Background: Health literacy is an increasingly important public health concern. However, little is known about the health literacy of general public in China. The aim of this study was to evaluate the prevalence of low health literacy and demographic associations in Shanghai, China. Methods: This study was a community-based cross-sectional health survey utilizing a multi-stage random sampling design. The sample consisted of 1360 individuals aged 15–69 years with the total community-dwelling Chinese as the sample frame. Health literacy was measured by a questionnaire developed on the basis of a national health literacy manual released by the Chinese Ministry of Health. Multiple logistic regression models were used to identify whether common socio-demographic features were associated with health literacy level. Results: The prevalence of low health literacy was 84.49% (95% CI, 82.56% to 86.41%). The prevalence of low health literacy was negatively associated with the level of education, occupation, and annual household income, but was not associated with gender, age, or the presence of non-communicable chronic disease. Conclusions: Simplifying health services, enhancing health education, and promoting interventions to improve health literacy in high-risk populations should be considered as part of the strategies in the making of health policy in China.

Neuropathic pain remains a prevalent and persistent clinical problem because it is often poorly responsive to the currently used analgesics. It is very urgent to develop novel drugs to alleviate neuropathic pain. Galectin-3 (gal3) is a multifunctional protein belonging to the carbohydrate-ligand lectin family, which is expressed by different cells. Emerging studies showed that gal3 elicits a pro-inflammatory response by recruiting and activating lymphocytes, macrophages and microglia. In the study we investigated whether gal3 inhibition could suppress neuroinflammation and alleviate neuropathic pain following peripheral nerve injury. We found that L5 spinal nerve ligation (SNL) increases the expression of gal3 in dorsal root ganglions at the mRNA and protein level. Intrathecal administration of modified citrus pectin (MCP), a gal3 inhibitor, reduces gal3 expression in dorsal root ganglions. MCP treatment also inhibits SNL-induced gal3 expression in primary rat microglia. SNL results in an increased activation of autophagy that contributes to microglial activation and subsequent inflammatory response. Intrathecal administration of MCP significantly suppresses SNL-induced autophagy activation. MCP also inhibits lipopolysaccharide (LPS)-induced autophagy in cultured microglia in vitro. MCP further decreases LPS-induced expression of proinflammatory mediators including IL-1β, TNF-α and IL-6 by regulating autophagy. Intrathecal administration of MCP results in adecreased mechanical and cold hypersensitivity following SNL. These results demonstrated that gal3 inhibition is associated with the suppression of SNL-induced inflammatory process andneurophathic pain attenuation.

Objectives: To investigate whether combined continuous venovenous hemofiltration and hemoperfusion among paraquat-poisoned patients would improve survival. Design: Prospective, controlled interventional study over 4 years. Setting: Single, tertiary, academic medical center. Patients: We recruited patients admitted to Shanghai Tenth People’s Hospital within 48 hours after paraquat ingestion. Exclusions were under 14 years old, ingestion of paraquat with other toxicants, pregnant, a history of chronic pulmonary disease, psychosis, hyperthyroidism, or diabetes with impaired liver or renal function. Interventions: All patients were assigned to receive continuous venovenous hemofiltration with hemoperfusion therapy (continuous venovenous hemofiltration group) and to receive conventional therapy (conventional group). The study outcomes were death from any cause within 90 days after paraquat ingestion and the frequencies of hypoxia, acute kidney injury, or adverse events. Measurements and Main Results: Of the 110 enrolled patients, 59 were assigned to continuous venovenous hemofiltration group and 51 to conventional group. The two groups had similar baseline demographics and clinical features. At 90 days after paraquat ingestion, 19 of 59 patients (32.2%) in the continuous venovenous hemofiltration group and 29 of 51 patients (56.9%) in the conventional group had died (hazard ratio, 0.43; 95% CI, 0.24–0.76; p = 0.004). In multivariable Cox proportional hazard models controlling for baseline characteristics, combined continuous venovenous hemofiltration and hemoperfusion was independently associated with reduced risk of death compared with conventional therapy (adjusted hazard ratio, 0.35; 95% CI, 0.19–0.64; p = 0.001). Patients in the continuous venovenous hemofiltration group, as compared to the conventional group, had a reduced occurrence rate of hypoxia (40.7% vs 72.5%; p = 0.001) and of acute kidney injury (59.3% vs 78.4%; p = 0.03). Hypophosphatemia and thrombocytopenia were more common in the continuous venovenous hemofiltration group (p < 0.05). Conclusions: In patients with paraquat poisoning, treatment with combined continuous venovenous hemofiltration and hemoperfusion significantly improved 90-day survival rates.

Marital status and survival in patients with non-small cell lung cancer: an analysis of 70006 patients in the SEER database Marital status and survival in patients with non-small cell lung cancer: an analysis of 70006 patients in the SEER database

Gout commonly manifests as a painful, self-limiting inflammatory arthritis. Nevertheless, the understanding of the inflammatory and immune responses underlying gout flares and remission remains ambiguous. Here, based on single-cell RNA-Seq and an independent validation cohort, we identified the potential mechanism of gout flare, which likely involves the upregulation of HLA-DQA1 ⁺ nonclassical monocytes and is related to antigen processing and presentation. Furthermore, Tregs also play an essential role in the suppressive capacity during gout remission. Cell communication analysis suggested the existence of altered crosstalk between monocytes and other T cell types, such as Tregs. Moreover, we observed the systemic upregulation of inflammatory and cytokine genes, primarily in classical monocytes, during gout flares. All monocyte subtypes showed increased arachidonic acid metabolic activity along with upregulation of prostaglandin-endoperoxide synthase 2 (PTGS2). We also detected a decrease in blood arachidonic acid and an increase in leukotriene B4 levels during gout flares. In summary, our study illustrates the distinctive immune cell responses and systemic inflammation patterns that characterize the transition from gout flares to remission, and it suggests that blood monocyte subtypes and Tregs are potential intervention targets for preventing recurrent gout attacks and progression.