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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

Comment by Dr. Krishna Kumari Challa on August 30, 2024 at 10:11am

Women with endometriosis at greater associated risk of heart attack and stroke, research finds

According to research presented at ESC Congress 2024, women with endometriosis have a 20% greater risk of significant cardiac outcomes compared with women without endometriosis.

The study used Danish nationwide registries of all women with a diagnosis of endometriosis between 1977 and 2021. They were matched with women from the background population without endometriosis in a 1:4 ratio based on year of birth. The primary outcome was a composite of acute myocardial infarction and ischemic stroke. The secondary outcomes were the individual components of the primary outcome, as well as arrhythmias, heart failure and mortality.

There were 60,508 women with endometriosis and 242,032 matched controls included in the analysis (median age, 37.3 years) who were followed for a median of 16 years and a maximum of 45 years.

Women with endometriosis had around a 20% increased risk of the composite endpoint of acute myocardial infarction and ischemic stroke compared with those without endometriosis (unadjusted hazard ratio [HR] 1.18; 95% confidence interval [CI] 1.14−1.23; adjusted HR 1.15; 95% CI 1.11−1.20). The 40-year cumulative incidence of the composite of acute myocardial infarction and ischemic stroke was 17.5% (95% CI 16.6−18.2%) and 15.3% (95% CI 15.0−15.7%) in women with and without endometriosis, respectively (p<0.0001).

When this was broken down to the individual components, women with endometriosis had around a 20% increased risk of ischemic stroke (adjusted HR 1.18; 95% CI 1.12−1.23) and around 35% increased risk of acute myocardial infarction (adjusted HR 1.35; 95% CI 1.31−1.40) compared with those without endometriosis. Moreover, women with endometriosis also had increased risk of arrhythmias (adjusted HR 1.21; 95% CI 1.17−1.25) and heart failure (adjusted HR 1.11; 95% CI 1.05−1.18) compared with those without endometriosis.

Growing evidence suggests there is a close relationship between endometriosis and the cardiovascular system and that they may share common disease pathways. 

Researchers suggest that women with endometriosis undergo CVD risk assessment, and it is now time for female-specific risk factors—such as endometriosis, but also gestational diabetes and pre-eclampsia—to be considered in cardiovascular risk prediction models. 

Havers-Borgersen, E. Endometriosis, a prevalent disease, is associated with significant cardiac disease, esc365.escardio.org/ESC-Congress/sessions/11951

Comment by Dr. Krishna Kumari Challa on August 30, 2024 at 10:04am

Scientists discover how the body's killer cells attack cancer

Scientists are on the verge of a cancer breakthrough after working out how the body's immune system targets cells devastated by the disease.

A new study has discovered that our natural killer cells, from the immune system which protect against disease and infections, instinctively recognize and attack a protein that drives cancer growth. The experts say that by hijacking this protein, known as XPO1, they may be able to activate more killer cells to destroy the disease.

These findings actually show how our body's immune system recognizes and attacks these cancer cells.

Killer cells are an emerging form of immunotherapy that shows huge promise. They don't attack healthy tissue in the way chemotherapy and other immunotherapies do, so are safer and have less side-effects than traditional forms of cancer treatment.

The XPO1 protein examined by the scientists is essential for normal cell function. However, in many cancers, it becomes overactive and allows malignant cells to multiply unchecked. The scientists found that a peptide—short chains of amino acids—derived from the XPO1 protein attracted the natural killer cells. This, they say, triggers the body's immune response against the cancerous cells.

Patients with cancer who had both active killer cells and high levels of XPO1 had significantly better survival rates. This holds true for a range of cancers including those with higher rates of death such as liver cancer, which has an average survival rate of only 18 months. As well as liver cancer, killer cell treatment in the future could be used to treat head and neck cancers, endometrial, bladder or breast cancer.

Matthew D. Blunt et al, The nuclear export protein XPO1 provides a peptide ligand for natural killer cells, Science Advances (2024). DOI: 10.1126/sciadv.ado6566

Comment by Dr. Krishna Kumari Challa on August 30, 2024 at 9:41am

How star fish perform Autotomy - the ability of an animal to detach a body part to evade predators.

Researchers have made a discovery about how starfish manage to survive predatory attacks by shedding their own limbs. The team has identified a neurohormone responsible for triggering this remarkable feat of self-preservation. The study is published in the journal Current Biology.

Autotomy, the ability of an animal to detach a body part to evade predators, is a well-known survival strategy in the animal kingdom. While lizards shedding their tails are a familiar example, the mechanisms behind this process remain largely mysterious.

Now, scientists have unveiled a key piece of the puzzle. By studying the common European starfish, Asterias rubens, they identified a neurohormone akin to the human satiety hormone, cholecystokinin (CCK), as a regulator of arm detachment.

Furthermore, the scientists propose that when this neurohormone is released in response to stress, such as a predator attack, it stimulates the contraction of a specialized muscle at the base of the starfish's arm, effectively causing it to break off.

Remarkably, starfish possess incredible regenerative abilities, allowing them to grow back lost limbs over time. Understanding the precise mechanisms behind this process could hold significant implications for regenerative medicine and the development of new treatments for limb injuries.

Discovery of a neuropeptide that acts as an autotomy-promoting factor, Current Biology (2024). DOI: 10.1016/j.cub.2024.08.003. www.cell.com/current-biology/f … 0960-9822(24)01079-0

Comment by Dr. Krishna Kumari Challa on August 30, 2024 at 9:32am

Nanoplastics put stress on trees and impair photosynthesis

It is well known that more and more plastic waste is ending up in soil and bodies of water. Researchers are particularly concerned about tiny micro- and nano-sized particles. It remains unclear how and to what extent they are able to enter living organisms—and what effect they may have on metabolism.

Researchers now been able to show how trees take up nanoplastics contained in water through their roots. They have demonstrated for the first time that this has a negative effect on photosynthesis. 

The team then added different concentrations of model metal-doped nanoplastics to the water and analyzed the content of plastic particles in different parts of the trees at varying intervals. They also determined photosynthesis activity throughout the study, which has now been published in Environmental Science: Nano.

Within just a few weeks, the researchers were able to detect 1 to 2 milligrams of nanoplastics per gram of plant material in the roots. The plastic content was around 10 to 100 times lower in the trunks, leaves and needles.

There were no significant differences between the two tree species.

The researchers also succeeded in proving that nanoplastics in the leaves and needles can affect important physiological processes. Their measurements showed that the effectiveness of photosynthesis in the wild service tree decreased by a third within two weeks, and in the Norway spruce by about 10% within four weeks—in each case they were compared with trees growing in water without the addition of nanoplastics.

The result indicated that some of the energy from sunlight is no longer used for photosynthesis, but is instead dissipated as heat. This is a typical stress reaction in trees.

Maria Elvira Murazzi et al, Uptake and physiological impacts of nanoplastics in trees with divergent water use strategies, Environmental Science: Nano (2024). DOI: 10.1039/D4EN00286E

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