Blog – Page 3

Obesity is a global epidemic and a major cause of morbidity and mortality because it increases the risk for comorbidities, including heart disease and fatty liver disease (MASLD). Rates of these disorders have risen as the world increasingly adopts energy-dense diets and sedentary lifestyles.

Nitric oxide is a gas molecule with pleiotropic actions in the body. These effects of nitric oxide are carried out through its binding to proteins. Too much or too little nitric oxide binding (to key proteins) causes disease.

In a study published in Science Signaling, a research team from University Hospitals and Case Western Reserve University discovered a novel enzyme (SCoR2) that removes nitric oxide from proteins controlling fat build up. Removal of nitric oxide turned on fat synthesis, establishing that SCoR2 is needed to make fat.

Current cardiac screening tools used to prevent myocardial infarction (MI) failed to identify nearly half of people who are at risk for MI, according to a new study. Those patients had low or borderline risk as per both standard and newer risk calculators for atherosclerotic cardiovascular disease (ASCVD). Most developed symptoms within 48 hours before the event, and many would not have been recommended statins or further testing if evaluated 2 days earlier.

Nearly half of adults with a first myocardial infarction show low or borderline risk on current risk estimators. Most develop symptoms only within 48 hours and would not qualify for statins earlier.

Two modeling studies suggest that making more people eligible for lung cancer screening would prevent tens of thousands of deaths in the US each year — but at what cost?

Two new modeling studies suggest that expanding lung cancer screening — to include more smokers or even lifelong nonsmokers — would save thousands more lives in the US every year. But not everyone is convinced the projected benefits would outweigh the harms.

In one study, published in JAMA, researchers at the American Cancer Society (ACS) found that only about 19% of currently eligible Americans underwent lung cancer screening in 2024.

That, the study projected, could translate to roughly 15,000 lung cancer deaths averted over 5 years. But 100% screening uptake would save three times as many lives.

Cao et al. show that Trichoderma harzianum detoxifies fusaric acid into the non-toxic metabolite 10OH-FSA, thereby suppressing disease and fostering beneficial microbial networks. This work reveals toxin neutralization as an ecological strategy for sustainable control of soil-borne plant diseases.

Like a phoenix rising from the ashes, our skin tissue—and in fact many types of epithelial tissue that lines and covers the body’s organs—can respond to death and destruction with a burst of regeneration. This phenomenon, known as compensatory proliferation, was first described in the 1970s in fly larvae, which regrew fully functional wings after their epithelial tissue had been severely damaged by high-dose radiation. Since then, this surprising ability has been documented in many species, including humans, yet its molecular basis has remained unclear.

A new study from the Weizmann Institute of Science, published in Nature Communications, reveals that the very enzymes responsible for cellular destruction—caspases—may also render certain cells resistant to death, enabling damaged tissue not only to regenerate but even to become more resilient.

Unfortunately, this same mechanism may be hijacked by many types of cancer and may help explain why some tumors recur in a more aggressive and treatment-resistant form. The new findings could thus open avenues for therapies that speed up wound repair and help prevent cancer relapse.

A new study published in Science Translational Medicine by researchers at The University of Texas MD Anderson Cancer Center details a therapeutic vulnerability in patients with an aggressive subtype of triple-negative breast cancer.

Led by Khandan Keyomarsi, Ph.D., professor of Experimental Radiation Oncology, the study shows that simultaneous inhibition of ATR and PKMYT1 triggers a type of cell death in Rb1-deficient breast cancer models.

Using genomic profiling, proteomics and patient-derived xenografts, the researchers found that loss of Rb1—a gene important for normal cell division—disrupts DNA repair processes and forces tumor cells to rely on ATR and PKMYT1 dependent pathways for survival, creating a vulnerability that can be selectively targeted.