Comment

Comment by Dr. Krishna Kumari Challa 18 minutes ago

Climate change is outpacing evolution

Evolution works over millennia. Climate change is moving far faster. That mismatch is killing some of the planet's most vital ecosystems that  store vast amounts of carbon and support complex webs of life.

Marine heat waves, record wildfires and coastal development are pushing these systems beyond their limits as climate change, driven by emissions of fuels like oil and gas, accelerates. An estimated 1 million species face extinction, many within decades, largely due to human activities such as habitat destruction, pollution and overuse of natural resources, according to a 2019 report by a United Nations-affiliated intergovernmental scientific body.

Scientists are working to close the gap with an emerging discipline called conservation genomics: sequencing an organism's complete genetic blueprint to pinpoint individuals with traits suited to survive drought, disease and other climate extremes, then using that information to guide restoration.

Coral reefs are among the first ecosystems where these genomic tools are being put to use. Repeated marine heat waves, which have caused mass bleaching, have devastated reefs worldwide. By sequencing corals and the algae that live inside them, researchers have identified colonies that naturally withstand higher temperatures and are beginning to test whether selectively breeding and growing those more resilient corals can support reef recovery.

However, conservation genomics alone cannot solve climate change
It can be helpful, but it's not a solution unto itself.

 What should be prioritized is reducing greenhouse gas emissions.

Genomic tools may help certain species, particularly long-lived ones like redwoods that cannot adapt quickly enough on their own, but they come with limits. Ecosystems are built on complex relationships among plants, animals, microbes and fungi. Engineering or selecting for climate resilient traits in one species does not guarantee the survival of the many others that depend on it.

 You can genetically engineer a few species that would be more tolerant. But that's not an ecosystem. "We're not going to engineer our way out of climate change," warn scientists

Source: News agencies

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Comment by Dr. Krishna Kumari Challa 53 minutes ago

Five warning signs that rivers are polluted—even when they look clean
Key indicators of river pollution, even when water appears clean, include the presence of sewage fungus, algal blooms, unusual water coloration or murkiness, persistent white foam with chemical odors, and signs of aquatic life distress or absence. Many pollutants are invisible, and these signs may overlap with natural phenomena, so additional context and caution are necessary for accurate assessment.

original article.

Comment by Dr. Krishna Kumari Challa 1 hour ago

Synthetic glucocorticoids are routinely given to pregnant women at risk of preterm birth, often without considering the time of day when these hormones naturally fluctuate. The authors found that giving these steroids daily to the mother accelerated the synchronization to local time of the daily rhythms in the pups. These findings may be important when considering how and when doctors administer medications to treat pregnancy conditions.

During the study, the researchers also observed a strong association between failure to develop circadian clock gene activity in the fetuses and failure to deliver. It is not clear yet whether the absence of rhythms contributes to developmental problems or simply reflects them. But the observation suggests that circadian clock activity may be closely linked to healthy fetal development.
The findings also highlight the importance of maintaining stable circadian rhythms during pregnancy. Over 80% of the world's population is exposed to artificial light at night that can disrupt daily rhythms, and this includes pregnant people.
Understanding when and how the body clock starts ticking helps scientists identify sensitive developmental windows when circadian disruption may have lasting effects. This knowledge could help guide medical treatments, inform clinical practices and shape public health policies aimed at protecting neonatal circadian health during pregnancy.

K. L. Nikhil et al, Fetoplacental Circadian Rhythms Develop and Then Synchronize to the Mother In Utero, Journal of Biological Rhythms (2026). DOI: 10.1177/07487304261435435

Part 2

Comment by Dr. Krishna Kumari Challa 1 hour ago

Baby's body clock begins to synchronize with local time while still in utero, study shows

Humans and most other organisms have internal biological clocks that track the daily cycle of sunrise and sunset. These clocks help time our sleep, metabolism and other essential body functions over the course of a day, creating daily patterns called circadian rhythms. Research shows that when these rhythms are disrupted—by jet lag, lack of sleep or irregular work schedules—people can suffer long-term negative health effects.

Scientists who study daily rhythms have long wondered about when the mammalian circadian clock starts ticking and synchronizes to local time. In a new study published in the Journal of Biological Rhythms, researchers reported that a mother helps to set the biological clock for her babies while they are still in the womb.

Disrupting circadian rhythms during pregnancy can affect how sleep and daily rhythms develop in infants, and these early disruptions are linked to a higher risk of mood disorders such as anxiety and depression later in life.

Understanding when the fetal clock begins to function helps us identify sensitive developmental windows when circadian disruption may have lasting effects and how those effects might be prevented or corrected.

In mouse models researchers  found clear day-night rhythms in the pups that synchronized to the mother's rest-activity cycle during the last week of pregnancy, equivalent to the third trimester in humans. This suggests that the clock machinery forms early in development and receives entraining cues from mom later.

Importantly, they found daily rhythms across the placenta from the mother to the baby before the fetus can sense light.

The researchers found that circadian synchronization of the pups to the mother coincided with when glucocorticoid hormones from the mother cross the placenta, potentially acting as timing signals for the fetal clock. These stress-related hormones normally rise and fall over the course of the day under the control of the mother's internal clock.

Part 1

Comment by Dr. Krishna Kumari Challa 1 hour ago

Orbital Mechanics

Comment by Dr. Krishna Kumari Challa 3 hours ago

Moon Joy, Courtesy of NASA's Artemis II Astronauts

Comment by Dr. Krishna Kumari Challa 4 hours ago

Artemis Re-Entry | NASA Most Dangerous 20 Minutes

Comment by Dr. Krishna Kumari Challa yesterday

People use the same neurons to see and imagine objects, study shows

Why can images of things we have seen seem so real when we later recall them from memory? A new study led by Cedars-Sinai Health Sciences University investigators sheds light on the answer. The research shows that the same brain neurons are activated when we imagine something and when we perceive something. The research, led by Cedars-Sinai, is the first to provide a detailed understanding of the shared mechanism that underlies visual perception and creation of mental images in the human brain. It was published in the journal Science.
Visual perception and imagination activate overlapping populations of neurons in the human fusiform gyrus, with about 40% of visually responsive neurons reactivating during mental imagery using the same neural code as during perception. This shared neural mechanism underlies the vividness of visual imagination and may inform understanding of psychiatric disorders involving altered mental imagery.
We generate a mental image of an object that we have seen before by reactivating the brain cells we used to see it in the first place.
The new study revealed the code that we use to re-create the images.
The findings provide a biological basis for visual imagination, a process that is also critical for creative arts.

"Further insight into this neural process has the potential to open pathways toward developing new therapies for post-traumatic stress disorder, obsessive-compulsive disorder, and other mental conditions that involve uncontrolled vivid imagery.
To conduct the study, investigators asked 16 adults with epilepsy, who had electrodes temporarily implanted in their brains for diagnosing their seizures, to view a series of images of faces and objects.

After viewing them, a subset of the participants were asked to imagine those same images from memory. Meanwhile, researchers recorded the electrical activity of hundreds of individual neurons in each participant's brain.

When the patients viewed the images, neurons were activated in their fusiform gyrus, an area of the brain essential for high-level visual processing, particularly for faces. For 80% of the visually responsive neurons recorded in the study, the researchers uncovered the aspects of the images they reacted to, thereby revealing their neural code.
When the patients later imagined the images, about 40% of these neurons reactivated using the same code, thereby recreating the pattern of activity that occurred during the initial viewing of the images.

V. S. Wadia et al, A shared code for perceiving and imagining objects in human ventral temporal cortex, Science (2026). DOI: 10.1126/science.adt8343. www.science.org/doi/10.1126/science.adt8343

Comment by Dr. Krishna Kumari Challa yesterday

Non-coding genes cause diabetes in babies, study reveals

Bi-allelic variants in the non-coding RNA genes RNU4ATAC and RNU6ATAC were identified as causes of syndromic monogenic autoimmune neonatal diabetes in 19 children. These mutations disrupt splicing and affect the expression of approximately 800 genes, many involved in immune function, highlighting the pathogenic potential of non-coding genomic regions in rare autoimmune diabetes.

Matthew B. Johnson et al, Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes, The American Journal of Human Genetics (2026). DOI: 10.1016/j.ajhg.2026.02.017

Comment by Dr. Krishna Kumari Challa yesterday

Non-coding genes cause diabetes in babies, study reveals

Bi-allelic variants in the non-coding RNA genes RNU4ATAC and RNU6ATAC were identified as causes of syndromic monogenic autoimmune neonatal diabetes in 19 children. These mutations disrupt splicing and affect the expression of approximately 800 genes, many involved in immune function, highlighting the pathogenic potential of non-coding genomic regions in rare autoimmune diabetes.

Matthew B. Johnson et al, Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes, The American Journal of Human Genetics (2026). DOI: 10.1016/j.ajhg.2026.02.017

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