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Comment by Dr. Krishna Kumari Challa on January 19, 2022 at 12:12pm

Research team identifies new mechanism for protecting DNA

Researchers  have identified a new mechanism by which a protein known for repairing damaged DNA also protects the integrity of DNA by preserving its structural shape.

The discovery, involving the protein 53BP1, offers insight into understanding how cells maintain the integrity of DNA in the nucleus, which is critical for preventing diseases like premature aging and cancer.

DNA, or deoxyribonucleic acid, is the chemical name for the molecule that carries genetic instructions in all living things.

The large protein 53BP1 is known for determining how cells will repair a particular type of DNA damage—DNA double-strand break (DSB), in which the two strands of DNA are both broken, leaving a free DNA end floating around in the cell's nucleus.

When DSB occurs, if it is not repaired, the DNA ends could fuse to what they should not under normal conditions, which could lead to the disruption of genetic information. In the short term, cells with unrepaired DNA may kill themselves off, but if a cell loses this self-surveillance, it may start the journey toward cancer.

In this study, the team discovered that 53BP1 has a biological function in mediating the structure of DNA, specifically at a highly compacted region called heterochromatin.

The researchers found that this new function involves a new form of activity of 53BP1, in which the protein accumulates at the condensed DNA regions and forms small liquid droplets—a process called liquid-liquid phase separation, similar to mixing oil with water for salad dressing.

The team determined how 53BP1 can form liquid droplets: They found that this process requires the participation of other proteins known to support the structure of the highly condensed DNA. But, in turn, they discovered that 53BP1 actually stabilized the gathering of these proteins at these DNA regions, which is important for keeping the overall function of the DNA.

They then carried out detailed molecular analysis to break the large protein into small pieces and determined which pieces are important for the liquid droplet formation of 53BP1. They further changed amino acid of a specific position of the 53BP1 protein and determined the contribution of several amino acids that are critical for this new function.

With this new information, Zhang and his team hope to better understand how diseases like cancer can be prevented, and even design therapies that use this new feature of 53BP1 to treat cancers in the future.

Lei Zhang et al, 53BP1 regulates heterochromatin through liquid phase separation, Nature Communications (2022). DOI: 10.1038/s41467-022-28019-y

https://phys.org/news/2022-01-team-mechanism-dna.html?utm_source=nw...

Comment by Dr. Krishna Kumari Challa on January 18, 2022 at 11:32am

This  Terrifying NEW Discovery on Neptune Changes Everything!

Comment by Dr. Krishna Kumari Challa on January 18, 2022 at 11:08am

Chal­lenging the the­ory of the nar­row host range of phages

Viruses that infect bacteria could one day replace antibiotics because they precisely attack only specific pathogens. Researchers  are now showing that this is not always the case. This new finding is important because bacterial viruses can transfer antibiotic resistance genes.

Bacteriophages—phages for short—are viruses that infect only bacteria. To capture a bacterial host, they first attach to specific molecules on its cell surface. Then they inject their genetic material into the bacterial cell. In order to reprogram the bacteria's cellular machinery to produce new virus particles, phages also have to outsmart the target bacteria's immune system.

The molecular entry points and the immune system differ from one bacterium to another, so it was commonly believed that most phages have a narrow host range—that is, that they infect only a single bacterial species or even subspecies. This is also what prompted the idea of using natural bacteria killers to treat infections—particularly when the disease-causing bacteria have acquired antibiotic resistances.

However, a new study challenges the theory of the narrow host range of phages. Phages within the Staphylococcus group of bacteria often infect multiple species simultaneously. The researchers recently published their results in the journal Nature Communications.

The findings could have direct consequences for phage therapy, which is not yet approved for use in Switzerland, but has long been in use in eastern Europe. Phages not only kill bacteria, they can also transfer antibiotic resistance genes from one bacterium to another. Accordingly, their unexpectedly broad range of prey means that phages could spread their resistance genes much further in the environment than was previously thought.

The mechanism through which phages can transfer antibiotic resistance among bacteria is already known. In short, when these viruses multiply in the bacterial cells, they not only inject their own genetic material into new virus particles; in some cases, they smuggle genetic material from the infected bacterium—a resistance gene, for instance—into the virus particles. If one of these virus particles then infects a new bacterium, the resistance may be transferred.

Therefore, if we want to assess the role of phages as vectors of antibiotic resistance, we have to look at the whole picture—not just the situation in human medicine. When using phages in medicine, one must be careful that they don't additionally act as vectors of antibiotic resistance genes. It is thus important to ensure that phages used in medicine have a propagation mechanism that functions as flawlessly as possible.

 Pauline C. Göller et al, Multi-species host range of staphylococcal phages isolated from wastewater, Nature Communications (2021). DOI: 10.1038/s41467-021-27037-6

https://phys.org/news/2022-01-theory-narrow-host-range-phages.html?...

Comment by Dr. Krishna Kumari Challa on January 18, 2022 at 10:56am

Are There Rainbows on Mars? 

Comment by Dr. Krishna Kumari Challa on January 18, 2022 at 10:50am

Nanotherapy offers new hope for the treatment of Type 1 diabetes

Individuals living with Type 1 diabetes must carefully follow prescribed insulin regimens every day, receiving injections of the hormone via syringe, insulin pump or some other device. And without viable long-term treatments, this course of treatment is a lifelong process.

Pancreatic islets control insulin production when blood sugar levels change, and in Type 1 diabetes, the body's immune system attacks and destroys such insulin-producing cells. Islet transplantation has emerged over the past few decades as a potential cure for Type 1 diabetes. With healthy transplanted islets, Type 1 diabetes patients may no longer need insulin injections, but transplantation efforts have faced setbacks as the immune system continues to eventually reject new islets. Current immunosuppressive drugs offer inadequate protection for transplanted cells and tissues and are plagued by undesirable side effects.

Now a team of researchers at Northwestern University has discovered a technique to help make immunomodulation more effective. The method uses nanocarriers to re-engineer the commonly used immunosuppressant rapamycin. Using these rapamycin-loaded nanocarriers, the researchers generated a new form of immunosuppression capable of targeting specific cells related to the transplant without suppressing wider immune responses.

The concept of enhancing and controlling side effects of drugs via nanodelivery is not a new one. But  in this study researchers are not enhancing an effect, they are changing it—by repurposing the biochemical pathway of a drug, in this case mTOR inhibition by rapamycin, they are generating a totally different cellular response.

The team's discovery could have far-reaching implications. This approach can be applied to other transplanted tissues and organs, opening up new research areas and options for patients.

Guillermo Ameer, Subcutaneous nanotherapy repurposes the immunosuppressive mechanism of rapamycin to enhance allogeneic islet graft viability, Nature Nanotechnology (2022). DOI: 10.1038/s41565-021-01048-2. www.nature.com/articles/s41565-021-01048-2

https://phys.org/news/2022-01-nanotherapy-treatment-diabetes.html?u...

Comment by Dr. Krishna Kumari Challa on January 18, 2022 at 9:52am

The researchers fed Rev-erbα/β knockout mice one of two high-fat diets. One diet was mostly high-fat. The other was a high-fat/high-sucrose diet, resembling human diets that promote obesity and insulin resistance. The high-fat/high-sucrose diet partially alleviated the cardiac defects, but the high-fat diet did not.

These findings support that the metabolic defect that prevents the heart cells from using fatty acids as fuel is causing the majority of the cardiac dysfunction we see in the Rev-erbα/β knockout mice. Importantly, we also show that correcting the metabolic defect can help improve the condition.

Chronotype Myocardial Rev-erb-mediated diurnal metabolic rhythm and obesity paradox, Circulation (2022). DOI: 10.1161/CIRCULATIONAHA.121.056076

https://medicalxpress.com/news/2022-01-circadian-clock-heart-failur...

Part2

Comment by Dr. Krishna Kumari Challa on January 18, 2022 at 9:51am

The circadian clock in heart failure

Disrupting circadian rhythms, which change naturally on a 24-hour cycle, has been implicated in heart disease, but it is unclear how it leads to the condition. A research team investigated the function of the protein Rev-erbα/β, a key component of the circadian clock, on heart disease development in animal models and human patients.

The team reports in the journal Circulation that Rev-erbα/β in cardiomyocytes mediates a normal metabolic rhythm that enables the cells to prefer lipids as a source of energy during the animal's resting time, daytime for mice. Removing Rev-erbα/β disrupts this rhythm, reduces the cardiomyocytes' ability to use lipids in the resting time and leads to progressive dilated cardiomyopathy and lethal heart failure.

They found that the Rev-erbα/β gene is highly expressed only during the sleep hours, and its activity is associated with fat and sugar metabolisms.

The heart responds differently to different sources of energy, depending on the time of the day. In the resting phase, which for humans is at night and for mice in the day, the heart uses fatty acids that are released from fats as the main source of energy. In the active phase, which is during the day for people and at night for mice, the heart has some resistance to dietary carbohydrates. The researchers found that without Rev-erbα/β, hearts have metabolic defects that limit the use of fatty acids when resting, and there is overuse of sugar in the active phase.

Scientists also found that when Rev-erbα/β knockout hearts cannot burn fatty acids efficiently in the resting phase, then they don't have enough energy to beat. That energy deficiency would probably lead to changes in the heart that resulted in progressive dilated cardiomyopathy.

To test this hypothesis, the researchers determined whether restoring the defect in fatty acid use would improve the condition.

Part 1

Comment by Dr. Krishna Kumari Challa on January 17, 2022 at 10:14am

How Salmonella overcomes host resistance

 The microbial species living in our gastrointestinal tract — the gut microbiota — help protect us against invading pathogens. One way they exert this “colonization resistance” is by producing antimicrobial products, such as the fatty acid propionate. The gut microbiota benefits the host by limiting enteric pathogen expansion (colonization resistance), partially via the production of inhibitory metabolites. Propionate, a short-chain fatty acid produced by microbiota members, is proposed to mediate colonization resistance against Salmonella enterica serovar Typhimurium (S. Tm).

Propionate is used in agricultural animals to limit infection by varieties of Salmonella bacteria, which cause food poisoning in humans.

Now, however, researchers have demonstrated that Salmonella can turn the tables and use propionate for its own purposes. The researchers showed in animal models that in the presence of inflammation, Salmonella changes its metabolism and uses propionate as a source of energy. They demonstrated that propionate metabolism supports expansion of Salmonella in the inflamed gut.

The findings, published in Cell Reports, show that in addition to promoting colonization resistance, propionate can fuel Salmonella growth, changing the understanding of propionate’s role and complicating its use as an antimicrobial treatment.

https://pubmed.ncbi.nlm.nih.gov/34986344/

https://researchnews.cc/news/11098/Salmonella-overcomes-host-resist...

Comment by Dr. Krishna Kumari Challa on January 17, 2022 at 9:58am

Tiger Shark Migrations Altered by Climate Change

Comment by Dr. Krishna Kumari Challa on January 16, 2022 at 11:35am

Your gut senses the difference between real sugar and artificial sweetener

 Your taste buds may or may not be able to tell real sugar from a sugar substitute like Splenda, but there are cells in your intestines that can and do distinguish between the two sweet solutions. And they can communicate the difference to your brain in milliseconds.

Not long after the sweet taste receptor was identified in the mouths of mice 20 years ago, scientists attempted to knock those taste buds out. But they were surprised to find that mice could still somehow discern and prefer natural sugar to artificial sweetener, even without a sense of taste.

The answer to this riddle lies much further down in the digestive tract, at the upper end of the gut just after the stomach, according to research.

The researchers have  identified the cells that make us eat sugar, and they are in the gut. The sensing cells are in the upper reaches of the gut. 

Having discovered a gut cell called the neuropod cell, researchers have been pursuing this cell’s critical role as a connection between what’s inside the gut and its influence in the brain. The gut talks directly to the brain, changing our eating behaviour. And in the long run, these findings may lead to entirely new ways to treat diseases.

Originally termed enteroendrocrine cells because of their ability to secrete hormones, specialized neuropod cells can communicate with neurons via rapid synaptic connections and are distributed throughout the lining of the upper gut. In addition to producing relatively slow-acting hormone signals, the  researchers have shown that these cells also produce fast-acting neurotransmitter signals that reach the vagus nerve and then the brain within milliseconds.

 These latest findings further show that neuropods are sensory cells of the nervous system just like taste buds in the tongue or the retinal cone cells in the eye that help us see colors. They sense traces of sugar versus sweetener and then they release different neurotransmitters that go into different cells in the vagus nerve, and ultimately, the animal knows ‘this is sugar’ or ‘this is sweetener.’”

Using lab-grown organoids from mouse and human cells to represent the small intestine and duodenum (upper gut), the researchers showed in a small experiment that real sugar stimulated individual neuropod cells to release glutamate as a neurotransmitter. Artificial sugar triggered the release of a different neurotransmitter, ATP.

Using a technique called optogenetics, the scientists were then able to turn the neuropod cells on and off in the gut of a living mouse to show whether the animal’s preference for real sugar was being driven by signals from the gut.

Sugar has both taste and nutritive value and the gut is able to identify both.
Many people struggle with sugar cravings, and now we have a better understanding of how the gut senses sugars (and why artificial sweeteners don’t curb those cravings).

1. Kelly L. Buchanan, Laura E. Rupprecht, M. Maya Kaelberer, Atharva Sahasrabudhe, Marguerita E. Klein, Jorge A. Villalobos, Winston W. Liu, Annabelle Yang, Justin Gelman, Seongjun Park, Polina Anikeeva, Diego V. Bohórquez. The preference for sugar over sweetener depends on a gut sensor cell. Nature Neuroscience, 2022; DOI: 10.1038/s41593-021-00982-7

https://researchnews.cc/news/11088/Your-gut-senses-the-difference-b...

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