
Background:Cellulitis is a common bacterial skin infection associated with substantial morbidity and economic burden in the United States, yet long-term national mortality trends remain poorly characterized. Methods:We analyzed multiple cause-of-death data from CDC WONDER from 1999 through 2024 using ICD-10 codes L03, H60, K12.2, and L98.3. Age-adjusted mortality rates (AAMRs) per 100 000 were calculated using the 2000 US standard population, with temporal trends assessed via Joinpoint regression across demographic, geographic, and urbanization subgroups. Results:A total of 139 485 cellulitis-related deaths were identified over the study period. The overall AAMR was 1.5 per 100 000, remaining stable from 1999 through 2011 before increasing significantly through 2024 [annual percent changes (APC): 2.39%, P = 0.0016]. Mortality rose sharply with age, with adults aged ≥85 years accounting for 31.0% of all deaths. Men had consistently higher AAMRs than women (1.7 vs. 1.4). NH American Indian or Alaska Native persons bore the greatest racial/ethnic burden (AAMR: 2.2), with rates rising from 2.2 in 1999 to 3.5 by 2024. The West and Midwest recorded the highest regional AAMRs (1.7 and 1.6, respectively), and nonmetropolitan areas sustained higher and more volatile mortality than metropolitan areas throughout (1.7 vs. 1.4). Conclusion:Cellulitis-related mortality increased significantly over recent decades and exhibits pronounced demographic and geographic disparities. Targeted prevention strategies, improved access to timely care for high-risk populations, and strengthened public health surveillance are needed to reduce this burden.
Background:Pediatric seizure disorders are clinically and genetically heterogeneous. Whole-exome sequencing has improved the detection of rare genetic variants in childhood epilepsy; however, data from pediatric populations in Southeast China remain limited. This study aimed to characterize the genetic landscape of pediatric seizure disorders in Southeast China and to evaluate the clinical diagnostic yield of whole-exome sequencing. Materials and methods:This retrospective observational study included 21 pediatric patients with seizure disorders who were recruited at the Fifth Hospital of Xiamen, Fujian, China, between January 2021 and June 2024. Clinical data were extracted from medical records. Whole-exome sequencing was performed on DNA extracted from peripheral blood. Sequence variants were annotated, filtered, and classified according to the guidelines of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. Copy-number variants were evaluated using exome-based algorithms. Descriptive statistics were used because of the limited sample size. Results:WES identified three clinically relevant, likely pathogenic findings in 3 of 21 patients, corresponding to a provisional diagnostic yield of 14.3%. The remaining 62 of 65 variants were of uncertain significance (VUS). The three retained variants included a GLI3 frameshift variant (exon 2: c.90_91insCAGATGTGAGC; p.Glu31Glnfs*3) and two copy-number variants (16p13.12-16p13.11 duplication and Xp22.31 deletion) with established clinical significance. Functional analysis of all 65 variants revealed that ion channel genes and neurodevelopmental genes were the most frequently affected categories. Conclusion:Whole-exome sequencing identified clinically relevant genetic findings in a subset of Southeast Chinese children with seizure disorders. The novel GLI3 frameshift variant may suggest an expansion of the GLI3-associated phenotypic spectrum, but further segregation, functional validation, and larger cohort studies are needed. The high proportion of variants of uncertain significance highlights the ongoing challenges of genetic interpretation in pediatric seizure disorders.
Introduction:Left-sided gallbladder (LSG) is a rare congenital anomaly that may not be detected by routine ultrasonography. Although uncommon, it has important implications for surgical safety due to associated variations in biliary anatomy. Case presentation:We report three patients with symptomatic cholelithiasis in whom preoperative ultrasonography suggested normal anatomy. In all cases, LSG was identified intraoperatively. Two patients underwent successful laparoscopic cholecystectomy following careful anatomical reassessment, while one required conversion to open surgery due to difficulty in safely identifying biliary structures. Discussion:These cases highlight the limitations of ultrasonography in identifying positional anomalies and emphasize the importance of intraoperative awareness. LSG can distort the usual anatomical landmarks and increase the risk of bile duct injury. A careful, anatomy-first approach is essential when such variations are encountered. Conclusion:Normal ultrasonography does not exclude anatomical variation. Safe surgical outcomes depend on early recognition, cautious dissection, and sound intraoperative judgment.
Background/objectives:Parkinson's disease (PD) is a neurodegenerative disorder with limited treatment options. This study investigated the therapeutic potential of astragalin (AST) in PD and explored its underlying mechanisms. Methods:Network pharmacology identified nine overlapping genes between the AST and PD target sets. Protein-protein interaction networks were constructed using Cytoscape and STRING. Based on KEGG pathway analysis, AST may influence PD through the IL-17 signaling pathway. Molecular docking simulations demonstrated a strong binding affinity between AST and key target proteins. In vitro, various concentrations of AST were applied to SH-SY5Y cells, and cell viability and inflammation-related factors were assessed using Cell Counting Kit-8 assays, RT-qPCR, immunoblotting, and enzyme-linked immunosorbent assay. In vivo, mice received intraperitoneal injections of AST, followed by behavioral assessments to evaluate AST's effects on PD symptoms. Results:Nine overlapping genes were identified. Molecular docking analyses revealed robust binding interactions between AST and PTGS2, PRSS1, PRKACA, and PIK3CG. In vitro results indicated that 40 μM and 60 μM concentrations of AST partially mitigated MPP+-induced cytotoxicity and morphological damage. Furthermore, treatment with AST led to a reduction in inflammatory factor expression while inhibiting IKKα/IκBα/p65 phosphorylation. In vivo experiments demonstrated that AST improved motor function and ameliorated cognitive impairments induced by MPTP administration, while enhancing tyrosine hydroxylase protein expression without causing significant organ damage. Conclusions:This study provides comprehensive evidence that AST may alleviate symptoms associated with PD by modulating the IL-17 signaling pathway. These findings highlight the potential of AST as a novel treatment for PD. Graphical abstract: Graphical abstract available at: https://links.lww.com/MS9/B316.
A 76-year-old male patient presented with a 16-year history of chronic, progressive urinary hesitancy requiring intermittent catheterization. After transabdominal ultrasonography, prostate MRI, and transrectal prostate biopsy were performed, he was diagnosed with benign prostatic hyperplasia (BPH). Preoperative computed tomography angiography of the prostatic arteries was performed to assess their origins and number. Subsequently, a prostate artery embolization (PAE) was performed. During the procedure, a contrast agent was infused into the catheter balloon, and three-dimensional digital subtraction angiography, along with C-arm rotation, was used to accurately locate the prostatic arteries. Super-selective embolization of the prostatic arteries was then performed under road-mapping to reduce procedure time, radiation exposure, and the risk of inadvertent embolization. At the 1-month postoperative follow-up, the patient was able to urinate independently. In this case, the patient's prostate volume measured 238 mL, and PAE was successfully performed under local anesthesia. Compared with previously reported cases in the literature, this patient exhibited a larger prostate volume and a longer history of urinary obstruction. During the procedure, the prostatic arteries were accurately identified, and embolization was performed. Postoperatively, the patient experienced significant relief from lower urinary tract symptoms, resulting in a remarkable improvement in quality of life.