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Comment by Dr. Krishna Kumari Challa yesterday

Study of nearly 60,000 women finds no association between COVID vaccine and decrease in childbirth

COVID-19 vaccination is not the cause behind a decrease in childbirth, according to a new study. The results, published in the journal Communications Medicine, speak to rumors about vaccination and reduced fertility. "Our conclusion is that it's highly unlikely that the mRNA vaccine against COVID-19 was behind the decrease in childbirth during the pandemic", say the researchers who conducted this study.

The researchers investigated the issue because, since the beginning of the COVID-19 pandemic, unfounded rumors have circulated, especially on social media, alleging that vaccination impairs chances of becoming pregnant. In the later stages of the pandemic, there was a decrease in the number of children born in some countries, including Sweden. This raised the question whether this could be due to the new vaccines.

In the study, the researchers analyzed all women aged 18 to 45 years in Region Jönköping County, a total of almost 60,000 women (of the region's total population of 369,000 people). Of these women, 75% were vaccinated once or more against COVID-19 from 2021 to 2024. The researchers used data on childbirths, vaccination, miscarriages and deaths from health care records.

When the researchers compared childbirths and miscarriages between vaccinated and unvaccinated women, they found no statistically significant difference between the groups. This is in line with several previous studies that have not found any association between the COVID vaccine and fertility.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Seeds 'listen' to mom: Study finds mother plants send ABA hormone signals that set seed dormancy
Maternal plants regulate seed dormancy by transferring abscisic acid (ABA) to developing seeds, with ABA levels increasing in maternal tissues under cooler temperatures. This hormonal signaling enables seeds to receive environmental information from the mother, promoting dormancy when conditions are unfavorable. The findings highlight a rapid, non-genetic mechanism for environmental adaptation in plants.

Xiaochao Chen et al, Adaptation of seed dormancy to maternal climate occurs via intergenerational transport of abscisic acid, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2519319122

Comment by Dr. Krishna Kumari Challa yesterday

News sites are locking out the internet archive to stop AI crawling. Is the 'open web' closing?
Major news publishers are blocking the Internet Archive to prevent AI companies from accessing their content for training, citing concerns over copyright and paywall circumvention. This shift reflects a broader trend toward monetizing digital archives and restricting public access, raising concerns about the preservation of internet history and the diminishing openness of the web.

News sites are locking out the Internet Archive to stop AI crawling...

Comment by Dr. Krishna Kumari Challa yesterday

Using comparative genomic data across primates, the researchers found examples of genes associated with burn injury responses which show signs of accelerated evolution in humans. These genes are involved in wound closure, inflammation and immune system response—likely helping to rapidly close wounds and fight infection; a major complication after burn injury, particularly before the widespread use of antibiotics.

These findings support the theory that exposure to burn injuries may have been a notable force on the evolution of humans.

Unlike other wounds from cuts or bites which would have also led to infections, the increased lifetime risk of burns experienced by humans and their hominin ancestors is unique as they are the only species to regularly experience burn injuries and survive them.

Burn Selection: How Fire Injury Shaped Human Evolution, BioEssays (2026).

Part2

Comment by Dr. Krishna Kumari Challa yesterday

Exposure to burn injuries played key role in shaping human evolution, study suggests

Humans' exposure to high temperature burn injuries may have played an important role in our evolutionary development, shaping how our bodies heal, fight infection, and sometimes fail under extreme injury, according to new research.

For more than one million years, the control of fire has powered human success, from cooking and heating to technology and industry, driving genetic and cultural evolution and setting us apart from all other species. But this relationship has also exposed humans to high temperature injuries at a scale unmatched in the natural world.

Humans burn themselves—and survive burns—with a frequency likely much greater than any other animal. Most animals avoid fire completely, while in contrast, humans live alongside fire and most humans will experience minor burns throughout their lives.

A new study published in BioEssays,  suggests that this increased exposure to burn injuries may have driven notable genetic adaptations which differentiated humans from other primates and mammals. This may also explain both beneficial and maladaptive responses to severe burn injury.

Burn injuries exist on a spectrum of severity, with most small injuries healing on their own, while severe burns can lead to lifelong disability or death. Burns damage the skin, the body's main protective barrier against infection, sometimes over large areas of the body. The longer the skin is damaged, the greater the risk that bacteria can enter the body and cause overwhelming infection.

The researchers argue that natural selection would have favored traits that helped humans survive small to moderate burns. These may include faster inflammation, faster wound closure (to prevent infection) and stronger pain signals.

However, while these traits are helpful for less severe injuries, they can become harmful for large burns, which may explain why modern humans can experience extreme inflammation, scarring, and organ failure from major burns.

Part 1

Comment by Dr. Krishna Kumari Challa on Thursday

Could fecal transplants be the new way to fight cancer?
Fecal microbiota transplants (FMT) are being explored as a method to modify gut microbes in cancer patients, potentially enhancing the effectiveness of immunotherapy, especially for those with less diverse gut microbiomes. Early clinical data indicate FMT may improve treatment response rates and outcomes, but safety concerns require that FMT be administered under medical supervision.

Could fecal transplants be the new way to fight cancer?

Comment by Dr. Krishna Kumari Challa on Thursday

High-dose antioxidants linked to offspring birth defects

Antioxidants have been marketed as miracle supplements, touted for preventing chronic diseases and cancers; treating COPD and dementia; and slowing aging.

While antioxidant therapies are widely used to treat male infertility, a new study  found that regularly consuming high doses of antioxidants negatively influences sperm DNA and may lead to offspring born with differences in craniofacial development.
Regular consumption of high doses of antioxidants such as N-acetyl-L-cysteine and selenium in male mice alters sperm DNA and is associated with craniofacial abnormalities in offspring, particularly in females. These effects occur without observable health changes in the fathers, indicating potential reproductive risks of excessive antioxidant supplementation prior to conception.

They found that offspring of male mice exposed to antioxidants for six weeks exhibited skull and facial shape differences, even while the father's health didn't change.

These findings suggest that men should exercise caution when consuming high doses of antioxidants, especially if they're planning to have children in the near future.

Destani D. Derrico et al, Therapy to teratology: chronic paternal antioxidant supplementation alters offspring placental architecture and craniofacial morphogenesis in a mouse model, Frontiers in Cell and Developmental Biology (2025). DOI: 10.3389/fcell.2025.1697843

Comment by Dr. Krishna Kumari Challa on Thursday

A minimalist bacterial defense strategy: Scientists discover single protein that disrupts viral assembly
A single bacterial protein, Rip1, can detect bacteriophage infection and disrupt viral assembly by binding to phage proteins and forming membrane pores. This dual-function mechanism causes premature bacterial cell death, halting phage propagation. Rip1 integrates both sensing and defense roles, representing a streamlined bacterial immune strategy.

Karen Maxwell, A pore-forming antiphage defence is activated by oligomeric phage proteins, Nature (2026). DOI: 10.1038/s41586-025-10075-1. www.nature.com/articles/s41586-025-10075-1

Comment by Dr. Krishna Kumari Challa on Thursday

Why snakes can go months between meals: A genetic explanation

Snakes may well be one of nature's greatest predators, capable of eating whole deer or even crocodiles, but just as impressive is that they can go months, or even a whole year, without a single meal. And now an international team of scientists thinks they know how they do it.

In a study published in the journal Open Biology, researchers report that snakes have lost the ghrelin gene, often called the hunger hormone gene, because it regulates appetite and signals when it is time to eat. Therefore, without a hormone signaling they are hungry, they can manage long periods between meals.

The team made their discovery after analyzing the genomes of 112 reptile species, including snakes, turtles, and crocodiles, using sequence comparison and gene-loss detection tools, among other methods.

In all the snakes they studied, which included pythons, boas, and vipers, genes for ghrelin and an enzyme called MBOAT4 (which activates ghrelin) were independently lost or heavily eroded. The same was true for chameleons and some toadhead agamas, a type of lizard.

Because the loss of these genes occurred in several different groups of reptiles, the study authors think it wasn't a mistake. It may have been an adaptation to their extreme feeding habits. For example, both snakes and chameleons adopt a sit-and-wait predation strategy, also known as ambush predation. Instead of actively hunting for prey, they remain concealed and wait to strike. This wait may go on for weeks or months. In these animals, a hormone that continually signals hunger would be counterproductive.
The researchers also suggest that losing the ghrelin system serves another vital purpose. Namely, helping these reptiles keep their energy use as low as possible while they wait for prey. In mammals, ghrelin normally tells the body to burn fat for fuel during a fast. However, snakes have evolved a different strategy. Instead of burning through their reserves, they enter into a state of extreme energy conservation.

"This study suggests that the intermittent feeding of these groups was accompanied by the loss of genes involved in energy homeostasis," commented the authors in their study.

Rui Resende Pinto et al, Ghrelin and MBOAT4 are lost in Serpentes, Open Biology (2026). DOI: 10.1098/rsob.250162

Comment by Dr. Krishna Kumari Challa on Thursday

One-third of dementia cases are linked to non brain-related diseases, study finds

Dementia is a term used to describe memory loss, impaired reasoning, difficulties communicating and other mental impairments that can be caused by Alzheimer's disease, other neurodegenerative disease, strokes, severe infections, head injuries or various other conditions. While most past studies investigating the causes and underpinnings of dementia focused on the brain, a growing body of research suggests that these mental impairments could sometimes be linked to diseases that affect other parts of the body, referred to as peripheral diseases.

Researchers recently carried out a systematic review and various meta-analyses of data collected over the past decades, to explore the link between dementia and 26 different peripheral diseases, including gum diseases, liver diseases, hearing loss, type 2 diabetes and various other conditions. Their results, published in Nature Human Behavior, suggest that in approximately one-third of cases, the risk of developing dementia is linked to other diseases that do not directly affect the brain.

Growing evidence suggests that peripheral diseases serve as risk factors for dementia.

As part of their study, the researchers analyzed data from PubMed, a publicly available medical database, which was collected as part of over 200 earlier research studies. Their analyses focused on 26 peripheral diseases and they found that 16 of these were associated with an increased risk of developing dementia.

The 16 diseases they identified were: periodontal diseases, cirrhosis and other chronic liver diseases, hearing loss, vision loss, type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), osteoarthritis, stroke, ischemic heart diseases, chronic obstructive pulmonary disease (COPD), asthma, atrial fibrillation and flutter, atopic dermatitis, rheumatoid arthritis, multiple sclerosis (MS), and inflammatory bowel disease.

Globally, these peripheral diseases collectively were related to a combined PAF of 33.18% (95% confidence interval (CI) 16.80–48.43) of dementia burden, corresponding to 18.8 million prevalent cases.

 Notably, the five diseases that were found to be most strongly correlated with an increased risk of developing dementia included gum disease, chronic liver diseases, hearing loss, vision loss and T2DM.

As dementia is not always caused by brain injuries or diseases, which means that it might in some cases be prevented by treating other diseases early.

Zhenhong Deng et al, Population attributable fractions of a wide range of peripheral diseases for the burden of dementia, Nature Human Behaviour (2026). DOI: 10.1038/s41562-025-02392-2.

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