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To explore the protective effects of live or pasteurizedA total of 96 Sprague-Dawley (SD) rats were randomly assigned to 8 groups, including 6 experimental groups and 2 control groups, with 12 rats in each group. HFD combined with STZ injection was given to the rats to create a simulated model of the progression of diabetes mellitus type 2. In addition, the rats were treated with different doses of live or pasteurizedCompared with the HFD control group, rats in the group treated withOral administration of

To investigate the effects ofINS-1 cells were divided into three groups, normal, repair, and protect groups, and subsequently every group was subjected withThere was no significant change in INS-1 cell morphology after co-incubation with 3 types of

Previous studies have shown that increasing estradiol concentrations had a toxic effect on the embryo and were deleterious to embryo adhesion. In this study, we evaluated the physiological impact of estradiol concentrations on endometrial cells to reveal that serum estradiol levels probably targeted the endometrium in controlled ovarian hyperstimulation (COH) protocols. An attachment model of human choriocarcinoma (JAr) cell spheroids to receptive-phase endometrial epithelial cells and Ishikawa cells treated with different estradiol (10−9 M or 10−7 M) concentrations was developed. Differentially expressed protein profiling of the Ishikawa cells was performed by proteomic analysis. Estradiol at 10−7 M demonstrated a high attachment rate of JAr spheroids to the endometrial cell monolayers. Using iTRAQ coupled with LC–MS/MS, we identified 45 differentially expressed proteins containing 43 significantly upregulated and 2 downregulated proteins in Ishikawa cells treated with 10−7 M estradiol. Differential expression of C3, plasminogen and kininogen-1 by Western blot confirmed the proteomic results. C3, plasminogen and kininogen-1 localization in human receptive endometrial luminal epithelium highlighted the key proteins as possible targets for endometrial receptivity and interception. Ingenuity pathway analysis of differentially expressed proteins exhibited a variety of signaling pathways, including LXR/RXR activation pathway and acute-phase response signaling and upstream regulators (TNF, IL6, Hmgn3 and miR-140-3p) associated with endometrial receptivity. The observed estrogenic effect on differential proteome dynamics in Ishikawa cells indicates that the human endometrium is the probable target for serum estradiol levels in COH cycles. The findings are also important for future functional studies with the identified proteins that may influence embryo implantation.

Background The existing reports about intergenerational or transgenerational effects of intrauterine hyperglycemia have included both intrauterine and postnatal metabolic exposure factors, while the impact of intrauterine hyperglycemia per se has not been assessed alone. A number of studies suggest DNA methylation reprogramming of gametes plays a crucial role in the metabolic inheritance, but it is unclear when and how DNA methylation patterns are altered when exposed to intrauterine hyperglycemia. In this study, we selected nondiabetic F1- and F2-gestational diabetes mellitus (GDM) male mice as founders to examine metabolic changes in the next generation and performed methylome sequencing of day 13.5 primordial germ cells (PGCs) from F1-GDM to explore the underlying epigenetic mechanism. Results We found that intrauterine hyperglycemia exposure resulted in obesity, insulin resistance, and/or glucose intolerance in F2 male mice, but no metabolic changes in F3 male mice at 8 weeks. Using reduced representation bisulfite sequencing, we found DNA methylome of day 13.5 PGCs from F1-GDM fetuses revealed differently methylated genes enriched in obesity and diabetes. Methylation validation of the insulin resistance and fat accumulation gene Fyn showed a consistent hypomethylation status in F1 PGCs, F1 fetal testes, sperm from F1/C-GDM mice, and somatic cells from F2-GDM male mice. In contrast, no methylation alteration was observed in F2-GDM male germ cells and F3-GDM somatic cells. Conclusion We provide evidence that intrauterine hyperglycemia exposure per se contributes to intergenerational metabolic changes in the F2 but not F3 generation. And the aberrant DNA methylation reprogramming occurs as early as day 13.5 in PGCs of the F1 generation. Our findings suggest that intrauterine exposure alone is sufficient to cause the epigenetic inheritance in F2 offspring, and the epigenetic memory carried by DNA methylation pattern could be erased by the second wave of methylation reprogramming in F2 PGCs during fetal development. Electronic supplementary material The online version of this article (10.1186/s13072-018-0192-2) contains supplementary material, which is available to authorized users.

In this work, a systematic approach to develop the teaching of general education courses via flipped classroom strategy is discussed. A series course of general chemistry is taken as examples for discussion. A conceptual framework for organizing and executing three-in-one combination teaching and studying systems, i.e., in-out class studying, on-off line studying, theoretical-practical studying, is presented. Problem based learning (PBL) and cooperative learning (CL) methods are applied. Overall, a student-centered environment is proposed which aims to train students’ innovative and critical thinking capabilities.

// Tanzil Ur Rahman 1, 2, * , Kamran Ullah 1, 2, * , Zhang-Hong Ke 4 , Meng-Xi Guo 1, 2 , Lu-Yang Jin 1, 2 , Jun Ren 1, 2 , Yu-Zhong Zhou 1, 2 , Yi Cheng 1, 2 , Xin-Yan Dong 1, 2 , Hai-Yan Pang 1, 2 , Ting-Ting Wang 1 , Jian-Zhong Sheng 1, 2, 3 and He-Feng Huang 1, 3 1 The Key Laboratory of Reproductive Genetics, Ministry of Education, Zhejiang University, Hangzhou, China 2 Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, China 3 The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China 4 Center of Reproductive Medicine, Fujian Maternity and Children Health Hospital, Fujian Medical University, Fuzhou, China * These authors have contributed equally to this work Correspondence to: Jian-Zhong Sheng, email: shengjz@zju.edu.cn He-Feng Huang, email: huanghefg@hotmail.com Keywords: triglyceridemia, leptin, hypothalamus, neuropeptide Y, pSTAT3 Received: February 08, 2017 Accepted: May 10, 2017 Published: June 16, 2017 ABSTRACT Maternal obesity influence the child’s long-term development and health. Though, the mechanism concerned in this process is still uncertain. In the present study, we explored whether overfeeding of a high-fat diet during pregnancy in female rats altered metabolic phenotypes in an F1 generation and authenticated the contribution of hypothalamic leptin signaling. Leptin responsiveness and the number of immunopositive neurons for phosphorylated signal transducer and activator transcription 3 (pSTAT3) were analyzed. Neuropeptide Y in the arcuate nucleus of the hypothalamus and in nucleus tractus solitaries was examined. Triglycerides and leptin levels were increased in the high-fat diet mother. The number of neuropeptide Y positive cell bodies and neurons was significantly increased in the high-fat diet-F1 offspring (HDF-F1) as compared to Chow-F1. Leptin administration significantly decreased the food intake and increased the pSTAT3 expression levels in neurons in the arcuate nucleus of Chow-F1. However, leptin did not show any effect on food intake and had a reduced effect on pSTAT3 expression levels in neurons in the arcuate nucleus of HDF-F1. From the present domino effect, we conclude that mothers exposed to high-fat diet during pregnancy may pass the obese phenotype to the succeeding generation via altering hypothalamic leptin signaling.

Self-ordering Anodic Aluminum Oxide Films Using Multi-step Anodizing MA Di,, LI Shu-bai, DONG Xin-yan HU Xiu-ying, WANG Bin, CHEN Xiang-yan (1School of Chem. & Environ. Engin., Jiangsu Univ. of Tech., Changzhou, Jiangsu, 213001 E-mail: amandama2008@gmail.com) (2Dept. of Chem. Engin., Changzhou Inst. of Engin. Tech., Changzhou 213164) (3 School of Biotech. & Environ. Engin., Ningbo Inst. of Tech., Zhejiang University, Ningbo 315100) Anodic aluminum oxide(AAO) film is known to have highly ordered pore arrangement, controllable pore diameter and well-characterized morphology when produced in acidic electrolytes. As a self-organized fine structure with a nanohole array, porous AAO has been used as a host material for many applications. Nevertheless, a full recognition of the potential of AAO a template for nano-fabrication only developed in the last few years since the pioneering work of Masuda’s group. A variety of nanostructures can be created using AAO templates by depositing metals, semiconductors, organics, or their combinations into the pores. For example, metallic nanowires and hollow nanotube arrays, were synthesized by controlled electrodeposition of a metal salt in an AAO template. In the present work, we studied the self-ordering process of the AAO films during multi-step anodization. During the leaching process, the porous alumina film was dipped in phosphoric acid and chromic acid solution for etching film. Each anodization process was followed by this leaching process.

The surface of porous anodic aluminum oxide (AAO) film anodizing in malonic acid, which is characterized by Scanning Electron Microscope (SEM) and ImageJ software. There are disorderly tiny pores or stripes on the first once anodizing surface. Pore diameter, pore density and porosity are decided by the first anodizing process. With anodizing step increased, pore diameter of the membrane decreased. Two-step anodization improves the order of PAA membrane greatly, which is processed on the basic of the ordered array pits at the aluminum that is observed after removing membrane of the one-step anodization. According to the experiments, porous anodic aluminum oxide (PAA) was prepared in 1.0 mol/L malonic acid, its pore diameter increased and porosity decreased with anodizing voltage increased.

Accumulating evidence suggests a role of bisphenol A (BPA) in metabolic disorders. However, the underlying mechanism is still unclear. Using a mouse BPA exposure model, we investigated the effects of long-term BPA exposure on lipid metabolism and the underlying mechanisms. The male mice exposed to BPA (0.5 μg BPA /kg/day, a human relevant dose) for 10 months exhibited significant hepatic accumulation of triglycerides and cholesterol. The liver cells from the BPA-exposed mice showed significantly increased expression levels of the genes related to lipid synthesis. These liver cells showed decreased DNA methylation levels of Srebf1 and Srebf2, and increased expression levels of Srebf1 and Srebf2 that may upregulate the genes related to lipid synthesis. The expression levels of DNA methyltransferases were decreased in BPA-exposed mouse liver. Hepa1-6 cell line treated with BPA showed decreased expression levels of DNA methyltransferases and increased expression levels of genes involved in lipid synthesis. DNA methyltransferase knockdown in Hepa1-6 led to hypo-methylation and increased expression levels of genes involved in lipid synthesis. Our results suggest that long-term BPA exposure could induce hepatic lipid accumulation, which may be due to the epigenetic reprogramming of the genes involved in lipid metabolism, such as the alterations of DNA methylation patterns.

Valone has a chronic and toxic anticoagulant rodenticide that has widely used in China and has resulted in some accidental and intentional intoxication in recent years. The literature reported so far lacks sensitive and selective method for the confirmation of valone. The purpose of this study was to establish a novel assay for the identification and quantification of valone in serum by ion chromatography–electrospray ionization tandem mass spectrometry (IC–MS/MS). After serum sample was extracted with methanol/acetonitrile (10:90, v/v) and cleaned by Oasis ® HLB solid-phase extraction cartridge, chromatographic separation was performed on an Ionpac ® AS11 column with an eluent of methanol/30 mmol/L KOH (10:90, v/v). The overall extraction efficiency was >81.0%, and the limit of quantification was 0.5 ng/mL for valone. Regression analysis of the calibration data revealed good correlation ( r 2 > 0.99) for valone. Intra- and inter-day precisions for quality-control samples were less than 8.0 and 13.7%, respectively. The proposed method enables the identification and quantification of valone in both clinical and forensic specimens.