Although anxiety disorders (ADs) have been recognized as one of the most prevalent mental disorders in mainland China, the prevalence of ADs has not been reported until now. The lack of a consolidated and comparable review on the prevalence of ADs in mainland China necessitated this meta-analysis to measure the prevalence. To identify the relevant studies on ADs for the analysis, we searched published studies in electronic databases up to July 2015. The pooled prevalence in the overall population and the prevalences by gender and location were estimated. A total of 21 studies were included in the analysis. The pooled current/lifetime prevalences of ADs, generalized AD, non-specific AD, panic disorder, social phobia, agoraphobia, specific phobia, post-traumatic stress disorder, and obsessive-compulsive disorder were 24.47‰/41.12‰, 5.17‰/4.66‰, 8.30‰/6.89‰, 1.08‰/3.44‰, 0.70‰/4.11‰, 0.19‰/2.15‰, 0.63‰/19.61‰, 0.49‰/1.83‰, and 0.90‰/3.17‰, respectively. Subgroup analyses indicated that compared with males, females had a consistently significantly higher prevalence of ADs. However, no difference was observed between those in urban and rural areas. The pooled prevalence of ADs was relatively lower than those of some other countries. A higher prevalence of ADs in women than in men was commonly observed, whereas the prevalences in urban and rural areas were nearly the same.

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Background: Impaired gut microbiota leads to pathogenic bacteria infection, pro-inflammatory response and postweaning diarrhea. Enterotoxigenic Escherichia coli (ETEC) K88 is a major cause of post-weaning diarrhea in weaned piglets. Fermented soybean meal (FSBM) could relieve diarrhea, alleviate inflammatory response, and modulate gut microbiota of weaned piglets. We used ETEC K88-challenged weaned piglet model to investigate the effects of FSBM on the growth performance, inflammatory response and cecal microbiota. Twenty-four crossbred piglets (6.8 ± 0.5 kg; 21 ± 2 days of age) were allotted into 2 treatment fed the diets with or without FSBM (6% at the expense of soybean meal). Six weaned piglets in each diet treatment were challenged by ETEC K88 (1 × 10 9 CFU/ piglets) on day 15. The experimental period lasted for 20 days.

Objective. The specific autoantibodies and antigens that mediate systemic lupus erythematosus (SLE)-related organ injuries remain largely unknown. This study was undertaken to investigate the antibodymediated immune response that leads to SLE skin lesions.Methods. The study included 85 SLE patients with lupus-specific skin lesions and 31 without skin lesions. The reactivity of serum antibody with skin antigens was determined by immunoblotting using human foreskin as the substrate. Skin antigens were identified using mass spectrometry. Serum antibody was isolated by affinity purification and was injected intracutaneously into mouse skin to determine pathogenicity. Serum antibody levels were monitored by enzyme-linked immunosorbent assay.Results. We determined that 78% of the patients with skin lesions had serum antibodies reactive with 35-kd and/or 25-kd skin antigens, which was significantly higher than the percentage of patients without skin lesions (P < 0.0001), suggesting a correlation between immune response and skin lesions. Acidic ribosomal protein P0 (RPLP0) and galectin 3 were 2 target antigens identified from 35-kd and 25-kd proteins, respectively. Purified serum anti-RPLP0 and anti-galectin 3 antibodies induced lupus-like histologic changes after intracutaneous injection. Anti-RPLP0 and anti-galectin 3 antibody levels were significantly higher in SLE patients than in healthy controls and decreased with skin recovery. Anti-galectin 3 antibody levels were not significantly higher in SLE patients than in patients with dermatomyositis or scleroderma, but strongly related to lupus cutaneous vasculitis. Additionally, levels of the 2 antibodies were positively correlated with leukopenia and C3 deficiency, and the anti-RPLP0 antibody level was also positively correlated with arthritis and SLE disease activity. Conclusion. Our findings indicate that the immune response mediated by serum anti-RPLP0 and anti-galectin 3 antibodies plays a key role in the pathogenesis of SLE skin lesions. These findings provide new insights into the mechanism of SLE-related organ disorders.Systemic lupus erythematosus (SLE) is a unique autoimmune disease characterized by extremely heterogeneous clinical manifestations and the most complex autoantibody profile (1-5). Autoantibodies not only serve as a marker of disease diagnosis, activity, and severity (6,7), but they also play a primary and pivotal role in the initiation and exacerbation of SLE disease (8,9). A cluster of anti-nuclear debris antibodies, including anti-double-stranded DNA (anti-dsDNA), anti-