Introduction: Data from last years suggested that early exposure to ENDOCRINE disruptors (EDs) can predispose newborns to ENDOCRINE dysfunction of adipocytes, obesity, and associated disorders. The implication of EDs at low doses on adipocyte development has been poorly investigated. For instance, vinclozolin (V) is a dicarboximide fungicide widely used in agriculture since the 90’ s, alone or in mixture with genistein (G), an isoflavonoid from Leguminosae. This study aims to identify the effect of vinclozolin alone or with genistein, on adipose tissue properties using cell culture.Methods: In steroid-free conditions, 3T3-L1 pre-adipocytes were induced to differentiate in the presence of EDs, singularly or in mixtures, for 2 days. DNA and triglyceride (TG) levels were measured on days 0, 2 and 8 of differentiation. Leptin secretion was measured only on the eighth day.Results: We show that low doses of G (25 mM) and V (0.1 mM) inhibit pre-adipocytes differentiation. This inhibition has been represented by a decreasing in DNA content (mg/well) and decreasing in TG accumulation (mg/mL) in 3T3-L1 cells. Nevertheless, V increased the anti-adipogenic properties of G.Conclusion: This study confirms that EDs singularly or in mixtures, introduced during early stages of life, could affect the differentiation and the ENDOCRINE activity of adipocytes, and can act as potential factors for obesity.

Infertility is defined as the inability to conceive after 12 months of unprotected sexual intercourse. The National Survey of Family Growth reports a 14% rate of infertility in the United States in married women aged 15-44 years. Infertility can be attributed primarily to male factors in 25%, female factors in 58% and is unexplained in about 17% of couples. The most common cause of female infertility is abnormalities in menstrual function (46%). These disorders include ovulatory dysfunction and abnormalities of the uterus or outflow tract. A careful history and physical examination and a limited number of hormonal tests will help to determine whether the abnormality is: 1/ hypothalamic or pituitary [low FSH, LH and estradiol with or without an increased PPL (51%)], 2/ PCOS (30%), 3/ ovarian (low estradiol with increased FSH) (12%), or 4/ uterus or outflow tract abnormality (7%).

Infertility is an emotionally charged problem affecting an estimated 15% of all couples. The man should be evaluated concurrently with the woman, since a male factor is the primary or contributing cause in 40% to 60% of cases. The evaluation of the infertile male continues to be a clinical challenge of increasing significance with considerable emotional and financial burdens. Many physiological, environmental and genetic factors are implicated.The infertility practitioner should have a thorough understanding of the advantages and limitations of various laboratory tests as well as the indications, costs and success rates of all treatment options. A complete medical history in conjunction with a focused examination can allow for an appropriate choice of laboratory and imaging studies. The semen analysis is a crucial first step, but it is by no means sufficient to determine cause or dictate therapy. Azoospermia factor (AZF) microdeletions of the Y chromosome, which occur in 1-55% of infertile men, are closely associated with severe spermatogenic failure and represent the most frequent molecular genetics causes of azoospermia and severe oligozoospermia. Researches on AZF and its related genes, approaching the mechanisms of spermatogenic failure at the molecular level, are of great significance for the diagnosis, treatment and prognosis of male infertility. The detection of AZF microdeletions can provide scientific basis for correct diagnosis and reasonable. Klinefelter, s syndrome and Y chromosome microdeletions are the most prevalent disorder, together accounting for 10-20% of patients evaluating for genetic cause of male infertility. Other cause of primary testicular failure such as undescended testis and orchiti should be considered as certain causes of infertility.Hypogonadotropic hypogonadism due to pituitary adenoma, panhypopituitarism hyperprolactinemia or idiopathic causes is another treatable etiology of male infertility. For part of infertile patients a genetic factor will be the underlying cause of the problems. The studies, focusing on men with fertility problems, can be subdivided into three groups: studies on deletions on the long arm of the Y chromosome, studies on X-linked genes and studies on autosomal genes. It is obvious that Yq microdeletions should be considered as a cause of male infertility. Therefore, couples with a component of male factor infertility need a systematic evaluation directed at the male partner to maximize their reproductive potential.

Background: Neuropeptide Y (NPY) is an ENDOCRINE peptide hormone that is produced by many parts of the bidy specially hypothalamus and has various physiological effects. Repeated intracerebroventricular (ICV) injections have shown NPY to be the most potent stimulator of feeding yet discovered. Chronic studies of many ENDOCRINE systems are frustrated by the lack of a reliable delivery sytem and the instability of many peptides. We have used transected cell line to model chronic over expression of NPY. To achieve the correct processing of NPY it was necessary ti use clonal ENDOCRINE cell line e.g, RIN 1056a. Material and Methods: Full length of NPY cDNA was isolated by PCR, cloned into the expression vector pCEP4 and transected into RIN 1056a cells. NPY gen expression was shown by total RNA extraction from transfected cells and Northern blotting, correct processing was also confirmed by reversed – phase FPLC and size exclusion chromatography. Since the syngeneic strains were not available for these cells, they had to be immunoisolated. Cells were micro- encapsulated in semipermiable PTFE hollow fibres (MWCO 500000) by resuspending freshly trypsinised cells at a concentration of 4x 107 cells/ml in 1% alginate and loaded into the fibres (internal diameter 1mm). The fibre was heat sealed approximately every 3mm and the alginate solidified by immersion in 0.05% Cac12 solution. Results: Individual 3mm sections were maintained in 1ml DMEM 10% FCS and retained their NPY screting activity for at least 28 days in vitro. Secreation of IR-NPY was measured by specific radioimmunoassay. Secretion of NPY was maintained for 28 days at approximately the same level with secretion maintained at 150 fmol/hour/fibre. Conclusion: Therefore we have successfully transected this cell line with NPY cDNA for the first time and measured the production and secretion of NPY from transected cell in high levels.