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To prevent similar incidents from reoccurring in the future, Cloudflare has improved credential logging and verification and now mandates the use of automated deployment tooling to avoid human errors.

The company is also updating standard operating procedures (SOPs) to require dual validation for high-impact actions like credential rotation and plans to enhance health checks for faster root cause detection.

Cloudflare’s R2 service suffered another 1-hour long outage in February, which was also caused by a human error.

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Study coauthors include UC’s Sreekar Puchala and Anca Ralescu and Ethan Muchnik of the University of Oregon. The study authors declare no competing interests.

This work was supported by the Office of the Assistant Secretary of Defense for Health Affairs, through the Defense Medical Research and Development Program under Award No. W81XWH-16–2–0020. Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the Department of Defense.

The researchers turned to a group of molecules called acylcarnitines, which are associated with declining cognition and breaking down or metabolizing fats and proteins for energy. To test if high acylcarnitine levels in the blood could predict who’s at risk of developing Alzheimer’s, the researchers used data from a large-scale study called the Alzheimer’s Disease Neuroimaging Initiative.

“It was fascinating,” the author said. “Dividing research participants into groups based on their specific acylcarnitine levels highlighted people with more severe Alzheimer’s disease and others with fewer symptoms.” This led the researchers to define a bioenergetic clock based on acylcarnitines—how old a person’s metabolism acts, compared to actual age. Higher bioenergetic age is linked to higher acylcarnitine levels, worsened Alzheimer’s pathology, cognitive decline and brain atrophy.

The researchers also quantified cognitive decline using a common test called the mini-mental state examination, on which a score below 24 out of 30 points indicates impairment. They found that people with low acylcarnitine levels to begin with declined more slowly, losing about 0.5 points less per year than people with high acylcarnitine levels. The benefit is on par with the Alzheimer’s drug lecanemab.

To some degree, a person’s bioenergetic clock ticks forward at a rate determined by their genetics, but having a healthy lifestyle—for example, eating a plant-based diet and exercising —can help keep acylcarnitine levels low, which means a younger bioenergetic age, the author explained.

They went on to identify a subgroup of participants, about 30% of the Alzheimer’s Disease Neuroimaging Initiative, with older bioenergetic age but favorable genetic background. These individuals may benefit more from early lifestyle interventions designed to decrease their bioenergetic age and potentially delay or prevent the onset of Alzheimer’s.

Moving forward, the senior author hopes to home in on the lifestyle interventions most effective for lowering bioenergetic age. For example, eating a low-carb diet may help maintain metabolic health, but just how low would carbohydrate consumption have to be for a person to see benefits?


A drug-resistant type of bacteria that has adapted to health care settings evolved in the past several years to weaponize an antimicrobial genetic tool, eliminating its cousins and replacing them as the dominant strain. University of Pittsburgh School of Medicine scientists made the discovery when combing through local hospital data—and then confirmed that it was a global phenomenon.

The finding, published in Nature Microbiology, may be the impetus for new approaches in developing therapeutics against some of the world’s deadliest . It also validates a new use for a system developed at Pitt and UPMC that couples genomic sequencing with computer algorithms to rapidly detect infectious disease outbreaks.

“Our lab has a front row seat to the parade of pathogens that move through the ,” said senior author Daria Van Tyne, Ph.D., associate professor of medicine in Pitt’s Division of Infectious Diseases. “And when we took a step back and zoomed out, it quickly became apparent that big changes were afoot with one of the world’s more difficult-to-treat bacteria.”

Additional experiments revealed that mice given access to an exercise wheel or treated with antidepressants also exhibited increased CB1 receptor levels in astrocytes. Furthermore, analysis of human brain tissue from the Douglas-Bell Canada Brain Bank indicated that individuals with major depression had lower astrocytic CB1 receptor levels compared to those without depression or those who had received antidepressant treatment.

Implications for mental health interventions

These findings raise the possibility of developing treatments that selectively activate CB1 receptors in astrocytes to mitigate anxiety and depression. However, the challenge remains in limiting activation to astrocytes, as prolonged CB1 receptor stimulation in neurons can lead to side effects affecting alertness, anxiety and appetite. Until targeted pharmacological interventions become available, engaging in physical activity may help protect against stress-related mental health conditions by enhancing CB1 receptor expression.