Melvingroth6008

In addition, a specific session has been devoted to the possible significance the OCN as a template agonist on its receptor GPRC6A, for the development of novel therapeutic and pharmacological approaches for the treatment of dismetabolic states and male infertility. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.The spermatozoon has classically been seen only as a paternal DNA transporter into the oocyte, thus underestimating the entire contribution of the male gamete to the embryo development. The advancement of the research supports that not only the sperm genome, but the entire sperm transcriptome and proteome carry crucial information for fertilization and embryo development. Altogether, 6871 proteins have been reported in spermatozoa so far. Their functional analysis has recently addressed to the sperm proteome a role in fertilization, preimplantation embryo development and paternal epigenetic inheritance. Targeted analysis of human spermatozoa is warranted to compile an evidence-based list of sperm-carried molecular targets in infertile patients. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Tuberculosis (TB) caused by Mycobacterium tuberculosis (MTB), especially the drug-resistant MTB, causes serious challenges for people healthcare worldwide. Cytotoxic T lymphocytes (CTLs) play a vital role in immune defense against MTB. OBJECTIVE To identify novel CTL epitopes that could induce cellular immunity against MTB infections. METHODS The HLA-A*0201 restricted CTL epitopes of the drug-resistant protein InhA from MTB were predicted by online algorisms and synthesized by the Fmoc solid phase method. The candidate peptides were used to induce CTLs from human peripheral blood mononuclear cells (PBMCs) of HLA-A*0201 healthy donors and the HLA-2.1/Kb mice. IFN-γ productions of CTLs were detected by enzyme linked immunospot assay (ELISPOT), flow cytometry and enzyme-linked immunosorbent assay (ELISA), and cytotoxicity was analyzed by lactate dehydrogenase (LDH) assay. RESULTS A group of 4 epitopes were screened out with high affinity to HLA-A*0201. ELISPOT and flow cytometry analysis indicated these peptides significantly induced IFN-γ release of CTLs from the HLA-A*0201+/PPD+ donors, as the mutant analogues had more potent stimulation effects. LDH assay showed that CTLs from PPD+ donors and the immunized mice exhibited significant cytotoxicity and low cross-reactivity. ELISA analysis revealed comparative levels of IFN-γ were released by CTLs isolated from the mice spleen. CONCLUSION Our study has identified 4 novel CTL epitopes of InhA that could elicited potent CTL immunity, establishing foundation for development for multivalent peptide vaccine against the drug-resistant MTB. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Obesity represents one of the most important health problems worldwide with increasing morbidity and mortality. signaling pathway Widespread prevalence of this disease justifies its actual definition of a "global epidemic". Adipose tissue is nowadays considered a complex organ with lots of endocrine and metabolic functions. In addition to fulfilling its task for energy storage and thermal regulation, by virtue of its constituent white and brown cells, adipose tissue represents, considering its size, the biggest endocrine gland in the body. Both adipocytes and surrounding resident cells (macrophages, endothelial cells and others) produce a huge number of molecules, or adipokines, with endocrine or paracrine functions, that regulate various aspects of metabolism whose clinical relevance is emerging. By balancing proinflammatory and anti-inflammatory effects, the adipokines control insulin sensitivity and related glucose metabolism changes, lipid accumulation in the liver and other organs, and finally gonadal function. Collectively, literature data remains cloudy because of still conflicting results of pre-clinical and clinical studies. The aim of this review was to summarize scientific evidence about adipokines' effects on human metabolism, by focusing on their role on either Metabolic Syndrome and NAFLD, or insulin-resistance in pregnancy, or finally, reproductive function disorders. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Male hypogonadism is "a clinical syndrome that results from failure of the testis to produce physiological concentrations of testosterone and/or a normal number of spermatozoa due to pathology at one or more concentrations of the hypothalamic-pituitary-testicular axis". The diagnostic protocol of male hypogonadism includes accurate medical history, physical exam, as well as hormone assays and instrumental evaluation. Basal hormonal evaluation of serum testosterone, LH, and FSH is important in the evaluation of diseases of the hypothalamus-pituitary-testis axis. Total testosterone levels less then 8 nmol/l profoundly suggest the diagnosis of hypogonadism. An inadequate androgen status is moreover possible if the total testosterone levels are 8-12 nmol/L. In this "grey zone" the diagnosis of hypogonadism is debated and the appropriateness for treating these patients with testosterone should be fostered by symptoms, although often non-specific. Up to now, no markers of androgen tissue action can be used in clinical practice. The identification of markers of androgens action might be useful in supporting diagnosis, testosterone replacement treatment (TRT) and clinical follow-up. The aim of this review is to analyze the main findings of recent studies in the field of discovering putative diagnostic markers of male hypogonadism in seminal plasma by proteomic techniques. The identified proteins might represent a "molecular androtest" useful as a seminal fingerprint of male hypogonadism, for the diagnosis of patients with moderate grades of testosterone reduction and in the follow-up of testosterone replacement treatment. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.