Immersive Technologies in Forensic Mental Health and Prison Settings: Scoping Review
Introduction of Nurse-Led Rehabilitation Services for Patients With Stroke After Discharge to Improve Self-Care Management in Bangladesh: Pilot Randomized Controlled Trial
Effects of Social Media Narratives on Affective and Behavioral Responses to Menopause Content: Randomized Online Experimental Study
Opinion: What the 20th-century war on smog tells us about today’s wildfire smoke
As wildfires burn millions of acres across Canada, smoke has descended upon cities across the United States, with air quality plummeting to unhealthy levels. In New York City, emergency room visits for asthma exacerbations jumped by 31% by the end of the first day. The timing could not have been worse for a city already in the throes of the second major heat wave of the season.
Extreme weather events represent the cyclical and compounding relationship between fossil fuel combustion, a warming climate, natural disasters, and related illnesses. Some may view them as proof the climate crisis has already become insurmountable. However, history teaches us to never let a health-related environmental crisis go to waste.
Genetic Study Links Excessive Sweating to Neurological Dysfunction
Data from a new study suggest that a form of hyperhidrosis, or excessive sweating, may be due to genetic mutations that result in the overstimulation of the nerves that control the sweat glands. These findings, which are reported in Science Advances, could open a door to targeted treatments for the condition using existing medicines. Full details of the findings are provided in the paper titled “A neurocutaneous NaV1.8 channelopathy underlies a genetic subtype of primary idiopathic hyperhidrosis.” The international study is led by scientists at Vrije Universiteit Brussel.
Excessive sweating, which affects roughly two to five percent of the population, causes more than just discomfort. The impact of the condition on the daily lives of people living with it can be very severe. Patients often sweat so profusely that they have to change clothes several times a day. Many avoid social contact, experience shame, and develop depression. Yet the condition is often seen as a superficial skin problem and patients often do not receive appropriate care.
That could change thanks to the findings from this study which is the culmination of 10 years of research done by scientists in the lab of Frank Bosmanbs, PhD, at Vrije Universiteit Brussel and their collaborators at Johns Hopkins University. To pinpoint a genetic basis for hyperhidrosis, the scientists analyzed the DNA of more than 180 patients. They discovered defects in the Nav1.8 ion channel, which normally functions as a biological gate that regulates electrical signals in the nervous system.
Specifically, in patients with hyperhidrosis, the gate is left too wide open due to a genetic predisposition. As a result of this, the nerves are constantly overstimulated and in a state of activity, which results in excessive sweating often triggered by emotional or stress-related stimuli. To dig deeper into their theory, the scientists developed an experimental mouse model. Because mice only sweat from their paws, the team developed a microscopic measurement method to count sweat droplets using an iodine-starch mixture.
They found that mice that had the same genetic defect as hyperhidrosis patients also sweated excessively. Furthermore, once the scientists administered a substance that blocked the overactive nerve signals, their symptoms decreased significantly and reversibly. However the genetic picture is more complex. Bosmanbs and his team found a patient who had inherited an inhibitory nerve mutation but still sweated excessively due to a separate mutation in a local water channel within the sweat gland. It suggests that there are different biological pathways that can lead to the same overstimulation that results in hyperhidrosis.
Though the genetic picture is a complex one, the scientists believe that their findings offer the prospect of better treatments for this condition. Currently, some severe forms of hyperhidrosis are treated by severing the sympathetic nerve pathways in the chest. While effective, this treatment is both invasive and can have unwanted side effects. With a deeper understanding of the genetic basis of the condition, scientists may be able to better predict which patients are likely to get the most benefit from localized treatment of the sweat glands, systemic medication or nerve-targeted therapies. Another potential treatment avenue is drug repurposing, which is supported by the evidence from the mouse studies. However, further testing via controlled clinical trials is required.
The post Genetic Study Links Excessive Sweating to Neurological Dysfunction appeared first on GEN – Genetic Engineering and Biotechnology News.
Why Microbot Medical thinks it can win the stroke telesurgery race
Microbot Medical says it has what it takes to win the race to treat stroke patients with a future version of its fully disposable, single-use endovascular navigation surgical robot, Liberty. Liberty earned FDA 510(k) clearance in September 2025 for “use in the remote delivery and manipulation of guidewires and catheters, and remote manipulation of guide…
The post Why Microbot Medical thinks it can win the stroke telesurgery race appeared first on Medical Design and Outsourcing.
Quitting smoking is hard. A Medicare change may push doctors to give more help
Pretty much everyone who cares about public health agrees that it’s a good idea to help people quit smoking, the No. 1 cause of preventable death in the U.S. Doctors may soon get some extra encouragement to lend a hand, thanks to proposed changes in Medicare’s physician fee schedules.
Physicians who offer counseling on quitting cigarettes or other tobacco products during visits with patients would get a 19% increase in reimbursement, according to a few paragraphs buried in the 1,592-page document released this week. The same adjustment would also apply to assessments of, and interventions for, alcohol and substance misuse during doctors’ visits.
“Given the evidence supported role these services play in preventing and managing chronic disease […] we believe that valuation should more accurately reflect the clinical intensity and work associated with these time-based services,” the proposal from the Centers for Medicare and Medicaid Services explains. Comments on the proposal are due Sept. 14.
“The prioritization of cessation as a service is long overdue, and we’re very excited about it,” said Anne DiGiulio, the American Lung Association’s senior director of nationwide tobacco cessation and health policy.
Dendritic Cells Identified as Key Organizers of Anti-Tumor Immune Hubs
Not all immune activity inside a tumor is disorganized. In some patients, tumors contain tertiary lymphoid structures, or TLSs: organized clusters of immune cells that resemble lymph-node-like sites of local immune coordination. Their presence has been associated with improved survival and better responses to immunotherapy in several cancers, making them an increasingly important feature of the tumor microenvironment.
A new study published in Science identifies a specialized immune cell population that helps build and sustain these structures. Researchers at the Icahn School of Medicine at Mount Sinai and collaborating institutions found that type 1 conventional dendritic cells, or cDC1s, act as central organizers of TLSs in cancer. The work helps explain how local anti-tumor immune responses are maintained within tumor tissue and points to potential strategies for improving immunotherapy.
Why TLSs matter in cancer immunity
TLSs are not normal anatomical lymph nodes. They arise in chronically inflamed tissues, including tumors, and can contain organized T-cell zones, B-cell follicles, germinal center-like regions, plasma cells, and specialized stromal networks. In cancer, their presence is often interpreted as evidence that the immune system is not only infiltrating the tumor but organizing a sustained local response.
Many tumors contain immune cells, but not all immune infiltrates are functionally productive. TLSs may provide a site where antigen presentation, T-cell activation, B-cell maturation, and antibody responses occur close to malignant cells. This could help explain why TLS-positive tumors are often associated with more favorable outcomes and greater sensitivity to immune checkpoint blockade.
Until now, however, it has been less clear what drives TLS formation and, just as importantly, what keeps these structures functional once they are established.
cDC1s as local immune architects
Dendritic cells are best known for antigen presentation: they capture tumor antigens and prime T-cell responses. This study expands that role. The researchers found that cDC1s do not only initiate anti-tumor immunity; they help organize the physical and functional immune architecture inside tumors.
“Our goal was to understand how these immune structures develop and persist inside tumors,” said lead author Raphael Mattiuz, PhD. “We found that a distinct subset of dendritic cells acts as the organizer, bringing together different immune cells and keeping the local anti-cancer response active.”
The team analyzed tumor samples from patients with lung, liver, colorectal, kidney, and ovarian cancers using multiplex imaging and spatial gene-expression approaches. These methods allowed them to map where dendritic cells were located, which immune cells surrounded them, and how those local neighborhoods related to TLS organization.
Across tumor types, mature dendritic cells accumulated within TLSs. The mechanistic work then focused on a mouse model of non-small cell lung cancer designed to reproduce mature TLS formation seen in human tumors. In this model, cDC1s were required both during the establishment of TLSs and later for their maintenance.
More than T-cell priming
The study suggests a two-stage role for cDC1s. Early in tumor development, TLS formation depended on IFNγ-driven maturation of cDC1s, migration to tumor-draining lymph nodes, and recruitment of primed T cells back into the tumor. As tumors progressed, however, the biology changed. TLSs could persist even when egress of T cells from tumor-draining lymph nodes was impaired, while cDC1s became retained within intratumoral stromal hubs enriched in CCR7 ligands.
This is clinically interesting because it positions cDC1s as tissue-resident coordinators of ongoing immunity, not merely transient antigen couriers. The researchers found that timed depletion of cDC1s after TLSs had formed disrupted TLS maintenance. Blocking their localization to stromal hubs had a similar effect.
The function of these cells also depended on antigen presentation. Genetic ablation of both MHC class I and II on cDC1s impaired TLS maintenance, T follicular helper cell preservation, germinal center formation, tumor-specific IgG production, and differentiation of progenitor exhausted CD8-positive T cells.
“We were surprised to see that these rare cells become permanent organizers within the tumor itself,” Mattiuz said. “They don’t just activate cancer-killing T cells. They also help coordinate antibody responses, allowing multiple parts of the immune system to work together where they’re needed most.”
Implications for immunotherapy
Checkpoint inhibitors have changed cancer care, but durable responses remain limited to a subset of patients. One reason is that reinvigorating T cells may not be enough if the tumor lacks the local immune organization needed to sustain productive responses. TLS biology offers a complementary framework: the issue may not only be whether immune cells are present, but whether they are organized into functional niches.
This study suggests that cDC1-directed therapies could help strengthen those niches. Potential strategies might include increasing cDC1 abundance, enhancing cDC1 maturation, improving their recruitment or retention in tumors, or combining cDC1 activation with checkpoint blockade, vaccines, radiotherapy, or other immune-modulating approaches.
The findings also add nuance to biomarker development. TLS presence is already being studied as a prognostic and predictive feature, but TLS quality may matter as much as TLS quantity. A tumor with cDC1-rich, antigen-presenting, germinal center-supporting TLSs may behave differently from a tumor with less mature or poorly maintained immune aggregates.
For medical oncology, this could eventually refine how TLSs are interpreted in pathology and translational studies. Rather than treating TLSs as a binary histological feature, future assays may need to assess their cellular composition, dendritic cell state, B-cell organization, and proximity to effector T-cell populations.
Still early, but mechanistically important
The work is not yet a clinical intervention. It does not show that activating cDC1s in patients will reliably generate TLSs or improve immunotherapy outcomes. Tumor type, antigenicity, stromal architecture, prior therapy, and immunosuppressive pathways will likely influence whether this biology can be therapeutically exploited.
Nevertheless, the study provides a clearer mechanistic target in a field that has often treated TLSs as useful but poorly controlled biomarkers. If cDC1s are required to form and maintain functional TLSs, then therapies aimed at dendritic cell biology may become a way to convert poorly organized tumor immune infiltrates into more coordinated anti-tumor responses.
The broader message is that effective cancer immunity is spatial as well as cellular. It is not only about having T cells, B cells, antibodies, or dendritic cells inside the tumor. It is about arranging them in the right place, in the right state, and for long enough to sustain pressure on malignant cells.
By identifying cDC1s as organizers of tumor-associated TLSs, the study offers a more concrete path toward therapies that help the immune system build its own infrastructure inside cancer.
The post Dendritic Cells Identified as Key Organizers of Anti-Tumor Immune Hubs appeared first on Inside Precision Medicine.

