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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.

FDA is announcing that it issued a “safe to proceed” letter to Revolution Medicines, allowing the sponsor to initiate an expanded access treatment protocol (EAP) for its experimental pancreatic cancer drug, daraxonrasib.

The U.S. Food and Drug Administration today approved an expanded use for Auvelity (dextromethorphan hydrobromide and bupropion hydrochloride) extended-release tablets to treat agitation associated with dementia due to Alzheimer’s disease in adults.

FDA is proposing to exclude semaglutide, tirzepatide, and liraglutide from the 503B bulks list, finding no clinical need for outsourcing facilities to compound these drugs from bulk substances.

FDA announces results from the largest and most rigorous examination ever conducted focused on chemical contaminants in infant formula available on the U.S. market.

The U.S. Food and Drug Administration today announced two major steps as part of an initiative to advance the implementation of real-time clinical trials (RTCT).

Omnipod Pods may not deliver insulin as intended due to a tear in the internal tubing.

Affected grafts may not unclasp from the delivery system, which may require conversion to open surgical repair and can result in patient death

FDA alerts of risks with use TRUE METRIX Blood Glucose Monitoring Systems by Trividia Health.

Trividia recommends that device users who receive an E-5 error code and are experiencing symptoms of high glucose should seek medical care immediately.

For Immediate Release - BETHLEHEM, PA – APRIL 28, 2026 – B. Braun Medical Inc. is voluntarily recalling two lots of Lactated Ringer’s Injection, E7500, 1L, to the hospital/healthcare facility level. The product has been found to have particulate matter in solution.

Scientists at Cornell University may be closing in on the long-sought “holy grail” of male contraception: a safe, reversible, nonhormonal method that completely halts sperm production. In a breakthrough mouse study, researchers used a compound called JQ1 to temporarily shut down meiosis—the critical process that produces sperm—without causing lasting harm. After treatment stopped, sperm production bounced back, fertility returned, and the animals produced healthy offspring.

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.

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.

ObjectiveTo explore the dynamic changes in excitability and viability of induced pluripotent stem cells (iPSC)-derived motor neurons from sporadic amyotrophic lateral sclerosis (ALS) and compare them with SOD1-related ALS patients and healthy control.MethodsPeripheral blood samples were collected from ALS patients and healthy controls (HC) to establish the iPSC-derived motor neurons (MNs). Whole-cell patch-clamp recordings at different culture stages was made using an Axopatch 700B amplifier in combination with pClamp 11 software (Molecular Devices). The frequency of action potentials (APs) was recorded. Additionally, Terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) Nick-End Labeling (TUNEL) was used to assess the apoptosis of MNs.ResultsALS patient-derived MNs exhibited significantly higher firing rates compared to HCs at both 4–7 weeks (p = 0.004) and 7–9 weeks (p = 0.009). Further analysis revealed that SOD1-derived MNs showed significantly higher firing frequencies than sALS (p = 0.009) and HCs (p < 0.001) in 4–7 weeks. In 7–9 weeks, it remained significant between SOD1 and HC-derived MNs (p = 0.015), but became insignificant between SOD1 and sALS (p = 0.855). The apoptotic rate of sALS (Day 30: 61.37% ± 9.63%; Day 60: 78.41% ± 6.63%) and SOD1 (Day 30: 73.69% ± 8.81%; Day 60: 60.37% ± 11.53%) -derived MNs was significantly higher than those of HCs at both Day 30 (30.72% ± 7.57%) and Day 60 (50.85% ± 19.36%) (p < 0.001).ConclusionMNs derived from both patients with mutant SOD1 and sporadic ALS exhibited increased excitability compared to HCs. The increased excitability of MNs derived from ALS patients with mutant SOD1 occurred earlier, and over time, became consistent with the excitability observed in MNs derived from sporadic ALS. The apoptosis rates of MNs showed similar trends. iPSC-derived MNs from both sporadic and mutant ALS may serve as useful cell models for ALS in future studies.

BackgroundDeer antlers have the potential to contribute to a range of novel biomedical models. Although androgen is undoubtedly an undisputed prerequisite for pedicle initiation (initial stage of antler formation), the molecular mechanisms underlying androgen stimulation remain unclear.MethodsFour juvenile male deer (Cervus nippon) were selected: one intact individual and three castrated ones. The castrates were further divided to receive either testosterone or vehicle injections. The antlerogenic periosteum (AP) tissues overlying each frontal crest were collected at successive time points for subsequent analyses. Proteomic analysis was performed using two-dimensional difference gel electrophoresis (2D-DIGE), while cell proliferation and differentiation were assessed through ex vivo tissue explant cultures, in vitro osteoblast induction, and transcriptomic analyses.ResultsExogenous androgen induced pedicle initiation. Among the differentially-expressed proteins (DEPs) identified, ACTB, VIM, p53, RNASEL, and CALR were notable for their direct interactions with the androgen receptor (AR). Pathways related to the cell cycle, gene expression, protein metabolism, and signal transduction were found to play key roles in activating pedicle initiation. In serum-free medium, testosterone promoted the proliferation of AP cells in ex vivo tissue explant cultures; however, it showed no effect on osteogenic differentiation of these cells.ConclusionOur findings indicate that testosterone serves as the key factor triggering pedicle initiation. However, this effect likely occurs through the promotion of AP cell proliferation rather than their osteogenic differentiation. Furthermore, the results suggest that CALR may play a pivotal role in regulating the transcription of AR downstream genes during pedicle initiation. These results provide new insights into androgen-regulated mechanisms in deer pedicle initiation.

IntroductionThe early stages of human embryonic development are challenging to study in pregnant women.MethodsA “disease-in-a-dish” model was utilized to investigate SARS-CoV-2 infection of human embryonic stem cells and the three germ layers (ectoderm, endoderm, and mesoderm).ResultsEctodermal cells showed significantly higher infection rates compared to the other cell types. This increased susceptibility was attributed to three key factors characteristic of the ectoderm: dual viral entry pathways (membrane fusion and endocytosis), elevated TMPRSS2 activity, and a markedly reduced glycocalyx, which facilitated viral access to host cell receptors.DiscussionOur findings provide strong evidence that cells in early post-implantation human embryos are susceptible to SARS-CoV-2 infection. The high level of infection in the ectodermal cells raises concern for potential teratogenic effects, particularly involving the nervous system. Future clinical studies should investigate neurological outcomes in infants born to mothers infected with SARS-CoV-2 during pregnancy.

IntroductionPeripheral nerve injuries remain a major clinical challenge, often leading to long-term motor and sensory deficits. Stem cell-based and cell-free approaches, combined with biomaterial scaffolds, have emerged as promising strategies for nerve repair.MethodsThis study evaluated the regenerative potential of human dental pulp stem cells (hDPSCs), their conditioned medium (hDPSCs-CM), and the combination of hDPSCs with olfactory mucosa mesenchymal stem cell conditioned medium (OM-MSCs-CM) in a rat model of sciatic nerve neurotmesis repaired with a chitosan-based nerve guide conduit (Reaxon®). Twenty-seven rats were allocated into experimental groups, including an uninjured control (contralateral limb), an end-to-end neurorrhaphy surgical control group, and treatment groups repaired with Reaxon® alone or combined with hDPSCs, hDPSCs-CM, or hDPSCs with OM-MSCs-CM suspended in Matrigel®. Following nerve transection, a 9–10 mm sciatic nerve gap was created. Functional recovery was monitored over 20 weeks through motor, nociceptive, behavioral, gait, stereological, histomorphometric, and electrophysiological evaluations.ResultsAll treatments promoted progressive motor recovery and partial restoration of nociceptive function compared to the untreated condition, although the magnitude of improvement differed among groups. The hDPSCs-CM–treated group (CMDP) showed the most favorable overall outcomes, including the lowest muscle mass loss, higher compound muscle action potential amplitudes, and functional indices approaching control values, indicating enhanced reinnervation and neuromuscular preservation. Histomorphometric and stereological analyses confirmed active regeneration across all groups, characterized by microfasciculation and thinner myelin sheaths typical of regenerating fibers.DiscussionDespite incomplete recovery, the combination of biological therapies with chitosan conduits provided an effective environment for axonal regrowth and functional improvement. These findings highlight the relevance of CMDP as a potent biological adjunct in peripheral nerve repair and support the development of cell-free, clinically translatable strategies for neuroregeneration.

IntroductionThe basement membrane is a specialized extracellular matrix that compartmentalizes epithelial and endothelial tissues and provides essential structural and signaling cues for tissue organization. Whereas fibrillar collagens (Col) of the interstitial matrix (such as Col I and Col III) are widely used in tissue modeling, the networking collagens that scaffold the basement membrane, including human Col IV and Col VI, remain difficult to access. Commercial basement membrane surrogates such as Matrigel® are derived from murine tumors and are ill defined, dilute, variable, and incompatible with animal-free biomanufacturing. Thus, there is a crucial need for human-derived basement membrane matrices that are free of xenogenic contaminants and do not rely on breeding animals.MethodsHere, we analyzed whether human mesenchymal stromal cells (MSCs) could serve as a platform to produce self-assembling basement membrane components under chemically defined, xeno-free conditions. MSCs from placental, umbilical cord, bone marrow, and adipose tissues were cultured as three-dimensional spheroids and adherent multilayered sheets.ResultsConfocal imaging of whole-mount, decellularized spheroid matrices showed complex networks of fibronectin (FN) and Col IV with topological and organizational features characteristic of basement membrane. Perinatal MSCs produced distinct matrix architectures consisting of apical FN sheets underlaid by continuous Col IV networks. Time-resolved imaging of umbilical cord MSC-derived matrix sheets demonstrated a reproducible sequence of basement membrane assembly that parallels developmental tissue organization.DiscussionTogether, these findings demonstrate that human MSCs cultured entirely without entirely animal-derived components can synthesize functional basement membrane proteins that self-assemble into ordered, tissue-like scaffolds. In this work, we establish MSCs as a scalable, sustainable, and cruelty-free platform for manufacturing human basement membrane matrices for bioengineering and regenerative medicine applications.