Background Weight regain (WR) and insufficient weight loss (WL) occur in 20–25% of patients after bariatric surgery due to various factors. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown promise in promoting WL; however, evidence regarding their effectiveness in managing WL and preventing WR post-bariatric surgery remains limited. Objective This study aims to evaluate the role of GLP-1RAs in treating and preventing WR following bariatric surgery. Methods A systematic search was conducted across PubMed, Scopus, and Web of Science for studies assessing the impact of GLP-1RAs on WR after bariatric surgery. Results Our search identified 27 original studies, with 10 included in the meta-analysis involving 769 participants (392 treated with GLP-1RAs). The mean age was 44.05 years, with 30.47% male. The time interval from surgery to the initiation of GLP-1RAs treatment ranged from 1.5 to 86.7 months, with treatment durations between 4 and 12 months. The analysis showed significantly greater WL in the GLP-1RAs group compared to placebo (SMD = 0.82, 95% CI 0.23 to 1.42). Subgroup analysis for treatment durations ≤ 6 months indicated a higher WL in the GLP-1RAs group (SMD = 0.79, 95% CI 0.25 to 1.34). Adverse events were primarily gastrointestinal, with nausea significantly more frequently in the GLP-1RAs group (OR = 2.01, 95% CI 1.24 to 3.27). Conclusion GLP-1RAs effectively promote WL among participants experiencing WR after bariatric surgery. Initiating GLP-1RAs therapy shortly after surgery may help prevent WR. Further research is warranted to explore long-term outcomes and optimize treatment protocols for this patient population. Graphical Abstract

Osteomyelitis (OM), an inflammatory condition of the bone tissue, is a complex orthopedic condition marked by chronic inflammation, diagnostic uncertainty, and recurrent infections. Despite standard treatments—including surgical debridement, antimicrobial therapy, and bone reconstruction—many patients continue to experience recurrence and treatment failure. Growing molecular evidence indicates that host genetic factors play a crucial role in shaping immune responses and influencing disease progression in OM. This narrative review synthesizes current knowledge from candidate gene single-nucleotide polymorphism (SNP) association studies to illustrate how specific genetic variations contribute to OM pathogenesis, diagnostic refinement, and treatment outcomes. We examined key immunogenetic variants within genes involved in inflammatory signaling, pathogen recognition, and neutrophil regulation. Our synthesis identifies a landscape of pro-inflammatory SNPs, such as IL-1β rs16944 and NLRP3 rs10754558, that are associated with increased susceptibility to chronic or post-traumatic OM, as well as SNPs that are associated with protective effects that may favor infection resolution, such as within the NOS2 and VDR genes. These SNP-driven differences in inflammasome activity, cytokine pathways, and oxidative stress responses highlight emerging opportunities for individualized therapeutic strategies. This review consolidates these variants, providing a genetic framework to analyze host susceptibility and differentiating high risk from protective genetic profiles. Integrating genomic insights into OM management represents a promising shift toward personalized medicine, enhancing diagnostic precision, informing targeted interventions, and improving prognostic assessment. Continued large-scale validation of candidate SNPs and translational genomic models will be essential to support their future clinical application.

Background: Chondroblastoma is a rare and benign bone tumor originating from immature chondroblasts. Chondroblastoma typically affects long bones; however, it can also occur in the skull, especially the temporal bone. The anterior skull base is a rare location for this tumor, with only two reported cases. Case Presentation: A 26‐year‐old woman presented with epiphora in her right eye and progressive proptosis on the same side. She had a previous biopsy that confirmed the presence of a giant cell tumor of the bone and had undergone an unsuccessful endoscopic surgery. A comprehensive endoscopic procedure subsequently revealed a cartilage‐producing neoplasm consistent with chondroblastoma. Conclusion: We presented a successful case of surgical resection of a chondroblastoma in the anterior skull base. Additionally, we reviewed the existing literature and previously documented cases.

Introduction: This study aims to determine whether incorporating physical therapy into a nonsurgical approach can effectively manage the course of glenohumeral osteoarthritis (OA) and potentially prevent patients from requiring total shoulder arthroplasty (TSA). Methods: This retrospective cohort consisted of patients diagnosed with glenohumeral OA between 2010 and 2021 using ICD-9, ICD-10, and current procedural terminology codes in the PearlDiver database. Two- and five-year TSA rates were compared between patients who had physical therapy within 1 year after glenohumeral OA diagnosis and patients who did not. Results: The study consisted of 2,710,463 patients with glenohumeral OA. After propensity score matching, among patients with corticosteroid injection, patients who received physical therapy had significantly higher 2- and 5-year TSA rates compared with those without physical therapy (2-year TSA: 0.60% vs. 0.35%, OR [95% CI]: 1.74 [1.50, 2.01] and 5-year TSA: 1.13% vs. 0.65%, OR [95% CI]: 1.74 [1.56, 1.93]). A similar association was also significant among patients without corticosteroid injection (0.35% vs. 0.16%, OR [95% CI]: 2.17 [2.03, 2.21] and 0.78% vs. 0.37%, OR [95% CI]: 2.11 [2.01, 2.21]). Conclusion: Individuals who had physical therapy as a part of their nonsurgical treatment did not have any decrease in the probability of requiring TSA.

Spinal dysraphism arises from neural tube closure defects occurring between 2 and 6 weeks of gestation, leading to severe complications after birth. It is typically classified as either open or closed, depending on whether the defect is covered by skin. Despite advances in diagnosis, current methods for detecting spinal dysraphism still lack the necessary sensitivity and specificity, driving the pursuit of more effective treatments. The complications, often arising from incomplete spine and brain formation or the exposure of the spinal cord to neurotoxic amniotic fluid, underscore the critical need for prenatal intervention. Current therapeutic approaches remain inadequate, underscoring the urgent need for novel strategies. Tissue engineering, a promising field of medical innovation, holds significant potential for enhancing neural regeneration and repair. Integrating advanced tissue engineering techniques with existing prenatal neurosurgical treatments offers a transformative opportunity to improve outcomes for patients affected by spinal dysraphism.