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Comment by Dr. Krishna Kumari Challa on May 8, 2022 at 1:39pm

Model finds COVID-19 deaths among elderly may be due to genetic limit on cell division

 Your immune system's ability to combat COVID-19, like any infection, largely depends on its ability to replicate the immune cells effective at destroying the SARS-CoV-2 virus that causes the disease. These cloned immune cells cannot be infinitely created, and a key hypothesis of a new University of Washington study is that the body's ability to create these cloned cells falls off significantly in old age.

According to a model created by UW research professor James Anderson, this genetically predetermined limit on your immune system may be the key to why COVID-19 has such a devastating effect on the elderly. Anderson is the lead author of a paper published March 31 in The Lancet eBioMedicine detailing this modeled link between aging, COVID-19 and mortality.

"When DNA split in cell division, the end cap—called a telomere—gets a little shorter with each division," explains Anderson, who is a modeler of biological systems in the School of Aquatic and Fishery Sciences. "After a series of replications of a cell, it gets too short and stops further division. Not all cells or all animals have this limit, but immune cells in humans have this cell life."

The average person's immune system coasts along pretty good despite this limit until about 50 years old. That's when enough core immune cells, called T cells, have shortened telomeres and cannot quickly clone themselves through cellular division in big enough numbers to attack and clear the COVID-19 virus, which has the trait of sharply reducing immune cell numbers, Anderson said. Importantly, he added, telomere lengths are inherited from your parents. Consequently, there are some differences in these lengths between people at every age as well as how old a person becomes before these lengths are mostly used up.

Anderson said the key difference between this understanding of aging, which has a threshold for when your immune system has run out of collective telomere length, and the idea that we all age consistently over time is the "most exciting" discovery of his research.

Part 1

Comment by Dr. Krishna Kumari Challa on May 7, 2022 at 9:19am

Global bird populations steadily declining

Staggering declines in bird populations are taking place around the world. So concludes a study from scientists at multiple institutions, published recently in the journal Annual Review of Environment and Resources. Loss and degradation of natural habitats and direct overexploitation of many species are cited as the key threats to avian biodiversity. Climate change is identified as an emerging driver of bird population declines.

We are now witnessing the first signs of a new wave of extinctions of continentally distributed bird species. Avian diversity peaks globally in the tropics and it is there that we also find the highest number of threatened species.

The study says approximately 48% of existing bird species worldwide are known or suspected to be undergoing population declines. Populations are stable for 39% of species. Only 6% are showing increasing population trends, and the status of 7% is still unknown. The study authors reviewed changes in avian biodiversity using data from the International Union for Conservation of Nature's "Red List" to reveal population changes among the world's 11,000 bird species.

Because birds are highly visible and sensitive indicators of environmental health, we know their loss signals a much wider loss of biodiversity and threats to human health and well-being.

The fate of bird populations is strongly dependent on stopping the loss and degradation of habitats.

Alexander C. Lees et al, State of the World's Birds, Annual Review of Environment and Resources (2022). DOI: 10.1146/annurev-environ-112420-014642

Comment by Dr. Krishna Kumari Challa on May 7, 2022 at 8:45am

Drugs targeting cell recycling could be used to suffocate cancer cells

Pancreatic cancers recycle resources to fuel their survival and growth, opening up the possibility of new treatments aimed at stopping them from doing so, scientists report.

New findings show that pancreatic cancers make use of a key "recycler" protein to keep pace with their constant demand for oxygen and energy, as they grow and spread. Blocking the recycler could suffocate pancreatic cancer cells by starving them of oxygen and energy—and the researchers now plan to create new drugs aimed at suffocating tumors. The new study is the first to investigate the role in pancreatic cancer of "deubiquitylating enzymes" (DUBs)—which stop other proteins from being "binned" by the body so they can be recycled instead.

Researchers identified a DUB called USP25 as a key "recycler" protein which supported the survival and growth of cancer cells.

Pancreatic tumors are known to have low oxygen "micro-environments." This is because the rapid growth of pancreatic cancer often outstrips the oxygen supply, which cancer cells need to survive and grow. Researchers found that USP25 can regulate a protein known as HIF-1a to help pancreatic cancer cells adapt to low oxygen levels in the tumor. USP25 does this by preventing HIF-1a from being "binned," so it can form new blood vessels to supply the cancer with oxygenated blood.

Scientists showed that genetically deleting USP25, or blocking it using drugs, meant mini-tumors were unable to grow, as they were starved of oxygen. They believe that by acting as a "recycler" protein, USP25 can reverse the protein modifications on HIF-1a that destine it to be degraded by the body, stabilizing HIF-1a and allowing it to continue supplying oxygen and nutrients to cancer cells. In this way, USP25 plays a role in helping pancreatic cancer grow and spread. Researchers think the mechanism may also be important for other low-oxygen tumor types, such as breast cancer, and plan to explore it further. They will seek to design USP25 inhibitors and ultimately to assess the new approach to treatment in patients with pancreatic cancer. They are also planning to investigate the role of other druggable DUBs in pancreatic cancer.

Jessica K. Nelson et al, USP25 promotes pathological HIF-1-driven metabolic reprogramming and is a potential therapeutic target in pancreatic cancer, Nature Communications (2022). DOI: 10.1038/s41467-022-29684-9

Comment by Dr. Krishna Kumari Challa on May 6, 2022 at 12:11pm

Miracle plant seagrass

Comment by Dr. Krishna Kumari Challa on May 6, 2022 at 9:46am

Comment by Dr. Krishna Kumari Challa on May 5, 2022 at 11:52am

Cancer origin identified through cell 'surgery'

Research sheds new light on a key cause of cancer formation during cell division (or mitosis), and points towards potential solutions for preventing it from occurring.

When a cell divides normally, it makes a copy of every chromosome and then shares them equally between the two new cells. This function is carried out by a complex machine in the cell called the mitotic spindle. If something goes wrong at this stage, the two new cells will be aneuploid, meaning that they will not have the correct number of chromosomes and will make mistakes when sharing genetic information.

Cancer cells are aneuploid, so understanding how and why this happens is hugely significant in finding out how the disease originates. This new work has identified exactly this.

Researchers found that some chromosomes can get lost and trapped in a tangle of membranes that exist in an area around the cell's spindle, preventing the chromosomes from being shared properly and leading to the abnormal cell division that can cause cancer.

They made their discovery by performing a sort of "surgery" on living cells. The researchers invented a way to remove the tangle of membranes in which chromosomes get trapped, and as a result the chromosomes were rescued by the spindle, thus enabling normal healthy cell division.

Researchers  found that chromosomes can get trapped in membranes and this is a disaster for the dividing cell. It has the potential to change a normal cell into a cancer cell. Preventing this process may be a way to treat disease.

This proved, for the first time, that chromosomes getting caught in these membranes is a direct risk factor for the formation of cancerous cells. Understanding this risk can lead to more effective cancer prevention.

Nuria Ferrandiz et al, Endomembranes promote chromosome missegregation by ensheathing misaligned chromosomes, Journal of Cell Biology (2022). DOI: 10.1083/jcb.202203021

https://researchnews.cc/news/12986/Cancer-origin-identified-through...

Comment by Dr. Krishna Kumari Challa on May 5, 2022 at 9:57am

What still remains a mystery is why humans evolved to have a BRCA2 gene that increases the risk of developing cancer, though there is the possibility that it was a tradeoff between an increased risk of cancer and an increase in fertility rates. Prior research has shown that women with a BRCA2 variant that makes them more susceptible to developing cancer can more easily become pregnant. The work also suggests that a means for treating cancer in the distant future may involve altering the BRCA2 gene to make it more like other primates, thereby reducing the overall risk of developing cancer.

 Christine A. Iacobuzio-Donahue, Evidence for Reduced BRCA2 Functional Activity in Homo Sapiens After Divergence from the Chimpanzee-Human Last Common Ancestor, Cell Reports (2022). DOI: 10.1016/j.celrep.2022.110771. www.cell.com/cell-reports/full … 2211-1247(22)00535-6

https://phys.org/news/2022-05-evidence-dna-humans-susceptible-cance...

Part 2

Comment by Dr. Krishna Kumari Challa on May 5, 2022 at 9:57am

Evidence that a DNA change made humans more susceptible to cancer

A team of researchers at the Sloan Kettering Institute working with a group at the American Museum of Natural History has found evidence of a change in human DNA after diverging from other primates that has made humans more susceptible to the development of cancerous tumors. In their paper published in the journal Cell Reports, the group compares human genes to those of other primates to learn more about why humans are more prone to developing cancer.

Prior research has shown that humans are more likely to develop cancerous tumors than any other primate, but the reason has remained a mystery until now. To find the answer, the researchers compared parts of the human genome with similar parts of 12 non-human primate genomes. They found a small difference in the BRCA2 gene that had to have arisen after humans diverged from other primates. The BRCA2 gene plays a role in tumor suppression due to coding for DNA repair.

The researchers then looked at the impact of the letter change in the human DNA and found that it lessened its effectiveness at coding for DNA repair by approximately 20%. And that, the researchers suggest, could explain why humans are more susceptible to the development of tumors. The findings align with results from prior research that has shown that humans with a certain BRCA2 variant are more likely to develop tumors, particularly of the ovaries and breast.

Part 1

Comment by Dr. Krishna Kumari Challa on May 5, 2022 at 9:14am

The study, published in the journal Microbiome, found that the microbiota from old donors led to loss of integrity of the lining of the gut, allowing bacterial products to cross into the circulation, which results in triggering the immune system and inflammation in the brain and eyes.

Age-related chronic inflammation, known as inflammaging, has been associated with the activation of specific immune cells found in brain. These cells were also over-activated in the young mice who received aged microbiome transplants.

In the eye, the team also found specific proteins associated with retinal degeneration were elevated in the young mice receiving microbiota from old donors.

In old mice, these detrimental changes in the gut, eye and brain could be reversed by transplanting the gut microbiota from young mice.

In ongoing studies, the team are now working to understand how long these positive effects can last, and to identify the beneficial components of the young donor microbiota and how they impact on organs distant from the gut.

The microbiota of young mice, and the old mice who received young microbiota transplants were enriched in beneficial bacteria that have previously been associated with good health in both mice and humans.

The researchers have also analyzed the products which these bacteria produce by breaking down elements of our diet. This has uncovered significant shifts in particular lipids (fats) and vitamin metabolism, which may be linked to the changes seen in inflammatory cells in the eye and brain.

Similar pathways exist in humans, and the human gut microbiota also changes significantly in later life, but the researchers caution about extrapolating their results directly to humans until similar studies in elderly humans can be performed.

Aimée Parker et al, Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain, Microbiome (2022). DOI: 10.1186/s40168-022-01243-w

https://medicalxpress.com/news/2022-05-fecal-transplants-reverse-ha...

Part 2

1. Aimée Parker, Stefano Romano, Rebecca Ansorge, Asmaa Aboelnour, Gwenaelle Le Gall, George M. Savva, Matthew G. Pontifex, Andrea Telatin, David Baker, Emily Jones, David Vauzour, Steven Rudder, L. Ashley Blackshaw, Glen Jeffery, Simon R. Carding. Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain. Microbiome, 2022; 10 (1) DOI: 10.1186/s40168-022-01243-w

Comment by Dr. Krishna Kumari Challa on May 5, 2022 at 9:13am

Fecal transplants reverse hallmarks of aging

In the search for eternal youth, poo transplants may seem like an unlikely way to reverse the aging process.

However, scientists  have provided evidence, from research in mice, that transplanting fecal microbiota from young into old mice can reverse hallmarks of aging in the gut, eyes, and brain.

In the reverse experiment, microbes from aged mice induced inflammation in the brain of young recipients and depleted a key protein required for normal vision.

These findings show that gut microbes play a role in the regulating some of the detrimental effects of aging and open up the possibility of gut microbe-based therapies to combat decline in later life.

It has been known for some time that the population of microbes that we carry around in our gut, collectively called the gut microbiota, is linked to health. Most diseases are associated with changes in the types and behavior of bacteria, viruses, fungi and other microbes in an individual's gut.

Some of these changes in microbiota composition happen as we age, adversely affecting metabolism and immunity, and this has been associated with age-related disorders including inflammatory bowel diseases, along with cardiovascular, autoimmune, metabolic and neurodegenerative disorders.

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To better understand the effects of these changes in the microbiota in old age, scientists  transferred the gut microbes from aged mice into healthy young mice, and vice versa. They then looked at how this affected inflammatory hallmarks of aging in the gut, brain and eye, which suffer from declining function in later life.

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