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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...

Comment by Dr. Krishna Kumari Challa on January 15, 2022 at 8:53am

ResearchNews Videos

Temperature Record 101: How We Know What We Know about Climate Change

Comment by Dr. Krishna Kumari Challa on January 15, 2022 at 8:38am

Being in space destroys more red blood cells

A world-first study has revealed how space travel can cause lower red blood cell counts, known as space anemia. Analysis of 14 astronauts showed their bodies destroyed 54 percent more red blood cells in space than they normally would on Earth, according to a study published in Nature Medicine.

Space anemia has consistently been reported when astronauts returned to Earth since the first space missions, but we didn't know why. This study shows that upon arriving in space, more red blood cells are destroyed, and this continues for the entire duration of the astronaut's mission.

Before this study, space anemia was thought to be a quick adaptation to fluids shifting into the astronaut's upper body when they first arrived in space. Astronauts lose 10 percent of the liquid in their blood vessels this way. It was thought astronauts rapidly destroyed 10 percent of their red blood cells to restore the balance, and that red blood cell control was back to normal after 10 days in space.

Now it was found that  the red blood cell destruction was a primary effect of being in space, not just caused by fluid shifts. They demonstrated this by directly measuring red blood cell destruction in 14 astronauts during their six-month space missions.

On Earth, our bodies create and destroy 2 million red blood cells every second. The researchers found that astronauts were destroying 54 percent more red blood cells during the six months they were in space, or 3 million every second. These results were the same for both female and male astronauts.

This discovery was made thanks to techniques and methods researchers developed to accurately measure red blood cell destruction. These methods were then adapted to collect samples aboard the International Space Station. They were able to precisely measure the tiny amounts of carbon monoxide in the breath samples from astronauts. One molecule of carbon monoxide is produced every time one molecule of heme, the deep-red pigment in red blood cells, is destroyed.

Trudel, G et al, Hemolysis contributes to anemia during long-duration space flight. Nat Med (2022). doi.org/10.1038/s41591-021-01637-7

https://phys.org/news/2022-01-space-red-blood-cells.html?utm_source...

Comment by Dr. Krishna Kumari Challa on January 15, 2022 at 8:23am

Copper-based chemicals may be contributing to ozone depletion

Copper released into the environment from fungicides, brake pads, antifouling paints on boats and other sources may be contributing significantly to stratospheric ozone depletion, according to a new study .

In a paper appearing this week in the journal Nature Communications, UC Berkeley geochemists show that copper in soil and seawater acts as a catalyst to turn organic matter into both methyl bromide and methyl chloride, two potent halocarbon compounds that destroy ozone. Sunlight worsens the situation, producing about 10 times the amount of these methyl halides.

The findings answer, at least in part, a long-standing mystery about the origin of much of the methyl bromide and methyl chloride in the stratosphere. Since the worldwide ban on chlorofluorocarbon (CFC) refrigerants and brominated halons used in fire extinguishers starting in 1989, these methyl halides have become the new dominant sources of ozone-depleting bromine and chlorine in the stratosphere. As the long-lived CFCs and halons slowly disappear from the atmosphere, the role of methyl halides increases.

Yi Jiao et al, Application of copper(II)-based chemicals induces CH3Br and CH3Cl emissions from soil and seawater, Nature Communications (2022). DOI: 10.1038/s41467-021-27779-3

https://phys.org/news/2022-01-copper-based-chemicals-contributing-o...

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