ed expression of ATG7 and unaltered expression of LC3II/LC3 may indicate that the autophagy pathway is initiated but not completely executed in spermatozoa of individuals with globozoospermia. A significant correlation of ATG7 expression with increased sperm DNA fragmentation, reduced sperm concentration, and sperm motility may associate with the activation of a compensatory mechanism for promoting deficient spermatozoa to undergo cell death by the autophagy pathway. Therfore, this pathway could act as a double-edged sword that, at the physiological level, is involved in acrosome biogenesis, while, at the pathological level, such as globozoospermia, could act as a compensatory mechanism.

Atherosclerosis (AS) is one of the most common causes of human death and disability. This study is designed to investigate the roles of aldosterone (Aldo) and oxidized low-density lipoprotein (Ox-LDL) in this disease by clinical data and cell model.

In this experimental study, clinical data were collected to investigate the Aldo role for the patients with primary aldosteronism or adrenal tumors. Cell viability assay, fluorescence-activated cell sorting (FACS) assay, apoptosis assay, cell aging analysis, and matrigel tube formation assay were performed to detect effects on human umbilical vein endothelial cells (HUVECs) treated with Aldo and/or Ox-LDL. Quantitative polymerase chain reaction (qPCR) and Western blot analysis were performed to figure out critical genes in the process of endothelial cells dysfunction induced by Aldo and/or Ox-LDL.

We found that the Aldo level had a positive correlation with the TG/HDL-C ratio. Endothelial cell growth, angiogenesis, senescence, and apoptosis were significantly affected, and eNOS/Sirt1, the value of Bcl-2/Bax and Angiopoietin1/2 were significantly affected when cells were co-treated by Aldo and Ox-LDL.

Elevated Aldo with high Ox-LDL together may accelerate the dysfunction of HUVEC, and the Ox-LDL, especially for those patients with high Aldo should be well controlled. The assessment of the role of Aldo may provide a theoretical basis for the effective prevention and investigation of a new treatment of AS.

Elevated Aldo with high Ox-LDL together may accelerate the dysfunction of HUVEC, and the Ox-LDL, especially for those patients with high Aldo should be well controlled. The assessment of the role of Aldo may provide a theoretical basis for the effective prevention and investigation of a new treatment of AS.

Patients with diabetes mellitus frequently have chronic wounds or diabetic ulcers as a result of impaired wound healing, which may lead to limb amputation. Human umbilical vein endothelial cell (HUVEC) dysfunction also delays wound healing. Here, we investigated the mechanism of miR-200b in HUVECs under high glucose conditions and the potential of miR-200b as a therapeutic target.

In this experimental study, HUVECs were cultured with 5 or 30 mM glucose for 48 hours. Cell proliferation was evaluated by CCK-8 assays. Cell mobility was tested by wound healing and Transwell assays. Angiogenesis was analyzed

Matrigel tube formation assays. Luciferase reporter assays were used to test the binding of miR-200b with Notch1.

miR-200b expression was induced by high glucose treatment of HUVECs (P<0.01), and it significantly repressed cell proliferation, migration, and tube formation (P<0.05). Notch1 was directly targeted and repressed by miR-200b at both the mRNA and protein levels. Inhibition of miR-200b restored Notch1 expression (P<0.05) and reactivated the Notch pathway. The effects of miR-200b inhibition in HUVECs could be reversed by treatment with a Notch pathway inhibitor (P<0.05), indicating that the miR-200b/Notch axis modulates the proliferation, migration, and tube formation ability of HUVECs.

Inhibition of miR-200b activated the angiogenic ability of endothelial cells and promoted wound healing through reactivation of the Notch pathway

. miR-200b could be a promising therapeutic target for treating HUVEC dysfunction.

Inhibition of miR-200b activated the angiogenic ability of endothelial cells and promoted wound healing through reactivation of the Notch pathway in vitro. miR-200b could be a promising therapeutic target for treating HUVEC dysfunction.

Sexual dimorphism in mammals can be described as subsequent transcriptional differences from their distinct sex chromosome complements. Following X inactivation in females, the Y chromosome is the major genetic difference between sexes. In this study, we used a male embryonic stem cell line (Royan H6) to identify the potential role of the male-specific region of the Y chromosome (MSY) during spontaneous differentiation into embryoid bodies (EBs) as a model of early embryonic development.

In this experimental study, RH6 cells were cultured on inactivated feeder layers and Matrigel. In a dynamic suspension system, aggregates were generated in the same size and were spontaneously differentiated into EBs. During differentiation, expression patterns of specific markers for three germ layers were compared with MSY genes.

Spontaneous differentiation was determined by downregulation of pluripotent markers and upregulation of fourteen differentiation markers. Upregulation of the ectoderm markers was observed on genes implied the potential responsibility of their gene co-expression clusters for EB differentiation. We suggest that these genes may play important roles in early embryonic development.

In customary assisted reproductive technology (ART), oocyte culture occurs in static micro drops of Petri dishes with vast media volume; while, the

condition is dynamic. In this study, we aimed to improve the maturation efficiency of mammalian oocytes by designing an optimal microchamber array to obtain the integration of oocyte trapping and maturation within a microfluidic device and evaluate the role of microfluidic culture condition in lipid peroxidation level of the culture medium,

matured oocytes apoptosis, and its comparison with the conventional static system.

In this experimental research, immature oocytes were collected from ovaries of the Naval Medical Research Institute (NMRI) mice. GSK2334470 concentration Oocytes were randomly laid in static and dynamic (passive and active)

maturation culture medium for 24 hours. The lipid peroxidation level in oocyte culture media was assessed by measuring the concentration of malondialdehyde (MDA), and the rate of apoptosis in

matured oocytes was assessed by the TUNEL assay after a-24 hour maturation period.