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The continuous development of urbanization has dramatically changed people’s living environment and lifestyle, accompanied by the increased prevalence of chronic diseases. However, there is little research on the effect of urbanization on gut microbiome in residents. Here we investigated the relation between living environment and gut microbiota in a homogenous population along an urban-rural gradient in Ningxia China. According to the degree of urbanization, the population is divided into four groups: mountainous rural (MR) represents non-urbanized areas, mountainous urban (MU) and plain rural (PR) represent preliminary urbanization, and plain urban (PU) is a representative of complete urbanization. Studies have found that with the deepening of urbanization, the prevalence of chronic diseases, such as diabetes, dyslipidemia, fatty liver, gallstones, and renal cysts, have gradually increased. The intestinal richness and diversity of the microbial community were significantly reduced in the PR and the PU groups compared with the MR and the MU groups. Based on linear discriminant analysis selection, the significantly enriched genera Faecalibacterium, Prevotella, and Pseudobutyrivibrio in the MR group gradually decreased in the MU, the PR, and the PU groups. Effect size results revealed that both residence and diet had an effect on intestinal microbiota. Our results suggested that the disparate patterns of gut microbiota composition were revealed at different levels of urbanization, providing an opportunity to understand the pathogenesis of chronic diseases and the contribution of the “rural microbiome” in potential protection against the occurrence of chronic diseases.

ObjectiveTo investigate the differences in gene expression between children and adults with Kashin-Beck disease (KBD).Methods12 children with KBD and 12 healthy children were selected and divided into 4 KBD vs. control pairs matched according to age and gender, with each pair having 3 KBD children and 3 healthy children. Additionally, 15 adults with KBD and 15 healthy adults were selected and divided into 5 KBD vs. control pairs matched according to age and gender, with each pair having 3 KBD adults and 3 healthy adults. Total RNA was isolated from peripheral blood mononuclear cells (PBMCs) respectively. A total of 367 target genes were selected based on previous genome-wide gene expression profile analysis. Expression levels of the 367 genes were evaluated by customized oligonucleotide microarray and the differentially expressed genes were identified. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was conducted to validate the microarray data.ResultsA total of 95 (25.9%) genes in KBD children and 158 (43.1%) genes in KBD adults were found to exhibit more than two-fold change in gene expression level relative to healthy controls. By comparing differentially expressed genes identified in KBD children to those of KBD adults, 42 genes were found to be differentially expressed only in KBD children. And 105 genes were found to be differentially expressed only in KBD adults. Further, 16 differentially expressed genes common to both KBD children and adults were found to be asynchronously expressed in KBD children compared to KBD adults.ConclusionSignificant differences in gene expression pattern were identified between KBD children and KBD adults, indicating different molecular mechanisms underlying cartilage lesions of KBD children and KBD adults. In addition, bone development-related genes GDF5 (expression ratio = 2.14±0.02) and DIO2 (expression ratio = 0.11±0.05) may contribute to the development of KBD in children rather than in adults.

Background In the northern region of China, many greenhouse vegetable farmers are exposed to high cumulative levels of pesticides due to long-term work in greenhouses that impacts their health. The aim of the current study was to identify the relationship between cumulative pesticide exposure and sleep disorders among farmers in Yinchuan, Northwest China. Methods A cross-sectional study was conducted for 3 consecutive years in 2015, 2016 and 2017. Using a random sampling to select the resident teams, 1366 participants were enrolled, and information was collected via face-to-face interviews by trained investigators. Ordinal logistic, multinomial logistic and poisson logistic regression models were used to identify the associations between cumulative exposure intensity (CEI) and sleep disorders. Results High CEI ( OR = 1.56, 95% CI : 1.02–3.38) was associated with short sleep duration when compared with low CEI in the Full Model. CEI was not associated with long sleep duration. Self-rated sleep quality was associated with medium ( OR = 1.46, 95% CI : 1.10–2.00) and high ( OR = 2.50, 95% CI : 1.83–3.40) CEI. Similarly, having difficulty sleeping was associated with medium ( OR = 1.52, 95% CI : 1.02–2.24) and high ( OR = 1.74, 95% CI : 1.16–2.62) CEI. Differences in the associations by gender were also noted. Conclusion CEI was associated with sleep disorders, and gender differences were observed. Efforts should be made by local governments to address sleep problems that result from cumulative pesticide exposure in farmers, and gender differences should be considered. Electronic supplementary material The online version of this article (10.1186/s12889-019-6712-6) contains supplementary material, which is available to authorized users.

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Abstract. Keshan disease (KD) is an endemic cardiomyopathy. The etiology of KD is selenium deficiency; however, it is not the only one and there is no effective approach to preventing and curing this disease. The aim of the present study was to explore the differences in the role of arachidonic acid (AA) by the cytochrome P450 enzyme between chronic KD (CKD), dilated cardiomyopathy (DCM) and control patients. Reverse transcription-quantitative polymerase chain reaction was used to detect the CYP1A1 and CYP2C19 gene expression levels in 6 CKD patients, 6 DCM and 6 healthy controls. An enzyme-linked immunosorbent assay kit was applied to detect serum protein expression of CYP1A1 and CYP2C19, AA and epoxyeicosatrienoic acids (EETs), and 20-hydroxyeicosatetraenoic acids (20-HETE) in 67 CKD patients, 28 DCM, and 58 controls. The present results showed that the expression levels of CYP1A1 and CYP2C19 genes were significantly upregulated compared with the control group (P<0.01). The expression level of the CYP1A1 protein in the CKD (49.55±35.11 pg/ml) and DCM (46.68 ±13.01 pg/ml) groups were enhanced compared with the control group (44.33±16.76 pg/ml) (P<0.01). The production of the CYP2C19 protein in the CKD (57.52±28.22 pg/ml) and DCM (56.36±11.26 pg/ml) groups was enhanced compared with the control group (51.43±10.76 pg/ml). The concentrations of AA in the CKD (126.27±47.91 ng/ml) and DCM (133.24±58.67 ng/ml) groups were also significantly increased compared to the control (78.16±23.90 ng/ml) (P<0.001). The concentration of 20-HETE in the CKD (198.34±17.22 ng/ml) and DCM (194.46±20.35 ng/ml) groups were also significantly increased compared to the control (130.10±16.10 ng/ml) (P<0.001). The only difference between CKD and DCM was for the expression of the CYP1A1 gene and protein.The maximum concentration of EETs was in the control group (44.37±6.14 pg/ml), and the other two groups were lower than the control group (P<0.001). These findings indicated that AA-derived CYP450 metabolites may have a critical role in the pathogenesis of KD and DCM. Upregulation of the CYP2C19 gene and frequent protein expression may be a protective compensation reaction, while CYP1A1 may aggravate myocardial injury.