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SMART breakthrough offers a promising pathway toward improved manufacturing of high‑quality cells for regenerative therapies to treat joint diseases.

Cultured from induced pluripotent stem cells, “miBrains” integrate all major brain cell types and model brain structures, cellular interactions, activity, and pathological features.

A new, highly efficient process for performing this conversion could make it easier to develop therapies for spinal cord injuries or diseases like ALS.

Lincoln Laboratory and MIT researchers are creating new types of bioabsorbable fabrics that mimic the unique way soft tissues stretch while nurturing growing cells.

Professor Li-Huei Tsai studies how brain waves can be used to treat neurodegenerative diseases such as Alzheimer’s.

The U.S. Food and Drug Administration today approved Foundayo (orforglipron) marking the fifth approval under the Commissioner's National Priority Voucher (CNPV) pilot program.

The U.S. Food and Drug Administration today approved Kresladi (marnetegragene autotemcel), the first gene therapy for the treatment of severe Leukocyte Adhesion Deficiency Type I (LAD-I).

The U.S. Food and Drug Administration approved Avlayah (tividenofusp alfa-eknm) to treat certain individuals with Hunter syndrome (Mucopolysaccharidosis type II or MPS II).

As part of the U.S. Food and Drug Administration’s continuous quality improvement efforts, the agency today published a Federal Register Notice seeking public comment on the Commissioner’s National Priority Voucher pilot program.

The U.S. Food and Drug Administration today approved a new higher dose (7.2 mg) of Wegovy (semaglutide) injection for weight loss and long-term maintenance of weight loss for certain adult patients.

Impella Generation 1 Purge Cassettes have an increased risk of purge leaks. Purge leaks can lead to low pump pressure and pump stops.

The differential pressure sensor in certain Impella devices may malfunction and cause sensor values to drift.

FOR IMMEDIATE RELEASE – 03/30/2026 - Flushing, New York, Aphreseller (Ebay seller ID), Buy-herbal.com is recalling all lots of Kian Pee Wan capsules to the consumer level. FDA analysis has found that the product contains the undeclared drug ingredients dexamethasone and cyproheptadine. Products cont

Erbe Cryoprobes may rupture during activation, leading to potential hearing loss, tinnitus, injury, or burns.

Navajo Manufacturing company is recalling certain heating pads that overheat when folded leading to potential burn injuries.

Scientists at Michigan State University have uncovered the molecular “switch” that powers sperm for their final, high-speed dash toward an egg. By tracking how sperm use glucose as fuel, the team discovered how dormant cells suddenly flip into overdrive, burning energy in a carefully controlled, multi-step process. A key enzyme, aldolase, helps convert sugar into the burst of power needed for fertilization, while other enzymes act like traffic controllers directing the flow of fuel.

Researchers have discovered a biological switch that explains why movement keeps bones strong. The protein senses physical activity and pushes bone marrow stem cells to build bone instead of storing fat, slowing age-related bone loss. By targeting this “exercise sensor,” scientists believe they could create drugs that mimic exercise at the molecular level. The approach could protect fragile bones in people who are unable to stay active.

Researchers have recreated a miniature human bone marrow system that mirrors the real structure found inside our bones. The model includes the full mix of cells and signals needed for blood production and even maintains this process for weeks. It could transform how scientists study blood cancers and test new drugs. In the future, it may support more personalized treatment strategies.

Researchers discovered that chronic inflammation fundamentally remodels the bone marrow, allowing mutated stem cell clones to quietly gain dominance with age. Reprogrammed stromal cells and interferon-responsive T cells create a self-sustaining inflammatory loop that weakens blood production. Surprisingly, the mutant cells themselves may not be the main instigators.

Groundbreaking research shows that as men age, harmful genetic mutations in sperm become more common—not just from random chance, but because some are naturally favored. Advanced sequencing revealed dozens of genes under selective pressure, many linked to serious disorders. The work reveals how evolution inside the testes can quietly shape the next generation’s genetic health.

A newly identified gene mutation may help explain why schizophrenia patients struggle to update their understanding of reality. The mutation disrupts a brain circuit involved in flexible decision-making, causing mice to stick with outdated choices even when conditions change. Researchers pinpointed the issue to a key thalamus–prefrontal cortex pathway. By reactivating this circuit, they were able to restore normal behavior—raising hope for future therapies.

Korean researchers found that low-dose radiation therapy eased knee pain and improved movement in people with mild to moderate osteoarthritis. The treatment, far weaker than cancer radiation, showed real benefits beyond placebo. With no side effects and strong trial results, the approach could provide a middle ground between painkillers and joint surgery.

For decades, scientists believed Alzheimer’s was driven mainly by sticky protein plaques and tangles in the brain. Now Purdue researchers have revealed a hidden culprit: fat. They found that brain immune cells can become clogged with fat, leaving them too weak to fight off disease. By clearing out this fat and restoring the cells’ defenses, researchers may have uncovered an entirely new way to combat Alzheimer’s — shifting the focus from plaques alone to how the brain handles fat.

Mayo Clinic scientists uncovered how excessive drinking triggers fatty liver disease by disrupting the enzyme VCP, which normally prevents harmful protein buildup on fat droplets in the liver. Alcohol blocks this protective process, allowing fat to accumulate and damage liver cells.

Switching clocks twice a year disrupts circadian rhythms in ways that harm health. Stanford scientists found permanent standard time would reduce obesity and stroke rates nationwide, making it the strongest option over permanent daylight saving time or seasonal shifts.

IntroductionMetabolic dysfunction-associated steatotic liver disease (MAFLD) has a high prevalence and high comorbidity for other diseases. Due to the complexity of this multifactorial disease, therapy options are still rather limited. We employed an in vitro pluripotent stem cell-based model to decipher potential disease-associated molecular pathways and study the mode of action of prospective drugs. Dipeptidyl peptidase 4 (DPP4) or cluster of differentiation 26 (CD26) is involved in inflammation, infections, immune disorders, type 2 diabetes, kidney disease, and cancer.MethodsWe induced the steatosis phenotype in human induced pluripotent stem cell (iPSC)-derived hepatocyte-like cells (HLCs) by oleic acid (OA) feeding and confirmed regulation of clinically relevant pathways by NGS-based global transcriptomic analyses. Analysis of the secretome of steatotic HLCs revealed DPP4 as a potential key mediator of the disease. To further elucidate its role in the development of MAFLD, we inhibited DPP4 activity with vildagliptin (VILDA) and analyzed the global transcriptomic changes and specific gene and protein gene expression of steatosis-associated genes with and without DPP4 inhibition.ResultsMAFLD-associated pathways such as PPAR and TNF signaling were differentially regulated in hiPSC-derived steatotic HLCs. We found increased hepatic DPP4 activity and secretion upon OA feeding. Gene expression of fatty acid and purine metabolism and inflammation-associated pathways was regulated upon DPP4 inhibition.DiscussionOur HLC model confirmed the association of DPP4 with metabolism and inflammation, which foster the development of MAFLD. Inhibiting DPP4 activity with VILDA partially relieved the steatotic phenotype on a global transcriptomic level.Impact and implicationsGiven the difficulties of identifying suitable anti-MAFLD drugs, novel model systems are urgently needed. Our in vitro HLC-model reproduced the DPP4-dependent aspects of the disease and responded positively to VILDA treatment. Further elucidation of the role of DPP4 in the etiology of MAFLD and other diseases is warranted.

IntroductionCD19-directed chimeric antigen receptor (CD19-CAR) T-cell therapy has markedly improved outcomes in relapsed and refractory B-cell malignancies, but its efficacy remains limited by insufficient in vivo persistence and functional exhaustion. We have generated functionally rejuvenated T-cells (rejTs) by reprogramming antigen-specific cytotoxic T lymphocytes (CTLs) into induced pluripotent stem cells (iPSCs) and redifferentiating them into CTLs with restored proliferative capacity. In this study, we explored a vaccine synergy strategy to enhance the persistence of CAR-rejuvenated CTLs (CARrejTs) through T-cell receptor (TCR) restimulation.MethodsSARS-CoV-2 spike protein-specific rejTs (COVID19-rejTs) were established from iPSCs derived from spike protein-specific CTLs. A CD19-CAR was introduced into these iPSCs to generate dual-antigen recognition CARrejTs targeting CD19 and COVID-19 spike protein (1919-CARrejTs). Subsequently, 1919-CARrejTs were assessed for cytotoxicity, proliferative capacity, and exhaustion phenotype using 51Cr release assays, sequential rechallenge assays, and CFSE-based proliferation analysis with CAR- or TCR-dependent stimulation.Results1919-CARrejTs uniformly expressed both CD19-CAR and spike protein-specific TCRs, retained antigen-specific cytotoxicity, and exhibited a rejuvenated phenotype with higher expression of granzyme B and perforin and lower expression of exhaustion markers compared with conventional CD19-CAR-T cells. Dual-antigen recognition enhanced cytotoxicity under matched antigen presentation, and 1919-CARrejTs maintained durable tumor control in sequential rechallenge assays. CFSE dilution analysis revealed that TCR-mediated stimulation by spike protein-specific peptide provided strong proliferative capacity of 1919-CARrejTs in an HLA-dependent manner.ConclusionThe combination of iPSC-mediated rejuvenation and dual-antigen recognition via CAR and native TCR confers superior cytotoxicity, persistence, and proliferative potential compared to conventional CD19-CAR-T cells. These findings provide a proof-of-concept for a vaccine-synergy strategy in which in vivo TCR restimulation supports selective expansion and sustained antitumor effect of dual-antigen recognition T-cells that can be a promising treatment approach for B-cell malignancies.

Mesenchymal stromal cells (MSCs) have emerged as promising therapeutic agents for inflammatory diseases because of their potent immunomodulatory properties. Although acute inflammation transiently enhances MSC functionality, the impact of chronic inflammatory exposure remains poorly defined. In this study, we investigated the effects of sustained TNF-α stimulation and indirect co-culture with M1 macrophages on MSC behavior. Comprehensive gene expression profiling was performed to assess the changes in immunoregulatory, apoptotic, and metabolic pathways. To determine functional reversibility, we also evaluated MSCs following the withdrawal of TNF-α. Short-term exposure led to upregulation of Tgf-β, Il-10, and Fasl, whereas prolonged stimulation suppressed these genes and significantly increased the expression of immune checkpoint genes Pd-1 and Ctla-4, indicative of an exhaustion-like phenotype. This phenotypic shift was associated with sustained NF-κB activation, upregulation of Stat3 and Ap-1, suppression of mTORC1/2 components, decreased Pd-l1 expression, and increased Pd-1 expression, raising the possibility that PD-1 upregulation is associated with MSC dysfunction under chronic inflammatory stress. These findings revealed that prolonged stimulation (48 h) induces an exhaustion-like dysfunction state in MSCs, characterized by checkpoint activation, transcriptional repression, and metabolic dysfunction. PD-1 may serve as a biomarker associated with inflammation-induced MSC impairment.