Lifeboat Foundation

A first-of-its-kind flexible sensor turns a pair of earbuds into a device capable of recording brain activity and analyzing sweat, making them useful for diagnosing diseases and health monitoring.

The background: Health monitoring wearables can measure our blood pressure, track our heart rates, and even detect infections before we start to feel sick, helping us take better care of ourselves and potentially even giving us a way to prevent the spread of diseases.

The devices are useless if no one wants to wear them, though, so finding designs that are comfortable and easy to integrate into daily life is key. Because earbuds are already popular, researchers have used them as the basis for health monitoring devices that record brain activity to predict strokes, epileptic seizures, or Parkinson’s disease.

Research published in Science Advances is the first to use a sophisticated human tissue model to explore the interaction between host and pathogen for six common species that cause urinary tract infections. The findings suggest that the “one size fits all” approach to diagnosis and treatment currently used in most health care systems is inadequate.

Urinary tract infection (UTI) is a growing problem, with around 400 million global cases per year and an estimated 250,000 UTI-related deaths associated with antimicrobial resistance (AMR). Although UTI is often perceived as a simple bacterial infection, 25–30% of UTIs recur within six months despite antibiotic therapy for reasons that are poorly understood.

A condition that primarily affects women, UTI has been historically understudied and underfunded, with no improved anti-infective treatments introduced since Alexander Fleming discovered antibiotics nearly a century ago. Diagnosis primarily rests on the midstream urine culture method (dipstick test), an early 20th century technique that is known to miss many infections.

Researchers at Weill Cornell Medicine have uncovered a novel route to stimulate the growth of healthy insulin-producing pancreatic beta cells in a preclinical model of diabetes. The findings hold promise for future therapeutics that will improve the lives of individuals with type 2 diabetes—a condition that affects more than half a billion people worldwide.

This study, published in the Journal of Clinical Investigation on Sept. 15, demonstrated that activating a pathway to promote cell division not only expanded the population of insulin-producing cells, but surprisingly, it also enhanced the cells’ function.

“That’s reassuring because there is a long-standing belief in the field that proliferation can lead to ‘de-differentiation’ and a loss of cell function,” said study senior author Dr. Laura Alonso, chief of the division of endocrinology, diabetes and metabolism, director of the Weill Center for Metabolic Health, and the E. Hugh Luckey Distinguished Professor in Medicine at Weill Cornell Medicine. “Our result flies in the face of that dogma and suggests if we can find a way to trigger replication of the beta cells in the body, we won’t impair their ability to produce and secrete insulin.”

Thyrotoxicosis was associated with 39% higher risk for cognitive disorders.

Thyrotoxicosis, defined as a low level of serum thyroid-stimulating hormone (TSH), can result from either a primary thyroid disorder (endogenous) or overtreatment of hypothyroidism (exogenous). Evidence suggests that thyrotoxicosis is a risk factor for dementia. In this U.S. longitudinal cohort study, researchers used data from electronic health records for 66,000 people (median age, 68) without low TSH levels or cognitive disorders at baseline and evaluated whether development of thyrotoxicosis was associated with excess risk for cognitive disorders.

During the study period (2014 to 2023), 2,700 patients had low TSH levels (60% exogenous), and 4,800 patients received diagnoses of cognitive disorders. The incidence of cognitive disorders among patients with and without thyrotoxicosis were 11% and 6% at age 75, and 34% and 26% at age 85. Adjusted for multiple variables, all-cause thyrotoxicosis was associated with a significant 39% excess risk for cognitive disorders. Exogenous thyrotoxicosis — and in particular, severe exogenous thyrotoxicosis (TSH 0.1 mIU/L) — were associated most strongly with excess risk for cognitive disorders.

While we all aspire for a long lifespan, what is most coveted is a long period of vigor and health, or “healthspan,” that precedes the inevitable decline of advancing age. Researchers at UC Santa Barbara have discovered that instruments of death that cells use to commit suicide when things go wrong contribute to making a longer and healthier life by revitalizing the specialized cellular compartments called mitochondria.

Mitochondria generate the energy for all of our activities, from movement to thought. These power plants inside our cells descended from what were once free-living bacteria.

“We are a sort of hybrid creature that arose from two independent evolutionary lineages: mitochondria, which were once bacteria, and the rest of the cell surrounding them,” notes Joel Rothman, a professor of molecular biology whose lab conducted the research.

UCLA scientists have developed a new method to engineer more powerful immune cells that can potentially be used for “off-the-shelf” cell therapy to treat challenging cancers.

“Off-the-shelf” cell therapy, also known as allogenic therapy, uses immune cells derived from healthy donors instead of patients. The approach can bring cell therapies, like chimeric antigen receptor (CAR) T cell therapy, to more patients in a timelier manner, which is one of the major barriers in getting these life-saving treatments to patients.

“Time is often of the essence when it comes to treating people with advanced cancers,” said Lili Yang, associate professor of microbiology, immunology and molecular genetics and member of the UCLA Health Jonsson Comprehensive Cancer Center. “Currently, these types of therapies need to be tailored to the individual patient. We have to extract white blood cells from a patient, genetically engineer the cells and then re-infuse them back into the patient. This process can take weeks to months and can cost hundreds of thousands of dollars to treat each patient.”

In nationwide projections, elderly and Black adults are most at risk for cardiovascular death due to extreme heat, finds a new study. Cardiovascular deaths from extreme heat in the U.S. may more than double by the middle of the century. Without reductions in greenhouse gas emissions, that number could even triple, according to new research published today in the American Heart Association’s flagship journal Circulation.

“Climate change and its many manifestations will play an increasingly important role on the health of communities around the world in the coming decades,” said lead study author Sameed Khatana, M.D., M.P.H., assistant professor of medicine at the University of Pennsylvania and a staff cardiologist at the Philadelphia Veterans Affairs Medical Center, both in Philadelphia. “Climate change is also a health equity issue as it will impact certain individuals and populations to a disproportionate degree and may exacerbate preexisting health disparities in the U.S.”

How much and how quickly greenhouse gas emissions increase in the next decades will determine the health impacts of extreme heat. More aggressive policies to reduce greenhouse gas emissions have the potential to reduce the number of people who may experience the adverse health effects of extreme heat, according to Khatana.

Researchers with the Translational Research in Neuroimaging and Data Science (TReNDs) Center at Georgia State have identified important new methods for accurately identifying possible biomarkers in adolescent brains that can reliably predict cognitive developments and psychiatric issues.

A new study, published in Nature Mental Health, represents the first large-scale analysis of its kind in which researchers analyzed functional network connectivity (FNC) across scans and identified associations with a diverse range of health measures in children. Researchers believe that inferences about early cognitive and psychiatric behaviors in children may be made using these intra-subject variabilities as a useful biomarker.

Researchers studied four scans from more than 9,000 subjects ages 9 to 11.

In a small study, researchers at the National Institutes of Health have found that positron emission tomography (PET) scans of the heart may identify people who will go on to develop Parkinson’s disease or Lewy body dementia among those at-risk for these diseases.

The findings, published in the Journal of Clinical Investigation and led by scientists at the National Institute of Neurological Disorders and Stroke (NINDS), part of NIH, may advance efforts to detect the earliest changes that years later lead to Parkinson’s disease and Lewy body dementia.

In 34 people with Parkinson’s disease risk factors, researchers conducted PET scans of the heart to gain insight into levels of the neurotransmitter norepinephrine. They found that the scans could distinguish individuals who would later be diagnosed with Parkinson’s or Lewy body dementia—both are brain diseases caused by abnormal deposits of the protein alpha-synuclein that form clumps known as Lewy bodies. The research was conducted at the NIH Clinical Center, currently the only location for ¹⁸ F-dopamine PET scanning.