SpaceX continues to dominate the global rocket launch market.
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.”
One person is injured after glue factory explosion, which sparked school evacuations and road closures.
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.
“You can see a very strong modulation, which is always there. As the modulation gets to be more profound, it eventually flattens out, and that’s when the brain reaches the deeper state,” Brown says.
When the amount of drug was reduced, the amplitude of the alpha waves began to increase again.
The researchers also found a distinctive pattern in the slow and delta waves seen in the patients’ EEG readings. Slow and delta oscillations are the slowest brain waves, and as the amount of drug was increased, the frequency of these waves became slower and slower, reflecting a decrease in brain activity.
Memory, a fundamental tool for our survival, is closely linked with how we encode, recall, and respond to external stimuli. Over the past decade, extensive research has focused on memory-encoding cells, known as engram cells, and their synaptic connections. Most of this research has centered on excitatory neurons and the neurotransmitter glutamate, emphasizing their interaction between specific brain regions.
To expand the understanding of memory, a research team led by KAANG Bong-Kiun (Seoul National University, Institute of Basic Science) developed a technology called LCD-eGRASP (local circuit dual-eGRASP) that can label synapses of neural circuits within a specific brain region. The team applied this new technology to identify the local synaptic connections between inhibitory interneurons and engram cells, shedding light on the role of inhibitory interneurons in memory expression.
The researchers targeted basolateral amygdala (BLA), an evolutionarily well-preserved brain region in vertebrates known for controlling positive and negative emotions in animals, especially fear. When a fear-related event occurs, neurons activated during that specific time point become engram cells, encoding the fear memory.
The prediction stems from a project to translate tests currently used in research into aids for routine diagnosis in hospitals.
In a recent study published in Frontiers in Psychology, researchers evaluate the association between paternal mental health and a child’s development during middle childhood.
Study: Longitudinal associations between paternal mental health and child behavior and cognition in middle childhood. Image Credit: PeopleImages.com — Yuri A/Shutterstock.com.