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Comment by Dr. Krishna Kumari Challa 13 hours ago

Why some people are more resistant to developing blood cancer even when they carry cancer-risk mutations

Blood cancer is an umbrella term for a variety of diseases that affect the blood, bone marrow and lymphatic system. Like most cancers, the cause is usually mutations in the DNA, which are genetic errors that accumulate as we age. However, some people are more resistant to developing blood cancer even when they carry cancer-risk mutations.

In a new study published in the journal Science, researchers discovered why. They identified a rare genetic variant that reduces the risk of several blood cancers, including leukemia, by slowing down a process called clonal hematopoiesis (CH).

CH occurs when a hematopoietic stem cell, which can develop into any type of blood cell, mutates and grows into a large population of identical mutated cells.

In their study, the team performed a large-scale analysis (known as a GWAS meta-analysis) of more than 640,000 individuals. By comparing 43,000 people with CH mutations to 600,000 without them, they pinpointed the genetic variant that protects against CH.

The researchers identified a noncoding regulatory variant, rs17834140-T, on chromosome 17q22.

The experiments revealed that rs17834140-T reduces the amount of a protein called MSI2, which acts as a growth booster in stem cells. In cancer, MSI2 causes mutated cells to multiply rapidly and take over the bone marrow. However, the protective variant results in lower levels of the protein, forcing these mutated cells to grow much more slowly and reducing their chances of progressing to leukemia. According to the study authors, people with the variant have up to a 30% lower risk of developing CH.

The research could lead to new ways to prevent cancer even before it starts. Now that we know that lowering MSI2 is protective, scientists may be able to develop drugs or other therapeutic approaches that mimic or enhance this natural protection.

Gaurav Agarwal et al, Inherited resilience to clonal hematopoiesis by modifying stem cell RNA regulation, Science (2026). DOI: 10.1126/science.adx4174

Francisco Caiado et al, Genetic resistance to leukemia, Science (2026). DOI: 10.1126/science.aed5244

Comment by Dr. Krishna Kumari Challa 13 hours ago

Patient-reported fatigue before cancer treatment was associated with increased risk of severe, life-threatening, and fatal adverse events during treatment.
Pre-treatment fatigue assessments could be seen as an early marker of vulnerability that could inform treatment strategies and symptom monitoring.

Joseph M. Unger et al, Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy, JAMA Oncology (2025). DOI: 10.1001/jamaoncol.2025.5549

Part 2

Comment by Dr. Krishna Kumari Challa 13 hours ago

Fatigue before cancer treatment linked to adverse events

Investigators found that higher patient-reported fatigue before cancer treatment aligned with higher odds of severe, life-threatening, and fatal treatment-related toxic effects.

Cancer-related fatigue harms quality of life and is a persistent tiredness or exhaustion tied to cancer or cancer treatment. It interferes with usual physical and mental functioning and does not match the patient's normal recent activity. Patients report that fatigue is among the most distressing symptoms of cancer and its treatment, yet physicians routinely underreport fatigue.

Some studies have suggested prevalence ranging from 25% to 50%. Separate estimates place moderate fatigue at 25% and severe fatigue at 15% to 20%, levels often associated with poor performance status.

In the study, "Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy," published in JAMA Oncology, researchers pooled baseline fatigue data to evaluate associations between pretreatment fatigue and subsequent adverse events in cancer treatment trials.

Across 17 trials, 103,738 adverse events were recorded. Higher baseline fatigue aligned with higher odds of severe toxic effects. Some or greater baseline fatigue, compared with less than some fatigue, yielded an odds ratio of 2.11 for grade 3 or higher toxic effects and 1.98 for life-threatening toxic effects.
Comparison between quite a lot or very much fatigue and no baseline fatigue produced an odds ratio of 4.99 for grade 5 toxic effects.
Fatal toxic effects were uncommon, though risk rose with higher fatigue to an odds ratio of 2.35.
Severe or worse toxic effects occurred in 34.2% of patients reporting no fatigue, 39.4% reporting a little fatigue, 52.8% reporting some fatigue, and 58.3% reporting quite a lot or very much fatigue.
Subset analyses did not show statistically significant differences in the fatigue to adverse event association by age, sex, race, ethnicity, or obesity status.
Cancer stage mattered in subgroup patterns. Advanced-disease trials showed clearer monotonic relationships between baseline fatigue and adverse events, while adjuvant or early-stage trials did not show statistically significant associations for grade 3 or higher or grade 4 or higher adverse events.

Part 1

Comment by Dr. Krishna Kumari Challa 13 hours ago

Researchers modeled four mitigation approaches that included plastic substitution or recycling, critical-metal substitution, modular designs for reuse and replacement, and a transition to green energy.

Chuanwang Yang et al, Quantifying the global eco-footprint of wearable healthcare electronics, Nature (2025). DOI: 10.1038/s41586-025-09819-w

Part3

Comment by Dr. Krishna Kumari Challa 13 hours ago

A single continuous glucose monitor from production to use carried a carbon footprint equivalent to about 2 kg CO2-equivalent, or driving a gas-powered car for around 5 miles. More than 95% of that impact was attributed to printed circuit boards and semiconductors inside the device, tied to energy required to purify raw materials and power manufacturing processes.

Single glucose monitor use lasted 14 days before being discarded and replaced. Repetition of that short cycle has stacked impacts across the scale of users. Wearable glucose monitor sales are estimated to exceed 1.4 billion devices a year by 2050.

Expected greenhouse-gas emissions from these units alone were around 2.7 million metric tons CO2-equivalent annually.

Per-device warming impacts ranged from 1.06 kg CO2-equivalent for a blood pressure monitor to 6.11 kg CO2-equivalent for a point-of-care ultrasound patch. Values of 1.30 kg CO2-equivalent for a continuous electrocardiogram monitor.

Annualized warming impacts, accounting for typical replacement frequencies, were 0.5 kg CO2-equivalent for the blood pressure monitor, 33.8 kg CO2-equivalent for the continuous electrocardiogram monitor, 50.6 kg CO2-equivalent for the non-invasive continuous glucose monitor, and 6.1 kg CO2-equivalent for the point-of-care ultrasound patch.

Greenhouse-gas emissions from all wearables in the model were 3.4 million metric tons CO2-equivalent annually, or about the carbon footprint of the transport sector of Chicago. Component-level analysis placed flexible printed circuit board assemblies at the center of warming impacts across all four devices, with hotspots tied to gold in integrated circuits, silicon wafers, polyimide, and batteries.
part 2

Comment by Dr. Krishna Kumari Challa 13 hours ago

The hidden carbon footprint of wearable health care

 Researchers analyzed wearable health care electronics and reported carbon impacts of 1.1–6.1 kg CO₂-equivalent per device. With global device consumption projected to rise 42-fold by 2050, approaching 2 billion units annually, their moderate projection adds 3.4 million metric tons of CO₂-equivalent emissions alongside ecotoxicity and e-waste.

Wearable electronics—glucose, heart and blood pressure monitors, integrated into patches, chest straps, clothes and smartwatches—are transforming health care through real-time monitoring, device interaction, and therapeutic interventions.

Compared with rigid consumer electronics, wearable health care systems—ranging from biophysical and biochemical sensors to e-textiles and biointegrated therapeutics—offer high compliance and continuous tracking and intervention capabilities.

With wireless integration, wearable health care electronics are evolving into digital infrastructure networks adopted globally by patients, older people, athletes, and health-conscious people.

Reliance on energy-intensive manufacturing, hazardous chemicals, fossil-based plastics, and critical metals can lead to substantial carbon emissions, ecological risks, and e-waste issues. Rising energy demands from artificial-intelligence-driven data processing and advanced digital infrastructures further enlarge the eco-footprint of even the smallest devices.

In the study, "Quantifying the global eco-footprint of wearable health care electronics," published in Nature, researchers integrated life-cycle assessment with forecasting adoption growth over time to quantify global eco-footprint hotspots and evaluate mitigation strategies.

Four devices anchored the assessment—a non-invasive continuous glucose monitor, a continuous electrocardiogram monitor, a blood pressure monitor, and a point-of-care ultrasound patch. Selection criteria included clinical relevance, diversity of sensing modalities, and coverage across an expanding technology spectrum.

Cradle-to-grave attributional life-cycle assessment covered raw-material acquisition, manufacturing, transportation, use, and end-of-life disposal. Monte Carlo simulation quantified uncertainty for environmental impacts, and diffusion modeling projected future scale of use.

Part 1

Comment by Dr. Krishna Kumari Challa yesterday

Roads can become more dangerous on hot days—especially for pedestrians, cyclists and motorcyclists

Road injury risk increases significantly on very hot days, with pedestrians, cyclists, and motorcyclists facing the greatest danger due to direct heat exposure. The risk rises sharply above 30°C, with pedestrian injuries more than doubling and cyclist and motorcyclist injuries increasing by 80% and 50%, respectively. Heat also elevates crash severity and fatality risk, especially on rural roads and among older drivers. Effects can persist for days due to fatigue and sleep disruption.

During heat waves, everyday life tends to feel more difficult than on an average day. Travel and daily movement are no exception.

But while most of us know rain, fog and storms can make driving conditions challenging, not many people realize heat also changes transport risk. At very high temperatures, overall crash risk is about 15% higher than on cool days.

In particular, research evidence consistently suggests roads, trips and daily commutes can become more dangerous on very hot days compared with an average day. Road injury risk rises much more steeply once temperatures move into the 30°C–40°C range.

Importantly, the increase is even larger for crashes linked to driver fatigue, distraction or illness.

Ambient temperature and risk of motor vehicle crashes: A countrywid...

Heat waves and fatal traffic crashes in the continental United Stat...

Comment by Dr. Krishna Kumari Challa yesterday

Genetic study uncovers unknown causes of blindness

Researchers have discovered new genetic causes of inherited blindness. Their study, published in Nature Genetics, shows that changes in specific pieces of DNA, which play a role in processing genetic information, can lead to retinitis pigmentosa.

This eye condition affects about one in 5,000 people worldwide, causing "tunnel vision" and often leads to legal blindness. The discovery provides clarity for dozens of families globally and opens new possibilities for diagnostics and counseling in hereditary conditions.

Retinitis pigmentosa (RP) is a disorder in which the rod and cone cells in the retina gradually die. Affected individuals first experience night blindness, followed by tunnel vision. Some eventually lose their sight completely.

Although more than a hundred genes are known to cause RP, in 30 to 50% of patients the genetic cause remains unresolved, even after extensive DNA testing. Researchers have now solved part of this puzzle.

Researchers found a variation in the gene RNU4-2. The change occurs in a special gene, RNU4-2, which does not produce a protein but only RNA. RNA from such genes associate with proteins and other RNAs and the whole resulting complex assists in editing genetic information (splicing), a step required before a cell can make proteins.

Other changes in RNU4-2 were recently linked to developmental disorders.

This breakthrough goes beyond these specific genetic variants causing RP. It shows that we should also look beyond protein-coding genes.

De novo and inherited dominant variants in U4 and U6 snRNA genes cause retinitis pigmentosa, Nature Genetics (2026). DOI: 10.1038/s41588-025-02451-4

Comment by Dr. Krishna Kumari Challa yesterday

Comment by Dr. Krishna Kumari Challa on Friday

Cancer Immunotherapy May Work Better Before 3PM

People with cancer receiving immunotherapy earlier in the day survived longer, suggesting that adjusting treatment timing may improve outcomes.

Mounting evidence suggests that the time of day at which cancer patients receive treatment could impact their outcomes. This effect is likely due to the circadian rhythm-dependent fluctuations in the function of immune cells as well as proteins that regulate their function, also called checkpoints.

In line with this, in a recent meta-analysis, researchers found that patients with various types of advanced cancer who underwent immune checkpoint inhibitor (ICI) infusions earlier in the day survived longer than their counterparts treated in the late afternoons or evenings.

In a new study, researchers discovered that patients with a highly aggressive lung cancer who received treatment before 3PM survived significantly longer than their counterparts who were treated later in the day.

Landré T, et al. Effect of immunotherapy-infusion time of day on survival of patient.... ESMO Open. 2024;9(2):102220.

Huang Z, et al. Overall survival according to time-of-day of immunochemotherapy for.... Cancer. 2025.

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