Comment

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 1:26pm

The investigations showed that a certain type of immune cell, so-called plasmacytoid dendritic cells, produce large amounts of the important antiviral messenger interferon-α (IFN-α) upon infection with influenza—regardless of the virus strain. This means that these immune cells generally respond strongly to influenza viruses without the need for the virus to productively infect them.

If this is the case, why do not all viruses cause the same severity of the disease? The research team found that other immune cells, namely myeloid dendritic cells and different types of macrophages, are infected with highly pathogenic influenza viruses and produce large amounts of IFN-α. Viral replication in these immune cells appears to be an important factor in the production of type I interferon and the development of an excessive immune response (cytokine storm).
These results provide an explanation of why some influenza viruses could be so much more dangerous than others: it might be their ability to replicate in certain immune cells and thereby trigger an extremely strong immune reaction that leads to severe inflammation and harm to health. This knowledge can help to develop targeted therapies and better identify risk groups.

Marc A. Niles et al, Influenza A virus induced interferon-alpha production by myeloid dendritic cells and macrophages requires productive infection, Emerging Microbes & Infections (2025). DOI: 10.1080/22221751.2025.2556718

Part 2

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 1:25pm

Why some influenza viruses are more dangerous than others

Serious infections with influenza A viruses are characterized by an excessive immune response, known as cytokine storm. It was previously unclear why some virus strains trigger these storms, while others do not. Researchers investigated 11 different influenza A virus strains and their effect on different human immune cells.

The results, published in Emerging Microbes & Infections, show that highly pathogenic avian influenza viruses infect specific kinds of immune cells and thus stimulate the production of type I interferon. This could explain why these viruses are particularly dangerous.

The new research results show that not only the immune cells that have always been the focus of attention regarding type I interferon production, but also other immune system cells could be decisive in whether an influenza infection triggers an excessive immune system response. This knowledge is important in order to be able to better assess the risk of dangerous virus variants.

Influenza viruses are some of the most significant respiratory disease pathogens worldwide. While most infections are relatively mild, certain virus strains can cause severe pneumonia, leading to acute respiratory failure. Highly pathogenic influenza viruses are particularly dangerous. They often spread from birds to humans and are associated with significantly higher mortality rates.

The immune system plays a crucial role in this danger: some virus strains cause the body to release an excessive amount of messenger substances known as cytokines. If a cytokine storm occurs, the immune response will end up damaging the body's tissue more than the virus itself.

But why do some influenza viruses trigger such excessive reactions, while others only cause infections with mild progression?

The researchers  tested how the flu viruses infect different immune cells and stimulate the release of messenger substances.

The aim of their research is to decipher the mechanisms behind mild and severe disease progression and to develop long-term approaches for better protection and treatment options.

Part 1

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 1:12pm

"Even after accounting for alcohol use by mothers during pregnancy, the father's drinking was still linked to lower child height, smaller head size and reduced verbal IQ. This suggests that paternal alcohol use may have its own, though limited, impact on a child's growth and development.

"Data analyses of children where both parents consumed alcohol during pregnancy had significantly negative effects on growth, head circumference, verbal intelligence and general birth defect scores than in children where neither parent consumed alcohol."

The researchers say that, while it is not yet clear whether the impact of a father's drinking on a child's growth and development stems from impaired sperm quality or other epigenetic influences (changes in how genes work that don't involve altering the DNA code itself), the father's role in the development of FASD cannot be overlooked.

Philip A. May et al, Does paternal alcohol consumption affect the severity of traits of fetal alcohol spectrum disorders?, Alcohol, Clinical and Experimental Research (2025). DOI: 10.1111/acer.70105

Part 2

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 1:11pm

Fathers' drinking plays role in fetal alcohol spectrum disorder, study shows

It's a well-known fact that fetal alcohol spectrum disorder (FASD) in children is caused by mothers who drink during pregnancy. But it turns out that the father's drinking habits could also affect a child's growth and development.

A team of international researchers found that a father's alcohol use may have a small but direct negative impact on a child's development by the age of seven. A father's drinking contributes to the harm caused by alcohol use during pregnancy.

The findings of their study were published recently in the journal Alcohol: Clinical & Experimental Research.

The researchers analyzed data from five studies on the prevalence and characteristics of FASD among Grade 1 learners in the Western Cape to explore whether a father's drinking affects children diagnosed with FASD. The children's biological mothers or legal guardians completed a questionnaire on the risk factors for FASD.

According to the researchers, there is a growing recognition that factors beyond pregnant women's drinking habits can affect their children's development. They add that increased attention is currently paid to the role of fathers, not only as a contributing factor to women's drinking habits, but also as an independent contributing factor to the growth and development of children.

The findings show that children whose fathers drank alcohol were more likely to be shorter, have smaller heads, and score lower on verbal IQ tests. It was also clear from the study that the highest risk to the child's development exists when both parents use alcohol during pregnancy. It also appeared that 'binge drinking' by the father, but especially by both parents, has the most detrimental effect on the child's development. 

Data analysis showed that between 66% and 77% of fathers of children on the FAS spectrum drank during their partner's pregnancy with the child in question. These fathers drank an average of 12 drinks per drinking day. The number of drinks that fathers drank per drinking day was significantly correlated with smaller head circumference in their children. Head circumference is used as a measure of brain development."

The researchers add that fathers who drank an average of five or more drinks per drinking day had shorter children with smaller head circumferences. These children also performed worse on measures in verbal intelligence tests.

"In general, it was found that the more fathers drank, the worse their children performed. However, it should also be noted that all these effects were observed in children whose mothers consumed alcohol during pregnancy."

They note that a father's drinking alone didn't increase the chances of a child being diagnosed with FASD. However, when the mother drank during pregnancy and the father was also a heavy drinker, the child was more likely to have the most serious symptoms of FASD.
"When looking at both parents' drinking patterns, the father's alcohol use alone didn't show a clear link to the child's physical or brain development problems. While both parents' drinking was considered, the main effects on a child's development and physical features were linked to the mother's alcohol use.
Part 1

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 11:45am

The role of telomeres in processes such as cancer development and aging, and what happens when they do not work properly, has long interested scientists. Diseases caused by disturbances in telomere maintenance are rare, but very serious, and include premature aging, blood cell deficiency called aplastic anemia and fibrosis in the lungs.

In about half of cases, the disease is explained by a known mutation that affects telomere stability, but in many cases, there is currently no known medical explanation for why the individual is sick.
Their research is also relevant to cancer research. On one hand, inappropriate "repair" of telomeres can trigger catastrophic events leading to the accumulation of mutations and cancer.

On the other hand, cancer cells are often less efficient at repairing damage to DNA compared to normal cells. This weakness is exploited in cancer treatments and many therapies kill tumor cells by causing DNA damage or inhibiting repair, or both.

In other words, knowledge of how cells regulate DNA repair and protect telomeres has a bearing on both prevention and treatment of cancer.

Increased understanding of which proteins play key roles in these cellular processes can, in the long term, contribute to more precise and targeted treatment strategies.

Patrik Eickhoff et al, Chromosome end protection by RAP1-mediated inhibition of DNA-PK, Nature (2025). DOI: 10.1038/s41586-025-08896-1

Part 2

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 11:44am

Discovery reveals how chromosome ends can be protected

Researchers have uncovered a previously unknown mechanism that safeguards the chromosome ends from being mistakenly repaired by the cell. While DNA repair is vital for survival, attempts to repair the chromosome ends—called telomeres—can have catastrophic outcomes for cells.

The research, published in Nature, increases the understanding of how cancer and certain rare diseases develop.

Cells constantly monitor their DNA. A DNA helix that ends abruptly is a signal that DNA has been severely damaged—at least in most cases. The most severe DNA damage a cell can suffer is when a DNA helix breaks up in two pieces. 

Normally, the cells would try to promptly repair all damage to DNA. The dilemma is that our chromosomes have ends that look just like broken DNA. If cells were to "repair" them, looking for another loose end to join them with, this would lead to the fusion between two or more chromosomes, making the cell susceptible to transform into a cancer cell.

Therefore, the chromosome ends—called telomeres—must be protected from the cell's DNA repair machinery.

The cells have to constantly repair DNA damage to avoid mutations, cell death, and cancer, while at the same time, they must not repair the chromosome ends by mistake, since that would result in the same catastrophic outcome. What's the difference between damaged DNA and the natural chromosome end? This problem has been known for almost a century, but some aspects are still not completely resolved.

Although the telomeres are not to be repaired as if they were broken DNA, several DNA repair proteins can be found at the chromosome ends. 

The research team has previously shown that a key repair protein, DNA Protein Kinase (called DNA-PK) helps in processing telomeres and in protecting them from degradation. But how DNA-PK at the same time is prevented from trying to repair these blunt DNA ends remained a mystery until now.

The researchers have now shown that two other proteins, called RAP1 and TRF2, have an important role to play in regulating DNA-PK.

They show genetically, biochemically and structurally how the protein RAP1, brought to telomeres by TRF2, ensure by  direct interaction that DNA-PK doesn't 'repair' the telomeres.

Part1

Comment by Dr. Krishna Kumari Challa on September 10, 2025 at 11:35am

Microbiome instability linked to poor growth in kids

Malnutrition is a leading cause of death in children under age 5, and nearly 150 million children globally under this age have stunted growth from lack of nutrition. Although an inadequate diet is a major contributor, researchers  found over a decade ago that dysfunctional communities of gut microbes play an important role in triggering malnutrition.

They  have discovered that toddlers in Malawi—among the places hardest hit by malnutrition—who had a fluctuating gut microbiome showed poorer growth than kids with a more stable microbiome. All of the children were at high risk for stunting and acute malnutrition.

The findings, published in Cell, establish a pediatric microbial genome library—a public health database containing complete genetic profiles of 986 microbes from fecal samples of eight Malawian children collected over nearly a year that can be used for future studies to help predict, prevent and treat malnutrition.

Culture-independent meta-pangenomics enabled by long-read metagenomics reveals associations with pediatric undernutrition, Cell (2025). DOI: 10.1016/j.cell.2025.08.020. www.cell.com/cell/fulltext/S0092-8674(25)00975-4

Comment by Dr. Krishna Kumari Challa on September 9, 2025 at 6:18am

Smart patch runs tests using sweat instead of blood

It is possible now to precisely assess the body's health status using only sweat instead of blood tests. 

A research team has now developed a smart patch that can precisely observe internal changes through sweat when simply attached to the body. This is expected to greatly contribute to the advancement of chronic disease management and personalized health care technologies. 

The researchers developed a wearable sensor that can simultaneously and in real-time analyze multiple metabolites in sweat. 

The research team developed a thin and flexible wearable sweat patch that can be directly attached to the skin. This patch incorporates both microchannels for collecting sweat and an ultrafine nanoplasmonic structure that analyzes sweat components using light. Thanks to this, multiple sweat metabolites can be simultaneously analyzed without the need for separate staining or labels, with just one patch application.

A nanoplasmonic structure is an optical sensor structure where nanoscale metallic patterns interact with light, designed to sensitively detect the presence or changes in concentration of molecules in sweat.

The patch was created by combining nanophotonics technology, which manipulates light at the nanometer scale (one-hundred-thousandth the thickness of a human hair) to read molecular properties, with microfluidics technology, which precisely controls sweat in channels thinner than a hair.

In other words, within a single sweat patch, microfluidic technology enables sweat to be collected sequentially over time, allowing for the measurement of changes in various metabolites without any labeling process. Inside the patch are six to 17 chambers (storage spaces), and sweat secreted during exercise flows along the microfluidic structures and fills each chamber in order.

The research team applied the patch to actual human subjects and succeeded in continuously tracking the changing components of sweat over time during exercise.

In this study, they demonstrated for the first time that three metabolites—uric acid, lactic acid, and tyrosine—can be quantitatively analyzed simultaneously, as well as how they change depending on exercise and diet.

In particular, by using artificial intelligence analysis methods, they were able to accurately distinguish signals of desired substances even within the complex components of sweat.

In the future,  this technology can be expanded to diverse fields such as chronic disease management, drug response tracking, environmental exposure monitoring, and the discovery of next-generation biomarkers for metabolic diseases.

Jaehun Jeon et al, All-flexible chronoepifluidic nanoplasmonic patch for label-free metabolite profiling in sweat, Nature Communications (2025). DOI: 10.1038/s41467-025-63510-2

Comment by Dr. Krishna Kumari Challa on September 9, 2025 at 6:08am

There is less room to store carbon dioxide, driver of climate change, than previously thought, finds a new study

The world has far fewer places to securely store carbon dioxide deep underground than previously thought, steeply lowering its potential to help stem global warming, according to a new study that challenges long-held industry claims about the practice.

The study, published last week in the journal Nature, found that global carbon storage capacity was 10 times less than previous estimates after ruling out geological formations where the gas could leak, trigger earthquakes or contaminate groundwater, or had other limitations. That means carbon capture and storage would only have the potential to reduce human-caused warming by 0.7 degrees Celsius (1.26 Fahrenheit)—far less than previous estimates of around 5-6 degrees Celsius (9-10.8 degrees Fahrenheit), researchers said.

Carbon storage is often portrayed as a way out of the climate crisis. These new findings make clear that it is a limited tool and reaffirms the extreme importance of reducing emissions as fast and as soon as possible.

 Matthew J. Gidden et al, A prudent planetary limit for geologic carbon storage, Nature (2025). DOI: 10.1038/s41586-025-09423-y

Comment by Dr. Krishna Kumari Challa on September 9, 2025 at 6:03am

Scientists discover why the flu is more deadly for older people

Scientists have discovered why older people are more likely to suffer severely from the flu, and can now use their findings to address this risk.

In a study published in PNAS, experts discovered that older people produce a glycosylated protein called apolipoprotein D (ApoD), which is involved in lipid metabolism and inflammation, at much higher levels than in younger people. This has the effect of reducing the patient's ability to resist virus infection, resulting in a more serious disease outcome.

ApoD is therefore a target for therapeutic intervention to protect against severe influenza virus infection in the elderly which would have a major impact on reducing morbidity and mortality in the aging population.

ApoD mediates age-associated increase in vulnerability to influenza virus infection, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2423973122

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