Mini review: The FDA-approved prescription drugs that induce ovulation in women with ovulatory problems.

Infertility is defined as not being able to become pregnant after 12 months or more of unprotected sexual intercourse. Female infertility as a serious health issue can result from ovulation disorders, menstrual cycle problems, structural problems, and environmental factors. Ovulation occurs once a month between the time of menarche and menopause. The release of a mature egg from the ovary is controlled with the hypothalamic-pituitary-ovarian axis. Several hormones such as gonadotropin-releasing hormone (GnRH), FSH (follicle-stimulating hormone), LH (luteinizing hormone), estrogen, and progesterone play fundamental roles in the ovulation process. Both FSH and LH are the main treatment for women with ovulation disorders. Depending on the reasons for infertility, several different types of treatment are available for infertile women. Fertility drugs as an important part of treatment work like the natural hormones to treat infertility. Several fertility drugs can regulate ovulation and the release of an egg from the ovary in women with polycystic ovary syndrome (PCOS) or undergoing in vitro fertilization (IVF) treatment. This mini-review is about the FDA-approved prescription drugs that induce ovulation in women with ovulatory problems.

Herpes B virus gD interaction with its human receptor--an in silico analysis approach.

BACKGROUND: The glycoprotein D (gD) is essential for Herpes B virus (BV) entry into mammalian cells. Nectin-1, an HSV-1 gD receptor, is found to be the receptor which mediated BV induced cell-cell fusion, while HVEM does not mediate fusion by BV glycoprotein. However, the specific sequence and structural requirements of the BV gD for the recognition of and binding to Nectin-1 are unknown. Moreover, the 3D structures of BV gD and the BV gD-receptor complex have not been determined. In this study, we propose a reliable model of the interaction of the BV gD with receptor using bioinformatics tools. RESULTS: The three-dimensional structures of two BV gD-receptor complexes were constructed using homology modelling and docking strategy. Based on the models of these complexes, the BV gD receptor interaction patterns were calculated. The results showed that the interface between the BV gD and nectin-1 molecule is not geometrically complementary. The computed molecular interactions indicated that two terminal extensions were the main region of BV gD that binds to nectin-1 and that hydrophobic contacts between the two molecules play key roles in their recognition and binding. The constructed BV gD-HVEM complex model showed that this complex had a lower shape complementarity value and a smaller interface area compared with the HSV-1 gD-HVEM complex, and the number of intermolecular interactions between BV gD-HVEM were fewer than that of HSV-1 gD-HVEM complex. These results could explain why HVEM does not function as a receptor for BV gD. CONCLUSION: In this study, we present structural model for the BV gD in a complex with its receptor. Some features predicted by this model can explain previously reported experimental data. This complex model may lead to a better understanding of the function of BV gD and its interaction with receptor and will improve our understanding of the activation of the BV fusion and entry process.

Dendrobium nobile-derived polysaccharides ameliorate spermatogenic disorders in mice with streptozotocin-induced diabetes through regulation of the glycolytic pathway.

Dysfunction of spermatogenesis is a major complication of diabetes mellitus (DM). This study characterized the protective effects of Dendrobium nobile-derived polysaccharides (DNP) against spermatogenetic dysfunction in mice with streptozotocin (STZ)-induced diabetes. The diabetic mice had lower body and testicular mass, and fewer spermatozoa with a higher incidence of malformation. The testicular histology showed disordered narrow seminiferous tubules covering a smaller area, and fewer spermatogenic cells. Moreover, the qRT-PCR analysis indicated that DM was associated with high expression of the pro-apoptotic factor Bax and low expression of the anti-apoptotic factor Bcl-2 in the testes. The qRT-PCR and immunohistochemical analysis clarified that DM was also associated with low testicular expression of the Sertoli cell (SC) markers GATA-4, WT1, and vimentin, and genes encoding the glycolytic rate-limiting enzymes LDHA, PKM2, and HK2. DNP treatment increased the body and testicular masses, sperm count, and number of spermatogenic cells of the mice, and reduced the proportion of abnormal sperm. DNP also reduced the expression of Bax, and increased that of Bcl-2, GATA-4, WT1, vimentin, LDHA, PKM2, and HK2, in the testes of the diabetic mice. Thus, DNP protects against spermatogenic dysfunction in diabetic mice by inhibiting apoptosis and activating the glycolytic pathway in their testes.

Long Non-Coding RNA SNHG14 Impedes Viability, Migration and Invasion of Endometrial Carcinoma Cells Through Modulating miR-93-5p/ZBTB7A Axis.

BACKGROUND: The function of long non-coding RNA small nucleolar RNA host gene 14 (SNHG14) in endometrial carcinoma (EC) has not been thoroughly reported. This research is designed to research the action mechanism of SNHG14 in EC development. METHODS: The expression of SNHG14 was estimated in The Cancer Genome Atlas and was verified by qRT-PCR in EC tissues. The correlation between SNHG14 expression and clinicopathological features of EC patients was analyzed. Cell viability, wound healing rate, and relative invasion rate were examined by MTT, wound healing, and transwell assay. StarBase, TargetScan, RNA pull-down, and dual luciferase reporter gene (DLR) assay were conducted to analyze the relationship among SNHG14, miR-93-5p and ZBTB7A. RESULTS: SNHG14 was underexpressed in EC. SNHG14 expression was significantly relevant to menstruation, FIGO stage, histological grade and lymphatic metastasis of EC patients. SNHG14 overexpression hampered viability, migration and invasion of EC cells. SNHG14 functioned as a sponge for miR-93-5p, and miR-93-5p inhibition restrained cell viability, migration and invasion in EC. In addition, miR-93-5p directly targeted to ZBTB7A, which was underexpressed in EC. The suppressive action of SNHG14 overexpression on the viability, migration and invasion of EC cells was partly rescued by miR-93-5p overexpression or ZBTB7A silencing. CONCLUSION: LncRNA SNHG14 hampered the viability, migration and invasion of EC cells via modulating miR-93-5p/ZBTB7A axis.

Inhibition of Microrna-766-5p Attenuates the Development of Cervical Cancer Through Regulating SCAI.

PURPOSE: MicroRNAs (miRNAs) are considered to play anti-tumor roles in cancers. This study is designed to illustrate the role and potential mechanism of miR-766-5p in cervical cancer (CC) progression. METHODS: MiR-766-5p expression in tissues and serum of CC patients was detected by quantitative reverse-transcription PCR (qRT-PCR). Receiver operating characteristic (ROC) curve was performed to evaluate the diagnostic value of serum miR-766-5p in CC. The 5-ethynyl-2'-deoxyuridine (EdU) assay, flow cytometry, wound healing as well as transwell assay were utilized to detect the proliferation, apoptosis, migration and invasion of CC cells, respectively. The interaction between miR-766-5p and SCAI was confirmed by dual-luciferase reporter gene assay. Xenografted tumor model was established to measure the growth of tumor xenograft in vivo. RESULTS: MiR-766-5p was significantly increased in tissues and serum of CC patients. ROC curve suggested that serum miR-766-5p could serve as a biomarker for the diagnosis of CC. Inhibition of miR-766-5p suppressed the proliferation, migration and invasion, and promoted the apoptosis of CC cells. SCAI was proved to be a target of miR-766-5p. Silencing of SCAI eliminated the inhibiting effects of miR-766-5p inhibitor on the proliferation, migration and invasion of CC cells in vitro. Additionally, down-regulation of SCAI also reversed the inhibitory effect of miR-766-5p inhibitor on the growth of tumor xenograft in vivo. CONCLUSIONS: Inhibition of miR-766-5p restrains the cell proliferation, migration and invasion, and promotes the apoptosis in CC through negatively regulating SCAI.