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Comment by Dr. Krishna Kumari Challa 5 hours ago

No single approach works for everyone, but several options have evidence behind them.

During perimenopause and after menopause, the National Institute for Health and Care Excellence (NICE) recommends considering vaginal estrogen for recurrent UTIs. NICE produces health and care guidance for England and recommends this approach when behavioral and personal hygiene measures have not been effective or are unsuitable. It has some of the strongest evidence among nonantibiotic approaches.
Drinking more water can help people who do not normally drink much. In a trial of 140 premenopausal women who drank less than 1.5 liters (51 fluid ounces) of fluid a day, those asked to add another 1.5 liters (51 fluid ounces) of water averaged 1.7 bladder infections over a year, compared with 3.2 among those who continued their usual intake.

Cranberry products may reduce recurrence for some women, although the evidence varies between studies and formulations. Current guidance from the European Association of Urology advises patients that the evidence remains contradictory and generally low quality.

D-mannose, a type of sugar sold as a dietary supplement, is thought to help prevent UTIs by making it harder for some E. coli bacteria to stick to the bladder lining. It looked promising in smaller studies but failed to prevent infections in a much larger U.K. randomized trial involving 598 women.

For people with recurrent infections, NICE says doctors can consider preventive treatment after any current infection has been treated. Options can include methenamine hippurate, a nonantibiotic urinary antiseptic, or preventive antibiotics. The choice depends on factors including how frequent and severe the infections are, previous urine test results, previous antibiotic use and whether measures such as vaginal estrogen or a single antibiotic dose after an identifiable trigger have helped.

Long-term antibiotic use also needs to be weighed against side effects and antimicrobial resistance, which the World Health Organization describes as a growing threat to global health.

The mini-bladder findings recast a UTI as a disease shaped by interactions between bacteria, bladder tissue, the immune system and the chemical and physical conditions inside the bladder.

Bladder-model study also investigated whether bacteria-killing viruses called bacteriophages, or phages, could help target bacteria persisting in bladder tissue. Phages reduced clusters of bacteria inside bladder cells, but adding them to nitrofurantoin did not consistently clear more bacteria from the bladder tissue than the antibiotic alone.

For someone whose infection keeps coming back, one possible explanation is that a small population of bacteria survived the original treatment and was able to start growing again.

original article.

Part 2

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Comment by Dr. Krishna Kumari Challa 5 hours ago

Lab‑grown 'mini‑bladder' helps explain why urinary tract infections keep coming back

UTIs affect more than 400 million people worldwide each year, according to a global analysis of UTI incidence. More than half of adult women will have at least one in their lifetime, and studies suggest around a quarter experience another within six months.

Antibiotics aren't simply failing. New research using a lab-grown human "mini-bladder" suggests part of the answer may lie inside the bladder wall itself.

Most UTIs are caused by a type of Escherichia coli that normally lives harmlessly in the gut. Problems start when bacteria travel up the urethra into the bladder.

A repeat infection can happen in two ways. New bacteria from the gut can make the same journey again, and many recurrences are reinfections. But sometimes bacteria from the original infection appear to survive treatment and later reemerge.
In 3D human bladder models, E. coli survived fosfomycin in deeper tissue in a cell-wall-deficient form and regrew after treatment ended. Concentrated urine weakened tissue barriers, while nitrofurantoin failed to eradicate tissue-associated bacteria in a separate model. These laboratory findings support a possible mechanism of UTI recurrence but do not establish its clinical frequency.
Why women are hit hardest
Anatomy is a major reason women tend to suffer more than men from UTIs. A woman's urethra is much shorter than a man's, so bacteria have a shorter distance to travel before reaching the bladder. The urethral opening is also close to the anus, where gut bacteria live.

Sexual activity and the use of spermicides are also established risk factors for recurrent infection in premenopausal women.

Risk rises again around and after menopause. Falling estrogen changes the tissues of the vagina and urinary tract and is associated with a reduction in protective Lactobacillus bacteria, creating conditions in which UTI-causing bacteria can become more established.
Part 1

Comment by Dr. Krishna Kumari Challa 6 hours ago

Inflammation can reactivate 'sleeping' cancer cells hidden in the bone

The spread of cancer from a primary tumour to another place in the body, called metastasis, remains one of the greatest challenges in cancer treatment and is responsible for most cancer-related deaths.
Cancer cells that have moved to another part of the body can stay dormant for years after the original tumour has been treated.
It's a worrying period for people, as they don't know if these metastatic cells will reactivate, leading to a relapse.
Breast cancer cells often spread to the bone marrow, where they can lie dormant for years within the tissue that normally supports the production of new blood cells. These disseminated cancer cells enter a "sleeping" state, which helps them evade the immune system and resist chemotherapy. What causes them to "wake up" is not only a key issue in cancer biology but also a huge challenge to study.

Injuries to the bone like fractures can lead to the growth of metastatic cancer cells hosted in the bone marrow, but the team wanted to establish if more indirect insults throughout the body, such as those caused by injury or infections, could also kick-start tumour development.
So researchers induced intestinal colitis—inflammation in the gut—in the mice with the extramedullary bone hosting dormant metastatic cells. Because the replica bone responds to the immune system, gut inflammation triggered a rapid production of immune cells from the bone.
The bone marrow environment needs to remodel to boost production of new immune cells, and it turned out that this change had a profound effect on the dormant cancer cells. More cancer cells started replicating, which increased the risk of a tumour forming.
In mice with engineered bone tissue, gut inflammation increased immune cell production and HMGB2, promoting reactivation of dormant breast cancer cells. Increased HMGB2 alone stimulated reactivation; it was also present in regions containing dividing cancer cells in human breast and prostate cancer bone samples.
By analyzing which genes were being switched on in the bone cells and the cancer cells, the team showed that a molecule that stimulates cell growth, HMGB2, increased as immune cell production surged, but also promoted the awakening of dormant cancer cells.

Even without inflammation elsewhere in the body, just the increased HMGB2 in the artificial bone was enough to stimulate more cancer cells to activate.
All of these findings suggest that boosting immune cell production in the bone, as part of a normal response to inflammation, comes at the cost of disrupting tumour dormancy, tipping the balance toward reactivation and metastatic growth.
The research suggests that monitoring people in this critical period after remission for infections, inflammation or injury anywhere in the body may indicate whether dormant cells are more likely to reactivate.

Stefania Di Blasio et al, An extramedullary bone model of metastatic dormancy reveals an increased rate of metastatic reactivation upon distant insults, Cell Reports (2026). DOI: 10.1016/j.celrep.2026.118088

Comment by Dr. Krishna Kumari Challa 6 hours ago

A food poisoning bacterium can cause severe wound infections

Bacteria belonging to the B. cereus group are found almost everywhere, including in soil, dust and food, and are best known for causing food poisoning. The same group of bacteria can also cause serious infections outside the gastrointestinal tract, including in open wounds.

The toxin NheABC, produced by Bacillus cereus, is particularly active in the pH conditions found in open wounds. Researchers found that the toxin damages both cell membranes and mitochondria and helps the bacterium establish infection in wounded tissue.

Bacillus cereus toxin NheABC forms pores in cell membranes and damages mitochondria, with cardiolipin enhancing toxicity. Its activity is greater at neutral or alkaline pH than under acidic conditions. In a mouse wound infection model, NheABC increased bacterial colonization and local inflammation.
The researchers showed that the NheABC toxin makes small holes in cell membranes and causes significant damage to mitochondria. Experiments using artificial membranes revealed that certain lipids in mitochondria, such as cardiolipin, enhance the damaging effects of the toxin.
The most surprising finding concerned acidity. The toxin's harmful activity was significantly lower under acidic conditions than at neutral or alkaline pH levels. Chronic wounds can develop a more alkaline environment due to the presence of blood, tissue fluids and metabolic byproducts such as ammonia. This may create conditions that favor bacterial growth and colonization. In a mouse model of wound infection, NheABC contributed to increased bacterial colonization and a stronger local inflammatory response.

These findings strengthen the view that disease-causing bacteria within the B. cereus group detected in deep or infected wounds should not always be dismissed as harmless contamination.

Naeem Ullah et al, NheABC is a pH-dependent cytotoxin that targets mitochondria and contributes to the virulence of Bacillus cereus in wound infections, Cell Communication and Signaling (2026). DOI: 10.1186/s12964-026-03235-x

Comment by Dr. Krishna Kumari Challa 7 hours ago

The research team then moved a step closer to humans and transplanted the organoids into a macaque monkey whose pituitary gland had been removed. To prevent rejection of the tissue because it came from a different species, they used immune-suppressing drugs already used in transplants of human insulin-producing cells for diabetes.

The transplanted tissue worked for six weeks and successfully elevated ACTH and cortisol levels in the blood. Additionally, significant weight loss caused by the hormone deficiency slowed during this period. Three months later, tissue samples still showed surviving transplanted cells, despite strong immune rejection common in cross-species transplants, which limited how well the transplant worked.

Stem cell treatments have a known risk of cells moving from the transplant site and growing uncontrollably elsewhere in the body. The researchers checked the lungs and liver for signs of stray organoid tissue and found none.

Functional analysis of adrenocorticotropic-hormone-producing pituitary cells derived from human pluripotent stem cells in murine and primate models of hypopituitarism, Stem Cell Research & Therapy (2026). DOI: 10.1186/s13287-026-05098-y

Part 2

Comment by Dr. Krishna Kumari Challa 7 hours ago

First successful primate transplant of human pituitary tissue boosts cortisol levels

Researchers in Japan have transplanted pituitary tissue grown from human stem cells into a primate whose pituitary gland had been surgically removed, successfully restoring critical hormone signals. Led by researchers from Nagoya University in Japan, the team showed that the same method worked in mice over a longer period.
This is the first time lab-grown human pituitary cells have been shown to work and survive after transplantation into a primate. The study, published in the journal Stem Cell Research & Therapy, may offer a new pathway for treating lifelong hormone disorders.

The pituitary gland controls hormones for stress, growth and metabolism. When it is damaged or removed, patients rely on daily hormone pills that do not accurately mimic the body's natural fluctuations. This study tested whether lab-grown pituitary tissue can be transplanted to produce hormones naturally instead.

The pituitary gland sits at the base of the brain and releases hormones into the bloodstream. One of them is ACTH, adrenocorticotropic hormone, which signals the adrenal glands to release cortisol. Cortisol helps the body manage stress, blood pressure and blood sugar. When the pituitary fails, patients lose this signal, leading to a condition called hypopituitarism.

Without enough ACTH, the body struggles to respond to stress, which can become dangerous. Daily hormone pills for life are the standard treatment, but these pills cannot fully match the changing needs of the body because demand for cortisol shifts with stress and time of day. As a result, patients face a higher risk of sudden death.
To find a better option, the researchers turned to stem cells. They grew small lab-made masses of tissue that can act as miniature organs, called organoids, from human stem cells. The organoids contained cells that produce ACTH. The team first tested the tissue in mice whose pituitary glands were removed.

The organoids were transplanted just under the skin, in fat or muscle tissue. They produced ACTH for more than six months and clearly extended the lifespans of these mice compared to those that did not receive the transplant. No unwanted tumours or unusual cell growth were observed.
Part 1

Comment by Dr. Krishna Kumari Challa 7 hours ago

Too little salt may hurt memory just as badly as too much

Salt can make or break a dish. A little too much or too little can throw everything off, leaving even the most luxurious ingredients tasting off. But get the balance right, and salt can bring out the flavour in even the simplest ingredients. The brain relies on a similar balancing act for healthy function and memory. While we are aware of the ill effects of having too much salt, what happens when we consume too little?
A recent study compared how long-term low-salt and high-salt diets affected memory, gut health and brain health in mice whose guts were colonized with human gut bacteria. The researchers focused on the gut–metabolite–brain axis, examining how dietary salt alters gut bacteria and their chemical products, and how those changes signal back to the brain.

Mice on either a low-salt or a high-salt diet struggled with memory. Compared with mice eating a normal amount of salt, they did worse on tests of short-term working memory and long-term recognition memory.

Inside the hippocampus, the brain's memory center, both diets lowered critical synaptic proteins like SYN1, PSD95 and BDNF and suppressed CREB activation. All of these are essential tools neurons use to build memories and adapt, so weakening them reduced the brain's ability to form memories.
Tests by researchers indicated that both eating too little salt and eating too much salt impair memory and brain function, but through two different biological pathways. With a low-salt diet, a drop in essential hippocampal synaptic proteins impaired long-term and short-term memory.

A high-salt diet significantly increased pro-inflammatory signals circulating in the blood and shifted the gut microbiota toward a pro-inflammatory state by lowering faecal levels of propionate and butyrate. This led to increased oxidative stress markers in the intestine, which can often trigger higher anxiety-like behaviour.
The results demonstrate the importance of a balanced, normal salt intake for one's overall brain and gut health. Too little salt starves the brain of vital gut-derived chemical signals, while too much salt causes inflammatory damage.

Anji Chen et al, Long-term low-salt and high-salt diets differentially disrupt the gut–metabolite–brain axis and induce cognitive impairment, Food Research International (2026). DOI: 10.1016/j.foodres.2026.119719

Comment by Dr. Krishna Kumari Challa yesterday

Gut bacterial compound worsens brain injury after stroke, study suggests

How much damage a stroke causes in the brain depends strongly on how quickly blood flow can be restored. The patient's own immune response that follows the stroke also plays an important role.

Researchers have discovered how a metabolite produced by gut bacteria can influence brain damage after stroke. Their paper is published in the journal Cell.

They have now identified a specific bacterial signal that shapes this immune response and influences stroke outcome.
Gut bacterial indole worsened brain injury after stroke in mice through AHR signaling in dendritic cells. Disabling AHR in these cells promoted protective immune responses and reduced injury. In patients with ischemic stroke, higher bacterial TnaA abundance was associated with poorer functional outcomes.

The researchers found that in mice with severe stroke, gut bacteria capable of producing indole, a metabolite that is only produced in the gut, become more abundant. These bacteria carry the gene tnaA, which allows them to convert the amino acid tryptophan, found in food, into indole. In mice, the team showed that indole-producing bacteria worsened brain injury after stroke.

Indole acts on a receptor called AHR (aryl hydrocarbon receptor), found in dendritic cells—immune cells that patrol the intestinal lining and help coordinate immune responses. When the researchers switched off AHR specifically in dendritic cells, mice were better protected against brain injury.

Dendritic cells have long extensions, like arms, that allow them to sense changes in their environment, including metabolites produced by gut bacteria. When scientists switched off AHR, the behaviour of these cells changed completely: Dendritic cells were better able to migrate from the intestine to the meninges, the membranes surrounding the brain. These dendritic cells also promoted protective T cells and helped reduce the damage in the brain.
The researchers also found evidence that this pathway may be relevant in humans. In a cohort of human patients with ischemic stroke, the ISD team found that a higher abundance of bacterial TnaA was associated with poorer functional outcomes.
The findings raise an important question for future research: Could changing the gut microbiome or the metabolites it produces in healthy individuals help prepare the immune system to respond differently if a stroke occurs?

Rosa Delgado Jiménez et al, Gut microbiota primes stroke severity via the AHR in intestinal dendritic cells, Cell (2026). DOI: 10.1016/j.cell.2026.09.013

Comment by Dr. Krishna Kumari Challa yesterday

The biological clock regulates phases of wakefulness

The circadian clock is an internal biological system that regulates sleep-wake cycles, as well as many physiological functions such as body temperature and hormone production. In many animals, this clock relies on a network of neurons that generates rhythms of approximately 24 hours.
These neurons must then transmit this information to other regions of the brain, allowing activity and behaviour to be adapted to the time of day.
A circuit linking the biological clock to wakefulness
Imaging techniques that measure neuronal activity allowed researchers to show that this activity varies throughout the day. They identified a connection between the biological clock neurons and a population of neurons that produce dopamine, a molecule that enables neurons to communicate with one another.
Researchers observed that the clock neurons inhibit these dopaminergic neurons, which in turn stimulate neurons in the mushroom body. This brain region plays a role in learning, memory and the regulation of sleep, and its activity contributes to promoting wakefulness during the day
When the clock neurons inhibit the dopaminergic neurons, the wake-promoting signal decreases. Conversely, when this inhibition is released, the dopaminergic neurons can more strongly stimulate the mushroom body and promote wakefulness. Through its neurons, the biological clock can therefore transmit information about the time of day to a brain circuit involved in regulating sleep and wakefulness.

These findings shed light on how the biological clock influences sleep and wake states. In particular, they highlight the central role of dopamine in promoting wakefulness and show how information from the biological clock is relayed through different neural circuits throughout the day.

Disruptions of the circadian clock are associated with various sleep disorders and alterations in brain function. A better understanding of these fundamental mechanisms could ultimately help explain how disturbances in biological rhythms affect the brain.

Blanca Lago Solis et al, Circadian control of dopaminergic signaling to the mushroom body regulates sleep through rhythmic Pka-C1 transcription in Drosophila, Current Biology (2026). DOI: 10.1016/j.cub.2026.09.014

Comment by Dr. Krishna Kumari Challa on Thursday

Skipping sweets during antibiotic treatment may help protect the gut microbiome

A new study by researchers suggests eating less sugar could protect the microbiome during antibiotic treatment. The study followed patients with blood cancer undergoing an intensive treatment called allogeneic hematopoietic cell transplant, a population at particularly high risk for severe gut microbiome disruption and associated side effects.

In stem cell transplant patients taking broad-spectrum antibiotics, each additional 100 g of sweets was associated with 24% lower gut bacterial diversity. High-sucrose diets promoted Enterococcus overgrowth in antibiotic-treated mice.
Published in Nature, the findings connect to the idea of "food as medicine" during cancer care and the ways diet can help us prevent and recover from illness. The research could lead to new treatment strategies for cancer patients and potentially others taking antibiotics.

Antibiotics disrupt the diversity of our gut bacteria, or microbiomes, which play an essential role in supporting our immune systems and overall health.
This new research supports emerging evidence that avoiding sugary foods during antibiotic treatment may protect the microbiome. Preserving microbiome diversity has previously been linked with improved clinical outcomes for patients with cancer.
Antibiotics are used to treat infections, but they also broadly destroy good bacteria in the gut, allowing harmful microbes to overgrow.

The five-year study, one of the largest of its kind, followed patients who were hospitalized for several weeks to receive intensive chemotherapy, sometimes with radiation, to wipe out their immune systems before undergoing a stem cell transplant.

To prevent and treat infections, each patient took at least one antibiotic during their hospital stay. Some 80% took one or more broad-spectrum antibiotics, which have the strongest effect on the microbiome because they target many types of bacteria.

The research team tracked 9,419 meals eaten by 173 hospitalized patients and profiled microbiome diversity in stool samples from 158 patients. Microbiome diversity is a key indicator of a healthy microbiome.

Using a variety of advanced statistical models, the researchers searched the data for patterns linked to injury to the gut microbiome.

What they found surprised them.
The patients who consumed more sweets while taking antibiotics were more likely to experience a loss of microbiome diversity as aggressive microbes crowded out other strains of bacteria.

One organism stood out: Enterococcus. When it takes over the microbiome, patients undergoing transplant face a higher risk of bloodstream infections, graft-versus-host disease and other life-threatening complications.

The combination of high-sugar foods and broad-spectrum antibiotics appeared to multiply injury to the microbiome, leading to a 24% drop in bacterial diversity for every 100-gram (3.5-ounce) increase in sweets (equivalent in sugar content to a large milkshake).
The researchers also tested their hypothesis that sugar exacerbates microbiome injury by giving broad-spectrum antibiotics to healthy mice and feeding them a variety of diets. Mice that ate a high-sucrose diet quickly developed an overgrowth of Enterococcus in their guts. Mice that ate the high-sugar diet without antibiotics, however, maintained normal bacterial diversity.

Jonathan Peled, Sugar-rich foods exacerbate antibiotic-induced microbiome disruption, Nature (2026). DOI: 10.1038/s41586-026-11077-3. www.nature.com/articles/s41586-026-11077-3

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