Aims: The aim of this meta-analysis is to evaluate the potential correlation between obesity and overweight, and the vulnerability to urinary incontinence (UI) in women aged middle-aged and above.Methods: We searched PubMed, Cochrane Library, and Embase for observational studies published between the inception of the databases and April 25, 2023. A fixed-effects model was used when the P>0.1 and the I² ≤ 50%. In cases where I² ≥ 50% (indicating significant heterogeneity), a random-effects model was applied. For the purpose of evaluating publication bias, a funnel plot and Egger’s test were used. Stata 14.0 was used for all statistical analyses.Findings: This meta-analysis includes 16 observational studies, covering29,618 individuals. The pooled analysis shows that being overweight(25 kg/m²≤BMI<30kg/m²) in middle-aged and elderly women is more likely to develop UI (OR=1.27; 95% CI: 1.17-1.37; I² = 51.8%, P=0.013). Middle-aged and elderly women with obesity(30 kg/m²≤BMI<35 kg/m²) are significantly more likely to develop UI (OR=1.60; 95% CI: 1.42-1.81; I² = 71.8%, P=0.000). In addition, the results indicated a higher probability of UI in middle-aged and older women with obesity class II (BMI≥35 kg/m²) (OR=1.85; 95% CI: 1.59-2.16; I^2 = 48.1%, P=0.103). In subgroup analysis, there is no direct relationship between the obesity in middle-aged and elderly women and an increased risk of stress urinary incontinence (SUI) (OR=1.31; 95% CI: 0.99-1.74; I² = 63.7%, P=0.011). In middle-aged and elderly women with obesity are more likely to develop urgent urinary incontinence (UUI) (OR=2.11; 95% CI: 1.54-2.89; I² = 80.2%, P=0.000).Conclusion: In this meta-analysis, overweight and obesity are associated with an increased risk of UI in middle-aged and elderly women. Obesity and overweight are independent risk factors for UI, as demonstrated by this study.Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42023421986.

Thyroid-associated ophthalmopathy (TAO), an ordinary extrathyroid syndrome of Graves' disease (GD), is closely associated with immunity. T helper (Th) 17, Th1, and Th2 cells in Th lineages are thought to be related to the disease pathogenesis. Recently, there has been growing evidence that Th17.1 cells are involved in the development and progression of TAO. The characteristics of this pathology are similar to those of Th1 and Th17 lymphocytes, which secrete interferon (IFN)-γ and interleukin (IL)-17A. This paper reviews the potential role of the Th17.1 subgroup pathogenesis of TAO. The therapeutic effects of drugs that can modulate Th17.1 cell populations are also highlighted. Rich Th17.1 cells exist in peripheral blood and ocular tissues of patients suffering from thyroid eye disease (TED), especially those with severe or steroid-resistant TAO. The bias of Th17.1 cells to secrete cytokines partly determines the pathological outcome of TAO patients. Th17.1 cells are important in regulating fibrosis, adipocyte differentiation, and hyaluronic acid production. In summary, the Th17.1 subpopulation is essential in the onset and progression of TED, and targeting Th17.1 cell therapy may be a promising therapeutic approach.

Fibrosis leads to organ failure and death, which is the final stage of many chronic diseases. Triptolide (TPL) is a terpenoid extracted from the traditional Chinese medicine Tripterygium wilfordii Hook. F (TwHF). Triptolide and its derivatives (Omtriptolide, Minnelide, (5R)-5-hydroxytriptolide) have been proven to have a variety of pharmacological effects. This study comprehensively reviewed the antifibrotic mechanism of TPL and its derivatives, and discussed the application of advanced nanoparticles (NPs) drug delivery system in the treatment of fibrotic diseases by TPL. The results show that TPL can inhibit immune inflammatory response, relieve oxidative stress and endoplasmic reticulum stress (ERS), regulate collagen deposition and inhibit myofibroblast production to play an anti-fibrosis effect and reduce organ injury. A low dose of TPL has no obvious toxicity. Under pathological conditions, a toxic dose of TPL has a protective effect on organs. The emergence of TPL derivatives (especially Minnelide) and NPs drug delivery systems promotes the anti-fibrosis effect of TPL and reduces its toxicity, which may be the main direction of anti-fibrosis research in the future.

Objective: The objective of this study is to investigate the ability of Ramulus Mori (Sangzhi) alkaloid tablets (SZ-A) to ameliorate obesity and lipid metabolism disorders in rats subjected to a high-fat diet (HFD) through metagenomics, untargeted lipidomics, targeted metabolism of bile acid (BA), and BA pathways, providing a novel perspective on the management of metabolic disorders.Methods: In this research, HFD-fed rats were concurrently administered SZ-A orally. We measured changes in body weight (BW), blood lipid profiles, and liver function to assess therapeutic effects. Liver lipid status was visualized through H&E and Oil Red O. Gut microbiota composition was elucidated using metagenomics. The LC-MS-targeted metabolomics approach was utilized to define the fecal BA profiles. Furthermore, the lipid metabolomics of adipose tissue samples was investigated using an LC-MS analysis platform. The expression levels of the BA receptor were determined by western blotting. Additionally, serum insulin (INS), glucagon-like peptide-1 (GLP-1), and inflammatory cytokines were quantified using an ELISA kit. The integrity of the colonic epithelial barrier was assessed using immunofluorescence.Results: SZ-A notably decreased BW and blood lipid levels in obese rats while also alleviating liver injury. Additionally, SZ-A reduced the serum levels of leptin (LEP), INS, and GLP-1, indicating its potential to modulate key metabolic hormones. Most notably, SZ-A substantially improved gut microbiota composition. Specifically, it reshaped the gut microbiota structure in HFD-fed rats by increasing the relative abundance of beneficial bacteria, such as Bacteroides, while decreasing the populations of potentially harmful bacteria, such as Dorea and Blautia. At the BA level, SZ-A decreased the levels of harmful BAs, including hyodeoxycholic acid (HDCA), deoxycholic acid (DCA), 12-keto lithocholic acid (12-KLCA), lithocholic acid (LCA), and muricholic acid (MDCA). Between the model group and SZ-A, 258 differentially abundant metabolites were detected, with 72 upregulated and 186 downregulated. Furthermore, these BAs are implicated in the activation of the FXR-FGF15 and TGR5-GLP-1 pathways in the intestine. This activation helps to alleviate HFD-fed intestinal inflammation and restore intestinal barrier damage by modulating inflammatory cytokines and bolstering the intestinal barrier’s capabilities.Conclusions: Our findings indicate that SZ-A effectively modulates BW, serum lipid profiles, and liver function in HFD-fed rats. Moreover, SZ-A exerts a positive influence on inflammatory cytokines, thereby mitigating inflammation and promoting the restoration of the intestinal barrier. Significantly, our research indicates that adjusting the gut microbiome and BA levels could serve as an effective approach for both preventing and treating obesity and related metabolic dyslipidemia.