Nerve growth factor (NGF) has important functions during embryonic development and on various tissues and organs under normal and pathological conditions during the extrauterine life. RT-PCR analysis and immunological methods demonstrate that human umbilical vein endothelial cells (HUVECs) express the NGF receptors trkA(NGFR) and p75NTR. NGF treatment caused a rapid phosphorylation of trkA(NGFR) in HUVECs, determining a parallel increase of phosphorylated ERK1/2. Accordingly, NGF induced a significant increase in HUVEC proliferation that was abolished by the trkA(NGFR) inhibitor K252a. Also, HUVECs express significant levels of NGF under standard culture conditions that were up-regulated during serum starvation. Endogenous NGF was responsible for the basal levels of trkA(NGFR) and ERK1/2 phosphorylation observed in untreated HUVEC cultures. Finally, NGF exerted a potent, direct, angiogenic activity in vivo when delivered onto the chorioallantoic membrane of the chicken embryo. The data indicate that NGF may play an important role in blood vessel formation in the nervous system and in several pathological processes, including tumors and inflammatory diseases. Unraveling mechanisms of NGF-dependent angiogenesis could provide valuable tools for novel therapeutic approaches in antiangiogenic therapy.

Azoospermic patients can now father children once spermatozoa have been retrieved from the epididymis or the testis. However, there are concerns about the risk of chromosomal abnormalities since an increase in sperm aneuploidy rate has been reported in samples from patients with abnormal sperm parameters. The purpose of this study was therefore to evaluate the sperm aneuploidy and diploidy rates for chromosomes 8, 12, 18, X and Y in spermatozoa extracted from the epididymes (n=10) or the testes (n=6) of patients with azoospermia. Ejaculated spermatozoa of healthy men (n=14) served as control. Epididymal and testicular spermatozoa had an aneuploidy rate significantly higher than that found in ejaculated spermatozoa. The aneuploidy and diploidy rates of testicular spermatozoa were higher, but not significantly different, than those found in epididymal spermatozoa. This study has shown that azoospermic patients have an increased sperm aneuploidy rate. They should therefore be given appropriate genetic counselling before entering in-vitro fertilisation programs.

Polycystic ovarian syndrome (PCOS) is a reproductive system disorder characterized by irregular menses, anovulation, clinical and/or biochemical signs of hyperandrogenism (hirsutism and/or acne), ovarian micropolycystic appearance and metabolic abnormalities, such as hyperinsulinaemia and obesity. The aetiopathogenesis of this syndrome is not well known. Several pathogenetic hypotheses have been proposed to explain the full array of symptoms and signs, but with elusive results. A genetic abnormality causing PCOS is supported by the observation that different members of the same family are often affected, and about half of the sisters of PCOS women have elevated serum testosterone concentrations. Therefore, the presence of gene abnormalities in women with PCOS has been widely explored in the attempt to establish whether their mutations or polymorphisms may cause PCOS. The main genes evaluated are those involved in steroidogenesis, steroid hormone effects, gonadotrophin release regulation and action, insulin secretion and action, and adipose tissue metabolism. Despite the vast body of literature produced, none of the genes evaluated seems to play a key role in PCOS pathogenesis. It is likely that PCOS may represent the final outcome of different, deeply inter-related genetic abnormalities that influence each other and perpetuate the syndrome.

1 Endothelium is a target for an array of factors involved in in¯ammation. Endothelial cells express receptors for CRH, a neuropeptide produced during in¯ammation. We report both the concentration-dependent inhibitory e ect of CRH upon cytokine-stimulated nitrite release by H5V murine endothelioma cells, and its stimulatory one in HUVEC cells. 2 Western blot analysis showed that CRH inhibits cytokine-stimulated iNOS protein in H5V cells, and, instead, potentiated it in HUVEC cells. 3 H5V cells expressed both CRH receptors (CRH-R1 and R2) mRNAs, whereas HUVEC cells expressed the CRH-R2 mRNA solely. 4 CRH increased medium nitrites and iNOS protein expression in H5V cells pretreated with the selective CRH-R1 antagonist CP 154,526. However, the selective CRH-R2 antagonist anti-Svg-30 failed to produce similar e ects. In fact, anti-Svg-30 inhibited CRH-induced increase of nitrite release and iNOS expression in HUVEC cells. 5 Our results con®rm the activating role of CRH on endothelial cells, although it suggests its possible inhibitory role in the late phase of the in¯ammatory response. NO-mediated e ects of CRH on endothelial cells could be exploited in therapeutic strategies related to in¯ammatory and/or degenerative diseases.

Background/Aim: The aim of this study is to improve the obstetrician-based cord blood collection system and an efficient recovery of CD34+ haematopoietic progenitor stem cells. Methods: CD34+ cells were purified from total blood using a positive selection enrichment method, called Mini-Macs. Results: The final yield of CD34+ cells we obtained was 10⁴ cells/ml, with a CD34+ purity of 99%. Conclusion: Our results confirm that, by using this method, it is possible to get a significant stem cell number, thus improving transplanting both peripheral stem cells and umbilical cord ones.