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Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 8:14am

The team also examined whether the brain's capacity for long-term potentiation (LTP), a cellular basis of learning and memory, changes with time of day. This represents the brain's potential for metaplasticity (the brain's ability to adjust how easily its networks change). Remarkably, repetitive optical stimulation induced LTP-like enhancement at sunrise, but not at sunset.

This was unexpected, as it suggests that although sleep pressure and fatigue peak at sunrise, the brain's metaplastic potential is heightened at this time. These findings indicate that the brain's ability to reorganize itself follows a daily rhythm, with specific periods more favorable for learning and adaptation.

These results imply that our brains have temporal windows that favor adaptability.
Knowing when the brain is most receptive to changing could help optimize training, rehabilitation, and stimulation-based therapies.
In humans, who are mainly active during daylight hours, the capacity for learning and memory formation may peak during the twilight period approaching sunset. In other words, the best time to study or learn something new may be before bedtime.

The study reveals how daily rhythms fine-tune the balance between excitability and plasticity in the cortex. Because adenosine levels and sleep pressure follow circadian patterns, this mechanism may synchronize brain adaptability with behavioral cycles such as rest and activity. The research provides new insight into how the brain coordinates energy use, neural signaling, and learning capacity across the day.

Yuki Donen et al, Diurnal modulation of optogenetically evoked neural signals, Neuroscience Research (2025). DOI: 10.1016/j.neures.2025.104981

Part 2

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 8:12am

The flexible brain: How circuit excitability and plasticity shift across the day

Our brains do not react in a fixed, mechanical way like electronic circuits. Even if we see the same scene every day on our commute to work, what we feel—and whether it leaves a lasting impression—depends on our internal state at that moment. For example, your commute may be a blur if you're too tired to pay attention to your surroundings.

The 24-hour cycle that humans naturally follow is one of the factors that shapes the brain's internal environment. These internal physiological cycles arise from the interplay between the body's intrinsic circadian clock and the external light-dark cycle that synchronizes it. Yet how such daily fluctuations influence brain chemistry and affect neuronal excitability and plasticity has remained largely unknown.

Now, researchers  have directly observed time-of-day-dependent changes in neural signal responses in the brains of nocturnal rats. Their findings are published in Neuroscience Research.

Using optogenetics, the team activated neurons in the visual cortexes of rats and recorded the resulting electrical activity. This approach allowed precise quantification of neural responsiveness. They found that identical neural stimuli evoked different responses depending on the time of day. Neural activity was reduced at sunrise and enhanced at sunset. Since rats are nocturnal, sunrise represents the period after a night of activity when they are preparing to sleep.

To explore the underlying mechanism explaining why this was occurring, the researchers looked at adenosine, a neuromodulator that accumulates during wakefulness and makes us feel sleepy.

When the researchers blocked the action of adenosine, neural activity at sunrise became disinhibited and enhanced, showing that adenosine helps regulate cortical excitability across the day.

So neural excitability is not constant; it depends on the brain's internal state. 

The results show that even identical neurons can respond differently depending on the time of day, governed by molecules like adenosine that link metabolism, sleep, and neuronal signaling.

Part 1

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 8:07am

Pancreatic cancer forms 'synapses,' scientists discover

Pancreatic cancer cells form pseudosynapses that exploit the nervous system by taking up glutamate via NMDA receptors, triggering calcium influx and sustained signaling that promotes tumor growth and metastasis. Blocking these receptors in mice slowed tumor progression and reduced metastases, suggesting a potential therapeutic target. Similar mechanisms may exist in other tumor types.

Lei Ren et al, Sensory neurons drive pancreatic cancer progression through glutamatergic neuron-cancer pseudo-synapses, Cancer Cell (2025). DOI: 10.1016/j.ccell.2025.09.003

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 8:04am

Paradoxical suppression refers to the attempt to suppress a thought, feeling or behavior and it results in the opposite outcome.

Higher activation in the reward system regions occurred when participants' teams scored against rivals versus non-rivals, suggesting in-group bonding and social identity reinforcement.
The effect is strongest in highly fanatic participants, predicting momentary self-regulatory failure precisely when identity is threatened and accounting for the puzzling ability of otherwise rational individuals to suddenly "flip" at matches.
Clinically, the pattern implies a state-dependent vulnerability whereby a brief cooling-off or removal from triggers might permit the dACC/salience control system to recover.
The same neural signature—reward up, control down under rivalry—likely generalizes beyond sport to political and sectarian conflicts, say the researchers.
The neural results identify mechanisms which may inform communication, crowd management, and prevention strategies around high-stakes events in the reward amplification and control down-regulation under rivalry, they conclude.

Brain Mechanisms across the Spectrum of Engagement in Football Fans: A Functional Neuroimaging Study, Radiology (2025).

Part 2

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 8:01am

Brain activity goes to extremes in soccer fans, neuroimaging reveals

Studying brain patterns in soccer fans, researchers found that certain circuit regions of the brain were activated while viewing soccer matches involving their favorite team, triggering positive and negative emotions and behaviors, according to a new study published in Radiology. The researchers say these patterns could apply to other types of fanaticism as well, and that the circuits are forged early in life.

Soccer is a global phenomenon, and its followers exhibit a broad spectrum of behaviors, from spectatorship to intense emotional engagement, providing a useful model for studying social identity and emotional processing in competitive situations.

Rivalries run deep in the history of sports, and fans can be very protective of their "home" team and favorite players. These same fans run the gamut of emotions watching their team succeed or fail over the course of a game or match, cheering when they score or raging at a bad call. Soccer fans are known for their team loyalty and enthusiasm, particularly in Europe and South America.

Soccer fandom provides a high-ecological-validity model of fanaticism with quantifiable life consequences for health and collective behaviour.

For the study, researchers used functional MRI (fMRI)—a technique that measures brain activity by detecting changes in blood flow—to examine 60 healthy male soccer fans (20–45 years) of two historical rivals. Fanaticism was quantified with the Football Supporters Fanaticism Scale, a 13-item scale that measures the fanaticism of football fans, assessing two sub-dimensions: "Inclination to Violence" and "Sense of Belongingness."

Brain imaging data were acquired while participants watched 63 goal sequences from matches involving their favorite team, a rival or a neutral team.

A whole-brain analysis was conducted to compare neural responses when participants viewed their favorite team scoring against an archrival (significant victory) versus when the archrival scored against their team (significant defeat), with control conditions for non-rival goals.

The fMRI results showed that brain activity changed when the fan's team succeeded or failed.

Rivalry rapidly reconfigures the brain's valuation–control balance within seconds. With significant victory, the reward circuitry in the brain is amplified relative to non-rival wins, whereas in significant defeat the dorsal anterior cingulate cortex (dACC)—which plays an important role in cognitive control—shows paradoxical suppression of control signals.

Part 1

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 7:39am

Turning up the power further, something curious happened: less frost jumped away, reducing to only 30% removal at 1,100 volts and 20% at 5,500 volts. The results contradicted the theoretical model, which predicted that the performance should continually improve with increasing voltage.

The team found a possible explanation for this plunge in frost removal at higher voltages. When growing frost on an insulating glass substrate, rather than a copper one, the higher voltages performed only slightly worse. This indicated that charge leakage from the polarized frost into the underlying substrate was occurring, especially at high voltages, which could be mitigated by using a more insulating surface.
Upgrading again to an air-trapping superhydrophobic substrate, now the highest voltage removed the most frost, as initially expected. Turning up the voltage now ripped off up to 75% of the frost.
This concept of electric deicing is still in a very early stage.
The research continues, toward the eventual goal of 100% ice removal. Part of this research will include the removal of frost on multiple types of surfaces, expanding the potential applications across both industrial and consumer use.

 Small Methods (2025). DOI: 10.1002/smtd.202501143

Part 2

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 7:36am

Electrostatic defrosting removes ice without heat or chemicals

During winter months, frost can unleash icy havoc on cars, planes, heat pumps, and much more. But thermal defrosting with heaters is very energy intensive, while chemical defrosting is expensive and toxic to the environment.

Now a research team may have found a new and improved method for deicing:

to combat ice by exploiting its own physics instead of using heat or chemicals, creating methods of frost removal that are more cost effective and environmentally friendly.

Their previous work leveraged the small amount of voltage that naturally exists within frost to polarize a nearby water film, creating an electric field that could detach microscopic ice crystals.

Now the team is amping up this concept by applying a high voltage to an opposing electrode to more forcibly dislodge frost from its surface. The result is a new method the team has named "electrostatic defrosting" (EDF). The approach to creating it has been published in Small Methods.

As frost crystals grow, the water molecules arrange into a tidy ice lattice. But sometimes a water molecule lands a little off-pattern—maybe it has an extra hydrogen nearby (H3O+) or is missing one entirely (OH–). These tiny errors create what scientists call ionic defects: places in the frost where there is a bit too much positive or negative charge.

The team hypothesized that when applying a positive voltage to an electrode plate held above the frost, the negative ionic defects would become attracted and "migrate" to the top of the frost sheet, while the positive ionic defects would be repelled and migrate toward the base of the frost.

In other words, the frost would become highly polarized and exhibit a strong attractive force to the electrode. If this attractive force is strong enough, frost crystals could fracture off and jump into the electrode.

Even without any applied voltage, the overhanging copper plate removed 15% of the frost. This is because frost can weakly self-polarize even without any applied electric field. However, applying voltage dramatically boosts the extent of polarization. When the team turned on 120 volts of power, 40% of the frost was removed. At 550 volts, 50% was removed. Part 1

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 7:26am

How climate change increased the risk of earthquakes in East Africa

Climate change is accelerating continental rifting, the geological process where landmasses slowly pull apart. According to a new study published in the journal Scientific Reports, the East African Rift System (EARS) became more tectonically active after its major lakes shrank due to a drier climate 4,000 to 6,000 years ago. This could have caused more frequent earthquakes and volcanic eruptions.

Researchers studied the Lake Turkana Basin in northern Kenya. This region is ideal for analyzing how climate and tectonics interact because it lies within the magmatically active eastern part of EARS and has witnessed dramatic lake-level shifts.

Scientists examined 27 underwater faults by comparing two time periods in the South Turkana Basin. The first was the wetter Late African Humid Period (9,631–5,333 years ago) and the second was the Post-African Humid Period (5,333 years ago to present), when the climate was much drier. Using geological data and computer models, they calculated how the reduced weight of the lake water affected fault activity.

The researchers discovered that the speed of faulting in the EARS accelerated significantly after the region's major lakes shrank, showing a mean increase of 0.17 mm/year in their slipping rate.

This work provides  the first empirical evidence of increased fault activity in response to climate-induced lake level changes in the East African Rift System over time scales of 10³–10⁴ years and reveal that climate-tectonic interactions are enhanced in magmatically active rift systems.

 James D. Muirhead et al, Accelerated rifting in response to regional climate change in the East African Rift System, Scientific Reports (2025). DOI: 10.1038/s41598-025-23264-9

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 6:58am

How climate change increased the risk of earthquakes in East Africa

Climate change is accelerating continental rifting, the geological process where landmasses slowly pull apart. According to a new study published in the journal Scientific Reports, the East African Rift System (EARS) became more tectonically active after its major lakes shrank due to a drier climate 4,000 to 6,000 years ago. This could have caused more frequent earthquakes and volcanic eruptions.

Researchers studied the Lake Turkana Basin in northern Kenya. This region is ideal for analyzing how climate and tectonics interact because it lies within the magmatically active eastern part of EARS and has witnessed dramatic lake-level shifts.

Scientists examined 27 underwater faults by comparing two time periods in the South Turkana Basin. The first was the wetter Late African Humid Period (9,631–5,333 years ago) and the second was the Post-African Humid Period (5,333 years ago to present), when the climate was much drier. Using geological data and computer models, they calculated how the reduced weight of the lake water affected fault activity.

The researchers discovered that the speed of faulting in the EARS accelerated significantly after the region's major lakes shrank, showing a mean increase of 0.17 mm/year in their slipping rate.

This work provides  the first empirical evidence of increased fault activity in response to climate-induced lake level changes in the East African Rift System over time scales of 10³–10⁴ years and reveal that climate-tectonic interactions are enhanced in magmatically active rift systems.

https://phys.org/news/2025-11-climate-earthquakes-east-africa.html?...

Comment by Dr. Krishna Kumari Challa on November 12, 2025 at 6:53am

Self-reactive T cells may explain why some patients can't reach undetectable HIV levels

Despite the capability of antiretroviral drugs to suppress HIV to undetectable levels, some people living with the human immunodeficiency virus can't reach the goal of viral imperceptibility even with daily doses of the potent medications.

It is a conundrum that has mystified virologists for years, but new research by a team of investigators It is a conundrum that has mystified virologists for years, but new research by a team of investigators.

Based on a study of eight people whose antiretroviral treatment did not drive down HIV to an undetectable level, the  researchers found that constant HIV in the blood is not the result of patients missing medication doses or the virus becoming drug resistant. It persists, they discovered, because of a population of insidious immune components known as "self-reactive CD4⁺ T cells".

These HIV-infected CD4⁺ T cells can release viral RNA that persists in the bloodstream, a phenomenon called nonsuppressible viremia. Simply put, nonsuppressible viremia refers to an ongoing presence of low levels of HIV in the blood.

Antiretroviral therapy halts HIV replication, reducing plasma virus concentrations to below the limit of detection, but it is not curative because of a reservoir of latently infected CD4⁺ T cells," writes lead author of the study, Dr. Fengting Wu, in Science Translational Medicine.

Even with 100% adherence to antiretroviral therapy, a large fraction of people living with HIV have residual viremia. Clinical options for managing nonsuppressible viremia are currently limited.

Even though the viremia may be low, it cannot be controlled by simply upping the dosage of antiretroviral medication. So, despite doctors' best efforts, viral RNA continues to persist in the blood. And more puzzling still, it may take years, even decades, for the viremia to emerge.

All eight patients examined by the researchers had been on long-term antiretroviral treatment for a median of 23 years before developing persistent viremia.

For the patient with the least amount of time on the therapy, it took nine years before nonsuppressible viremia occurred. Another spent 31 problem-free years on the treatment before viremia loomed as an inescapable fact of life. Yet, during the study period, some research participants who had lab-confirmed evidence of nonsuppressible viremia, had no signs of it at all.

Several possibilities could explain the lack of detectable virus production from infected CD4⁺ T cells in some study participants," write the investigators in their paper. "These include a low frequency of infected self-reactive cells, the antigen of interest not being present in the lysate, or the antigen being present at very low concentrations."

Complicating matters further, CD4⁺ T cells make clones of themselves in HIV infection, a process known as clonal expansion. A small fraction of CD4⁺ T cells infected with HIV survive and divide, creating clones of infected cells that form the viral reservoir, the source of the nonsuppressible viremia.

 Fengting Wu et al, Proviruses in CD4⁺ T cells reactive to autologous antigens contribute to nonsuppressible HIV-1 viremia, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adu4643

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