Endoscopic Surveillance for Premalignant Esophageal Lesions: A Community-Based Multicenter, Prospective Cohort Study.

BACKGROUND & AIMS: Mild and moderate dysplasia are major premalignant lesions of esophageal squamous cell carcinoma (ESCC); however, evidence of the progression risk in patients with these conditions is extremely limited. We aimed to assess the incidence and risk factors for advanced neoplasia in patients with mild-moderate dysplasia. METHODS: This prospective cohort study included patients with mild-moderate dysplasia from 9 regions in rural China. These patients were identified from a community-based ESCC screening program conducted between 2010 and 2016 and were offered endoscopic surveillance until December 2021. We estimated the incidence of advanced esophageal neoplasia, including severe dysplasia, carcinoma in situ, or ESCC, and identified potential risk factors using the Cox regression model. RESULTS: The 1183 patients with mild-moderate dysplasia were followed up over a period of 6.95 years. During follow-up evaluation, 88 patients progressed to advanced neoplasia (7.44%), with an incidence rate of 10.44 per 1000 person-years. The median interval from the progression of mild-moderate dysplasia to advanced neoplasia was 2.39 years (interquartile range, 1.58-4.32 y). A total of 74.47% of patients with mild-moderate dysplasia experienced regression to nondysplasia, and 18.09% showed no lesion progression. Patients with mild-moderate dysplasia who had a family history of esophageal cancer and were age 55 years and older showed 97% higher advanced neoplasia yields than all patients with mild-moderate dysplasia. CONCLUSIONS: In a country with a high incidence of ESCC, patients with mild-moderate dysplasia showed an overall risk of advanced neoplasia progression of 1.04% per year. Patients with mild-moderate dysplasia would be recommended for endoscopic surveillance during the first 2 to 3 years.

Hippocampal Crhr1 conditional gene knockout ameliorated the depression-like behavior and pathological damage in male offspring mice caused by chronic stress during pregnancy.

Numerous studies have demonstrated that chronic stress during pregnancy (CSDP) can induce depression and hippocampal damage in offspring. It has also been observed that high levels of corticotropin-releasing hormone (CRH) can damage hippocampal neurons, and intraperitoneal injection of a corticotropin releasing hormone receptor 1 (CRHR1) antagonist decreases depression-like behavior and hippocampal neuronal damage in a mouse depression model. However, whether CSDP causes hippocampal damage and depression in offspring through the interaction of CRH and hippocampal CRHR1 remains unknown and warrants further investigation. Therefore, hippocampal Crhr1 conditional gene knockout mice and C57/BL6J mice were used to study these questions. Depression-related indexs in male offspring mice were examined using the forced swim test (FST), sucrose preference test (SPT), tail suspension test (TST) and open field test (OFT). Serum CRH levels were measured by enzyme-linked immunosorbent assay (ELISA). Golgi-Cox staining was used to examine the morphological changes of hippocampal neuronal dendrites. Neuronal apoptosis in the hippocampal CA3 regions was detected by terminal deoxynucleotidy transferase dUTP nick end labeling (TUNEL) staining. The levels of mammalian target of rapamycin (mTOR), phosphorylated mTOR (p-mTOR) and protein kinase B (AKT) proteins were measured by Western blot analysis. This study showed that CSDP induces depression-like behavior, hippocampal neuronal dendrite damage and apoptosis in male offspring mice. Conditional gene knockout of hippocampal Crhr1 in mice reduced CSDP-induced depression-like behavior, hippocampal neuronal dendrite damage and apoptosis in male offspring, and counteracted the CSDP-induced decreased expression of p-Akt and mTOR activity in male offspring hippocampus. These findings demonstrated that CSDP might inhibit the Akt/mTOR pathway by increasing the levels of CRH, leading to increased CRH-mediated activation of hippocampal CRHR1, thereby inducing synaptic impairment and apoptosis in hippocampal neurons, which in turn leads to depression-like behavior in offspring.

The effects of air pollution on the lung cancer mortality in rural areas of eastern China: a multi-region study.

Recently, the burden of lung cancer (LC) has attracted global attention. Meanwhile, LC has become the leading cause of death in China. Many studies found a strong link between air pollutants and the risk of LC mortality in some large cities, but the results have been inconsistent, and most studies have only focused on the daily effects of six pollutants in large cities, ignoring their potential cumulative effects. This study was to investigate the weekly effects of six air pollutants (CO, NO2, O3, PM2.5, PM10, and SO2) on LC mortality in rural areas of eastern China and to further clarify which population groups were susceptible to air pollution and seasonal trends. First, a generalized additive model was combined with a distributed lag nonlinear model to evaluate the individual impact of air pollution on LC deaths in each area. The random-effect model was then used to pool the associations between air pollutants and LC mortality risk in ten counties or districts. The results showed that six air pollutants had a statistically significant effect on the risk of LC mortality at different lag weeks. The effects of NO2, PM10, and CO on weekly LC mortality were strongest at a cumulative lag of 1, 0, and 1 week, respectively, the maximum cumulative risk ratio (RR) of 1.37 (95%CI: 1.23 to 1.52), 1.30 (95%CI: 1.15 to 1.46), and 1.30 (95%CI: 1.17 to 1.43), with interquartile concentrations increasing. In summary, air pollution was an important factor in LC mortality, and the effect was stronger on males, the elderly, and during cold season. It was suggested that relevant departments should formulate air pollution management measures for the elderly, males, and in different seasons in rural areas and reduce the burden of lung cancer caused by air pollution.

Light therapy in non-seasonal depression: An update meta-analysis.

The effect of light therapy in treating seasonal affective disorder has been demonstrated amongst previous studies. However, the effect of light therapy in treating non-seasonal depression remains unclear. This meta-analysis aimed to determine the efficacy of light therapy in non-seasonal depression. We searched for randomized controlled trials (RCTs) in the PubMed, Web of Science, Chinese National Knowledge Infrastructure, and Chinese Biomedical Database up to February 2020. The pooled post-trial standardized mean difference in depression scores with corresponding 95% confidence intervals was calculated to evaluate the efficacy of light therapy in non-seasonal depression. A total of 23 RCTs with 1120 participants were included. The meta-analysis demonstrated the light therapy was significantly more effective than comparative treatments. Subgroup analyses revealed that none of the factors explained the significantly heterogeneity. Light therapy has a statistically significant mild to moderate treatment effect in reducing depressive symptoms, can be used as a clinical therapy in treating non-seasonal depression. But the quality of evidence is still low, more well-designed studies with larger sample size and high quality are needed to confirm the efficiency of light therapy in treating non-seasonal depression.