[Clinical development of the malignant process in retained testis with a contribution of 5 cases].
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The sources of origin and the peculiarities of formation of the seminal ducts and rete testis during the prenatal period of ontogenesis in man were studied. It has been established that the seminal duct sand the ducts of the rete testis form from the cellular cords of the coelomic epithelium and the primordial germ cells which appear simultaneously in the septum of the testis and the primordial germ cells which appear simultaneously in the septum of the testis and central part of its parenchyma in the embryos, 13.0--17.0 mm long. By plastic and graphic reconstruction, as well as by methods of subtle preparation under binocular microscope MBC-I control it was revealed that the seminal ducts anastomosed between themselves both within the limits of one and the adjacent lobules. The ducts of the rete testis do not form anastomoses, but superimpose over one another, creating an impression of a rete. Approaching the tunica albuginea they merge, continuing into the cuctuli efferentes testis.
Pseudohermaphroditic Stanley-Gumbreck male rats showed infrequent and incomplete copulatory responses to receptive females. Administration of testosterone propionate produced no increase in this behavior. Injections of estradiol and progesterone induced the pseudohermaphrodites to exhibit lordosis when mounted by stimulus males, but feminine responses were no more frequent than those of normal males given the same hormonal treatment. The hypothesis is suggested that early in development sufficient endogenous testis hormone is produced to cause normal desensitization of feminine behavioral mechanisms to estradiol, but that mechanisms for male behavior are not normally sensitized to testosterone.
85 cases of this syndrom have been published since the original case in 1964. The main clinical symptoms are those of Klinefelter's disease from which it differs by the caryotype only. Azoospermie is the rule. 3 mechanisms can be implicated: Mosaic 46 XX/47 XY with secondary loss of Y chromosome; Translocation of a part of Y chromosome upon an autosome or Y chromosome; Autosomal mutant gene acting upon the masculinizing site of X chromosome and inducing the primitive development of the testis as the short arm and proximal part of the long arm of Y chromosome normally do. These mechanisms perhaps are distinct origins of a syndrom which clinic alone cannot dissociate.
A 42 year old (46 XY) subject with 17-ketosteroid reductase deficiency was investigated. The patient reared as female, has developed masculine features (facial hair, male distribution of body hair, male body habitus, acne and clitoridomegaly) at about 15 years of age but never consulted. She married at 22 years and for 20 years thought to have a "normal" female sex life. Only when her 14 year old "niece" was investigated (1) and treated for similar problems she realized hers. She had a small phallus with perineal urethra, vaginal pouch absence of labia minora and undescended testis, no breast development. Baseline peripheral studies showed plasma testosterone (T) in the range of Tanner II stade of puberty (150 ng/dl), elevated delta 4-androstenedione (delta 4) (930 ng/dl) and estrone (E1) (33,5 NG/DL) LEVELS 6--8 times above normal, but subnormal estradiol levels. Increased basal gonadotropins showed an hyper-response to LHRH stimulation. Dynamic tests (ACTH test, Dexamethasone suppression, and hCG stimulation) showed that abnormal delta 4 and E1 were not of adrenal origin. In the spermatic veins delta 4 levels were extremely high (239 micrograms/dl) but T levels low (11.4 micrograms/dl). delta 4/T ratio in the spermatic vein was much higher than in the peripheral blood suggesting intact peripheral conversion of delta 4 to T. After castration all hormone levels returned to the range usually seen in agonadic male or female adults.
A reliable and uniform vascular perfusion fixation method for the testis has been developed by using an initial washout solution containing a vasodilator and an anticoagulant. This is followed by a brief fixation with a sodium phosphate buffered formaldehyde-glutaraldehyde solution of conventional strenght, and then a second more concentrated aldehyde fixative solution containing picric acid. The method takes into account some of the unique features of the vascular supply of the male genital tract for its favorable perfusion and fixation. The advantages of this method are: (1) consistently favorable preservation of the testis; (2) simple and inexpensive apparatus; and (3) stable and relatively innocuous stock solutions.
Fetal decapitation in utero has enabled us to study the role of fetal pituitary hormones in the development of the fetal testis. Testes from males decapitated near 80 days of gestational life and later delivered at 150 days were smaller than normal and about one-tenth the normal weight. The size of the seminiferous tubules was similar in both groups; however, the number of Leydig cells seemed reduced. In addition, the Leydig cells of the experimental group contained smaller mitochondria with reduced tubular cristae, fewer lipid droplets, and reduced agranular endoplasmic reticulum. Androgen production was inhibited. Measured by radioimmunoassay, the testosterone level in the umbilical vein was 329 +/- 82 pg/ml in six decapitates fetuses, 412 +/- 62 pg/ml in ten normal fetuses. The level in the umbilical artery was 328 +/- 56 pg/ml in five decapitated fetuses, 658 +/- 140 pg/ml in normal fetuses. These studies suggest that chronic deprivation of fetal pituitary hormones inhibits the growth and development of the testis in general and of the Leydig cells in particular.
Micropuncture techniques developed for the study of renal physiology have been adapted for investigation of the male reproductive tract. Ultramicro specimens were obtained in vivo from the tubules of the rat testis and epididymis. These samples were analyzed for sperm morphology and concentration. The new methods developed to conduct these studies are discussed in detail. The mean in vivo spermatocrits were 0.411 plus and minus 0.029, 0.355 plus and minus 0.019, and 0;731 plus and minus 0.028 in the seminiferous tubule, caput epididymidis, and caudal spermatocrit was significantly higher than the spermatocrit in the caput or seminiferous tubule. The percentages of abnormal spermatozoa in the caput and cauda were 5.5% plus and minus .7% and 4.3% plus and minus .6%, respectively.
Several lines of evidence suggest that catecholamines are involved in the regulation of the development of the testis. We have therefore investigated the ability of testicular parenchyma (decapsulated pieces of testes) from 18 to 20-day-old golden hamsters to respond to catecholaminergic stimuli in vitro. Norepinephrine and epinephrine, as well as the beta-receptor agonist isoproterenol and the alpha-adrenoreceptor agonist phenylephrine were able to significantly stimulate testicular testosterone production. Dopamine and serotonin were not effective. The stimulatory action of norepinephrine on testosterone production was dependent on the concentration. In incubations of testes with human chorionic gonadotropin (hCG) and norepinephrine, no synergistic effects on testosterone release were observed. The stimulatory effect of norepinephrine could be partially blocked by incubation with beta-receptor antagonist propranolol, or with alpha-receptor antagonist prazosin, while a combination of propranolol and prazosin completely inhibited the norepinephrine-induced testosterone production. Moreover, isoproterenol and phenylephrine in combination stimulated testosterone more than either drug did alone. Measurements of concentrations of norepinephrine and epinephrine in testicular homogenates revealed higher values for these catecholamines than in the plasma, implying that catecholamine levels in the interstitial spaces of the testis might be in the range of concentrations effectively stimulating testosterone production in vitro. This suggests that in the immature testis of the golden hamster, catecholamines acting through both alpha- and beta-adrenergic receptors may be potent physiological stimulators of testosterone production.
The pairing mechanism of the XY bivalent, the possibility of crossing-over between X and Y chromosomes during meiotic prophase, and the location of the H-Y locus are of interest with regard to genetic control mechanisms, male gametogenesis, and testicular organization. A whole-mount electron microscope technique has permitted the study of a large number of mouse and hamster spermatocytes to evaluate the spatial relationship of sex chromosomes and autosomes. X and Y chromosomes showed a transient, extensive side-by-side pairing segment along most of the length of the Y chromosome. This extensive pairing segment may cause genetic exchange between X and Y chromosomes. The finding of a small unpaired paracentromeric region of the Y chromosome could be related to a locus of totally sex-linked gene(s) that determine the development of the testis from the undifferentiated embryonic gonad.
The anatomical structure of the ejaculatory groove region (EGR) of the drake was investigated macro- and microscopically in connection with its function. The EGR covers a part of the urodeum and the second fold of the cloaca. The EGR is unique to the males and is characterized by red colored appearance and less smooth surface of the mucosa. The mucosa of EGR forms folds giving less smooth surface to it and is lined with psuedostratified columnar epithelium. A vascular layer which contains many capillaries and lymphocytes and gives red color to the mucosa lies just beneath the epithelium. The EGR develops at puberty together with the developments of the testis and the penis. Blood supply and the arrangement of the lymphatic sinuses of EGR were described and their functions were discussed.
After a brief review of the pertaining literature, the case of a 63 year old male patient with a histologically confirmed mesothelioma starting from the tunica vaginalis of the testis is described. The rare tumour developed after an injury of the testis suffered 15 years earlier.
A distinctive Mn-2+-sensitive adenylate cyclase [ATP pyrophosphate-lyase(cyclizing), EC 4.6.1.1] system insensitive to fluoride has been found in rat seminiferous tubules and epididymal sperm. The development of this distinctive adenylate cyclase in testis was studied during spermatogenesis. It was first detectable in seminiferous tubules in immature rats at about the time of the first reductive divisions and the appearance of spermatid cells. The specific activity of the enzyme increased substantially during the period of spermatogenesis when spermatids develop into mature spermatozoa, and reached maximal values in the testis of adult rats. After centrifugation of testis tissue homogenates at 105,000 X g for 60 min, the Mn-2+-sensitive adenylate cyclase activity was found in the cytosol. The enzyme remains in solution after centrifugation at 300,000 X g for 5 hr or at 180,000 X g for 24 hr and passes through a 0.22 mum Millipore filter. Electron microscopic examination showed no visible membrane fragments or vesicles in the filtered supernatant. The Mn-2+-sensitive adenylate cyclase system is also present in epidiymal sperm. However, in the sperm obtained from either the caput or the cauda of epididymis, the adenylate cyclase is membrane-associated and found in particulate fractions of sperm homogenates. It therefore appears that the Mn-2+-sensitive adenylate cyclase is initially present in the cytoplasm either unattached or loosely bound to intracellular membranes and becomes firmly attached to sperm membranes later in development. This occurs either during the process of maturation of spermatids into sperm or during the transport of the testicular sperm into the epididymis.
Repeated amputation of the lower incisors in rats, 11- and 14-days old, caused hypertrophy of the testis only in the presence of the submaxillary salivary glands. Bilateral submaxillary and sublingual sialadenectomy prevented hypertrophy of the testis. After the unilateral removal of these glands the weight of the testis increased, but its hypertrophy developed always. The absence of hypertrophy of the testis in the sialadenectomized animals led to the conclusion that the growth stimulating action on the testis of repeated amputations of the lower incisors was in some way mediated through the function of the salivary glands.
It has now been clearly demonstrated that cryptorchidism is accompanied by a very marked increase in malignancy of the ectopic testis as well as in that in place. Amongst 80 patients undergoing surgery for carcinoma of the testis 14 (17.5%) had a past history of unilateral undescended. The risk of malignancy developing in an ectopic testis is 12 to 48 times greater than that of a testis which has descended normally. It would appear that the higher the position of the testis, the greater is the risk. Orchidopexy may decreased the risk if performed before the age of 11. When the tumour is situated in an ectopic testis, the clinical picture is often misleading. When the ectopic testis has been brought down the special feature of these tumours is the frequency of spread to inguinal lymph nodes. In terms of its basic principles the treatment of these tumours does not differ from that of those affecting normal testis. The aetiology of these tumours remains uncertain. There would seem to be a consensus in favour of a disgenetic origin, possible secondary to hormonal deficiency.
Transformation of the rete ovarii into a rete testis and of the epoophoron into an epididymis after experimental sex reversal in Gallus domesticus is described. After castration of female chicks, the medulla of the left ovary and/or the right gonadal rudiment develop into a testoid or an ovotestis. From general view, this is observed as sex reversal. In case of formation of a testoid, the epoophoron develops into an epididymis and the rete ovarii develops into a rete testis which consists of intra- and extratesticular and intracapsular parts. Thus, a luminated duct system is developed which allows the transport of semen. In case of formation of an ovotestis, the discontinuously side-by-side located parts of the rete ovarii and of the epoophoron are maintained.
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