19043 research outputs found
Sort by
Risk of Postoperative Complications Following Total Knee or Hip Arthroplasty Associated with Patients Who Consume Alcohol: A Systematic Review Protocol
InTouch Week of October 6, 2025
NYMC Goes Pink for Breast Cancer Awareness Month Summer Research Fellowships Empower Medical Students to Explore, Innovate, and Lead International Symposium on Adolescent and Young Adult NHL Has Far Reach A Look Inside NYMC with the 2025-2026 Social Media Ambassadors SOM Welcomes New Faculty Pet the Stress Away Brings Joy to NYMC Stay Warm with Savings on Hoodies In The Community: College Joins Forces at Westchester Heart Walk to Fight Heart Disease and Stroke In The Community: SHSP Students and Faculty Partner with the White Plains Youth Bureau for Community Health and Wellness Day Faculty Spotlight: Christopher Whitehurst, Ph.D., Cracks the Code of EBV Student Spotlight: Isabella Perea Caicedo, on Pride, Identity, and Community during Hispanic Heritage Monthhttps://touroscholar.touro.edu/in_touch/1376/thumbnail.jp
12-LIPOXYGENASE (12-LOX) PLAYS A KEY ROLE IN TISSUE INFLAMMATION AND DYSFUNCTION
Inflammation and immune cell activation in islets lead to pancreatic β-cell dysfunction and loss of mass, leading to type 2 diabetes development. Lipoxygenases, group of enzymes, that catalyze the oxygenation of cellular poly-unsaturated fatty acids to form lipid inflammatory mediators. 12-Lipoxygenase protein (12-LOX) converts arachidonic acid to 12-hydroperoxyeicasatetranoic acid (12-HPETE), which is then reduced to a more stable 12-hydroxyeicosatetraenoic acid (12-HETE) by glutathione peroxidase. In the islets, increased expression or activity of 12-LOX catalyzes the production of 12-HETE to accelerate inflammation and promote oxidative stress. 12-LOX has been identified in both rodent and human endocrine pancreas and is upregulated in both species in pre-diabetes and T2D. Also, evidence suggests that SARS-CoV-2 infection aggravates diabetes, and diabetic patients have severe outcomes. In addition, SARS-CoV-2 infection increases 12-LOX products in platelets, lungs, and vascular system. Elevated levels of 12-HETE are reported in serum and lung-derived fluids of patients undergoing severe SARS-CoV-2 infection. With this information, we hypothesized that Increased 12-LOX expression contributes to insulin resistance and β-cell dysfunction, and it plays an important role in exacerbating tissue inflammation and β-cell dysfunction in COVID-19 infection. Specifically, Insulin resistance is associated with increased 12-LOX expression, and 12-LOX participates in the pathology of SARS-CoV2 infection and may lead to β-cell dysfunction associated with diabetic pathology. In this study, I evaluated the molecular mechanisms leading to activation and downstream functions of human 12-LOX in the human beta cell in insulin resistance using an insulin receptor antagonist, S961, in non-diabetic and T2D pancreatic islet donors. To test this hypothesis, we analyzed human islet 12-LOX protein expression, mRNA levels, and eicosanoid levels to link human ALOX12 expression and 12-LOX production to impaired insulin receptor signaling. There was a significant increase of ALOX12 mRNA and 12-LOX in the presence of S961-induced insulin resistance in non-diabetic islets and an increase in 12-HETE in T2D islet donors xiv compared to the non-diabetic donors. Next, to determine the link between insulin resistance and 12-LOX in vivo, I used samples from a β-cell specific insulin receptor knockout mouse that manifests a local β-cell signaling defect and spontaneously develops T2D. Using this novel mouse model, we studied ALOX12 expression by PCR and 12-LOX protein by immunostaining in isolated islets at various time points. Freshly isolated islets from βIRKO and littermate control mice were examined at ages 4, 9-11, and 18 weeks. There was a peak increase of 12-LOX in the islets at 9-11 weeks of age in the βIRKOs compared to control mice. The data also suggests ALOX12 but not ALOX 15 expression in the βIRKO mouse islets compared to control mice. Immune cell activation or inflammation is also observed in βIRKO mice compared to the wild type, specifically in the pancreatic islet. These new data suggest that 12-LOX plays a key role in inducing inflammation and β-cell dysfunction in this mouse model of localized insulin resistance and T2D. In a follow-up aim, we investigated the potential role of 12-LOX in inflammation associated with SARS-CoV-2 infection in decedents with diabetes. We obtained lung and pancreatic sections of COVID-19 decedents without diabetes and with diabetes and determined 12-LOX protein and mRNA levels. The studies demonstrated an elevated expression of 12-LOX protein and mRNA levels in lungs and pancreas samples from COVID-19 + decedents with diabetes. These interesting findings led us to move into in-vivo studies in the K-18hACE2 transgenic mice, a mouse model of COVID-19. Both male and female mice were inoculated with a high dose of SARS-CoV-2 and were treated with a specific 12-LOX small molecule inhibitor, VLX-1005 (30mg/kg; i.p) for 24-48 hours post-infection for 7-12 days. The results revealed significantly higher survival with minimal body weight loss in the VLX-1005-treated male mice compared to the vehicle-treated mice group, especially when the treatment was initiated 48 hours after the infection and continued for 12 days. The survival rates were higher in VLX-1005-treated male than female mice. In VLX-1005-treated male mice, there was a significant reduction in the expression of key chemokines and cytokines known to be associated with severe COVID-19 infection. Histopathological evaluation of the lung showed resolution of inflammation in xv VLX-1005 treated mice 14 days post-infection. 12-LOX expression was also increased in the pancreas of infected mice. These results suggest that inhibition of 12-LOX could provide therapeutic efficacy against COVID-19 infection by reducing hyper-inflammatory response. In conclusion, this study provides evidence that 12-LOX plays a key role in inflammation and may lead to β-cell dysfunction in a diabetic pathology, including COVID-19 infection-associate diabetic complications
Live in the Moment
Great blue heron in Pleasantville, NY on a beautiful autumn day.
Spending time in nature has been proven to boost overall well-being
Hazy Summer Sunset at Scarborough
The faint glimmers of the setting sun reflect off a northbound Metro-North passenger train as it travels through Scarborough, NY, with the Mario M. Cuomo Tappan Zee Bridge and Sleepy Hollow Lighthouse visible in the background. // Summer 202
Gut Microbiome Dysbiosis and Its Contribution to Carcinogenesis
The gut microbiome, a diverse community of microorganisms within the gastrointestinal (GI) tract, plays a pivotal role in maintaining health through digestion, immune regulation, and homeostasis. Emerging evidence links gut microbiome dysbiosis—a disruption in its composition and function—to the development and progression of various cancers, particularly within the GI tract. This review explores the multifaceted relationship between the gut microbiome and carcinogenesis, highlighting key microbial mechanisms, including chronic inflammation, production of carcinogenic metabolites, and immune modulation. Specific pathogens such as Fusobacterium nucleatum, Escherichia coli, and Helicobacter pylori are implicated in colorectal, gastric, and esophageal cancers, respectively, through pathways that promote tumor initiation and progression.
Diagnostic advances, including microbial biomarkers and non-invasive stooland breath-based tests, offer significant promise for early detection. Therapeutically, interventions targeting the microbiome, such as probiotics, prebiotics, fecal microbiota transplantation, and dietary modifications, have demonstrated potential in restoring microbial balance, enhancing immune responses, and improving treatment efficacy. However, challenges persist in distinguishing causation from correlation and standardizing methodologies. It can be noted that future research must prioritize longitudinal studies, personalized microbiome-based therapies, and exploration of microbial metabolites to fully leverage the gut microbiome in cancer prevention and treatment. This research has provided critical insights that underscore the transformative potential of microbiome when it comes to advancing precision oncology and reducing cancer burden
Comprehensive Approaches to Pain Management in Postoperative Spinal Surgery Patients: Advanced Strategies and Future Directions
Effective postoperative pain management remains a major clinical challenge in spinal surgery, with poorly controlled pain affecting up to 50% of patients and contributing to delayed mobilization, prolonged hospitalization, and risk of chronic postsurgical pain. This review synthesizes current and emerging strategies in postoperative spinal pain management, tracing the evolution from opioid-centric paradigms to individualized, multimodal approaches. Multimodal analgesia (MMA) has become the cornerstone of contemporary care, combining pharmacologic agents, such as non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and gabapentinoids, with regional anesthesia techniques, including erector spinae plane blocks and liposomal bupivacaine. Adjunctive nonpharmacologic modalities like early mobilization, cognitive behavioral therapy, and mindfulness-based interventions further optimize recovery and address the biopsychosocial dimensions of pain. For patients with refractory pain, neuromodulation techniques such as spinal cord and peripheral nerve stimulation offer promising results. Advances in artificial intelligence (AI), biomarker discovery, and nanotechnology are poised to enhance personalized pain protocols through predictive modeling and targeted drug delivery. Enhanced recovery after surgery protocols, which integrate many of these strategies, have been shown to reduce opioid use, hospital length of stay, and complication rates. Nevertheless, variability in implementation and the need for individualized protocols remain key challenges. Future directions include AI-guided analytics, regenerative therapies, and expanded research on long-term functional outcomes. This review provides an evidence-based framework for pain control following spinal surgery, emphasizing integration of multimodal and innovative approaches tailored to diverse patient populations
Clinical Validation of a Vaginal Cervical Cancer Screening Self-Collection Method for At-Home Use: A Nonrandomized Clinical Trial
Importance: One-quarter of US women who are at risk for cervical cancer delay screening. Self-collected (SC) cervical screening was recently US Food and Drug Administration (FDA)-approved in the US for use in a health care setting only; an at-home SC option is crucial to address clinic-related barriers to screening. Objective: To clinically validate the use of an SC device that was designed for optimal at-home performance, safety, ease-of-use, and dry storage and transport. Design, Setting, and Participants: This nonrandomized clinical trial used a prospective method comparison study design. Participants aged 25 to 65 years were recruited from 16 clinical sites in the US including community and academic practices from November 20, 2023, to April 5, 2024. Data analysis was conducted from April to August 2024. Intervention: Eligible participants collected a sample with the SC method, followed by a clinician-collected (CC) sample. The SC sample was eluted into PreservCyt at the laboratory and both samples were tested on an FDA-approved high risk human papillomavirus (hrHPV) test approved for primary screening. Participants were followed up for safety and completed usability and screening preference surveys. Main Outcome and Measures: The primary outcome measures were positive percentage agreement (PPA) and negative percentage agreement for detection of hrHPV between the SC and CC samples. Other study measures included clinical sensitivity for high grade cervical dysplasia and usability. Results: Of 609 screening-eligible participants, 599 (262 aged 30-39 years [43.7%]; 583 identified as female [97.3%]) had paired SC-CC samples, of which 582 had valid paired samples included in the end point analysis. Among the 582 evaluable paired samples, the PPA between SC compared with paired CC samples for detection of hrHPV was 95.2% (95% CI, 92.1%-97.1%; 278 of 292 participants). The absolute clinical sensitivity for detection of high-grade cervical dysplasia was 95.8% (95% CI, 86.0%-98.8%; 46 of 48 participants), equivalent to the CC (relative sensitivity, 1.00). Nearly all participants (555 of 601 participants [92.3%]) reported that the device instructions were easy or very easy to understand and also that they would choose SC if they knew the results were comparable to CC results (560 of 602 participants [93.0%]). Conclusions and Relevance: In this nonrandomized clinical trial, SC samples collected with the device showed equivalent clinical sensitivity and exceeded the PPA end point for cervical screening. This SC method was found to be easy to use and to be a preferred option with high clinical performance intended for use in an at-home setting. Trial Registration: ClinicalTrials.gov Identifier: NCT06120205