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Implant design helps fight ovarian cancer from the inside

Researchers have developed an implant that could deliver next-generation therapies for ovarian cancer precisely where they are needed while simultaneously monitoring how the disease responds.

The project was carried out by a team at CÚRAM, the Research Ireland Centre for Medical Devices based at the University of Galway, along with collaborators from the University of Minnesota, Massachusetts Institute of Technology (MIT) and the Wyss Institute.

The research was published in the journal Device. It showed how the team developed a flexible, porous implant designed to sit inside the peritoneal cavity—the space surrounding the abdominal organs in a woman’s body where ovarian cancer predominantly occurs. The device is designed to connect to an external port through the skin so it can be replenished with therapeutic agents as often as needed without requiring further surgery.

The End of High Cholesterol? The First Oral PCSK9 Drug Could Change Heart Medicine Forever

Dr. Norman Lepor, MD — Founder and Director of the National Heart Institute, Clinical Professor of Medicine at UCLA, and Attending Cardiologist at Cedars-Sinai.


Heart disease remains the leading cause of death worldwide, and one of its most important modifiable risk factors is elevated LDL cholesterol — the so-called \.

Neuraspace raises $18 million to expand sovereign space awareness

TAMPA, Fla. — Neuraspace, the Portuguese space traffic management startup, announced 15.6 million euros ($18 million) in fresh funding Aug. 5 to expand European space domain awareness (SDA) and defense capabilities.

The financing comprises a six million euro Series B round from venture capitalists and 9.6 million euros from Portugal’s Recovery and Resilience Plan, an EU-backed national program created in response to the COVID-19 pandemic.

A Neuraspace spokesperson said the public funding will directly support NeuraspaceDEF, an AI-powered, SDA platform for civil and defense users.

IL-1 pathway may stop Candida fungus from turning fatal in weakened immunity

An immune pathway has been discovered that prevents a normally harmless fungus from developing into a fatal infection. The King’s College London study, published in Nature Microbiology, provides the first potential clue as to why only certain patients with weakened immune systems, including those undergoing chemotherapy or living with HIV, are at risk of life-threatening Candida albicans infections.

Candida albicans is a fungus that normally lives harmlessly in areas such as the mouth and gut but can sometimes spread through the body and cause fatal disease.

If the results are confirmed in humans, they could provide a test to identify who is at risk of developing fatal fungal infections and represent a potential therapeutic target to reduce the risk of developing the disease.

Restoring Saliva Flow May Improve Oral Health in Down Syndrome

However, Carpenter was not entirely convinced that hyposalivation drives periodontitis. “I don’t think there’s much evidence for that in…literature about human studies,” he said. Instead, he said that inflammation—which is present in Dp16 salivary glands—could cause hyposalivation. “There’s lots of literature that shows that inflammatory cells can affect salivary secretion,” he noted.

According to Yule, next steps could include looking at whether dysregulated calcium signaling—which is linked with several other diseases—also underlies other Down syndrome-related complications like Alzheimer’s disease. While drugs targeting calcium signaling could potentially help, there is a complexity to it, he noted. “Knowing what the target is [is] good, but the fact that the target is almost universal in cells, then that makes you think about whether it’s something that could be targeted,” explained Yule.

Lacruz agreed that disrupted calcium signaling occurs in other tissues as well. “Understanding why calcium is dysregulated is an important part of what we need to do [next],” he said. More work needs to be done to translate the findings to the clinic, “but we see that as a way forward to potentially impacting the lives of individuals with Down syndrome,” said Lacruz.

Chronic Stress and Headaches: The Role of the HPA Axis and Autonomic Nervous System

Chronic stress significantly influences the pathogenesis of headache disorders, affecting millions worldwide. This review explores the intricate relationship between stress and headaches, focusing on the dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis and autonomic nervous system (ANS). Persistent stress could lead to neuroinflammation, increased pain sensitivity, and vascular changes that could contribute to headache development and progression. The bidirectional nature of this relationship creates a vicious cycle, with recurrent headaches becoming a source of additional stress. Dysregulation of the HPA axis and ANS imbalance could amplify susceptibility to headaches, intensifying their frequency and severity. While pharmacological interventions remain common, non-pharmacological approaches targeting stress reduction, such as cognitive-behavioral therapy, biofeedback, and relaxation techniques, offer promising avenues for comprehensive headache management. By addressing the underlying stress-related mechanisms, these approaches provide a sustainable strategy to reduce headache frequency and improve patients’ quality of life.

JCI: Department of Immunology and Inflammation, Imperial College London, London, United Kingdom

2 School of Medicine, Chang Gung University and Division of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.

3Imperial Lupus Centre, Imperial College Healthcare NHS Trust, London, United Kingdom.

3D DNA mapping in rare immune cells reveals new genes linked with autoimmune disease risk

Our DNA is often pictured as a simple spiral, like a piece of rope held taut. But inside cells, it folds into a complex three-dimensional structure, with 2 meters (6.6 feet) of DNA scrunched like a headphone wire in a pocket. This bundled architecture plays a crucial role in how genes are switched on and off. Understanding these interactions is key to interpreting genetic studies of disease and can help develop targeted treatments.

Genes—the instructions for making proteins—are regulated by two types of DNA regions, called promoters and enhancers. Promoters are located at the start of each gene and directly load the machinery that reads it to produce RNA, a template for making proteins. In contrast, enhancers, which act like “molecular switches” boosting gene activity in the right cell and condition, may be found much further from the genes they control: sometimes many thousands or even millions of DNA letters away. When DNA folds in the 3D space of the cell’s nucleus, these enhancers loop around to physically contact the genes they regulate.

Understanding how enhancers work and which genes they control is particularly important because genome-wide association studies—large-scale efforts comparing the DNA of thousands of people to identify small genetic differences linked to disease—have revealed many genetic variants associated with complex conditions such as Crohn’s disease that sit within these regions. Crohn’s disease is a common form of inflammatory bowel disease, which affects around 1 in 100 people globally and currently has no known cure.

Abstract: Section of Nephrology, Yale University School of Medicine, New Haven, Connecticut, USA

2 Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.

3Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.

A crossvertebrate brain protein interaction map identifies conserved neural and nonneural complexes

Dang et al. use co-fractionation and immunoprecipitation mass spectrometry to map protein interactions conserved across vertebrate brains. This resource, dubbed VerteBrain, offers insights into brain protein function and new links between proteins and disease, identifying candidate genes and pathways involved in epilepsy, deafness, and developmental disorders.

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