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Comment by Dr. Krishna Kumari Challa 3 hours ago

Climate change is overhauling marine nutrient cycles, scientists say

Computer models reveal how human-driven climate change will dramatically overhaul critical nutrient cycles in the ocean. In the Proceedings of the National Academy of Sciences,  researchers report evidence that marine nutrient cycles—essential for sustaining ocean ecosystems—are changing in unexpected ways as the planet continues to warm.

Model studies have suggested that when the ocean warms it gets more stratified, which can drain certain parts of the surface ocean of nutrients. 

Although models suggest a connection between ocean temperatures and surface ocean nutrients, this is the first study to confirm climate change's impacts on nutrient cycles.

The researchers  discovered that over the last half-century, there's been a major decline in phosphorus—a nutrient that plays a key role in the health of marine food webs—in southern hemisphere oceans.

There can be cascading effects up the food web, they say. Because plankton—microorganisms that form the bases of many marine food webs—rely on phosphorous as a food source. "When phytoplankton have less phosphorus, they become less nutritious, which can impair zooplankton and fish growth rates."

Surprisingly, concentrations of nitrate—a nutrient the team expected to decline—appear to remain steady. Nitrate is crucial for ecosystem functioning, so that it's not in decline is a good sign.

Nevertheless, nitrate concentrations may still decline in the future as the climate continues to change.

Skylar D. Gerace et al, Observed declines in upper ocean phosphate-to-nitrate availability, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2411835122

Comment by Dr. Krishna Kumari Challa 4 hours ago

Half a degree rise in global warming will triple area of Earth too hot for humans, scientists warn

An international group of scientists has revealed how continued global warming will lead to more parts of the planet becoming too hot for the human body over the coming decades.

The paper, published in Nature Reviews Earth & Environment, finds that the amount of landmass on our planet that would be too hot for even healthy young humans (18 to 60-year-olds) to keep a safe core body temperature will approximately triple (to 6%)—an area almost the size of the US—if global warming reaches 2°C above the preindustrial average.

Under these conditions, they also warn that the area of land where the over 60s will be at risk will increase to about 35%.

Last year was the first calendar year with a global mean temperature of more than 1.5°C above the preindustrial average, and at current rates of warming, 2°C could be reached by mid to late century.

These findings show the potentially deadly consequences if global warming reaches 2°C. Unsurvivable heat thresholds, which so far have only been exceeded briefly for older adults in the hottest regions on Earth, are likely to emerge even for younger adults.

In such conditions, prolonged outdoor exposure—even for those in the shade, subject to a strong breeze, and well hydrated—would be expected to cause lethal heatstroke. It represents a step-change in heat-mortality risk, they warn.

Earth's most extreme heat events and mortality impacts under climate warming, Nature Reviews Earth & Environment (2025). DOI: 10.1038/s43017-024-00635-w

Comment by Dr. Krishna Kumari Challa 4 hours ago

The link between renal failure and Parkinson's disease: Researchers illuminate the underlying mechanisms

Lewy body diseases (LBDs) are a class of debilitating neurodegenerative disorders linked to the abnormal aggregation of the protein α-synuclein in nerve cells. When misfolded, this protein can produce clumps known as Lewy bodies, which can adversely impact the functioning of cells, contributing to neurodegeneration.

Recent studies also showed that LBDs, particularly Parkinson's disease, often initiate in the gut and that, in some cases, kidney failure contributes to their emergence. So far, however, the exact physiological processes connecting kidney failure to PD are being studied now.

Researchers  recently carried out a study to better understand these mechanisms by further examining the link between kidney failure and LBDs. Their findings, published in Nature Neuroscience, show that renal dysfunction can cause the accumulation of α-synuclein in the kidneys, which can in turn cause the protein to spread to the brain, in some cases facilitating the development of PD.

Building on previous studies that unveiled a link between kidney function and the incidence of PD, researchers now carried out experiments to further illustrate the mechanisms behind this connection. To do this, they first stained kidney samples extracted from patients diagnosed with PD and those extracted from people with chronic renal diseases.

They found that α-synuclein was deposited in the kidneys of these patients. 

To illustrate the role of renal failure in PD, they induced renal failure in mouse models of PD and found that renal failure exacerbates PD-like pathology. Injection of α-synuclein fibrils into the kidney induced the spread of α-synuclein pathology to the brain, whereas deletion of α-synuclein in blood cells alleviated PD pathology in a mouse model of PD.

Essentially, the researchers found that the kidneys of patients presenting renal failure contained a large amount of the protein α-synuclein. They were then able to shed light on how this α-synuclein accumulation could lead to PD, specifically following the spread of this protein to the brain.

They also showed that severing the connections between the kidneys and the brain in male mice blocked the accumulation of α-synuclein in the brain following renal failure.

Xin Yuan et al, Propagation of pathologic α-synuclein from kidney to brain may contribute to Parkinson's disease, Nature Neuroscience (2025). DOI: 10.1038/s41593-024-01866-2.

Comment by Dr. Krishna Kumari Challa yesterday

Compared to singleton pregnancies with normal blood pressure, people with twins with normal blood pressure were around twice as likely to be hospitalized with cardiovascular disease. For those with twins with high blood pressure during pregnancy, the risk is more than eight times higher.

However, one year after birth, deaths from any cause, including heart disease, were higher among patients with singleton pregnancies who had high blood pressure conditions compared to patients with twins with high blood pressure conditions. This suggests that the risk to mothers of twins decreases in the longer term, while the mothers of singletons may have other pre-existing cardiovascular risk factors.
Recommendations: People with twin pregnancies should be aware of the short-term increase in cardiovascular disease complications in the first year after birth, even if they had a pregnancy that was not complicated by high blood pressure conditions, such as pre-eclampsia. For patients having fertility treatments, especially for those with other cardiovascular risk factors, such as older age, obesity, diabetes, high blood pressure or heart disease, patients should be advised that twin pregnancies may increase cardiovascular disease complications in the short term.

Given these higher risks, health care providers and health insurance companies should continue to provide follow-up for up to a year after birth for high-risk pregnancies such as twin pregnancies.

 Cande V. Ananth et al, Hospitalization for cardiovascular disease in the year after delivery of twin pregnancies, European Heart Journal (2025). DOI: 10.1093/eurheartj/ehaf003

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

Mothers of twins face a higher risk of heart disease in the year after birth

The risk of being admitted to the hospital with heart disease is twice as high the year after birth for mothers of twins compared to singleton births, according to research published in the European Heart Journal. The risk is even higher in mothers of twins who had a high blood pressure condition during pregnancy.

The rate of twin pregnancies worldwide has risen in recent decades, driven by fertility treatments and older maternal ages. Previous studies have shown no long-term increased risk of cardiovascular disease when following people with twin pregnancies for decades after delivery. However, this is counterintuitive to what we observe clinically when caring for patients with twin pregnancies.

Given the unacceptably high rate of maternal mortality in the first year after birth due to cardiovascular disease, researchers wanted to examine whether twin pregnancies increase this risk.

The researchers studied data on 36 million hospital deliveries taken from the US Nationwide Readmissions Database of US hospitals from 2010 to 2020. They divided pregnant patients into four groups: those who had twins but normal blood pressure during pregnancy, those who had twins and hypertensive disease of pregnancy (high blood pressure conditions), those who had singleton pregnancies with normal blood pressure, and those who had singleton pregnancies with hypertensive disease of pregnancy.

Hypertensive disease of pregnancy includes gestational hypertension, pre-eclampsia, eclampsia, and superimposed pre-eclampsia.

For each group, researchers calculated the proportion of patients who were readmitted to the hospital within a year of childbirth with any type of cardiovascular disease, including heart attack, heart failure, or stroke.

Researchers found that the proportion of readmissions for cardiovascular disease within a year of giving birth was higher overall for those with twins (1,105.4 per 100,000 deliveries) than singleton pregnancies (734.1 per 100,000 deliveries).

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Scientists find more microplastics in human brains than in kidneys and livers—and levels are rising

Tiny plastic particles may accumulate at higher levels in the human brain than in the kidney and liver, with greater concentrations detected in postmortem samples from 2024 than in those from 2016, suggests a paper published in Nature Medicine. Although the potential implications for human health remain unclear, these findings may highlight a consequence of rising global concentrations of environmental plastics.

The amount of environmental plastic nano- and microparticles, which range in size from as small as 1 nanometer (one billionth of a meter) up to 500 micrometers (one millionth of a meter) in diameter, has increased exponentially over the past 50 years. However, whether they are harmful or toxic to humans is unclear. Most previous studies used visual microscopic spectroscopy methods to identify particulates in human tissues, but this is often limited to particulates larger than 5 micrometers.

Researchers now  used novel methods to analyze the distribution of micro- and nanoparticles in samples of liver, kidney, and brain tissues from human bodies that underwent autopsy in 2016 and 2024. A total of 52 brain specimens (28 in 2016 and 24 in 2024) were analyzed.

The team detected these particles in all of the samples and found similar concentrations in the samples of liver and kidney tissues obtained in 2016. However, brain samples taken from that time, all derived from the frontal cortex region, contained substantially higher concentrations of plastic particles than the liver and kidney tissues.

They  also found that liver and brain samples from 2024 had significantly higher concentrations of plastic micro- and nanoparticles than those from 2016. They compared these findings with those of brain tissue samples from earlier time frames (1997–2013) and noted that there were higher concentrations of plastic particles in the more recent tissue samples. They also found a higher concentration of micro- and nanoplastic particles in brains from 12 individuals with a documented dementia diagnosis than in those without.

The authors note that the findings identify an association but do not establish a causal link between plastic particles and health effects.

Alexander J. Nihart et al, Bioaccumulation of microplastics in decedent human brains, Nature Medicine (2025). DOI: 10.1038/s41591-024-03453-1

Comment by Dr. Krishna Kumari Challa yesterday

How the hippocampus coordinates memory encoding and retrieval

A team of scientists has unveiled how the hippocampus orchestrates multiple memory processes, including encoding new information, forming memories, and retrieving them. The study is published in Nature Communications.

 By applying advanced dimensionality reduction techniques to fMRI data, the researchers demonstrated the hippocampus's critical role in coordinating these processes.

The human brain processes and integrates diverse information simultaneously to form memories. For example, while watching a movie, the brain integrates multiple pieces of information, such as identifying the characters and understanding the evolution of their relationships, to later recall the storyline.

The team hypothesized that the hippocampus coordinates these processes by aligning low-dimensional subspaces of neural activity, which represent different memory functions.

And their results showed that -
Aligned subspaces for the two types of novelty, suggesting that the hippocampus integrates diverse forms of novel information.
Alignment between novelty and memory formation subspaces, with participants showing better memory performance when these alignments were stronger.
Distinct alignment patterns for retrieval, where the subspace for memory retrieval aligned with memory formation but not with novelty, suggesting process-specific coordination by the hippocampus.

This work expands our understanding of memory by uncovering the hippocampus's coordinating role and the neural dynamics supporting it.

 Dasom Kwon et al, Coordinated representations for naturalistic memory encoding and retrieval in hippocampal neural subspaces, Nature Communications (2025). DOI: 10.1038/s41467-025-55833-x

Comment by Dr. Krishna Kumari Challa yesterday

Out of four microRNAs located on the X chromosome, the researchers homed in on miR-871. This microRNA reduces the amount of sarcalumenin or SRL, a protein, produced in the heart. SRL helps the heart cells recharge and reset after each muscle contraction and keeps the heart "in rhythm." MiR-888, the human equivalent of miR-871, similarly regulates SRL levels in the human heart.

Researchers confirmed their findings by manipulating the levels of miR-871. They used genetic techniques to inhibit the production of miR-871 in female mice. This intervention increased SRL levels and improved the heart's ability to recharge between beats. Consequently, the hearts of the female mice began to resemble the beating pattern and functionality of male hearts.
Researchers may use this information to develop therapies that modify human microRNA levels to treat heart diseases. MicroRNA-based therapies are already being explored for other conditions.

James I. Emerson et al, X-Chromosome–Linked miRNAs Regulate Sex Differences in Cardiac Physiology, Circulation Research (2024). DOI: 10.1161/CIRCRESAHA.124.325447

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

Heart health differences in men and women: Tiny RNA molecules play key role, study finds

There are notable differences between men and women in their susceptibility to many human diseases, including cardiovascular disease. For example, women typically have smaller hearts that pump faster, while men have larger hearts that pump more blood with each heartbeat.

Researchers have been making massive efforts to understand what, in the underlying biology, predisposes people to sex-specific cardiovascular disease.

They recently made a large stride in the field, uncovering one of the molecular reasons behind sex disparities in heart disease.

They discovered that a microRNA called miR-871—one of the smallest RNAs found in cells—plays a significant role in the physiological and pathological differences observed between men's and women's hearts. Their findings were published in Circulation Research.

The findings demonstrate that miRNAs on the X chromosome can directly control male-female differences in the heart. The findings also show that male-female differences in biology can be established after a gene is turned on.

MicroRNAs are small, single-stranded nucleic acids that play a crucial role in regulating gene expression, effectively turning genes down to fine-tune protein production in the body. Although these tasks may seem minor, they significantly influence most bodily functions, from the cellular development of organs to the rhythmic beating of our hearts.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Many animals and plants are losing their genetic diversity, making them more vulnerable

Two-thirds of animal and plant populations are declining in genetic diversity, which makes it harder to adapt to environmental changes, according to research published this week.

Long before a species goes extinct, the population becomes smaller and more fragmented, shrinking the number of potential mates and therefore genetic mixing. This leaves a species more vulnerable to future threats such as disease.

A surprising trend was that we saw genetic diversity declining even among many species that aren't considered at risk. 

Researchers examined data for 628 species studied between 1985 and 2019. The greatest losses in genetic variation were seen in birds and mammals.

Findings were published in the journal Nature.

When a species has different genetic solutions, it's better able to deal with changes. 

If a new disease spreads through a population or climate change alters summer rainfall, some individuals will fare better than others, in part because of their genes. Higher genetic diversity also means there's a greater chance of a species' survival.

Conservation efforts to connect isolated populations—basically expanding the dating pool for a particular species—can help maintain or even restore genetic diversity.

Isolated populations suffer. The solution is to reconnect them, stress the biologists.

Catherine Grueber, Global meta-analysis shows action is needed to halt genetic diversity loss, Nature (2025). DOI: 10.1038/s41586-024-08458-x. www.nature.com/articles/s41586-024-08458-x

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