Lifeboat Foundation

The AI tool can indicate the risk of heart attacks, as well as information on narrowings of the arteries and other clinical risk factors.

Stevanovicigor/ iStock.

In a development that could help the people at risk, an artificial intelligence technology has been created that can gaze into the future and predict the 10-year risk of deadly heart attacks.

Colon cancer remains a leading cause of cancer-related deaths, and there has been a rise in the incidence of early-onset colon cancer or colon cancer diagnosed before the age of 50 years old. Early-onset colon cancer has several differences in clinical presentation, as well as histopathology, genetic alteration, and molecular profiling. Early-onset colon cancer can be differentiated into familial type that includes hereditary familial syndrome and sporadic type. Demographic variance also exists in both developing and developed countries. Due to the rising incidence of colon cancer diagnosed in younger age, it is imperative to examine the available evidence regarding the mortality rate of early-onset colon cancer. Colon cancer is affected by numerous modifiable and non-modifiable risk factors.

At Oak Ridge National Laboratory (ORNL), quantum biology, artificial intelligence, and bioengineering have collided to redefine the landscape of CRISPR Cas9 genome editing tools. This multidisciplinary approach, detailed in the journal Nucleic Acids Research, promises to elevate the precision and efficiency of genetic modifications in organisms, particularly microbes, paving the way for enhanced production of renewable fuels and chemicals.

CRISPR is adept at modifying genetic code to enhance an organism’s performance or correct mutations. CRISPR Cas9 requires a guide RNA (gRNA) to direct the enzyme to its target site to perform these modifications. However, existing computational models for predicting effective guide RNAs in CRISPR tools have shown limited efficiency when applied to microbes. ORNL’s Synthetic Biology group, led by Carrie Eckert, observed these disparities and set out to bridge the gap.

“A lot of the CRISPR tools have been developed for mammalian cells, fruit flies, or other model species. Few have been geared towards microbes where the chromosomal structures and sizes are very different,” explained Eckert.

Boston, MA—We’ve known for more than a century that women outlive men. But new research led by Harvard T.H. Chan School of Public Health and UC San Francisco shows that, at least in the United States, the gap has been widening for more than a decade. The trend is being driven by the COVID-19 pandemic and the opioid overdose epidemic, among other factors.

In a research paper, to be published online on November 13 in JAMA Internal Medicine, the authors found the difference between how long American men and women live increased to 5.8 years in 2021, the largest it’s been since 1996. This is an increase from 4.8 years in 2010, when the gap was at its smallest in recent history.

The pandemic, which took a disproportionate toll on men, was the biggest contributor to the widening gap from 2019–2021, followed by unintentional injuries and poisonings (mostly drug overdoses), accidents, and suicide.

A pair of studies from the laboratory of Evangelos Kiskinis, Ph.D., associate professor in the Ken and Ruth Davee Department of Neurology’s Division of Neuromuscular Disease and of Neuroscience, have uncovered novel cellular mechanisms that are involved in two types of genetic amyotrophic lateral sclerosis, or ALS.

The findings, published in Science Advances and Cell Reports, improve the understanding of ALS, a progressive neurodegenerative disease that attacks motor neurons in the brain and spinal cord, and provides support for the future development of targeted therapies.

An estimated 32,000 individuals are currently living with ALS in the U.S., according to the Les Turner ALS Foundation. There are two types of ALS: sporadic (non-genetic), which makes up more than 90% of all ALS cases, and familial (genetic).

Nephrologists — know the CTRX encephalopathy risk in ESRD patients. This case of a hemodialysis patient found blood and CSF concentrations 10 times usual — dose adjustment may be needed. Monitor for neuro changes when using CTRX in renal failure. pharmacology.

Ceftriaxone (CTRX) does not require dose adjustment based on the renal function status and is used to treat infections. Recently, several studies reported the incidence of antibiotic-associated encephalopathy due to CTRX in patients with end-stage renal disease (ESRD). We experienced a case of CTRX-related encephalopathy in a patient on hemodialysis. When CTRX-related encephalopathy was discovered, the CTRX concentrations were measured in the blood and cerebrospinal fluid (CSF). The highest blood and CSF CTRX concentrations in this patient were 967 and 100.7 μg/mL, respectively, which were approximately 10 times higher than the CSF concentrations in a previously evaluated patient with CTRX encephalopathy. The concentration of CTRX may be increased in patients with ESRD. Hence, encephalopathy must be suspected in this patient group when CTRX is used.

The wait time for a heart transplant is long — from many months to over a year. Some patients will never get the transplant they need.

But researchers may have come up with an artificial heart solution: a titanium, pumpless, device with spinning magnets — and it looks nothing like a bonafide heart.

The problem: Heart failure affects over six million people every year in the U.S., and treatment options are slim. Medication can help, but some people need a heart transplant for a full recovery. Still, donor hearts are hard to come by. The number of people who need a heart far exceeds what’s available. And, donor hearts aren’t one-size-fits-all. The blood type and size need to be just right.

Having healthy mitochondria, the organelles that produce energy in all our cells, usually portends a long healthy life whether in humans or in C. elegans, a tiny, short-lived nematode worm often used to study the aging process.

Researchers at the Buck Institute have identified a new drug-like molecule that keeps mitochondria healthy via mitophagy, a process that removes and recycles damaged mitochondria in multicellular organisms. The compound, dubbed MIC, is a natural compound that extended lifespan in C. elegans, ameliorated pathology in neurodegenerative disease models of C. elegans, and improved mitochondrial function in mouse muscle cells. Results are published in the November 13, 2023, edition of Nature Aging.

Defective mitophagy is implicated in many age-related diseases. It’s tied to neurodegenerative disorders such as Parkinson’s and Alzheimer’s; it plays a role in cardiovascular diseases including heart failure; it influences metabolic disorders including obesity and type 2 diabetes; it is implicated in muscle wasting and sarcopenia and has a complex relationship with cancer progression.

The AI tools were complemented by quantum biology and bioengineering approaches.

Philip Gray/ORNL, U.S. Dept. of Energy.

Combining several advances.

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