No abstract

Background: Although psoriasis occurs worldwide, the prevalence varies considerably between different peoples and regions. In China, a questionnaire-based study was carried out in 1987 and the prevalence of psoriasis was found to be 0.12%. Since then, no large-scale, populationbased study has been reported. Objectives: To obtain the accurate figures for the prevalence of psoriasis in China. Methods: A population-based survey was conducted in 6 cities. The cluster sampling method was used to select communities in each city. The subjects were required to fill out self-reporting questionnaires during a face-to-face interview and also received physical examination by dermatologists. Results: 19,974 subjects were visited and 17,345 completed the questionnaires and received dermatological examination. 102 subjects (0.59%) were found to have psoriasis. After standardization, the prevalence of psoriasis was 0.47%. The prevalence of psoriasis in males and females was 0.54% and 0.44% respectively. 97.06% of the patients had psoriasis vulgaris. 28.43% of the patients reported a family history of psoriasis. 59.80% of patients experienced a negative influence on the quality of life. Conclusions: This population-based and dermatologist-confirmed study showed that the prevalence of psoriasis in China is 0.47%, which is higher than that reported in 1987.

It is unknown whether transforming growth factor ␤1 (TGF-␤1) signaling uniformly participates in fibrogenic chronic liver diseases, irrespective of the underlying origin, or if other cytokines such as interleukin (IL)-13 share in fibrogenesis (e.g., due to regulatory effects on type I pro-collagen expression). TGF-␤1 signaling events were scored in 396 liver tissue samples from patients with diverse chronic liver diseases, including hepatitis B virus (HBV), hepatitis C virus (HCV), Schistosoma japonicum infection, and steatosis/steatohepatitis. Phospho-Smad2 staining correlated significantly with fibrotic stage in patients with HBV infection (n ‫؍‬ 112, P < 0.001) and steatosis/steatohepatitis (n ‫؍‬ 120, P < 0.01), but not in patients with HCV infection (n ‫؍‬ 77, P > 0.05). In tissue with HBx protein expression, phospho-Smad2 was detectable, suggesting a functional link between viral protein expression and TGF-␤1 signaling. For IL-13, immunostaining correlated with fibrotic stage in patients with HCV infection and steatosis/steatohepatitis. IL-13 protein was more abundant in liver tissue lysates from three HCV patients compared with controls, as were IL-13 serum levels in 68 patients with chronic HCV infection compared with 20 healthy volunteers (72.87 ؎ 26.38 versus 45.41 ؎ 3.73, P < 0.001). Immunohistochemistry results suggest that IL-13-mediated liver fibrogenesis may take place in the absence of phospho-signal transducer and activator of transcription protein 6 signaling. In a subgroup of patients with advanced liver fibrosis (stage >3), neither TGF-␤ nor IL-13 signaling was detectable. Conclusion: Depending on the cause of liver damage, a predominance of TGF-␤ or IL-13 signaling is found. TGF-␤1 predominance is detected in HBV-related liver fibrogenesis and IL-13 predominance in chronic HCV infection. In some instances, the underlying fibrogenic mediator remains enigmatic. (HEPATOLOGY 2009;50:230-243.)

Regulated necrosis has been reported to exert an important role in the pathogenesis of various diseases, including renal ischemia-reperfusion (I/R) injury. Damage to renal tubular epithelial cells and subsequent cell death initiate the progression of acute kidney injury (AKI) and subsequent chronic kidney disease (CKD). We found that ferroptosis appeared in tubular epithelial cells (TECs) of various human kidney diseases and the upregulation of tubular proferroptotic gene ACSL4 was correlated with renal function in patients with acute kidney tubular injury. XJB-5-131, which showed high affinity for TECs, attenuated I/R-induced renal injury and inflammation in mice by specifically inhibiting ferroptosis rather than necroptosis and pyroptosis. Single-cell RNA sequencing (scRNA-seq) indicated that ferroptosis-related genes were mainly expressed in tubular epithelial cells after I/R injury, while few necroptosis- and pyroptosis-associated genes were identified to express in this cluster of cell. Taken together, ferroptosis plays an important role in renal tubular injury and the inhibition of ferroptosis by XJB-5-131 is a promising therapeutic strategy for protection against renal tubular cell injury in kidney diseases.