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Comment by Dr. Krishna Kumari Challa on November 27, 2020 at 10:15am

High blood pressure in midlife is linked to increased brain damage in later life

Higher than normal blood pressure is linked to more extensive brain damage in the elderly, according to a new study published.

In particular, the study found that there was a strong association between diastolic blood pressure (the blood pressure between heart beats) before the age of 50 and brain damage in later life, even if the diastolic blood pressure was within what is normally considered to be a healthy range.

The findings come from a study of 37,041 participants enrolled in UK Biobank, a large group of people recruited from the general population aged between 40 and 69 years, and for whom medical information, including MRI brain scans was available.

Karolina Agnieszka Wartolowska et al, Midlife blood pressure is associated with the severity of white matter hyperintensities: analysis of the UK Biobank cohort study, European Heart Journal (2020). DOI: 10.1093/eurheartj/ehaa756

https://medicalxpress.com/news/2020-11-high-blood-pressure-midlife-...

Comment by Dr. Krishna Kumari Challa on November 27, 2020 at 10:10am

New Hubble data explains missing dark matter

New data from the NASA/ESA Hubble Space Telescope provides further evidence for tidal disruption in the galaxy NGC 1052-DF4. This result explains a previous finding that this galaxy is missing most of its dark matter. By studying the galaxy's light and globular cluster distribution, astronomers have concluded that the gravity forces of the neighbouring galaxy NGC 1035 stripped the dark matter from NGC 1052-DF4 and are now tearing the galaxy apart.

The galaxy "missing dark matter" NGC1052-DF4 is undergoing tidal disruption arXiv:2010.09719 [astro-ph.GA] arxiv.org/abs/2010.09719

https://phys.org/news/2020-11-hubble-dark.html?utm_source=nwletter&...

Comment by Dr. Krishna Kumari Challa on November 27, 2020 at 10:07am

Ancient Earth had a thick, toxic atmosphere like Venus—until it cooled off and became liveable

A rocky planet like Earth is born through a process called "accretion", in which initially small particles clump together under the pull of gravity to form larger and larger bodies. The smaller bodies, called "planetesimals", look like asteroids, and the next size up are "planetary embryos". There may have been many planetary embryos in the early Solar System, but the only one that still survives is Mars, which is not a fully fledged planet like Earth or Venus.

The late stages of accretion involve giant impacts that release enormous amounts of energy. We think the last impact in Earth's accretion involved a Mars-sized embryo hitting the growing Earth, spinning off our Moon, and melting most or all of what was left.

The impact would have left Earth covered in a global sea of molten rock called a "magma ocean". The magma ocean would have leaked hydrogen, carbon, oxygen and nitrogen gases, to form Earth's first atmosphere.

This ratio of CO₂ to N₂ is strikingly like the present atmosphere on Venus. So why did Venus, but not Earth, retain the hellishly hot and toxic environment we observe today?

The answer is that Venus was too close to the Sun. It simply never cooled down enough to form water oceans. Instead, the H₂O in the atmosphere stayed as water vapour and was slowly but inexorably lost to space.

On the early Earth, the water oceans instead slowly but steadily drew down CO₂ from the atmosphere by reaction with rock – a reaction known to science for the past 70 years as the “Urey reaction”, after the Nobel prizewinner who discovered it – and reducing atmospheric pressure to what we observe today.

So, although both planets started out almost identically, it is their different distances from the Sun that put them on divergent paths. Earth became more conducive to life while Venus became increasingly inhospitable.

Paolo A. Sossi et al. Redox state of Earth's magma ocean and its Venus-like early atmosphere, Science Advances (2020). DOI: 10.1126/sciadv.abd1387

https://theconversation.com/ancient-earth-had-a-thick-toxic-atmosph...

Comment by Dr. Krishna Kumari Challa on November 27, 2020 at 10:00am

Foreign vs. own DNA: How an innate immune sensor tells friend from foe

How do molecules involved in activating our immune system discriminate between our own DNA and foreign pathogens? Researchers deciphered the structural and functional basis of a DNA-sensing molecule when it comes in contact with the cell's own DNA, providing crucial insights into the recognition of self vs. non-self DNA.

DNA within our cells is compacted and stored in the nucleus in the form of chromatin (DNA wraped around histone proteins, forming nucleosomes, the basic unit of chromatin). DNA found outside the nucleus, in the cytoplasm, is an important signal that triggers immune responses indicating the presence of an intracellular pathogen or a potentially cancerous cell. DNA sensing is carried out by cGAS, an enzyme responsible for recognizing and binding naked DNA. When activated, cGAS synthesizes cyclic GMP-AMP, which in turn initiates the body's so-called "innate" immune system—the first-line-of-defense part of our immune system.

Until now, cGAS was thought to function predominantly in the cytoplasm, detecting foreign, non-self, DNA such as viruses. But recent studies suggested that cGAS is also present inside the nucleus. This was puzzling given the possibility that the enzyme is activated by its own DNA triggering an unwanted inflammatory response against its own DNA. Intrigued by this observation, researchers used structural biology as a discovery tool and found that cGAS is present in the nucleus in an inactive state. They teamed up with the Ablasser lab at the EPFL to decipher the mechanism of cGAS inactivation by chromatin in cells.

Taking advantage of  cryo-electron microscopy (cryo-EM), the researchers derived the structure of cGAS bound to a nucleosome. They found that cGAS directly engages the histone proteins of nucleosomes. Once bound to the nucleosome, cGAS is "trapped" in a state in which it is unable to engage or sense naked DNA. It is then also unable to synthesize GMP-AMP and remains inactivated. cGAS, when present in the nucleus of healthy cells, is thus inactivated by chromatin, and does not participate in innate immune signaling in response to its own DNA.

 Ganesh R. Pathare et al. Structural mechanism of cGAS inhibition by the nucleosome, Nature (2020). DOI: 10.1038/s41586-020-2750-6

https://phys.org/news/2020-11-foreign-dna-innate-immune-sensor.html...

Comment by Dr. Krishna Kumari Challa on November 27, 2020 at 9:54am

Study is the first to link microbiota to dynamics of the human immune system

Researchers have uncovered an important finding about the relationship between the microbiota and the immune system, showing for the first time that the concentration of different types of immune cells in the blood changes in relation to the presence of different bacterial strains in the gut.

In recent years, the microbiota—the community of bacteria and other microorganisms that live on and in the human body—has captured the attention of scientists and the public, in part because it's become easier to study. It has been linked to many aspects of human health.

A multidisciplinary team from Memorial Sloan Kettering has shown for the first time that the gut microbiota directly shapes the makeup of the human immune system. Specifically, their research demonstrated that the concentration of different types of immune cells in the blood changed in relation to the presence of different bacterial strains in the gut. The results of their study, which used more than ten years of data collected from more than 2,000 patients, is being published November 25, 2020, in Nature.

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The data that were used in the study came from people receiving allogeneic stem cell and bone marrow transplants (BMTs). After strong chemotherapy or radiation therapy is used to destroy cancerous blood cells, the patient's blood-forming system is replaced with stem cells from a donor. For the first few weeks until the donor's blood cells—including the white blood cells that make up the immune system—have established themselves, the patients are extremely vulnerable to infections. To protect them during this time, patients are given antibiotics.

But many of these antibiotics have the unwanted side effect of destroying healthy microbiota that live in the gut, allowing dangerous strains to take over. When the patient's immune system has reconstituted, the antibiotics are discontinued, and the gut microbiota slowly starts to grow back.

The parallel recoveries of the immune system and the microbiota, both of which are damaged and then restored, gives us a unique opportunity to analyze the associations between these two systems.

Jonas Schluter et al. The gut microbiota is associated with immune cell dynamics in humans, Nature (2020). DOI: 10.1038/s41586-020-2971-8

https://medicalxpress.com/news/2020-11-link-microbiota-dynamics-hum...

Comment by Dr. Krishna Kumari Challa on November 27, 2020 at 9:43am

Scientists develop new gene therapy for eye disease

Scientists  have developed a new gene therapy approach that offers promise for one day treating an eye disease that leads to a progressive loss of vision and affects thousands of people across the globe.

The study also has implications for a much wider suite of neurological disorders associated with aging.

Characterized by degeneration of the optic nerves, DOA typically starts to cause symptoms in patients in their early adult years. These include moderate vision loss and some color vision defects, but severity varies, symptoms can worsen over time and some people may become blind. There is currently no way to prevent or cure DOA.

A gene (OPA1) provides instructions for making a protein that is found in cells and tissues throughout the body, and which is pivotal for maintaining proper function in mitochondria, which are the energy producers in cells.

Without the protein made by OPA1, mitochondrial function is sub-optimal and the mitochondrial network which in healthy cells is well interconnected is highly disrupted.

For those living with DOA, it is mutations in OPA1 and the dysfunctional mitochondria that are responsible for the onset and progression of the disorder. 

The scientists, led by Dr. Daniel Maloney and Professor Jane Farrar from Trinity's School of Genetics and Microbiology, have developed a new gene therapy, which successfully protected the visual function of mice who were treated with a chemical targeting the mitochondria and were consequently living with dysfunctional mitochondria.

The scientists also found that their gene therapy improved mitochondrial performance in human cells that contained mutations in the OPA1 gene, offering hope that it may be effective in people.

They used a clever lab technique that allows scientists to provide a specific gene to cells that need it using specially engineered non-harmful viruses. This allowed them to directly alter the functioning of the mitochondria in the cells theytreated, boosting their ability to produce energy which in turn helps protects them from cell damage.

These results  demonstrate that this OPA1-based gene therapy can potentially provide benefit for diseases like DOA, which are due to OPA1 mutations, and also possibly for a wider array of diseases involving mitochondrial dysfunction

https://www.frontiersin.org/articles/10.3389/fnins.2020.571479/full

https://www.tcd.ie/news_events/articles/scientists-develop-new-gene...

https://medicalxpress.com/news/2020-11-scientists-gene-therapy-eye-...

Comment by Dr. Krishna Kumari Challa on November 27, 2020 at 9:35am

**Study revealing the secret behind a key cellular process refutes biology textbooks

New research has identified and described a cellular process that, despite what textbooks say, has remained elusive to scientists until now—precisely how the copying of genetic material that, once started, is properly turned off.

The finding concerns a key process essential to life: the transcription phase of gene expression, which enables cells to live and do their jobs.

During transcription, an enzyme called RNA polymerase wraps itself around the double helix of DNA, using one strand to match nucleotides to make a copy of genetic material—resulting in a newly synthesized strand of RNA that breaks off when transcription is complete. That RNA enables production of proteins, which are essential to all life and perform most of the work inside cells.

Just as with any coherent message, RNA needs to start and stop in the right place to make sense. A bacterial protein called Rho was discovered more than 50 years ago because of its ability to stop, or terminate, transcription. In every textbook, Rho is used as a model terminator that, using its very strong motor force, binds to the RNA and pulls it out of RNA polymerase. But a closer look by these scientists showed that Rho wouldn't be able to find the RNAs it needs to release using the textbook mechanism.

Researchers started studying Rho, and realized it cannot possibly work in ways people tell us it works!

The research determined that instead of attaching to a specific piece of RNA near the end of transcription and helping it unwind from DNA, Rho actually "hitchhikes" on RNA polymerase for the duration of transcription. Rho cooperates with other proteins to eventually coax the enzyme through a series of structural changes that end with an inactive state enabling release of the RNA.

The team used sophisticated microscopes to reveal how Rho acts on a complete transcription complex composed of RNA polymerase and two accessory proteins that travel with it throughout transcription.

It answers a fundamental question—transcription is fundamental to life, but if it were not controlled, nothing would work. RNA polymerase by itself has to be completely neutral. It has to be able to make any RNA, including those that are damaged or could harm the cell. While traveling with RNA polymerase, Rho can tell if the synthesized RNA is worth making—and if not, Rho releases it.

"Steps toward translocation-independent RNA polymerase inactivation by terminator ATPase ρ" Science (2020). science.sciencemag.org/lookup/ … 1126/science.abd1673

https://phys.org/news/2020-11-revealing-secret-key-cellular-refutes...

Comment by Dr. Krishna Kumari Challa on November 26, 2020 at 10:35am

Covid-19 pandemic could be stopped if at least 70% public wore face...
The Covid-19 pandemic could be stopped if at least 70 per cent of the public wore face masks consistently, according to research published in the journal Physics of Fluids. The study suggests that the type of material used and the duration of mask use play key roles in their effectiveness. While surgical masks were said to be more efficient, cloth masks could also slow transmission.

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Humans are polluting the environment with antibiotic-resistant bacteria, and scientists are  finding them everywhere

https://theconversation.com/humans-are-polluting-the-environment-wi...

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** Keyhole wasps may threaten aviation safety

Over a period of 39 months, invasive keyhole wasps (Pachodynerus nasidens) at the Brisbane Airport were responsible for 93 instances of fully blocked replica pitot probes—vital instruments that measure airspeed—according to a study published November 25 in the open-access journal PLOS ONE by Alan House of Eco Logical Australia and colleagues. As noted by the authors, the results underscore the importance of risk-mitigating strategies, such as covering pitot probes when aircraft arrive and setting up additional traps to intercept the wasps.

Comment by Dr. Krishna Kumari Challa on November 26, 2020 at 10:23am

Researchers uncover the unique way stem cells protect their chromosome ends

Telomeres are specialized structures at the end of chromosomes which protect our DNA and ensure healthy division of cells. According to a new study from researchers at the Francis Crick Institute published in Nature, the mechanisms of telomere protection are surprisingly unique in stem cells.

For the last 20 years, researchers have been working to understand how telomeres protect chromosome ends from being incorrectly repaired and joined together because this has important implications for our understanding of cancer and aging.

In healthy cells, this protection is very efficient, but as we age our telomeres get progressively shorter, eventually becoming so short that they lose some of these protective functions. In healthy cells, this contributes to the progressive decline in our health and fitness as we age. Conversely, telomere shortening poses a protective barrier to tumor development, which cancer cells must solve in order to divide indefinitely.

In somatic cells, which are all the cells in the adult body except stem cells and gametes, we know that a protein called TRF2 helps to protect the telomere. It does this by binding to and stabilizing a loop structure, called a t-loop, which masks the end of the chromosome. When the TRF2 protein is removed, these loops do not form and the chromosome ends fuse together, leading to "spaghetti chromosomes" and killing the cell.

However, in this latest study, Crick researchers have found that when the TRF2 protein is removed from mouse embryonic stem cells, t-loops continue to form, chromosome ends remain protected and the cells are largely unaffected.

As embryonic stem cells differentiate into somatic cells, this unique mechanism of end protection is lost and both t-loops and chromosome end protection become reliant on TRF2. This suggests that somatic and stem cells protect their chromosome ends in fundamentally different ways.

Phil Ruis et al. TRF2-independent chromosome end protection during pluripotency, Nature (2020). DOI: 10.1038/s41586-020-2960-y

https://phys.org/news/2020-11-uncover-unique-stem-cells-chromosome....

Comment by Dr. Krishna Kumari Challa on November 26, 2020 at 10:19am

Scientists discover potential method to starve the bacteria that cause tuberculosis

The infectious disease Tuberculosis (TB) is one of the leading causes of death worldwide.

Researchers have known for some time that the bacteria that causes TB (Mycobacterium tuberculosis) uses our body's cholesterol—a steroid—as a food source. Other relatives of the bacteria that do not cause disease share its ability to break down steroids. In this study scientists identified the structure of an enzyme (acyl CoA dehydrogenase) involved in steroid degradation in another member of the same bacteria family, called Thermomonospora curvata.

Determining the structure of enzymes that metabolize steroids moves scientists and pharmaceutical companies one step closer to creating drugs that can inhibit a similar enzyme found in M. tuberculosis, which would effectively starve TB of its food source. 

Alexander J. Stirling et al. A Key Glycine in Bacterial Steroid-Degrading Acyl-CoA Dehydrogenases Allows Flavin-Ring Repositioning and Modulates Substrate Side Chain Specificity, Biochemistry (2020). DOI: 10.1021/acs.biochem.0c00568

https://phys.org/news/2020-11-scientists-potential-method-starve-ba...

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