Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels, the sperm count and the histologic appearance of the testis were studied in 56 patients with azoospermia or oligospermia.FSH is elevated in those cases of azoospermia where gametogenesis is arrested prior to spermatid differentiation. Serum FSH is normal, however, in most patients in whom spermatids and spermatozoa are detectable on testicular biopsy. There is no relationship between the sperm count and the concentration of serum FSH.No correlation exists between serum LH and either the sperm count or the stage of spermatogenesis as evaluated on testicular biopsy. (/ Clin Endocrinol Metab 34: 1003, 1972

Three monoclonal antibodies against human protamines were obtained by immunization with total human basic nuclear proteins or purified protamine HP3. The specificity of antibodies was assessed by enzyme-linked immunosorbent assay (ELISA) and Western blot. They recognized three distinct epitopes: One was specific for the protamine P1 family, another was specific for the protamine P2 family and the third was common to both families. All were specific for the human species. Antibodies were used to detect protamines in germ cells by indirect immunofluorescence and by immunoelectron microscopy. Protamines appeared in spermtid nuclei at steps 4-5 of spermiogenesis, i.e., during the chromatin condensation process, and were not accumulated in the cytoplasm before entering the nucleus.

A 25 year old man presented hypogonadotropic hypogonadism with complete anosmia (Kallman's syndrome). His chromosomic type was 47 XXY (Klinefelter's syndrome). Clinical findings were: height 183 cm, weight 62 kg, increased length of lower limbs, P2\p=n-\A2pilosity and micropenis. Only a left testis was present (1.5\p=n-\1.5cm). Bone age was 15. Testicular biopsy showed that the signs were more related to the gonadotropic deficit than to the gonadal dysgenesis; tubular hyalinization was not observed. Plasma levels of testosterone and oestradiol were very low. Plasma gonadotropin levels were below normal ranges and did not respond to an infusion test of GnRH. GnRH was administrated iv every 90 min for 3 weeks by an auto syringe infusion pump and induced a pulsatile response of FSH and LH. Plasma levels of testosterone and oestradiol were unaffected. It may be concluded that the results of pulsatile injection of GnRH confirmed in this patient a unique association of Kallmann's syndrome with complete 47 XXY Klinefelter's syndrome.Idiopathic hypogonadotropic hypogonadism re¬ sult in absent or incomplete puberal development. The disease is characterized by low plasma gona¬ dotropin and sexual steroid levels; it appears to be due to a deficiency in GnRH. This type of hypo¬ gonadism may be associated with other inherited abnormalities such as hypo-or complete anosmia, cleft palate or cranio-facial deformities and in rare cases gonadal dysgenesis.In the present study we observed the effects of pulsatile low doses GnRH administration in a male with hypogonadotropic hypogonadism and complete anosmia (Kallmann's syndrome) asso¬ ciated with a 47 XXY gonadal dysgenesis (Klinefelter's syndrome). Material and MethodsHormones assays FSH and LH were determined in vitro in human serum by the principle of competitive protein-binding analysis (RIA-gnost hFSH and RIA-gnost hLH Tachisorb kits from Hoechst-Behring Laboratories) normal male adult range: 0.3-2.3 ng/ml for FSH; 1 ng of hFSH was equivalent to 4 mU hFSH MRC 69/104; normal male adult range 1.1 -3.1 ng/ml for LH; 1 ng of hLH was equivalent to 3.5 mU hLH MRC 68/40. Plasma testosterone was measured by radio-immunoassay as previously described (Abraham et al. 1972) normal male adult range 12 to 41 nmol/1. Plasma oestradiol was measured by a radioimmunoassay; nor¬ mal male adult range 36 to 183 pmol/1.

Introduction.

RESUMELa formation des gonades est intimement li4e ~ celle du m4son4phros ou rein interm4diaire.Les testicules apparaissent dans la r4gion dorsale de l'embryon, en arri~re de la cavit6 coelomique abdominale. Pour gagner leur situation d4finitive les testicules descendent dans la cavit4 pelvienne, franchissent la paroi abdominale par ranneau inguinal et se fixent au fond de la poche scrotale. La migration testiculaire se fait ainsi en trois phases successives ayant chacune leur m4canisme propre. Les organes annex4s aux testicules (4pididyme et d4f6rent) et surtout les ligaments qui les relient ~ la paroi (gubernaculum testis) jouent un r61e essentiel dans ces d4placements.