Objective To explore the role of enteral nutrition in the treatment of functional delayed gastric emptying. Methods Among 15 patients with functional delayed gastric emptying after resection of esophageal or gastric cardiac carcinoma, 10 patients were treated with enteral nutrition( EN group),5 patients were treated with parenteral nutrition (PN group). Postoperative hospital stay, gastrointestinal decompression amount, recovering time of postoperative gastric emptying were observed to assess the efficacy of enteral nutrition. Results The average postoperative hospital stay was ( 14. 4 ± 4. 6) days in the EN group, whereas (20. 3 ±6. 6) days in the PN group. The average recovering time of postoperative gastric emptying was (19 ±9)days in the PN group and( 12 ± 4)days in the EN group. Conclusion The method of EN can enhance gastric emptying and is effective for functional delayed gastric emptying after resection of esophageal or gastric cardiac carcinoma

Objective To investigate the mechanism underlying the inhibitory effects of Demethylzeylasteral(T-96)on non-small cell lung cancer(NSCLC)cells.Methods We first examined the effects of different concentrations(1,3,10,and 30 μmol/L)of demethylzeylasteral on morphology and cell number of A549 and H1299 cells.The changes in proliferation,cell viability,migration,invasion,and apoptosis of A549 and H1299 cells following demethylzeylasteral treatment were detected using clone formation,CCK-8,cell scratch,Transwell,and flow cytometric assays,and the effect of SC79 treatment against demethylzeylasteral-induced cell apoptosis was assessed.Western blotting was performed to detect the changes in expressions of E-cadherin,N-cadherin,vimentin,Bax,Bcl-2 and cleaved caspase-3 and phosphorylation of AKT/CREB in demethylzeylasteral-treated A549 and H1299 cells and the cellular expressions of apoptotic proteins following treatment with both demethylzeylasteral and SC79.Results T-96 treatment caused elongation of the cell body and widening of the intercellular space and significantly inhibited cell viability,proliferation,migration and invasion of A549 and H1299 cells(P<0.05).Flow cytometry showed that demethylzeylasteral induced apoptosis in both A549 and H1299 cells,whereas SC79 treatment obviously attenuated its pro-apoptotic effect(P<0.05).Western blotting revealed up-regulated expressions of Bax and cleaved caspase-3 proteins and lowered Bcl-2 expression level in demethylzeylasteral-treated A549 and H1299 cells,but co-treatment with SC79 obviously attenuated the expressions of the apoptotic proteins.T-96 significantly up-regulated the expression level of E-cadherin,down-regulated the expressions of N-cadherin and vimentin,and inhibited the phosphorylation of AKT and CREB in the two cell lines(P<0.05).Conclusion T-96 inhibits the proliferation,migration and invasion and induces apoptosis of NSCLC cells possibly by inhibiting the AKT/CREB signaling pathway.

Objective To investigate the mechanism underlying the inhibitory effects of Demethylzeylasteral(T-96)on non-small cell lung cancer(NSCLC)cells.Methods We first examined the effects of different concentrations(1,3,10,and 30 μmol/L)of demethylzeylasteral on morphology and cell number of A549 and H1299 cells.The changes in proliferation,cell viability,migration,invasion,and apoptosis of A549 and H1299 cells following demethylzeylasteral treatment were detected using clone formation,CCK-8,cell scratch,Transwell,and flow cytometric assays,and the effect of SC79 treatment against demethylzeylasteral-induced cell apoptosis was assessed.Western blotting was performed to detect the changes in expressions of E-cadherin,N-cadherin,vimentin,Bax,Bcl-2 and cleaved caspase-3 and phosphorylation of AKT/CREB in demethylzeylasteral-treated A549 and H1299 cells and the cellular expressions of apoptotic proteins following treatment with both demethylzeylasteral and SC79.Results T-96 treatment caused elongation of the cell body and widening of the intercellular space and significantly inhibited cell viability,proliferation,migration and invasion of A549 and H1299 cells(P<0.05).Flow cytometry showed that demethylzeylasteral induced apoptosis in both A549 and H1299 cells,whereas SC79 treatment obviously attenuated its pro-apoptotic effect(P<0.05).Western blotting revealed up-regulated expressions of Bax and cleaved caspase-3 proteins and lowered Bcl-2 expression level in demethylzeylasteral-treated A549 and H1299 cells,but co-treatment with SC79 obviously attenuated the expressions of the apoptotic proteins.T-96 significantly up-regulated the expression level of E-cadherin,down-regulated the expressions of N-cadherin and vimentin,and inhibited the phosphorylation of AKT and CREB in the two cell lines(P<0.05).Conclusion T-96 inhibits the proliferation,migration and invasion and induces apoptosis of NSCLC cells possibly by inhibiting the AKT/CREB signaling pathway.

Objective:To investigate the changes of serum miR-33 in patients with type 2 diabetes mellitus (T2DM) with non-alcoholic fatty liver disease (NAFLD), and analyze the relationship between miR-33 and non-alcoholic fatty liver disease and type 2 diabetes mellitus.Methods:From July 2019 to January 2020, 25 healthy subjects (control group), 25 NAFLD patients (NAFLD group), 25 T2DM patients hospitalized in the department of endocrinology (T2DM group) and 25 T2DM patients with NAFLD (NAFLD combined with T2DM group) were selected. The basic data of the subjects were collected, and the levels of miR-33 and other biochemical indexes in the serum of the four groups were detected. The risk factors for type 2 diabetes mellitus with nonalcoholic fatty liver disease were analyzed.Results:There was no significant difference between T2DM group and T2DM group with NAFLD in course of disease, medication history and incidence of complications ( P<0.05). The levels of serum miR-33 in T2DM group, NAFLD group and T2DM combined with NAFLD group were higher than those in healthy people, and the level of serum miR-33 in the combined group was the highest ( P<0.05). The differences in systolic blood pressure, total cholesterol (TC), fasting blood glucose (FPG), glycosylated hemoglobin, triglycerides (HbA1c), triglycerides (TG), high density lipoprotein (HDL-C), uric acid (UA), serum creatinine (Scr), gamma-glutamyl transpeptidase (GGT), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in the four groups were statistically significant ( P<0.05). The level of miR-33 was positively correlated with systolic blood pressure, FPG, HbA1c, TG, UA and GGT ( P<0.05), and negatively correlated with the level of HDL-C ( P<0.05). MiR-33, systolic blood pressure and FPG increased the risk of NAFLD in T2DM patients ( OR=8.999, 1.083, 2.071, P<0.05). Conclusions:Serum miR-33 is the influencing factor of T2DM and NAFLD diseases and the risk factor of T2DM patients with NAFLD. It may affect the occurrence and development of metabolic diseases by participating in the regulation of glycolipid metabolism.

Objective:To analyze and compare the association between different obesity-related indices and vitamin D deficiency in middle-aged and elderly population dwelled in Lanzhou city.Methods:From May, 2011 to September, 2012, middle-aged and elderly individuals with complete baseline data were included via randomly cluster sampling from 3 communities in Lanzhou. The subjects were divided into 4 subgroups by vitamin D levels and various obesity-related indices were compared across subgroups with the same gender. The relationship between the obesity-related indices and the severity of vitamin D deficiency was analyzed using Spearman correlation analysis, and the effects of different obesity-related indices on the severity of vitamin D deficiency was analyzed using multivariate logistic regression analysis.Results:A total of 9 437 residents were included. The overall prevalence of vitamin D deficiency was 97.7%. Compared with the group with lower vitamin D level, participants in the group with higher vitamin D level showed evidently lower body mass index (BMI), waist circumference (WC), lipid accumulation product (LAP), visceral adiposity index (VAI) and triglyceride/ high density lipoprotein cholesterol (TG/HDL-C) ratio in the total population and females, while only WC, LAP, VAI and TG/HDL-C in the males (all P<0.05). Spearman correlation analysis showed that BMI, WC, LAP, VAI and TG/HDL-C were positively correlated with the severity of vitamin D deficiency in the total population and the females, while only LAP, VAI and TG/HDL-C in the males (all P<0.05) . Multivariate logistic regression analysis showed that higher levels of these obesity related indices were correlated with more severe vitamin D deficiency in the total population and the females, while only higher LAP, VAI and TG/HDL-C in the males (all P<0.05). The effects of higher LAP was the most prominant in the total population ,the females and the males. Conclusion:Various obesity phenotypes are closely related to vitamin D deficiency in middle-aged and elderly women, while only visceral obesity and abnormal lipid metabolism are related to vitamin D deficiency in middle-aged and elderly men, with LAP being the most important influencing factor.

The accurate annotation of transcription start sites(TSSs)and their usage are critical for the mechanistic understanding of gene regulation in different biological contexts.To fulfill this,specific high-throughput experimental technologies have been developed to capture TSSs in a genome-wide manner,and various computational tools have also been developed for in silico pre-diction of TSSs solely based on genomic sequences.Most of these computational tools cast the problem as a binary classification task on a balanced dataset,thus resulting in drastic false positive predictions when applied on the genome scale.Here,we present DeeReCT-TSS,a deep learning-based method that is capable of identifying TSSs across the whole genome based on both DNA sequence and conventional RNA sequencing data.We show that by effectively incorporating these two sources of information,DeeReCT-TSS significantly outperforms other solely sequence-based methods on the precise annotation of TSSs used in different cell types.Furthermore,we develop a meta-learning-based extension for simultaneous TSS annotations on 10 cell types,which enables the identification of cell type-specific TSSs.Finally,we demonstrate the high precision of DeeReCT-TSS on two independent datasets by correlating our predicted TSSs with experimentally defined TSS chromatin states.The source code for DeeReCT-TSS is available at https://github.-com/JoshuaChou2018/DeeReCT-TSS_release and https://ngdc.cncb.ac.cn/biocode/tools/BT007316.