In this systematic review and meta-analysis of EDI initiatives in health care institutions, programs were associated with an increased workforce diversity.
This systematic review and meta-analysis assesses equity, diversity, and inclusion initiatives in health care institutions that aimed to promote a more inclusive and equitable health care culture for individuals who beloing to racial and ethnic minority groups.
A new study published in the journal Social Cognitive and Affective Neuroscience provides evidence that the human brain processes romantic partners differently than close friends, specifically within the reward system. The research suggests that while the brain creates a unique neural signature for a partner early in a relationship, this distinction tends to fade as the bond matures. These findings offer insight into how the biological drivers of romantic love may evolve from passion to companionship over time.
Relationships involve complex psychological states that differentiate a committed partner from a platonic friend. Scientists have sought to map these differences in the brain to understand the biological foundations of human bonding. Much of this research focuses on the nucleus accumbens. This small region deep within the brain, which relies heavily on the neurotransmitter dopamine, plays a central role in processing rewards and motivation.
Evidence from animal studies indicates that the nucleus accumbens is essential for forming pair bonds. Research on monogamous prairie voles shows that neurochemical signaling in this area drives the preference for a specific partner. The brain appears to undergo plastic changes that reinforce the bond.
Paulsen et al. present the process development and clinical application of an hiPSC-derived OSC product, Fertilo. They describe the raw material upgrades, process consistency and reproducibility, and analytical assessment required for the generation of a clinically suitable product, as well as favorable outcomes from the first-in-human application of Fertilo.
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Ovarian cancer kills more women than any other gynecological cancer. Most patients receive their diagnosis only after the disease spreads throughout the abdomen. Until now, scientists have never fully understood why this cancer advances so fast.
A new study led by Nagoya University explains why. Published in Science Advances, the study shows that cancer cells recruit help from protective mesothelial cells that normally line the abdominal cavity. Mesothelial cells lead the invasion and cancer cells follow the pathways they create. These hybrid cell clusters resist chemotherapy better than cancer alone.
Researchers examined abdominal fluid from ovarian cancer patients and found something unexpected. Cancer cells do not float alone in the abdominal cavity. Instead, they often grab onto mesothelial cells and form hybrid spheres. About 60% of all cancer spheres contain these recruited mesothelial cells. The cancer cells release a protein called TGF-β1 that transforms the mesothelial cells and causes them to develop spike-like structures that cut through tissue.
In recent years, cancer researchers have made major breakthroughs by using the body’s immune system to fight cancer. One of the most promising approaches, known as immune checkpoint blockade, works by releasing molecular “brakes” on T cells. This allows them to better recognize and attack cancer cells. While these therapies can be very effective for some patients, many solid tumors, including most forms of breast cancer, remain largely unaffected. Cancer Center at Illinois (CCIL) Program Co-leader Erik Nelson and his research group are working to understand why these treatments fail.
Elevated blood concentrations of cholesterol have long been linked to cancer outcomes. In a new study, they found that a protein called ABCA1 is involved in transporting cholesterol out of a type of immune cell called macrophages, and in so-doing shifts them to an “attack cancer” mode.
“Immune based therapies have revolutionized how we can treat cancer, basically taking the brakes off of a type of immune cell called T cells so they can attack cancer,” Nelson said. “While this approach works well for some patients, many so-called solid tumors fail to respond or develop resistance mechanisms.”
A new study has detected a DNA marker in a gene encoding a key enzyme known as cytochrome P450 that helps mosquitoes to break down and survive exposure to pyrethroids, the main insecticides used for treating bed nets. This new finding, published on the bioRxiv preprint server and slated for publication in Science Translational Medicine, will help to better implement insecticide resistance management strategies and contribute to reducing the burden of malaria in sub-Saharan Africa, home to 90% of cases globally.
The work was jointly led by Liverpool School of Tropical Medicine and the Centre for Research in Infectious Diseases (CRID) in Cameroon.
Professor Charles Wondji, Professor of Genetics and Vector Biology at Liverpool School of Tropical Medicine and lead author on the study, said, “Our study designed field-applicable tools to easily track the spread of metabolic resistance in the major malaria mosquito species and assess its impact on control interventions. These important findings can help to maintain the effectiveness of insecticide-based tools such as bed nets, which remain a cornerstone of malaria prevention.”
A study led by the Center for Astrobiology (CAB), CSIC-INTA, using modeling techniques developed at the University of Oxford, has uncovered an unprecedented richness of small organic molecules in the deeply obscured nucleus of a nearby galaxy, thanks to observations made with the James Webb Space Telescope (JWST).
The work, published in Nature Astronomy, provides new insights into how complex organic molecules and carbon are processed in some of the most extreme environments in the universe.
The study focuses on IRAS 07251–0248, an ultra-luminous infrared galaxy whose nucleus is hidden behind vast amounts of gas and dust. This material absorbs most of the radiation emitted by the central supermassive black hole, making it extremely difficult to study with conventional telescopes.
A hallmark of Parkinson’s disease is the buildup of Lewy bodies—misfolded clumps of the protein known as alpha-synuclein. Long before Lewy bodies form, alpha-synuclein can interfere with neurons’ ability to transport proteins and other cargo along their axons to the synapses. When present at high levels, alpha-synuclein binds too tightly to structures inside the axon, creating the cellular equivalent of traffic jams. These disruptions may even help set the stage for the later accumulation of Lewy bodies in the brain.
Now, University at Buffalo researchers have identified a way to reduce these traffic jams and restore flow—by altering how alpha-synuclein interacts with another Parkinson’s-related protein known as leucine-rich repeat kinase 2 (LRRK2).
In a study published last month, the researchers increased levels of specific mutant forms of LRRK2 in fruit fly larvae. They found that one mutation had a downstream effect on alpha-synuclein, limiting its ability to bind to cargo and disrupt axonal transport. The research is published in the journal Frontiers in Molecular Neuroscience.