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Comment by Dr. Krishna Kumari Challa on November 23, 2020 at 9:55am

Astronomers discover new 'fossil galaxy' buried deep within the Milky Way

Scientists working with data from the Sloan Digital Sky Surveys' Apache Point Observatory Galactic Evolution Experiment (APOGEE) have discovered a "fossil galaxy" hidden in the depths of our own Milky Way.

The proposed fossil galaxy may have collided with the Milky Way ten billion years ago, when our galaxy was still in its infancy. Astronomers named it Heracles, after the ancient Greek hero who received the gift of immortality when the Milky Way was created.

The remnants of Heracles account for about one third of the Milky Way's spherical halo. But if stars and gas from Heracles make up such a large percentage of the galactic halo, why didn't we see it before? The answer lies in its location deep inside the Milky Way.

"To find a fossil galaxy like this one, we had to look at the detailed chemical makeup and motions of tens of thousands of stars. That is especially hard to do for stars in the center of the Milky Way, because they are hidden from view by clouds of interstellar dust. APOGEE lets us pierce through that dust and see deeper into the heart of the Milky Way than ever before.

APOGEE does this by taking spectra of stars in near-infrared light, instead of visible light, which gets obscured by dust. Over its ten-year observational life, APOGEE has measured spectra for more than half a million stars all across the Milky Way, including its previously dust-obscured core and finally discovered this fossil galaxy .

"Evidence from APOGEE for the Presence of a Major Building Block of the Halo Buried in the Inner Galaxy," Danny Horta et al., 2020 Nov. 20, Monthly Notices of the Royal Astronomical Society: arxiv.org/abs/2007.10374].

https://phys.org/news/2020-11-astronomers-fossil-galaxy-deep-milky....

Comment by Dr. Krishna Kumari Challa on November 22, 2020 at 10:12am

3D-printed, lifelike heart models could help train tomorrow’s surgeons

Comment by Dr. Krishna Kumari Challa on November 21, 2020 at 10:55am

** Asymptomatic Children Can Spread Malaria to Mosquitoes

Children infected with malaria can become 'superspreaders' and pass the parasite to droves of local mosquitoes, even if the kids never develop symptoms of the disease, a new study suggests. 

Since this disease is passed from humans to mosquitoes and then back again, rather than from person to person, this finding is worrisome. If malaria goes untreated in these asymptomatic children, the parasites will continue to circulate among mosquitoes, even in places that employ intensive malaria controls like insecticides, bednets, and free diagnostic tests and treatments. According to new research, presented Wednesday (Nov. 18) at the annual meeting of the American Society of Tropical Medicine and Hygiene (ASTMH), even a small number of infected children can transmit malaria parasites to a mob of mosquitoes, which can then go on to infect more humans. From their new research in Uganda, the researchers concluded that asymptomatic children between ages 5 and 15 are the main source of infection for local mosquitoes in the region they studied. Some of these children were so-called superspreaders, meaning they infected a much larger number of mosquitoes than others; in experiments where mosquitoes were fed blood samples from infected people, more than 60 percent of the resulting mosquito infections could be traced back to just four asymptomatic children, two of whom were school-age. The other two superspreaders were ages 3 and 4.

Despite some children becoming infected with multiple malaria clones during the study, these kids never fell ill and continued to lead a "normal life … somehow living with all these parasites

https://www.livescience.com/asymptomatic-children-malaria-reservoir...

Comment by Dr. Krishna Kumari Challa on November 21, 2020 at 10:52am

**In a First, Scientists Say They've Partially Reversed a Cellular Aging Process in Humans

Every time a cell inside your body replicates, a slither of your youth crumbles to dust. This occurs via the shortening of telomeres, structures that 'cap' the tips of our chromosomes.

Now, scientists in Israel say they've been able to reverse this process and extend the length of telomeres in a small study involving 26 patients.

The participants sat in a hyperbaric oxygen chamber for five 90 minutes sessions per week over three months, and as a result, some of their cell's telomeres were extended by up to 20 percent.

It's an impressive claim - and something many other researchers have attempted in the past without success. But of course it's worth flagging that this is a small sample size, and the results will need to be replicated before we can get too excited. 

However, the fact that hyperbaric oxygen therapy appears to affect telomere length is a compelling link worth investigating further. 

Telomeres are repeating chunks of code that act as the DNA equivalent of the plastic or metal aglet capping the end of a shoelace.

They copy themselves along with the rest of the chromosomes whenever a cell divides. Yet with every replication, tiny fragments of code from the very tip of the sequence fail to make it into the new copy, leaving the freshly minted chromosome a touch shorter than its predecessor.

As anybody who has lost the cap of their shoelace knows, it doesn't take long for the shoelace to lose its integrity. Similarly, shorter telomeres put sequences further down the chromosome at higher risk of hazardous mutations.

These mutations coincide with changes that predispose us to a bunch of age-related conditions, not least of all diseases such as cancer.

That's not necessarily to say that we age because our telomeres shrink, but there is a connection between telomere length and health that researchers are keen to investigate further.

"Longer telomeres correlates with better cellular performance. There are plenty of ways to accelerate the erosion of our telomeres. Failing to get adequate sleep could do it, as might chowing down on too much processed food, and maybe even having kids.
Slowing down the loss takes a bit more effort, but engaging in regular exercise and eating well are sound bets if you want your chromosomes to remain as long as possible.

A real achievement would be to flip our chromosomal hourglass completely and return lost sections of telomere. The fact that high-turnover tissues lining our gut do this naturally using an enzyme called telomerase has fuelled research over the years.

There have been plenty of milestones in attempts to achieve this task. Gene therapy in mice has shown it could one day be feasible in humans. More recently, stem cells from a supercentenarian woman had their telomeres completely reset outside of her body.

Some studies have found potential for tiny increases of maybe a few percent with provision of nutritional supplements such as vitamin D.

https://www.aging-us.com/article/202188/text

https://www.sciencealert.com/oxygen-therapy-found-to-turn-back-the-...

Comment by Dr. Krishna Kumari Challa on November 21, 2020 at 7:35am

How rotavirus causes severe gastrointestinal disease

Rotavirus is a major cause of diarrhea and vomiting, especially in children, that results in approximately 128,000 deaths annually. The virus triggers the disease by infecting enterocyte cells in the small intestine, but only a fraction of the susceptible cells has the virus. In the mid-90s, scientists proposed that the small portion of infected cells promotes severe disease by sending out signals that disrupt the normal function of neighbouring uninfected cells, but the nature of the signal has remained a mystery.

In the current study published in the journal Science, a team led by researchers at Baylor College of Medicine discovered that rotavirus-infected cells release signaling molecules, identified as adenosine diphosphate (ADP), which binds its cellular receptor P2Y1 on neighboring cells. Activating P2Y1 by ADP results in signals called intercellular calcium waves in these uninfected cells. Disrupting ADP binding to its receptor reduced the severity of diarrhea in a mouse model of the disease, suggesting that targeting the P2Y1 may be an effective strategy to control viral diarrhea in human populations.

Further studies revealed previously unknown roles of ADP on rotavirus infection and replication, shining a spotlight on ADP as an important trigger of the multiple factors involved in severe diarrhea and vomiting caused by rotavirus. For instance, the researchers found evidence that ADP signaling increases rotavirus infection, the expression of inflammatory cytokine IL1-alpha and the secretion of serotonin, an inducer of diarrhea. ADP signaling also increases the expression of enzymes that produce prostaglandin and nitric oxide, potentially causing the increases in those compounds observed in rotavirus infection. Preventing ADP signaling and intercellular calcium waves reduced the production of the compounds mentioned above.

 Alexandra L. Chang-Graham et al, Rotavirus induces intercellular calcium waves through ADP signaling, Science (2020). DOI: 10.1126/science.abc3621

https://medicalxpress.com/news/2020-11-rotavirus-severe-gastrointes...

Comment by Dr. Krishna Kumari Challa on November 20, 2020 at 10:13am

Your Tears Might Save Your Life Someday

They could ultimately be used to find diseases the way blood tests do now—but cheaper and more easily

At any given moment, about seven microliters of tears are present in each of our eyes—about a tenth of a drop of water. You might think of them as nothing more than salty water, but it’s more accurate to think if them filtered blood; they deliver oxygen and nutrients to our eyes, removing waste, serving as the first line of defense against pathogens and helping to heal injuries.

Tears also contain traces of the various chemicals originally present in blood, some of which serve as markers of illness—glucose, for example, which can signal diabetes, or enzymes that point to possible liver disease. That’s a primary reason doctors order blood tests. But it also that means that physicians—and maybe, in the near future, you—can look for indicators of illness by looking at your tears.

https://www.scientificamerican.com/article/your-tears-might-save-yo...

Comment by Dr. Krishna Kumari Challa on November 20, 2020 at 9:37am

Scientists identify brain cells that drive wakefulness and resist general anesthetics
Neuroscientists don’t know precisely what brain circuits control wakefulness and sleep, nor exactly how drugs for general anesthesia affect those circuits. But a new study from Penn Medicine researchers brings neuroscience a step closer to solving that important conundrum.

A team of researchers from the Perelman School of Medicine at the University of Pennsylvania, in a study published online Nov. 13 in Current Biology, identified a population of neurons in the hypothalamus region of the brain that keeps mice from sleeping when they normally would when they are activated. Activating these neurons also “wakes” them from ongoing exposure to inhaled anesthetics like isoflurane or sevoflurane, and even helps maintain the alert state when animals are dosed with anesthetics.

The study also supports a hypothesis long debated by neuroscientists: that the parts of the brain regulating sleep and waking are also capable of regulating the brain’s response to general anesthetics.

https://www.pennmedicine.org/news/news-releases/2020/november/scien...

https://researchnews.cc/news/3673/Scientists-identify-brain-cells-t...

Comment by Dr. Krishna Kumari Challa on November 20, 2020 at 9:30am

Gut microbiome manipulation could result from virus discovery

Scientists have discovered how a common virus in the human gut infects and takes over bacterial cells – a finding that could be used to control the composition of the gut microbiome, which is important for human health.

The Rutgers co-authored research, which could aid efforts to engineer beneficial bacteria that produce medicines and fuels and clean up pollutants.
CrAssphages are the most abundant viruses infecting bacteria in the human gut. As such, they likely control our intestinal community of microbes (the microbiome).Understanding how these tiny viruses infect bacteria may allow scientists to control and manipulate the makeup of the microbiome, either by increasing the proportion of beneficial bacteria in our intestines or decreasing the number of harmful bacteria, thus promoting health and fighting disease.
Scientists found that crAssphages use their own enzyme (an RNA polymerase) to make RNA copies of their genes. RNA has the genetic information to make proteins. All cells, ranging from bacterial to human, use such enzymes to make RNA copies of their genes. And these enzymes are very similar in all living matter, implying that they’re ancient and related by common ancestry.
The atomic structure of a crAssphage enzyme is distinct from other RNA polymerases but closely resembles an enzyme in humans and other higher organisms that is involved in RNA interference. Such interference silences the function of some genes and may lead to certain diseases.

This is a startling result. It suggests that enzymes of RNA interference, a process that was thought to occur only in cells of higher organisms, were ‘borrowed’ from an ancestral bacterial virus early in evolution. The result provides a glimpse of how cells of higher organisms evolved by mixing and matching components of simpler cells and even their viruses.

In addition to deep evolutionary insights, phage (viral) enzymes such as crAssphage RNA polymerase may be used in synthetic biology to generate genetic circuits that do not exist in nature.

https://www.rutgers.edu/news/gut-microbiome-manipulation-could-resu...

https://researchnews.cc/news/3670/Gut-microbiome-manipulation-could...

Comment by Dr. Krishna Kumari Challa on November 20, 2020 at 8:00am

The fundamental chemistry behind electrocatalytic water splitting

https://phys.org/news/2020-11-fundamental-chemistry-electrocatalyti...

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New system can sterilize medical tools using solar heat

Comment by Dr. Krishna Kumari Challa on November 20, 2020 at 7:27am

Undesirable rejection mechanism identified in stem cell transplantation

In the treatment of leukemia, stem cell transplantation subsequent to chemotherapy and radiation can often engender severe adverse inflammatory reactions—especially in the skin or in the gut, since these so-called barrier organs are more frequently affected. Up until now, the reason for this was unclear till now. Scientists now identified an immune mechanism that is partially responsible for this.

The term leukemia is used to describe a group of malignant diseases of the haematopoietic system, in which precursors of the white blood cells (leucocytes) proliferate uncontrollably. Chemotherapy and radiotherapy are used to destroy the abnormal blood cells, which are then replaced by means of a stem cell transplant. In leukemia, the transplantation of healthy bone marrow stem cells or haematopoietic stem cells is often the only hope of recovery for patients. The process involves "replacing" all the recipient's blood cells that were previously destroyed by the treatment with donor cells.

However, the MedUni Vienna dermatologists have now found that there are so-called skin-resident and inactive T cells in the endogenous immune system that survive chemotherapy and radiotherapy intact and go on to survive for a further ten years between and beneath the epithelial cells of the skin, while the circulating T cells are destroyed.

"We were able to demonstrate that T cells surviving in the skin tissue are responsible for the inflammatory reaction following a stem cell transplant. These phenomena often occur within the first 100 days and can cause anything from mild eczema through to extensive fibrosis, hardening of the tissue, or blistering on the surface of the skin. In other words, the endogenous T cells attack the recipient (host) following stem cell transplantation." In specialist jargon, the condition is also referred to as Graft versus Host Disease (GvHD), and, for the first time, this study identified an inverse "Host-versus-graft reaction."

There were also cases in which the donor T cells further "supported," and thus intensified, this reaction. Affected patients are treated with cortisone, which causes an additional burden for patients who are already immunosuppressed following the transplantation. The study found that in patients who do not develop graft-versus-host disease, tissue-resident T cells remaining after treatment even proved to be beneficial to the recipient, in that they assumed their role in immune defense and protecting against infection.

In the future, the exemplary study results could lead to new treatment strategies that help to avoid, or at least to minimize, undesirable and violent inflammatory reactions following stem cell transplants by manipulating the recipient's inactive T cells in advance. In addition, the manipulation of tissue-resident T cells might lead to new therapeutic approaches for other chronic inflammatory skin diseases, such as psoriasis or neurodermatitis.

Johanna Strobl et al. Long-term skin-resident memory T cells proliferate in situ and are involved in human graft-versus-host disease, Science Translational Medicine (2020). DOI: 10.1126/scitranslmed.abb7028

https://medicalxpress.com/news/2020-11-undesirable-mechanism-stem-c...

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