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Comment by Dr. Krishna Kumari Challa yesterday

Despite such striking results, reprogramming the immune system is no simple matter. In early treatment of cancer patients, CAR T cells produced life-threatening side effects, as outlined in a 2026 article in the Annual Review of Medicine. As CAR T cells attack their targets, the associated inflammation can cause symptoms like high fevers and low blood pressure. If that inflammation reaches the brain, it can cause additional problems such as confusion and drowsiness.

Fortunately, physicians now have a decade's worth of experience recognizing and treating these problems. They're certainly reversible and don't cause long-term damage most of the time.
Physicians and patients also must contend with decreased immunity as both a side effect of the treatment and its desired outcome. In CAR T treatment, doctors typically use powerful chemotherapy drugs to temporarily reduce the body's immune cell population to make room for the new, engineered cells, leaving patients temporarily immunosuppressed. And if the treatment works, it will decimate B cell populations. Patients can be vulnerable to infections for up to a year after treatment.
These effects are manageable with preventive antibiotics, antivirals and vaccines. Patients also retain antibodies that their B cells made before the treatment, which provide residual protection for a few months. And for reasons that are not yet fully understood, CAR T seems to leave older B cells, which provide immune memory of past infections, intact in some cases. One study found that autoimmune patients treated with CAR T still made antibodies for diseases they'd been previously vaccinated against, like chicken pox and measles. These are signs that the treatment did not completely return the immune system to its factory settings.

When evaluating CAR T risk, it's important to consider that many existing treatments for autoimmune disease also suppress the immune system for as long as a person takes them, experts note.
Researchers are already working on second- and third-generation versions of CAR T that they expect to be safer for both cancer and autoimmunity.

Source: https://knowablemagazine.org/content/article/health-disease/2026/ca...

Part 2

Comment by Dr. Krishna Kumari Challa yesterday

CAR T moves beyond cancer, targeting autoimmune disease with immune system reset
CAR T cell therapy, originally developed for cancer, is being investigated for autoimmune diseases by targeting and eliminating pathogenic B cells, potentially resetting immune function. Early trials show promising symptom improvement and reduced need for other immunotherapies, but risks include severe inflammation, immunosuppression, and uncertain long-term effects such as secondary malignancies. Newer approaches aim to enhance safety and reduce costs, including mRNA-based CAR T and off-the-shelf donor cell therapies. Long-term efficacy and safety in autoimmunity remain under investigation.

Originally designed to target and wipe out cancer by reprogramming the patient's immune cells, CAR T is now being offered to patients in hundreds of clinical trials for autoimmune conditions like multiple sclerosis, lupus, Graves' disease, vasculitis and many others. The hope is that CAR T can duplicate the success it has demonstrated in a range of blood cancers by hunting down and eliminating cells that target the self in autoimmune diseases. This would essentially reset the body's defenses to a state like the one that existed before the disease took hold.
But along with CAR T's promise come risks, questions and challenges. There's uncertainty about how well it will work for autoimmunity and how long any benefits might last, as well as what long-term side effects might arise.
The basic premise of CAR T is to activate the power of key immune cells called T cells. T cells normally recognize other cells that have been infected by a virus or bacterium, or are otherwise abnormal, and either destroy them or recruit other parts of the immune system to do so.

In CAR T for cancer, scientists engineer those T cells to specifically hunt and destroy malignant cells. The technology got its start when cancer researchers figured out how to take out a patient's own T cells, insert DNA instructions for a "chimeric antigen receptor," or CAR, and put them back into the person's circulation. The CAR, which sits on the T cell's surface and latches on to a specific molecular partner on the surface of cancerous cells, activates the T cell to attack.

Today CAR T cells are most commonly programmed to attack B cells, another key immune player. B cells are normally responsible for making antibodies, but in certain blood cancers, they proliferate out of control. By giving T cells a CAR that recognizes one of a couple of molecules unique to the B cell surface, the cells are reprogrammed to find and eliminate those cancerous cells.

B cells are also the central problem in many autoimmune conditions: They mistakenly make antibodies against normal tissues instead of against invading pathogens. So as CAR T began to succeed against B cell cancers, it didn't take long for doctors to reason that CAR T therapy might also be able to wipe out bad B cells in people with autoimmunity.
A German team pioneered autoimmune CAR T in a woman with lupus, reporting positive results in 2021. Since then, that team and others have worked to translate the oncology success of CAR T to tackle a broad spectrum of autoimmune diseases.
Part 1

Comment by Dr. Krishna Kumari Challa on Saturday

The left and right ventricles differ in their ability to withstand the effects of cardiac arrest, study finds
The right ventricle demonstrates greater resistance to ischemia and better preservation of electrical activity than the left ventricle during cardiac arrest caused by ventricular fibrillation. Electrical gradients between heart regions can be detected via surface ECG, which may help predict neurological recovery outcomes. These findings suggest potential for targeted therapies to improve left ventricular resistance during cardiac arrest.

https://medicalxpress.com/news/2026-05-left-ventricles-differ-abili...

Comment by Dr. Krishna Kumari Challa on Saturday

What separates dreaming from deep sleep? Brain rhythm offers new clue to consciousness

Neuropsychology researchers have discovered a rhythm in the midbrain that could serve as a biophysiological signature for specific states of consciousness.
A rapid oscillation in the human thalamus, occurring at 20–45 Hz, is present only during wakefulness and REM sleep, but absent during non-REM sleep. This thalamic rhythm may serve as a biophysiological marker distinguishing conscious states from deep, unconscious sleep.
The thalamus is a deep-lying structure in the center of the brain which gathers and relays signals from many different areas of the brain. It functions like a gate for perception and attention and is thought to play a key role in supporting conscious states.
The researchers discovered a previously unknown rapid activity pattern in the human thalamus.
This rapid oscillation, in the frequency range of 20 to 45 Hertz, occurs exclusively during waking hours and REM sleep, the phase of sleep with rapid eye movements and intensive dreams. It is entirely absent in non-REM sleep, when eye movements are absent and consciousness is strongly reduced. In this sleep phase, the brain activity is dominated instead by slower oscillations.
The results show that the central thalamus plays an important role in regulating brain states. In the context of existing research, our results show that this small deep-lying brain structure could actively influence our states of consciousness.
These characteristic rhythm patterns can be reliably attributed to specific states and thus have the potential to serve as a measurable biological signature of states of consciousness.

Aditya Chowdhury et al, Thalamic oscillations distinguish natural states of consciousness in humans, Nature Human Behaviour (2026). DOI: 10.1038/s41562-026-02446-z

Comment by Dr. Krishna Kumari Challa on Saturday

Humans reshape predator-prey rules across food webs, creating a challenging new world for wildlife

The relationship between predators and prey in the wild is underscored by an evolutionary arms race spanning millions of years, but new research has found modern human activity is reshaping the rules.
The review found that physical and behavioural traits of both predator and prey have been altered by human interference, and this has affected how they interact with each other.

Human activities such as selective hunting, fishing, habitat alteration, and pollution are altering the physical and behavioural traits of both predators and prey, disrupting established predator-prey interactions. These trait shifts can cascade through food webs, leading to population declines, food web restructuring, and potential local extinctions, fundamentally altering ecosystem function.
Predator–prey interactions underpin the evolution of entire ecosystems.
They influence everything from species abundance to vegetation and nutrient cycling—if we change how predators and prey interact, those effects can cascade through food webs and fundamentally alter ecosystems.

One of the key takeaways from the study was that changes in animal behavior and physiology weren't always obvious or immediate, but could have long-term consequences.

Trait shifts can build over time, leading to cascading effects like population declines, food web restructuring, or even local extinctions.
By understanding how human activities drive these changes, we can design better conservation strategies.

Eamonn I.F. Wooster et al, Human-induced trait shifts reshape predator–prey interactions, Trends in Ecology & Evolution (2026). DOI: 10.1016/j.tree.2026.01.005

Comment by Dr. Krishna Kumari Challa on Saturday

Tardigrades reveal extreme heat-blocking survival trick while in tun state

The tun state is a form of suspended animation used by tardigrades (water bears) to survive harsh environmental conditions. When faced with extreme drought, freezing, or radiation, they expel nearly all their water and curl into a dry, lifeless ball, dropping their metabolism to virtually zero.
A biological process that allows tardigrades to survive in extreme environments is anhydrobiosis. This is a reversible process via which the animals lose most of their body water and their metabolism temporarily stops, which in turn allows them to survive in dry environments. When tardigrades undergo this process, they curl up and enter what is known as a "tun" state.
Researchers at the Indian Institute of Science recently carried out a study aimed at better understanding how a species of tardigrade—called Paramacrobiotus sp. BLR strain—survives extreme heat while in the tun state. Their findings, published in the Journal of the Royal Society Interface, suggest that reductions in thermal conductivity are central to the survival of this species at high temperatures and under extreme heat.

Tardigrades in the tun state exhibit significantly reduced thermal conductivity, enabling survival at extreme temperatures up to 85°C, unlike their active counterparts. This physical adaptation limits heat flow, protecting internal cellular structures and contributing to their extremotolerance beyond known biochemical mechanisms.
Researchers found that active tardigrades did not survive high temperatures for one hour, even the lowest experimental temperature of 45°C. Instead, 90% of tardigrades in the tun state survived under the same conditions, and some of them were still alive after one hour at 85°C.
Interestingly, the researchers found that tardigrades in the tun state exhibited a higher thermal resistance and a reduced flow of heat through their bodies. In their paper, they propose that the observed lower thermal conductivity protects the animals' internal cellular structures and prevents heat-related damage.
The results of this study suggest that the ability to survive extreme temperatures is supported not just by biochemical, but also by physical processes.

Harikumar R. Suma et al, Thermal conductivity modulation as a mechanism of inducible thermotolerance in the eutardigrade Paramacrobiotus sp., Journal of the Royal Society Interface (2026). DOI: 10.1098/rsif.2025.1033

Comment by Dr. Krishna Kumari Challa on Friday

Ming Dynasty Surgeons Used Poison as an Anesthetic

Traces of red material crusted on ancient surgical tools may not be a record of pain, but rather the absence thereof.

Metal scissors and tweezers recovered from a Ming Dynasty tomb in Jiangyin County, China, retain what scientists think may be the earliest direct chemical evidence of surgical anesthesia – a substance used for painless medical treatment.

It's the first discovery of its kind and highlights the sophisticated medicine of the Ming Dynasty.

 That substance appears to be aconitine, a highly toxic compound derived from the group of plants that includes wolfsbane.

Its presence on the tools of a revered surgeon – Xia Quan, who lived around 1348 to 1411 and in whose tomb the tools were found in 1974 – implies a very high level of skill and precision.
Six centuries ago, a Ming Dynasty surgeon performed an operation with a pair of iron scissors and tweezers, and today researchers have read the traces of anesthetic medicine left on those instruments using a beam of laser light.
This is the first time humanity has found direct chemical evidence of anesthetics on ancient surgical tools, proving that our ancestors already knew how to safely alleviate patients' pain with highly toxic herbs.

https://www.cambridge.org/core/journals/antiquity/article/surgical-...

Comment by Dr. Krishna Kumari Challa on Friday

AI can mass-produce finance research papers indistinguishable from human work, reports study
AI and large language models can rapidly generate large volumes of finance research papers that closely resemble human-authored work, including plausible hypotheses and theoretical justifications. This capability raises concerns about the scalability of HARKing, the integrity of scientific contribution, and increased strain on the peer-review system, suggesting a need for adaptation in academic standards and evaluation processes.

Robert Novy-Marx et al, Artificial Intelligence–Powered (Finance) Scholarship, Journal of Economic Literature (2026). DOI: 10.1257/jel.20251821

Comment by Dr. Krishna Kumari Challa on Friday

Why do you get so tired while driving?
Driving requires sustained attention and coordination across multiple brain regions, making it mentally demanding and prone to fatigue. Fatigue impairs attention, decision-making, and reaction time, increasing crash risk and the likelihood of microsleeps, which can be catastrophic. Risk factors include insufficient sleep, long driving periods, circadian disruption, dehydration, and stress. Regular breaks, adequate sleep, and hydration are essential for maintaining alertness while driving.

 original article.

Comment by Dr. Krishna Kumari Challa on Friday

Oral inflammation may reach ovaries, speeding fertility decline, mouse study suggests
Chronic oral inflammation in mice induces systemic immune responses that reach the ovaries, elevating ovarian inflammatory cytokines, altering immune cell populations, and causing oxidative and DNA damage in oocytes. These changes impair follicle development, reduce oocyte quality, and significantly lower fertility, suggesting oral inflammation may accelerate reproductive aging and contribute to infertility.

P. Kles et al, Chronic Oral Inflammation Impairs Female Reproduction in a Murine Model, Journal of Dental Research (2026). DOI: 10.1177/00220345251412768

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