IMPORTANCE The origins and development of autism spectrum disorder (ASD) remain unresolved. No individual-level study has provided estimates of additive genetic, maternal, and environmental effects in ASD across several countries. OBJECTIVE To estimate the additive genetic, maternal, and environmental effects in ASD.

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In view of the high incidence of diabetic retinopathy and the functionality of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) in different disease models, the present study aimed to investigate the role of MEG3 in diabetic retinopathy. In the study, patients with diabetic retinopathy, diabetic patients without retinopathy as well as healthy people were included. Fasting blood was extracted from each participant. Serum MEG3 levels were detected by everse transcription-quantitative polymerase chain reaction (RT-qPCR) and serum vascular endothelial growth factor (VEGF) and transforming growth factor-β1 (TGF-β1) levels were detected by ELISA. Also, the effects of high glucose treatment on the expression of MEG3 and VEGF and the effects of MEG3 overexpression on expression of VEGF and TGF-β1 in high glucose-treated ARPE-19 cells were detected by RT-qPCR and western blot analysis to determine the mRNA and protein levels, respectively. It was indicated that serum levels of MEG3 were significantly lower, while the serum levels of VEGF and TGF-β1 were significantly higher in patients with diabetic retinopathy and diabetic patients without retinopathy compared with the healthy controls. Furthermore, slight differences were found between patients with diabetic retinopathy and diabetic patients without retinopathy; however, these differences were not significant. The findings indicated that high glucose upregulated the expression of VEGF mRNA and downregulated the expression of MEG3, MEG3 overexpression reduced the increased expression levels of VEGF and TGF-β1 induced by high glucose treatment. Therefore, it was concluded that lncRNA MEG3 overexpression may inhibit the development of diabetic retinopathy by inhibiting TGF-β1 and VEGF expression.

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There was modest, if any, contribution of maternal effects to liability for ASD, including subtypes AD and SD, and there was no support for shared environmental effects. These results show liability to ASD arises largely from additive genetic variation.

Objective: Familial recurrence risk is an important population-level measure of the combined genetic and shared familial liability of autism spectrum disorder (ASD). Objectives were to

In vivo, cells are located in a dynamic, three-dimensional (3D) cell microenvironment, and various biomaterials have been used to engineer 3D cell microenvironments in vitro to study the effects of the cell microenvironment on the regulation of cell fate. However, conventional hydrogels can only mimic the static cell microenvironment without any synchronous regulations. Therefore, novel hydrogels that are capable of responding to specific stimuli (e.g., light, temperature, pH, and magnetic and electrical stimulations) have emerged as versatile platforms to precisely mimic the dynamic native 3D cell microenvironment. Among these novel hydrogels, photoresponsive hydrogels (PRHs) that are capable of changing their physical and chemical properties after exposure to light irradiation enable the dynamic, native cell microenvironment to be mimicked and show great promise in deciphering the unknown mechanisms of the 3D cell microenvironment in regulating the cell fate. Several reviews have already summarized the advances of PRHs and have focused on specific photosensitive chemical groups and photoresponsive elements or on the reaction categories and mechanism of PRHs. However, a holistic view of novel PRHs, which highlights the multiple physical and chemical properties that can be tuned by remote light activation, as well as their applications in engineering a dynamic cell microenvironment for the regulation of cell behaviors in vitro is still missing and is the focus of this review.

INTRODUCTION: Besides Helicobacter pylori and Epstein-Barr virus, other viruses might play potential roles in gastric carcinogenesis. This systematic review and meta-analysis was conducted to compare the prevalence of the viruses between gastric cancer (GC) and any controls. METHODS: Comprehensive literature was searched up to January 25, 2019, and search was updated on April 6, 2020. The studies that compared the prevalence of viruses other than Epstein-Barr virus between GC and healthy or nonmalignant controls were eligible. Stata 12.0 software was used for heterogeneity tests and meta-analyses. Meanwhile, subgroup analysis, sensitivity analysis, and publication bias evaluation were performed where applicable. The power (1–β) was estimated by the PASS 11 software for each individual study. RESULTS: A total of 41 eligible studies were included, concerning 11 kinds of viruses. Prevalence were significantly higher in GC for hepatitis B virus (odds ratio [OR] = 1.39, 95% confidence interval [CI] 1.11–1.75), human cytomegalovirus (OR = 2.25, 95% CI 1.14–4.43), human papillomavirus (HPV) (OR = 1.63, 95% CI 1.05–2.54), and John Cunningham virus (OR = 2.52, 95% CI 1.26–5.04). In subgroup analyses, HPV-16 infection was significantly associated with GC (OR = 2.42, 95% CI 1.00–5.83). DISCUSSION: This study demonstrated that hepatitis B virus, human cytomegalovirus, HPV, and John Cunningham virus were more prevalent in GC. However, the causal relationship between their infection and risk of GC remains inconclusive, and further investigations are required.