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Comment by Dr. Krishna Kumari Challa 16 hours ago

How Plantago asiatica plants communicate with each other to respond to salt stress

Plants exchange adaptive information, helping them to adjust to environmental challenges. Salt stress in plants, caused by soil salinity, often results in water loss. Plants often cope with this situation by closing the stomatal aperture.

In a study appearing in Plant Signaling & Behavior, the scientists wanted to understand how Plantago asiatica plants utilize both above- and below-ground communication to differentially respond to salt stress cues perceived from neighbors with variable genetic identities.
Interplant cueing or communication is a fascinating method through which neighboring plants exchange adaptive information. Plants can send and receive information through both aboveground and belowground pathways: via the shoot system (involving stems and leaves) and the root system, respectively.
Communication usually relies on volatile organic compounds aboveground and fungal networks in the soil of the root system. This exchange of information helps plants to respond quickly to certain stress situations and enhance their resistance by activating adaptive mechanisms.
Plants exchange information regarding altered nutrient availability, impending competition, neighbor proximity, drought stress, and salt stress. Plant stomata refer to microscopic pores on leaf surfaces that control gas exchange and transpiration. Closure of stomata due to salt stress was previously recorded as a stress response in many plants.
Some studies also reported that unstressed plants show this adaptive mechanism, which is a result of communication with stressed plants.

Plantago asiatica plants communicate salt stress signals through both aboveground and belowground pathways, the new study shows. Aboveground cues induce stomatal closure in neighboring plants regardless of genetic relatedness, while belowground signaling is more effective among genetically similar individuals, suggesting root-mediated communication depends on genetic background.

Kai Ito et al, Integrated above- and below-ground interplant cueing of salt stress, Plant Signaling & Behavior (2025). DOI: 10.1080/15592324.2025.2542560

Comment by Dr. Krishna Kumari Challa 16 hours ago

How harmful bacteria know where to cluster and cause infection

The bacterium known as Pseudomonas aeruginosa is an unwelcome visitor in the human body. Serious infections can result when a bunch of these bugs settle together on a surface to form a biofilm—a community of microbes like the slime on spoiled food, but in this case residing inside a person.

The grouped-up bacteria attack the lungs of patients with cystic fibrosis and conditions that require the use of ventilators, such as severe COVID-19. Worse still, the World Health Organization lists Pseudomonas among the antibiotic-resistant bacteria presenting the biggest threat to human health.

Now, however, new findings by researchers reveal just how Pseudomonas goes from exploring a surface to committing to it and building a community—a key finding that can help pave the way to understanding how to tackle these types of infections.

The new study revealed how Pseudomonas detects and binds to specific sugars left behind by others from its species that arrived earlier. The cell senses these sugar trails using proteins on its body, and then identifies the sugars using hairlike appendages called pili. These pili are normally used to crawl along a surface, but in this case double as mechanical sensors that test the strength of the sugar bonds.

All of this information is translated into chemical signals inside the cell that guide the operation of other bacterial machinery, such as the controlled secretion of more sugars to make biofilms.

Reported in the journal Nature Microbiology, the results may inform applications in human health and industry. For Pseudomonas, the findings could lead to better approaches for undermining the dangerous bugs' ability to resist drug treatments.

William C. Schmidt et al, Pseudomonas aeruginosa senses exopolysaccharide trails using type IV pili and adhesins during biofilm formation, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02087-4

Comment by Dr. Krishna Kumari Challa 16 hours ago

Sinking Indian megacities pose 'alarming' building damage risks

Sinking land is quietly destabilizing urban infrastructure in India's largest cities, putting thousands of buildings and millions of people at risk, according to Virginia Tech scientists.

Groundwater overuse is a critical driver of the problem, say the researchers in their paper published in Nature Sustainability.

When cities pump more water from aquifers than nature can replenish, the ground quite literally sinks. This study shows that this overexploitation of groundwater is directly linked to structural weakening in urban areas.

Using satellite radar data from 2015–23, the research team assessed differential ground sinking, or subsidence, in New Delhi, Mumbai, Chennai, Kolkata, and Bengaluru, covering more than 13 million buildings and home to nearly 80 million people.
Results revealed that 878 square kilometers of urban land, or about 339 square miles, is sinking, with nearly 1.9 million people exposed to subsidence rates greater than 4 millimeters per year.
The study estimates that 2,406 buildings in New Delhi, Mumbai, and Chennai are already at high risk of structural damage. If current subsidence trends continue, over 23,000 buildings could face a very high risk within the next 50 years.

Land subsidence compounds the threats from flooding and earthquakes. When the ground beneath a city sinks unevenly, it weakens foundations, damages utility lines, and amplifies structural vulnerability.

The silent strain we see today could lead to tomorrow's disasters if cities do not adapt their infrastructure and groundwater management policies, say the researchers.

The study demonstrates the value of cutting-edge satellite techniques in preventing tragedy.

The findings extend beyond India, warning that subsidence-driven building damage is an emerging global urban challenge. As more cities depend on stressed aquifers and expand rapidly, subsidence will continue to erode infrastructure resilience worldwide.

 Building damage risk in sinking Indian megacities, Nature Sustainability (2025). DOI: 10.1038/s41893-025-01663-0.

Comment by Dr. Krishna Kumari Challa 17 hours ago

Caught on camera: Rats snatching bats from the sky 

For the first time, brown rats have been filmed actively hunting bats, snatching some from the air and capturing others on the ground. The rodents were caught on camera at bat hibernation sites in northern Germany. According to a paper published in the journal Global Ecology and Conservation, researchers think this predation could be significant enough to threaten local bat populations.

This study is the first to systematically document brown rats hunting in urban Europe. Scientists set up infrared and thermal imaging cameras to monitor bats at two hibernation sites in the towns of Segeberg and Lüneburg-Kalkberg. Observations were made during peak bat activity over several months between 2020 and 2024.

The cameras revealed two distinct hunting strategies. Some rats stood upright, using their tails for balance as they grabbed the bats while they were flying. Others attacked them when they were resting on the ground. At the Segeberg site, the team recorded 13 confirmed kills over five weeks and found a cache of 52 bat carcasses. Similar remains and evidence of bat predation were also discovered at the Lüneburg-Kalkberg site.

The number of kills may not sound large, but the researchers calculated that even a small rat colony could kill up to 7% of the roughly 30,000 bats at the Segeberg site in a single winter. The attacks also occurred at a time when the bats were most vulnerable—during swarming and hibernation—meaning even limited predation could threaten the long-term survival of the population.

The study highlights the importance of bat conservation strategies. The flying mammals help control insect populations and support healthy ecosystems by pollinating plants and dispersing seeds. But protecting bats is not only good for the environment; it also benefits human health, as the researchers point out.

Florian Gloza-Rausch et al, Active predation by brown rats (Rattus norvegicus) on bats at urban mass hibernacula in Northern Germany: Conservation and one health implications, Global Ecology and Conservation (2025). DOI: 10.1016/j.gecco.2025.e03894

Comment by Dr. Krishna Kumari Challa 17 hours ago

Dermal white fat beneath the skin shifted into lipolysis. Lipid droplets in adipocytes shrank, staining showed less stored fat, phosphorylated PLIN1 increased, triglycerides fell, and free fatty acids rose. Blocking the rate-limiting lipase ATGL with a drug or by genetic deletion prevented lipolysis and halted hair regeneration. A deeper thermal injury model showed the same dependence on adipocyte lipolysis.

Measurements of norepinephrine and chemical sympathectomy indicated no required role for sympathetic nerves.

Inflammatory signals in the skin rose after irritation. Single knockouts of tumor necrosis factor-alpha (TNFα) and Interleukin-1 (IL-1), cytokines required for activating the innate immune response, did not stop lipolysis or hair regrowth. Broad anti-inflammatory steroid treatment to dampen cytokine induction blocked adipocyte lipolysis, and prevented hair renewal.

Macrophages emerged as key drivers. Transcriptomic analyses pointed to macrophage signatures, with spatial data showing infiltration into dermal fat.

Depleting macrophages with clodronate liposomes reduced serum amyloid A3 (SAA3) induction, suppressed lipolysis, and stopped hair regrowth, while neutrophil depletion and loss of adaptive immunity did not block regrowth.

Authors conclude that a macrophage-to-adipocyte-to-stem cell axis converts injury signals into localized metabolic communication that activates epithelial hair follicle stem cells. Topical monounsaturated fatty acids promoted hair growth in mice, suggesting therapeutic potential for hair loss.

Validation with human skin was not tested and the suggested mechanistic linchpin found is SAA3-dependent lipolysis in mice, whereas human skin mainly uses SAA1/2.

Kang-Yu Tai et al, Adipocyte lipolysis activates epithelial stem cells for hair regeneration through fatty acid metabolic signaling, Cell Metabolism (2025). DOI: 10.1016/j.cmet.2025.09.012

Part 2

Comment by Dr. Krishna Kumari Challa 18 hours ago

Fat breakdown in skin cells restarts hair growth in mice

Researchers  report that adipocyte lipolysis activates epithelial hair follicle stem cells and drives hair regeneration via monounsaturated fatty acid signaling.

Healthy hair follicles are still present in balding men, but they are often miniaturized, producing thinner, weaker hairs that eventually stop producing. For a while, even though the follicles stop growing visible hair, previous studies show they still contain stem cells and could, theoretically, be reactivated.

Skin is a lipid-rich organ where fatty tissue cushions, insulates, and secretes endocrine factors. Previous studies have linked inflammation after minor injury to hair regrowth and have described crosstalk between dermal white adipose tissue and hair follicle stem cells with both stem cell activation and dormancy. Specific roles for adipocytes in regeneration remained unclear.

In the study, "Adipocyte lipolysis activates epithelial stem cells for hair regeneration through fatty acid metabolic signaling," published in Cell Metabolism, researchers employed mouse models of skin injury to determine whether inflammation-triggered adipocyte lipolysis promotes hair regrowth and to define the downstream metabolic pathway in epithelial hair follicle stem cells.

Mouse experiments were conducted using topical sodium dodecyl sulfate (SDS) irritation and controlled dermal laser injury, with female mice used predominantly. Mice were shaved on postnatal day 49 to synchronize with the start of the second telogen phase, when hair follicles are naturally resting and hair doesn't normally regrow for about six weeks.

Investigators applied 7.5% SDS to induce contact dermatitis, tracked timing of epidermal and follicular responses by histology, EdU labeling, lipid testing and immunostaining, and profiled transcripts with bulk and spatial transcriptomics.
Skin irritation produced rapid skin redness and scaling at the surface, outer skin thickened and immune cells flooded in. Several days later, growth of new hair was observed.
Part1

Comment by Dr. Krishna Kumari Challa 18 hours ago

Over 3.5 years, the team studied 8,073 older adults aged 73 to 91. They tracked how quickly participants lost teeth over time, measuring this as the average number of teeth lost per year. Based on the tooth loss pattern, the participants were divided into four groups: stable (no teeth lost per year), slow loss (more than zero but less than two teeth lost per year), moderate loss (two to under four teeth lost per year), and rapid loss (4 or more teeth lost per year).

The data were then entered into a Cox regression analysis—a statistical method that accounts for the relative risk of an event—to determine whether faster tooth loss was associated with a higher mortality risk. They found that those with rapid tooth loss had a 33% higher risk of death compared to those who lost none. Also, with each tooth lost per year, the risk increases by 4%.

The researchers note that further investigation into the mechanisms underlying this relationship is needed to develop effective interventions. Until then, raising awareness of the hidden health risks of rapid tooth loss among both health care professionals and the public could go a long way toward encouraging habit modification.

Linjia Duan et al, Tooth loss progression and mortality among older adults: results from the Chinese longitudinal healthy longevity survey (CLHLS), BMC Geriatrics (2025). DOI: 10.1186/s12877-025-06419-1

Part 2

Comment by Dr. Krishna Kumari Challa 18 hours ago

Rapid tooth loss linked to higher risk of death in older people

In older adults, tooth loss may be linked to serious health risks. A team of  researchers analyzed data from 8,073 older participants and found that people who lost their teeth more quickly had a higher risk of dying, regardless of how many teeth they started with.

The researchers emphasize the need to closely monitor the progression of tooth loss among older adults, as it is an important indicator of broader physiological decline.

Modifiable habits like regular brushing, avoiding smoking, and routine dental checkups play a key role in how quickly teeth are lost. Studies show that consistent oral care can lower mortality rates among older adults with missing teeth. Making oral health a stronger focus of public health efforts could be an easy way to improve overall well-being, suggests the study published in BMC Geriatrics.

Old age or not, oral health is a major problem in humans across the globe. In 2022, the World Health Organization released a "Global Oral Health Status Report," which showed that almost half of the world's population (~3.5 billion people) has some form of dental disease. It highlighted tooth loss as one of the most common problems.

While losing teeth with age is often inevitable, its impact can be far-reaching. It not only affects quality of life by making it harder to chew and enjoy food, but has also been linked to higher death rates—not just overall mortality, but from specific causes like heart disease, lung cancer, and pneumonia.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Exploring mechanisms behind attachment issues

Stoicism says attachment is not good. But  overcoming biochemistry is extremely difficult. Especially when you are young. 

And then not giving enough care also makes people detached. 

Children can sometimes develop health, behavioral, and attachment issues that persist when their needs are not met by their caregiver. Now from eNeuro, researchers explored whether mouse pups also experience these issues from early life adversity.

Their discoveries provide an opportunity for researchers to explore the mechanisms of health and behavioral deficits from early life adversity.

When the researchers limited bedding for making nests, this impaired maternal care and increased stress hormone signaling in pups after just one week. Offspring also experienced long-term stunted growth trajectories.

Behaviorally, while some attachment behaviors remained unchanged, many were affected: Pups vocalized less when they were separated from their mothers after one week, did not approach their mothers after about two weeks, and had anxiety-like behavior by week three.

Giving credit where credit is due, work in rats relates an increased stress response from impaired maternal care to attachment deficits. But this work was only done in one age group. Researchers used thorough, 24/7 videotape footage of moms and their pups to show how impaired maternal care leads to attachment deficits at different timepoints.

This isn't a linear relationship. It seems that there is a threshold for how bad maternal care must be to disrupt the offspring's behavior. This supports an existing hypothesis that you don't have to be a perfect parent, you just need to provide adequate care.

Erratic Maternal Care Induces Avoidant-Like Attachment Deficits in a Mouse Model of Early Life Adversity, eNeuro (2025). DOI: 10.1523/ENEURO.0249-25.202

Comment by Dr. Krishna Kumari Challa yesterday

Most often the behavior was directed at the chimpanzee's own open wound. However, in one rare instance, an adolescent female applied an insect to her brother's wound. A study on the same community has shown that chimpanzees also dab the wounds of unrelated members with leaves, prompting the question of whether insect application of these chimpanzees, too, might extend beyond family members. Acts of care, whether directed towards family or others, can reveal the early foundations of empathy and cooperation.

 Kayla Kolff et al, Insect applications to open wounds by chimpanzees in the wild: first insights from East African chimpanzees, Scientific Reports (2025). DOI: 10.1038/s41598-025-16582-5

Part2

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