Western University of Health Sciences (WesternU) is a private medical school and health sciences university with its main campus in Pomona, California, with an additional osteopathic medical school in Lebanon, Oregon. With an enrollment of 3,814 students (2020–21), WesternU offers more than twenty academic programs in multiple colleges.Under the banner of WesternU Health, the university operates a variety of patient care facilities in California and Oregon. The Pomona and Portland (Oregon) campuses both include a medical center, dental center, eye care institute, pharmacy, and travel health center. WesternU-Pomona also is home to the Pet Health Center, which provides veterinary services. Dental services are offered at the Rancho Mirage campus, while a Los Angeles campus provides optometry services.Several nonprofit organizations are based at the WesternU Pomona campus, including the Harris Family Center for Disability and Health Policy. The Center for Oral Health, moved from the Bay area to the WesternU Pomona campus in 2012. In 2015, the Southern California Medical Museum moved to the Pomona campus.Founded in 1977, the first program at WesternU was its medical school, the College of Osteopathic Medicine of the Pacific (COMP). Since that time, the College of Veterinary Medicine opened in 2003, and colleges of dental medicine, optometry, and podiatric medicine opened in 2009. In 2011, the university opened an additional campus in Lebanon, Oregon, the College of Osteopathic Medicine of the Pacific - Northwest (COMP-Northwest). In 2015, the university's founding president, Philip Pumerantz, retired.All of the programs at WesternU have professional accreditation and the university is accredited by the Western Association of Schools and Colleges. The medical school (COMP) is also accredited by the American Osteopathic Association's Commission on Osteopathic College Accreditation.
Diabetic foot ulcers are a major cause of morbidity in patients with diabetes mellitus and remain challenging to treat despite advances in wound care. Growing evidence suggests that impaired axonal regeneration, along with chronic inflammation, impaired angiogenesis, and altered extracellular remodeling, is an important mechanism contributing to the chronic, nonhealing nature of cutaneous wounds. However, the mediators involved and the mechanisms by which they impair wound healing in the presence of hyperglycemia are poorly understood. Peripheral nerves coordinate inflammation, angiogenesis, and extracellular matrix remodeling during repair, and their dysfunction in diabetes disrupts these processes. This review examines how hyperglycemia and oxidative stress impair neuroregeneration ( mainly axonal and nerve regeneration), highlighting the downstream consequences for vascular and structural repair. Particular attention is given to the altered expression of activin A (associated with nerve growth and neural inflammation), TNFRSF10B (associated with neuronal damage and apoptosis, and synaptophysin (a marker of synaptic vesicles and involved in nerve regeneration, particularly in the early stages of axonal regrowth) as representative mediators linking neuronal injury to defective wound healing. By integrating findings across neural, vascular, and inflammatory pathways, this review supports impaired neuronal regeneration as an important contributor to nonhealing diabetic foot ulcer pathogenesis to identify potential molecular targets that may improve healing outcomes.
Mechanosensitive PIEZO channels are thought to open via tension-induced flattening of peripheral transmembrane arm domains, yet the structural basis of this activation remains unclear. Here, by leveraging hybrid-resolution molecular dynamics simulations, we uncover how large-scale PIEZO2 arm movements funnel into subtle gating motions in the central pore under physiological tension. Arm flattening correlates with anticlockwise rotation of the pore relative to the arms and with clockwise twisting of inner pore helices. These clockwork motions open the pore in a two-step fashion, yielding a fully conducting state and a stable subconducting state populated at a low tension, which was detected electrophysiologically. The fully open PIEZO2 pore is walled by both lipids and amino acids and recapitulates minimal pore size, conductance, ion selectivity and outward rectification of chloride currents measured electrophysiologically. These findings provide structural insights into PIEZO2 gating and demonstrate hybrid-resolution molecular dynamics as a powerful approach to study large-scale membrane protein dynamics and guide drug discovery.
Measles remains a significant global health threat due to its extreme transmissibility and the potential for severe, long-term complications. This review synthesizes the most up-to-date literature on the host response, immunological impact, current treatments, and prevention of the measles virus (MeV). The review details host immune evasion mechanisms, including the antagonism of interferon signaling, discusses genetic associations with vaccine failure, and explores adjunctive treatments like vitamin A and ribavirin. Despite the success of the two-dose MMR vaccine, recent resurgences in the United States, peaking at 2065 cases in 2025, underscore a critical decline in herd immunity driven by vaccine hesitancy and pandemic-related disruptions. However, with no FDA-approved antiviral, primary prevention via vaccination remains the only effective strategy. This paper emphasizes the necessity of strengthening public health outreach and standardizing international surveillance to mitigate the rising incidence of this preventable disease.
Diabetes mellitus and inflammatory bowel disease are chronic inflammatory disorders characterized by immune dysregulation and rising global prevalence. Epidemiological studies increasingly suggest a bidirectional association between the two conditions, linked through shared mechanisms of intestinal barrier dysfunction, microbial dysbiosis, and sustained innate immune activation. Activated macrophages play a central role in driving mucosal inflammation through polarization toward a pro-inflammatory M1 phenotype, accompanied by increased production of inflammatory cytokines. These mediators disrupt tight junctions, induce epithelial apoptosis, and perpetuate cycles of immune activation and tissue injury. This macrophage–cytokine axis not only amplifies local inflammation but also sustains chronic barrier dysfunction, creating a pathogenic overlap between diabetes mellitus-associated intestinal injury and intestinal bowel disease. In this study, we used a low dose streptozotocin and high-fat diet-induced diabetic Sprague–Dawley rat model in both sexes to investigate the effects of chronic hyperglycemia on intestinal inflammation, with particular emphasis on macrophage activation and pro-inflammatory cytokine responses. We found inflammation in both small and large intestines with mucosal injury and barrier disruption, and immune activation involving macrophages and enhanced expression of CD68, iNOS, TNF-α, and IL-6. Female rats were more susceptible to gut-related inflammatory changes due to diabetes. These findings suggest a complex interplay between epithelial stress, immune signaling, and microbial factors supporting the role of intestinal inflammation in the immune–metabolic interaction in diabetes-associated intestinal changes, which may contribute to the pathogenesis of inflammatory bowel disease.
Background:Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide, arising from complex interactions among demographic, clinical, behavioral, and social determinants. Leveraging large, nationally representative datasets such as the 2022 Behavioral Risk Factor Surveillance System (BRFSS) offers a unique opportunity to identify emerging risk patterns, monitor population-level disparities, and inform more targeted prevention strategies. Methods:A total of 221,643 participants from the BRFSS 2022 survey were included after excluding records with missing data. Thirteen key predictors spanning demographics, chronic conditions, and social factors were selected. Data were split into training (80%) and testing (20%) sets. Four machine learning models, XGBoost, Random Forest, Logistic Regression, and Naive Bayes, were developed and evaluated using stratified 10-fold cross-validation. Model performance was assessed via accuracy, F1 score, precision, sensitivity, and ROC AUC. Synthetic Minority Over-sampling Technique (SMOTE) addressed class imbalance. SHAP values provided insights into feature importance and model interpretability. Results:XGBoost demonstrated the best predictive performance (accuracy 94.2%, F1 score 85.3%, ROC AUC 0.94). SHAP analysis highlighted age ≥ 65, male gender, and diabetes as the strongest predictors, with additional contributions from kidney disease, employment status, and social isolation. Protective effects were observed for never smoking and higher education. Stratified analyses revealed that while overweight/obesity (BMI ≥25) was generally associated with higher CVD prevalence, the association was attenuated in older adults, smokers, and those with diabetes or kidney disease, suggesting illness-related weight loss, frailty, and behavioral confounding. These subgroup insights contextualize the apparent "BMI paradox" observed in the aggregate data. Conclusions:Findings from the BRFSS 2022 highlight both established and emerging determinants of CVD risk, including the modifying effects of comorbidities, social isolation, and BMI-related heterogeneity. Beyond algorithmic performance, these results underscore the value of national surveillance data for informing applied, actionable strategies in CVD prevention and risk stratification.
