Samer Al-Dury

Background: Assistant performance is important for endoscopy workflow, yet nurse training is often informal. We evaluated whether a structured simulation-and-theory program improves nurse-dependent workflow during live endoscopy. Methods: In this prospective parallel-group study, 20 endoscopy nurses were grouped 1:1 into Simulation+Theory or Control. Each nurse assisted 10 recorded live procedures performed by the same endoscopist (5 gastroscopies and 5 colonoscopies; 200 nurse–procedure observations). The prespecified procedure mix included diagnostic biopsies, dilation, cold-snare polypectomy, hot-snare polypectomy, endoscopic mucosal resection, and endoscopic submucosal dissection. The primary endpoint was device-to-field time, defined at the procedure level using one predefined index request per procedure. The primary analysis was performed at the nurse level, comparing within-nurse change from baseline (cases 1–3) to post-training (cases 4–10). Results: Groups performed similarly at baseline. From case 4 onward, the Simulation group showed shorter device-to-field times and maintained this advantage through case 10. In the primary nurse-level analysis, the between-group difference in change from baseline to post-training corresponded to a time ratio of 0.80 (95% confidence interval 0.76–0.85; p < 0.001), indicating approximately 20% faster device readiness after structured training. Supportive sensitivity analyses showed the same directional pattern. Conclusions: A brief structured simulation-and-theory program was associated with faster nurse device readiness during live endoscopy. These findings support ongoing structured nurse training as a practical strategy to improve workflow efficiency in endoscopy services.

Methotrexate (MTX) remains a cornerstone therapy for chronic inflammatory diseases (e.g. , rheumatoid arthritis, psoriasis). However, long-standing concerns about MTX hepatotoxicity - especially liver fibrosis - have historically led to conservative monitoring and routine invasive liver biopsies at predefined cumulative dose thresholds. These practices often prompted early discontinuation of MTX therapy. These concerns originated from early liver biopsy studies in high-dose MTX patients that did not adequately account for metabolic risk factors. Emerging evidence indicates that advanced fibrosis is rare in MTX-treated patients and usually attributable to coexisting metabolic comorbidities (e.g. , obesity, insulin resistance) rather than the cumulative MTX dose itself. Moreover, noninvasive fibrosis assessment modalities and recent large cohort studies demonstrate that MTX at standard doses with folate supplementation seldom drives fibrogenesis independently. This review reappraises MTX-related fibrosis risk in light of contemporary data and highlights a shift from dose-driven biopsy protocols to risk-based, noninvasive monitoring strategies. Recognizing that MTX is less hepatotoxic than historically assumed can prevent unnecessary drug discontinuation and refocus management on modifiable metabolic risk factors.

Metabolic pressure shifts signaling pathways of nuclear receptors, including the bile acid receptor FXR, which are sensitive to nutritional inputs. We performed an FXR ChIP-seq–centered multiomic analysis of liver biopsy samples from individuals with or without obesity, who were treated with either placebo or the FXR agonist obeticholic acid, to define metabolic adaptions of FXR signaling pathways. FXR occupied substantially more DNA binding sites in individuals with obesity, and FXR activation by OCA robustly changed the transcriptional output. Integration of ChIP-seq and RNA-seq data showed that mitochondrial function and substrate oxidation were the top metabolic pathways selectively modulated by FXR activation in individuals with obesity. FXR activation restored compromised substrate oxidation by enhancing β-oxidation and oxidative phosphorylation along with antagonizing ROS production. In line with this, the amount of reduced glutathione in patients with obesity normalized after OCA treatment. In summary, FXR signaling profoundly differs in patients with obesity, consisting of changes in DNA binding profiles and transcriptional programs, which enhance energy substrate utilization in this patient cohort.

This review addresses the vital role of vaccinations in managing patients with chronic liver disease (CLD), especially in the context of the post-COVID-19 landscape. The pandemic has highlighted the unique vulnerabilities of CLD patients, including those awaiting liver transplantation and post-transplant individuals, who face heightened risks of infection due to compromised immune responses. Recent advancements in vaccine technology, such as mRNA platforms, novel adjuvants, and advanced delivery systems, have significantly accelerated vaccine development, enhancing both speed and efficacy. Moreover, the emergence of personalized vaccines, tailored to everyone’s unique immunological profile, presents new opportunities, particularly for those with chronic conditions. This review synthesizes the current state of evidence regarding vaccine recommendations for CLD patients, focusing on their response to vaccinations and proposing effective strategies to protect this vulnerable group from vaccine-preventable diseases. It also explores the challenges in implementing these strategies and considers the impact of emerging vaccine delivery systems on improving outcomes for CLD patients. The paper aims to provide nuanced guidance on vaccination in the rapidly evolving healthcare landscape, addressing both technological innovations and comprehensive patient care strategies.

Recipients of allogeneic hematopoietic stem cell transplantation (allo-HSCT) for hematological diseases are at risk of severe disease and death from COVID-19. To determine the safety and immunogenicity of BNT162b2 and mRNA-1273 COVID-19 vaccines, samples from 50 infection-naive allo-HSCT recipients (median, 92 months from transplantation, range, 7-340 months) and 39 healthy controls were analyzed for serum immunoglobulin G (IgG) against the receptor binding domain (RBD) within spike 1 (S1) of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; anti–RBD-S1 IgG) and for SARS-CoV-2–specific T-cell immunity, reflected by induction of T-cell–derived interferon-γ in whole blood stimulated ex vivo with 15-mer SI-spanning peptides with 11 amino acid overlap S1-spanning peptides. The rate of seroconversion was not significantly lower in allo-transplanted patients than in controls with 24% (12/50) and 6% (3/50) of patients remaining seronegative after the first and second vaccination, respectively. However, 58% of transplanted patients lacked T-cell responses against S1 peptides after 1 vaccination compared with 19% of controls (odds ratio [OR] 0.17; P = .009, Fisher’s exact test) with a similar trend after the second vaccination where 28% of patients were devoid of detectable specific T-cell immunity, compared with 6% of controls (OR 0.18; P = .02, Fisher’s exact test). Importantly, lack of T-cell reactivity to S1 peptides after vaccination heralded substandard levels (<100 BAU/mL) of anti–RBD-S1 IgG 5 to 6 months after the second vaccine dose (OR 8.2; P = .007, Fisher’s exact test). We conclude that although allo-HSCT recipients achieve serum anti–RBD-S1 IgG against SARS-CoV-2 after 2 vaccinations, a deficiency of SARS-CoV-2–specific T-cell immunity may subsequently translate into insufficient humoral responses.