials have raised, and we expound on how to address them. We further discuss ethical considerations of microbiome surveys and provide practical recommendations for public engagement.
    Keywords

    Microbiome Metagenome Built environment PublicMetaSUBConcerns Ethics

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