Comment

Comment by Dr. Krishna Kumari Challa on September 1, 2024 at 2:38pm

Racing may slightly increase the chances a runner will suffer a rare event like heatstroke or cardiac arrest.
Runners and athletes are at reduced risk of having not only cardiac arrest, but all forms of heart disease compared to non-runners.
Taking care will reduce these chances of falling into dangerous situations.

Part 2

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Comment by Dr. Krishna Kumari Challa on September 1, 2024 at 2:35pm

A warming climate can make running deadly

A normal routine of runners can suddenly become deadly because of excess heat.

The body temperatures can cross 105 - sometimes can get as high as 107 degrees (41.6 Celsius).

Heat stroke is a deadly illness associated with extreme heat, and climate change is worsening the risk. 

Exertional heatstroke happens during exercise when the body can't properly cool, rising above 104 degrees (40 Celsius) and triggering a central nervous system problem such as fainting or blacking out. It can be effectively treated by rapidly cooling a victim, but lots of races lack the resources or expertise to do it. And many runners, in a culture that esteems grit and suffering, may ignore conditions that put them at risk.

Muscles can break down, releasing proteins that damage kidneys. The lining of the digestive system may weaken and leak bacteria. Brain cells may die. It can damage organs and, ultimately, kill.

Races are   magnets for heatstroke. At several miles, they are long enough to give the body time to heat up dangerously and short enough that many runners are pushing hard. Odds are good that some who haven't trained to acclimate to hot weather, or show up dehydrated,  become simply more vulnerable.

And  problem is lots of races don't have the equipment or expertise to offer the right lifesaving care.

Getting victims into a tub of ice water is the best way to quickly cool them. And it needs to happen fast, with quick diagnoses to treat runners on the spot. Medical staff need rectal thermometers to gauge temperature when skin can be deceptively cool.

But based on over 3,000 cases researchers have tracked, if someone's temp gets under 104 within 30 minutes of the presentation of heatstroke, no one has ever died.

Comment by Dr. Krishna Kumari Challa on September 1, 2024 at 2:13pm

Home stress testing

Modern day life style increases stress. Ignoring these high stress levels can lead to serious health issues like depression and Alzheimer's disease. So what if checking your stress levels at home became the norm? Thanks to nanoparticles, this possibility is drawing closer.

In a new study published in the journal Talanta, a team of researchers have produced a new and improved detector that can accurately measure levels of cortisol—a stress biomarker in the blood.

This is a  cost-effective, easily reproducible, and easy-to-use point-of-care testing device that accurately measures cortisol levels.

The devices currently available generally contain electrodes that have poor stability in different and fluctuating conditions, such as changing pH and temperature. This gives the devices a short shelf life and makes them difficult to produce commercially.

In this study, researchers used iridium oxide nanoparticles to cover the silver layer. This modification improves the stability, sensitivity and reproducibility of cortisol detection in point-of-care devices.

Tong Ji et al, Iridium oxide-modified reference screen-printed electrodes for point-of-care portable electrochemical cortisol detection, Talanta (2024). DOI: 10.1016/j.talanta.2024.126776

Comment by Dr. Krishna Kumari Challa on September 1, 2024 at 10:42am

Home stress testing

Modern day life style increases stress. Ignoring these high stress levels can lead to serious health issues like depression and Alzheimer's disease. So what if checking your stress levels at home became the norm? Thanks to nanoparticles, this possibility is drawing closer.

In a new study published in the journal Talanta, a team of researchers have produced a new and improved detector that can accurately measure levels of cortisol—a stress biomarker in the blood.

This is a  cost-effective, easily reproducible, and easy-to-use point-of-care testing device that accurately measures cortisol levels.

The devices currently available generally contain electrodes that have poor stability in different and fluctuating conditions, such as changing pH and temperature. This gives the devices a short shelf life and makes them difficult to produce commercially.

In this study, researchers used iridium oxide nanoparticles to cover the silver layer. This modification improves the stability, sensitivity and reproducibility of cortisol detection in point-of-care devices.

Tong Ji et al, Iridium oxide-modified reference screen-printed electrodes for point-of-care portable electrochemical cortisol detection, Talanta (2024). DOI: 10.1016/j.talanta.2024.126776

Comment by Dr. Krishna Kumari Challa on September 1, 2024 at 10:33am

Astronomers spot merging galaxies from 12.8 billion years ago

Astronomers have spotted a pair of galaxies in the act of merging 12.8 billion years ago. The characteristics of these galaxies indicate that the merger will form a monster galaxy, one of the brightest types of objects in the universe.

These results, which have been detailed in The Astrophysical Journal, are important for understanding the early evolution of galaxies and black holes in the early universe.

Quasars are bright objects powered by matter falling into a supermassive black hole at the center of a galaxy in the early universe. The most accepted theory is that when two gas-rich galaxies merge to form a single larger galaxy, the gravitational interaction of the two galaxies causes gas to fall towards the supermassive black hole in one or both of the galaxies, causing quasar activity.

To test this theory, an international team of researchers led by Takuma Izumi used the ALMA (Atacama Large Millimeter/submillimeter Array) radio telescope to study the earliest known pair of close quasars.
This pair was discovered by Yoshiki Matsuoka, at Ehime University in Japan, in images taken by the Subaru Telescope. Located in the direction of the constellation Virgo, this pair of quasars existed during the first 900 million years of the universe.

The pair is dim, indicating that the quasars are still in the early stages of their evolution. The ALMA observations mapped the host galaxies of the quasars and showed that the galaxies are linked by a "bridge" of gas and dust. This indicates that the two galaxies are in fact merging.

The ALMA observations also allowed the team to measure the amount of gas, the material for new star formation. The team found that the two galaxies are very rich in gas, suggesting that in addition to more vigorous quasar activity in the future, the merger will also trigger a rapid increase in star formation, known as a "starburst."

The combination of starburst activity and vigorous quasar activity is expected to create a super-bright object in the early universe known as a monster galaxy.

Takuma Izumi et al, Merging Gas-rich Galaxies That Harbor Low-luminosity Twin Quasars at z = 6.05: A Promising Progenitor of the Most Luminous Quasars, The Astrophysical Journal (2024). DOI: 10.3847/1538-4357/ad57c6

Comment by Dr. Krishna Kumari Challa on September 1, 2024 at 10:22am

However, it remains possible that other factors, such as genetic profile or lifestyle, might modulate the effects of clonal hematopoiesis, and future studies are planned to examine this possibility.

In the new study published in the European Heart Journal, the CNIC group, in partnership with the team led by Dr. Pradeep Natarajan at the Broad Institute in Boston, show that the adverse effects of TET2 mutations on cardiovascular health can be alleviated by treatment with the anti-inflammatory drug colchicine.

The  team demonstrated that administration of colchicine to animals with TET2 mutations slows the development of atherosclerosis to a rate similar to that seen in non-mutated animals. In parallel, the Broad Institute scientists showed that individuals with TET2 mutations and who had been treated with colchicine for other conditions had a lower risk of myocardial infarction than untreated patients with similar mutations.

Unidirectional association of clonal hematopoiesis with atherosclerosis development, Nature Medicine (2024). DOI: 10.1038/s41591-024-03213-1

M A Zuriaga et al, Colchicine prevents accelerated atherosclerosis development in TET2-mutant clonal hematopoiesis, European Heart Journal (2023). DOI: 10.1093/eurheartj/ehad655.3264

Part 2

Comment by Dr. Krishna Kumari Challa on September 1, 2024 at 10:20am

Scientists discover a new cardiovascular risk factor and identify a drug able to reduce its effects

To the known risk factors for cardiovascular disease—high blood pressure, high cholesterol, diabetes, overweight and obesity, smoking, and physical inactivity—a new one has to be added, clonal hematopoiesis. This condition is triggered by acquired mutations in blood stem cells and was already known to be associated with an elevated cardiovascular risk.

However, until now it was uncertain if clonal hematopoiesis was a cause or consequence of cardiovascular disease.

Now, a new study published in Nature Medicine and carried out by researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) resolves this critical debate by establishing clonal hematopoiesis as a new risk factor for atherosclerosis—the formation of lesions in the arterial wall that underlies most cardiovascular disorders.

In a second study, published in the European Heart Journal, the CNIC scientists propose the ancient medication colchicine as the central plank of personalized strategies to alleviate the effects of clonal hematopoiesis associated with acquired mutations in the TET2 gene. The results of these important studies were presented at the European Society of Cardiology meeting in London, UK.

An adult person produces hundreds of thousands of blood cells every day. This high rate of cell division unavoidably entails the accumulation of DNA mutations in the dividing cells. These mutations are known as somatic mutations, and are acquired, not inherited.

Although most somatic mutations are innocuous, some give the affected cells a competitive advantage that allows them to expand and progressively accumulate, generating clonal populations of mutated blood cells, a phenomenon known as clonal hematopoiesis.

These mutations had already been proposed as a possible risk factor for cardiovascular disease.

Some earlier studies suggested that somatic mutations linked to clonal hematopoiesis contribute directly to cardiovascular disease and thereby accelerating the development of atherosclerosis. On the other hand, others proposed that it is atherosclerosis that causes clonal hematopoiesis by increasing the proliferation of blood stem cells and thereby generating a higher proportion of mutated blood cells.

The Nature Medicine study clarifies the relationship between clonal hematopoiesis and atherosclerosis through a longitudinal analysis of data from the PESA-CNIC-Santander study. PESA (Progression of Early Subclinical Atherosclerosis) is a prospective study of more than 4000 apparently healthy middle-aged participants who have undergone periodic examinations using advanced imaging technology since 2010 to detect the presence and progression of asymptomatic atherosclerosis. PESA is a collaborative initiative of the CNIC and Santander Bank.

The results of the study clearly demonstrate that participants who had mutations linked to clonal hematopoiesis at the start of the study were more likely to develop atherosclerosis in the following years. On the other hand, the presence and extent of atherosclerosis had no influence on the expansion of mutated blood cells.

"These results indicate that the mutations contribute to the development of atherosclerosis but are not a consequence of it.

Part1

Comment by Dr. Krishna Kumari Challa on August 31, 2024 at 8:56am

Computer Scientists  show evidence That Heat Destroys Quantum Entanglement

While devising a new quantum algorithm, four researchers accidentally established a hard limit on the "spooky" phenomenon.

 When quantum particles such as atoms interact, they shed their individual identities in favor of a collective state that’s greater, and weirder, than the sum of its parts. This phenomenon is called entanglement.

When quantum particles such as atoms interact, they shed their individual identities in favor of a collective state that’s greater, and weirder, than the sum of its parts. This phenomenon is called entanglement.

Researchers have a firm understanding of how entanglement works in idealized systems containing just a few particles. But the real world is more complicated. In large arrays of atoms, like the ones that make up the stuff we see and touch, the laws of quantum physics compete with the laws of thermodynamics, and things get messy.

At very low temperatures, entanglement can spread over long distances, enveloping many atoms and giving rise to strange phenomena such as superconductivity. Crank up the heat, though, and atoms jitter about, disrupting the fragile links that bind entangled particles.

Physicists have long struggled to pin down the details of this process. Now, a team of four researchers has provided evidence that entanglement doesn’t just weaken as temperature increases. Rather, in mathematical models of quantum systems such as the arrays of atoms in physical materials, there’s always a specific temperature above which it vanishes completely. “It’s not just that it’s exponentially small,” say the researchers, “It’s zero.”

Researchers had previously observed hints of this behavior and dubbed it the “sudden death” of entanglement. But their evidence has always been indirect. The new finding, by contrast, has the force of a mathematical proof. It establishes the absence of entanglement in a much more comprehensive and rigorous way.

https://arxiv.org/abs/2403.16850

Comment by Dr. Krishna Kumari Challa on August 31, 2024 at 8:40am

The physics of fish hearing

Comment by Dr. Krishna Kumari Challa on August 30, 2024 at 10:23am

Trouble with trembling hands originates in the brain: Research IDs genetic variations associated with essential tremor

New research by the National Neuroscience Institute (NNI) of Singapore has identified for the first time how gene variations cause changes in the brain that are linked to essential tremor—a common condition that causes uncontrollable shaking of the hands, such as when writing or holding items.

Essential tremor is one of the most common movement disorders, affecting more than 60 million people worldwide. More than half of the total diagnosed cases have a family history of tremor, and those with a parent or sibling with essential tremor are nearly five times more likely to have the condition.

Hand tremor affects both the young and the old. It is not only socially embarrassing but impacts one's quality of life. Some patients also develop voice and head tremor. While some medical conditions can cause tremors, scientists are still trying to understand the underlying mechanism. 

The NNI study, which was published in the journal Movement Disorders, used brain MRI scans and genetic data of more than 33 000 adults to identify genetic variations associated with essential tremor and their links with structural changes in the brain.

The team identified genes related to differences in specific parts of the brain involved in tremor. For example, there is a specific set of genes that are related to a thinner cortex (outer region of the brain) and a smaller cerebellum (hind brain), the part of the brain involved in balance and movement.

The study also identified how these genetic variations affect the brain at the cellular pathway level, revealing new potential drug targets to treat the condition.

Normally, the body is able to dispose of faulty proteins, but scientists found that this 'quality control' system is faulty in tremor-related parts of the brain. This may affect cell function and disrupt the flow of messages along a key neural pathway between the cerebellum, thalamus and motor cortex, and result in uncontrollable shaking of the hands.

Thomas Welton et al, Association of Gene Expression and Tremor Network Structure, Movement Disorders (2024). DOI: 10.1002/mds.29831

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