Euthanasia, suicide or death are not the solutions to one's suffering from health conditions - SCI-ART LAB2024-03-28T17:47:36Zhttps://kkartlab.in/forum/topics/euthanasia-suicide-or-death-are-not-the-solutions-to-one-s-suffer?groupUrl=some-science&feed=yes&xn_auth=noResearchers discover a new wa…tag:kkartlab.in,2023-03-24:2816864:Comment:2472402023-03-24T05:25:16.737ZDr. Krishna Kumari Challahttps://kkartlab.in/profile/DrKrishnaKumariChalla
<h1 class="text-extra-large line-low mb-2">Researchers discover a new way to fight the aging process and cancer development</h1>
<p class="article-byline text-low">by<span> </span><a class="article-byline__link" href="http://www.portal.uni-koeln.de/uoc_home.html?&L=1" rel="noopener" target="_blank">University of Cologne</a></p>
<div class="mt-4 article-main"><div class="article-gallery lightGallery"><div style="box-sizing: border-box;"><img alt="Researchers discover a new way to fight the aging process and cancer development" height="530" src="https://scx1.b-cdn.net/csz/news/800a/2023/researchers-discover-a-3.jpg" title="lin-52 mutant worms retained motility upon DNA damage induction. lin-52(n771) and WT day 1 adult worms were irradiated or mock-treated with UV-B and their motility was measured after 72 h. Maximum speed per individual is presented (mean +/− SD in red). Two-tailed Mann-Whitney test was used. From left to right, n = 20, 23, 29, 32. Credit: Nature Structural & Molecular Biology (2023). DOI: 10.1038/s41594-023-00942-8" width="800"></img> lin-52 mutant worms retained motility upon…</div>
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<h1 class="text-extra-large line-low mb-2">Researchers discover a new way to fight the aging process and cancer development</h1>
<p class="article-byline text-low">by<span> </span><a class="article-byline__link" href="http://www.portal.uni-koeln.de/uoc_home.html?&L=1" target="_blank" rel="noopener">University of Cologne</a></p>
<div class="mt-4 article-main"><div class="article-gallery lightGallery"><div style="box-sizing: border-box;"><img src="https://scx1.b-cdn.net/csz/news/800a/2023/researchers-discover-a-3.jpg" alt="Researchers discover a new way to fight the aging process and cancer development" title="lin-52 mutant worms retained motility upon DNA damage induction. lin-52(n771) and WT day 1 adult worms were irradiated or mock-treated with UV-B and their motility was measured after 72 h. Maximum speed per individual is presented (mean +/− SD in red). Two-tailed Mann-Whitney test was used. From left to right, n = 20, 23, 29, 32. Credit: Nature Structural & Molecular Biology (2023). DOI: 10.1038/s41594-023-00942-8" width="800" height="530"/>
lin-52 mutant worms retained motility upon DNA damage induction. lin-52(n771) and WT day 1 adult worms were irradiated or mock-treated with UV-B and their motility was measured after 72 h. Maximum speed per individual is presented (mean +/− SD in red). Two-tailed Mann-Whitney test was used. From left to right, n = 20, 23, 29, 32. Credit:<span> </span><i>Nature Structural & Molecular Biology</i><span> </span>(2023). DOI: 10.1038/s41594-023-00942-8<br />
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<p>A protein complex prevents the repair of genome damage in human cells, in mice and in the nematode Caenorhabditis elegans, a team of researchers at the University of Cologne has discovered. They also successfully inhibited this complex for the first time using a pharmaceutical agent.</p>
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<p>"When we suppress the so-called DREAM complex in body cells, various repair mechanisms kick in, making these cells extremely resilient towards all kinds of DNA damage," said Professor Dr. Björn Schumacher, Director of the Institute for Genome Stability in Aging and Disease at the University of Cologne's CECAD Cluster of Excellence in Aging Research.</p>
<p>Because it contains all of our<span> </span><a href="https://phys.org/tags/genetic+information/" rel="tag" class="textTag">genetic information</a>, our DNA must be well protected. However, it constantly faces damage caused by environmental influences—or our normal metabolism. Hence, DNA repair is essential for the stability of our genome and the functioning of our cells.</p>
<p>"Our findings for the first time allow us to improve DNA repair in body cells and to target the causes of aging and cancer development," Schumacher added. Still, more research is needed until these results can be translated into new therapies for<span> </span><a href="https://phys.org/tags/human+patients/" rel="tag" class="textTag">human patients</a>. The study 'The DREAM complex functions as conserved master regulator of somatic DNA repair capacities' has appeared in<span> </span><i>Nature Structural & Molecular Biology</i>.</p>
<h2>DNA damage leads to aging and disease</h2>
<p>Our genetic material is passed on from generation to generation. That is why it is particularly well protected in our germ cells. Highly precise DNA repair mechanisms are at work there, ensuring that only very few changes in the genetic material are passed on to offspring. Thanks to DNA repair, our<span> </span><a href="https://phys.org/tags/human+genome/" rel="tag" class="textTag">human genome</a><span> </span>has been passed on to us by our ancestors for two hundred thousand years. It has always ensured that the genetic information is preserved. DNA is also constantly repaired in our body cells, but only for the duration of the individual's life.</p>
<p>Sometimes, children are born with faulty DNA repair systems, making them age more quickly and develop typical age-related diseases such as neuro-degradation and arteriosclerosis already in childhood. In some cases, they also have an extremely increased risk of cancer. These are all consequences of DNA damage not being properly repaired.</p>
<h2>The DREAM complex prevents repairs</h2>
<p>Schumacher and his team explored why body cells do not have the same repair mechanisms as<span> </span><a href="https://phys.org/tags/germ+cells/" rel="tag" class="textTag">germ cells</a>. In experiments with the nematode C. elegans, they found out that the DREAM<span> </span><a href="https://phys.org/tags/protein+complex/" rel="tag" class="textTag">protein complex</a><span> </span>limits the quantity of DNA repair mechanisms in body cells: the complex attaches to the DNA's construction plans containing instructions for the repair mechanisms. This prevents them from being produced in large quantities.</p>
<p>Germ cells, however, do not have the DREAM complex. Hence, they naturally produce large quantities of DNA repair mechanisms.</p>
<h2>Mammals also have a DREAM complex</h2>
<p>In further experiments with human cells in the laboratory (cell culture), the scientists showed that the DREAM complex functions in the same way in human cells. They were also able to override the DREAM complex with a pharmaceutical agent.</p>
<p>"We were very pleased to see the same effect as we did in C. elegans. The<span> </span><a href="https://phys.org/tags/human+cells/" rel="tag" class="textTag">human cells</a><span> </span>were much more resilient towards DNA damage after treatment," said Arturo Bujarrabal, a postdoc in Schumacher's team and lead author of the study. Treatment with the DREAM complex inhibitor also showed amazing effects in mice: The DNA in the retina of mice could be repaired and the function of the eye preserved.</p>
<p>The test was carried out in mice that, like some patients, age prematurely and show a typical degeneration of the eye's retina.</p>
<p>Genome damage also plays a major role in<span> </span><a href="https://phys.org/tags/manned+spaceflight/" rel="tag" class="textTag">manned spaceflight</a><span> </span>because of the extremely high radiation in space. A longer stay in space without improved DNA repair is hardly imaginable. Schumacher says, "Therapies that target and improve this newly discovered master regulator of DNA repair could reduce the risk of cancer because genes remain intact."</p>
<p>In addition, the risk of age-related diseases would be reduced because cells can only fulfill their function with an intact genome.</p>
<div class="article-main__more p-4"><p><strong>More information:</strong><span> </span>Björn Schumacher, The DREAM complex functions as conserved master regulator of somatic DNA-repair capacities,<span> </span><i>Nature Structural & Molecular Biology</i><span> </span>(2023).<span> </span><a href="https://dx.doi.org/10.1038/s41594-023-00942-8" target="_blank" rel="noopener">DOI: 10.1038/s41594-023-00942-8</a>.<span> </span><a href="https://www.nature.com/articles/s41594-023-00942-8" target="_blank" rel="noopener">www.nature.com/articles/s41594-023-00942-8</a></p>
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</div> Aging: What underlies the mit…tag:kkartlab.in,2021-02-17:2816864:Comment:2311982021-02-17T03:15:52.294ZDr. Krishna Kumari Challahttps://kkartlab.in/profile/DrKrishnaKumariChalla
<h1 class="text-extra-large line-low mb-2">Aging: What underlies the mitochondrial stress response</h1>
<p><span>Scientists at EPFL have discovered certain enzymes that play a central role in the stress responses that defend mitochondria from stress, and promote health and longevity.</span></p>
<p>Probably the most well-known organelle of the cell,<span> mitochondria </span>play a critical role in producing energy from food. So, it's no surprise that mitochondria can get stressed and damaged.…</p>
<h1 class="text-extra-large line-low mb-2">Aging: What underlies the mitochondrial stress response</h1>
<p><span>Scientists at EPFL have discovered certain enzymes that play a central role in the stress responses that defend mitochondria from stress, and promote health and longevity.</span></p>
<p>Probably the most well-known organelle of the cell,<span> mitochondria </span>play a critical role in producing energy from food. So, it's no surprise that mitochondria can get stressed and damaged. When stressed, mitochondria turn on multiple defense mechanisms: biochemical "domino" pathways that help them repair their defects and recover or improve their health.</p>
<p>Stressed mitochondria are particularly linked to aging and many age-related diseases. Problematic mitochondria are the cause of diseases in metabolism, the cardiovascular and neuromuscular systems, and even certain cancers. Because of how central mitochondria are to survival and health, they have evolved multiple<span> stress response</span><span> </span>pathways to adapt their function to the ever-changing environment of the cell. But how these stress responses are regulated is still largely unknown.</p>
<p><span>Now, a team of scientists has discovered that mitochondrial stress induces global but also very specific epigenetic changes, which involve enzymes that unravel compacted DNA in the cell's nucleus to activate genes. These enzymes are called histone acetyltransferases because they interact with the histone proteins that pack DNA into a structure called chromatin. The findings are published in </span><i>Nature Aging</i><span>.</span></p>
<p>Looking at the chromatin of the nematode C. elegans—a highly popular organism for studying aging—the scientists found that a histone acetyltransferase named CBP-1 is essential for the epigenetic changes caused by stress response of mitochondria, translating their stress signal into a coordinated transcription of a number of genes that are known to be involved in mitochondrial stress response.</p>
<p>The beneficial effects of the mitochondrial stress response, such as resistance to pathogen infections, improved proteostasis against amyloid-β aggregation—one of the culprits of Alzheimer's—and extending lifespan are almost completely dependent on these epigenetic changes. <span>Moreover, analysis in mouse and human populations</span><span>, as well as genetic and pharmacological loss-of-function studies in mammalian cells, strongly suggest that this epigenetic mechanism involved in the regulation of the stress response, health and lifespan is also conserved in the mouse and human.</span></p>
<p><span>This work identifies an evolutionarily conserved node for mitochondrial stress signaling that defends mitochondrial function, and promotes health and longevity. Drugs that target these mitochondrial stress pathways may be interesting to curb the aging process.</span></p>
<p><span>Terytty Yang Li et al. The transcriptional coactivator CBP/p300 is an evolutionarily conserved node that promotes longevity in response to mitochondrial stress, <i>Nature Aging</i> (2021). <a href="http://dx.doi.org/10.1038/s43587-020-00025-z" target="_blank" rel="noopener">DOI: 10.1038/s43587-020-00025-z</a></span></p>
<p><span><a href="https://phys.org/news/2021-02-aging-underlies-mitochondrial-stress-response.html?utm_source=nwletter&utm_medium=email&utm_campaign=daily-nwletter" target="_blank">https://phys.org/news/2021-02-aging-underlies-mitochondrial-stress-response.html?utm_source=nwletter&utm_medium=email&utm_campaign=daily-nwletter</a></span></p> 621
Our young cells survive o…tag:kkartlab.in,2015-11-04:2816864:Comment:1322362015-11-04T05:01:14.314ZDr. Krishna Kumari Challahttps://kkartlab.in/profile/DrKrishnaKumariChalla
<p>621</p>
<p>Our young cells survive only because they have a slew of trusty mechanics on call. Take DNA, which provides the all-important instructions for making proteins. Every time a cell divides, it makes a near-perfect copy of its three-billion-letter code. Copying mistakes happen frequently along the way, but we have specialised repair enzymes to fix them, like an automatic spellcheck. Proteins, too, are ever vulnerable. If it gets too hot, they twist into deviant shapes that keep them…</p>
<p>621</p>
<p>Our young cells survive only because they have a slew of trusty mechanics on call. Take DNA, which provides the all-important instructions for making proteins. Every time a cell divides, it makes a near-perfect copy of its three-billion-letter code. Copying mistakes happen frequently along the way, but we have specialised repair enzymes to fix them, like an automatic spellcheck. Proteins, too, are ever vulnerable. If it gets too hot, they twist into deviant shapes that keep them from working. But here again, we have a fixer: so-called ‘heat shock proteins’ that rush to the aid of their misfolded brethren. Our bodies are also regularly exposed to environmental poisons, such as the reactive and unstable ‘free radical’ molecules that come from the oxidisation of the air we breathe. Happily, our tissues are stocked with antioxidants and vitamins that neutralise this chemical damage. Time and time again, our cellular mechanics come to the rescue.<br/> <br/> Which leads to the biologists’ longstanding conundrum: if our bodies are so well tuned, why, then, does everything eventually go to hell.<br/> One theory is that it all boils down to the pressures of evolution. Humans reproduce early in life, well before ageing rears its ugly head. All of the repair mechanisms that are important in youth – the DNA editors, the heat shock proteins, the antioxidants – help the young survive until reproduction, and are therefore passed down to future generations. But problems that show up after we’re done reproducing cannot be weeded out by evolution. Hence, ageing.<br/> Most scientists say that ageing is not caused by any one culprit but by the breakdown of many systems at once. Our sturdy DNA mechanics become less effective with age, meaning that our genetic code sees a gradual increase in mutations. Telomeres, the sequences of DNA that act as protective caps on the ends of our chromosomes, get shorter every year. Epigenetic messages, which help turn genes on and off, get corrupted with time. Heat shock proteins run down, leading to tangled protein clumps that muck up the smooth workings of a cell. Faced with all of this damage, our cells try to adjust by changing the way they metabolise nutrients and store energy. To ward off cancer, they even know how to shut themselves down. But eventually cells stop dividing and stop communicating with each other, triggering the decline we see from the outside.</p>