Frozen shoulder (FS), characterized by pain and restricted mobility, remains a challenging condition with unclear optimal treatment. This study aims to investigate the development of FS research, identify hotspot treatments, and verify their efficacy. Analyzing 3139 FS-related publications from the Web of Science Core Collection revealed a significant rise in publications (R² = 0.9478), with the United States as a leader in this research area. Our keyword analysis pinpointed suprascapular nerve block (SSNB) as a notable research focus since 2021. To assess the effectiveness of SSNB, we conducted a meta-analysis of eight randomized controlled trials including 435 patients. The results at the 6-8 weeks follow-up showed SSNB significantly reduced pain and improved active shoulder function compared to intra-articular corticosteroid injections (IACI). Specifically, SSNB led to considerable enhancements in abduction (SMD: 12.88; 95 % CI: 4.13, 21.64; p = 0.004; I² = 54 %), flexion (SMD: 9.16; 95 % CI: 6.50, 11.82; p < 0.00001; I² = 0 %), and external rotation (SMD: 18.03; 95 % CI: 6.59, 29.48; p = 0.008; I² = 59 %). Additionally, there was a significant reduction in Shoulder Pain and Disability Index (SPADI) scores (SMD: 4.46; 95 % CIs: 7.75, -1.17; p = 0.008; I² = 59 %). Despite these findings, no differences were observed in the improvement of passive activities between the SSNB and IACI groups at any follow-up. This study supports the short-term benefits of SSNB for FS, prompting further investigation into its long-term efficacy and comparison with other treatments.

Background: Osteoporosis (OP) is a systemic bone disease often undiagnosed until fractures occur. Metabolites may influence OP, offering potential biomarkers or therapeutic targets. This study investigates the causal relationship between circulating metabolites and OP-related phenotypes using Mendelian Randomization (MR). Methods: GWAS data on 233 metabolic traits from 136,016 participants were analyzed through two-sample MR. Linkage disequilibrium score regression (LDCS) was used to estimate genetic correlations between metabolic traits and OP-related phenotypes, leveraging European ancestry linkage disequilibrium scores to account for polygenicity and stratification. MR employed the inverse-variance weighted (IVW) method, with sensitivity analyses via MR-Egger, MR-PRESSO, and weighted median methods to address pleiotropy and confounders. Results: LDCS identified significant genetic correlations between metabolites and bone mineral density (BMD) phenotypes, with total body BMD (toBMD) showing the strongest associations. Thirty-five metabolite traits, including apolipoprotein A-I, exhibited significant linkages. Among 79 metabolites influencing BMD, serum acetate levels were significantly associated with femoral neck BMD (OR: 1.28, 95% CI: 1.02–1.62), lumbar spine BMD (OR: 1.73, 95% CI: 1.32–2.27), and total body BMD (OR: 1.21, 95% CI: 1.04–1.42). Creatinine levels were consistently linked to reduced BMD, including lumbar spine BMD (OR: 0.88, 95% CI: 0.79–0.99). Triglycerides in IDL and VLDL particles also contributed to BMD variation. Conclusions: Significant genetic correlations and causal relationships were observed between specific metabolites and OP, highlighting key traits as potential biomarkers of bone health. These findings enhance the understanding of OP pathogenesis and suggest future preventive strategies.

The gut–brain axis is a key interface between neuropsychiatric and digestive disorders, however, the underlying shared genetic mechanisms and microbial mediators remain poorly understood. Utilizing genome-wide association study (GWAS) data from 18 neuropsychiatric and 24 digestive disorders, along with microbial quantitative trait loci (mbQTL) data encompassing 211 taxa (N = 18,340), we conducted a comprehensive analysis integrating linkage disequilibrium score regression, MAGMA gene-based pleiotropy mapping, and Mendelian randomization. We identified 12 significant genetic correlations between gut–brain disorder pairs, including attention-deficit/hyperactivity disorder (ADHD) and fatty liver disease. In total, 5339 pleiotropic genes were discovered, with MSH5 appearing in 28 disorder pairs. Pathway enrichment analysis implicated immune regulation and synaptic signaling as core biological processes. Novel causal relationships were also uncovered, such as ADHD increasing the risk of irritable bowel syndrome. Co-localization analysis validated three causal associations. Microbiota-focused analyses further demonstrated a protective role of Actinobacteria against stroke, resolving previous inconsistencies in the literature. Collectively, these findings highlight the dual role of the gut microbiota—as both modulator and contributor—and provide critical genetic insights that may guide the development of targeted interventions across the gut–brain axis.

Chondrosarcoma is 1 of the most common malignant bone tumors, with dedicated research being conducted by scientists worldwide. The purpose of this study was to guide researchers in identifying valuable scholars, institutions, and countries, provide recommendations for journal submissions, and explore research trends and hotspots in chondrosarcoma studies through literature analysis. Data for this study were collected from the Web of Science Core Collection website. The R package bibliometrix was utilized for citation metrics analysis, VOSviewer for network analysis, and CiteSpace for generating keywords citation burst maps. The analysis focused on publications from 2000 to 2023, identifying trends, authorship patterns, and collaboration networks. A total of 2085 articles were initially identified, but after excluding non-English articles and those outside the study’s time range, 2022 articles were included. The field comprised 9954 author records, with an average of 6.37 coauthors per document and 13.9% international co-authorships. Publications in chondrosarcoma research have shown an average annual growth rate of 3.9%. The most influential author identified was Tang Chih-Hsin from China Medical University. Significant contributions came from China Medical University and Leiden University, with China showing a dramatic increase in publications while the United States maintained a leading position in the field. The study highlights an increasing trend in chondrosarcoma research publications and identifies key contributors and institutions. Cancer emerged as 1 of the most influential journals in the field. Future research is likely to focus on targeted therapy for refractory chondrosarcomas, indicating a potential new hotspot in the ongoing efforts to understand and treat this malignancy.

Background Previous investigations have elucidated epidemiological associations linking smoking to neuropsychiatric and gastrointestinal diseases, yet the underlying causal relationships remain enigmatic. To shed light on this matter, we undertook a Mendelian randomisation(MR) study with the aim of gauging the potential causal association between smoking and the susceptibility to neuropsychiatric and gastrointestinal tract diseases. Methods We meticulously collected and preprocessed genome-wide association study (GWAS) data encompassing smoking (280,508 cases and 180,558 controls) as well as neuropsychiatric and gastrointestinal phenotypes (n = 6,681 to 87,3341). To investigate the genetic correlation between smoking and diseases, we employed linkage disequilibrium score regression. We further applied multi-trait analysis of GWAS to identify the shared risk single-nucleotide polymorphisms (SNPs) implicated in both smoking and diseases. Pleiotropic genes were annotated by enrichment analysis. Subsequently, bidirectional MR analysis was performed to infer causality. Results Our findings, supported by robust evidence derived from an expansive sample size, demonstrate that smoking exerts a causal influence on merely six of these diseases, while no disease was found to causally impact smoking. Intriguingly, we discovered 513 pleiotropic genes enriched in pathways such as the regulation of growth and synapses, suggesting a potential shared genetic basis between smoking and these diseases, leading to aberrant neural development. Remarkably, among the 42 diseases scrutinized, a significant genetic correlation was exclusively observed with gastroesophageal reflux disease (GRED). Furthermore, we identified risk SNPs shared by smoking and GRED. Conclusions This study revealed the shared genetic basis and causal effects connecting smoking to neuropsychiatric and gastrointestinal diseases, thereby providing novel etiological insights into the role of smoking in these diseases.