Severe hydrops foetalis treated with peritoneal dialysis and positive-pressure ventilation.
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Biomedical subjects
Publications and source records attributed to E Nathan.
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This study was conducted to determine the effects of lead on Sertoli cell function. Androgen binding protein and inhibin in testicular fluids and classical parameters of the hypothalamic-pituitary-gonadal axis were measured in adult male rats. For 10 wk, the rats were given water that contained 0.05%, 0.1%, 0.5%, and 1% lead acetate. Serum follicle-stimulating hormone, luteinizing hormone, and testosterone levels in all animals that ingested lead were normal at the middle and end of the experiment, as was the pituitary content of follicle-stimulating hormone and luteinizing hormone. Histologic examination revealed no disruption of spermatogenesis. Distribution of androgen binding protein in serum, seminiferous tubular fluid, and interstitial fluid was normal, as was the concentration of inhibin in interstitial fluid and seminiferous tubular fluid. However, a significant increase in epididymal androgen binding protein level and a decrease in seminal vesicle weight were observed in rats that ingested water containing 1% lead acetate. These results suggest that the effect of lead on spermatogenesis is not marked in adult Sprague Dawley rats, nor does Sertoli cell function appear to be affected adversely. Lead has been reported to alter in vitro metabolic function of Sertoli cells obtained from 16- to 21-d-old Sprague Dawley rats, and the Sertoli cells of juvenile animals may be more susceptible to lead than those of adult animals. The significant decrease in seminal vesicle weight and the abnormal epididymal androgen binding protein content indicate that lead could affect the male reproductive function in Sprague Dawley rats via its action on male accessory organs.
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This study examines the effects of a potent gonadotropin releasing hormone (GnRH)-antagonist (GnRH-A, Ac-D[2] Nal1, 4-CL-D Phe2, D-Trp3, D-Arg6, D-Ala10) upon the distribution of androgen binding protein (ABP) in serum, testis, and epididymis, and its relationship with the completion of spermatogenesis in Sprague-Dawley rats. After 2 weeks of daily injections of 10 micrograms/kg, 50 micrograms/kg, 100 micrograms/kg, or 500 micrograms/kg of GnRH-A, testicular ABP content was either unchanged or elevated (P less than 0.05), and serum ABP levels were elevated (P less than 0.01). Spermatogenesis was maintained in animals administered 10 micrograms/kg or 50 micrograms/kg GnRH-A, and epididymal ABP content remained unchanged. On the other hand, daily injections of 100 micrograms/kg or 500 micrograms/kg GnRH-A resulted in a significant decrease in epididymal ABP content (P less than 0.05), and spermatogenesis was arrested at early spermiogenesis. After 4 weeks of GnRH-A administration, both testicular and epididymal ABP were decreased in a dose-dependent manner in animals receiving doses of 50 micrograms/kg or higher of GnRH-A. In order to evaluate the normalcy of the bidirectional release of ABP in GnRH-A treated rats, additional rats were given daily injections of 25 micrograms/kg or 250 micrograms/kg of GnRH-A for 2 weeks. Concentrations of ABP in interstitial fluid (ITF) and seminiferous tubular fluid (STF) remained unchanged, but serum ABP levels were significantly increased (P less than 0.05) in rats administered 25 micrograms/kg GnRH-A. Qualitatively normal spermatogenesis was maintained and epididymal ABP content did not differ from that of control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
The investigation of the brain from a seven-day-old girl who died from a disorder in the metabolism of methylmalonic acid revealed a severe reactive gliosis of the cerebral white matter and the deeper layers of the cortex, incomplete development of the fetal granular layer of the cerebellum and the Bergmann glial cells, and delayed myelination of the cerebellum, the brainstem, and the cervical spinal cord. We suggest that some of the described neuropathological findings are an immediate consequence of a disturbed methylmalonic acid metabolism starting in utero, and not exclusively a secondary phenomenon due to accumulation of metabolites and acidosis postpartum.
One of the side effects of cisplatinum-based chemotherapy is the impairment of spermatogenic function. In order to understand the mechanisms responsible for this side effect, the present study examined the short- and long-term effects of five daily injections of 2 mg/kg cisplatinum upon the functional normality of Leydig cells and Sertoli cells in intact adult rats, and their relationship with the status of spermatogenesis. Results of the present study demonstrate that cisplatinum treatment resulted in a progressive but reversible loss of germ cells from the seminiferous epithelium. Although testicular testosterone contents reduced transiently after the adminisration of cisplatinum, these testosterone levels are otherwise sufficient to support complete spermatogenesis. Thus, the cisplatinum-induced germinal regression cannot be accounted for by hypoandrogenism. The testicular ABP contents of the drug-treated rats remained unchanged during the treatment period, decreased transiently 30 days after the treatment, and returned to normal 120 days after treatment. A decrease in epididymal ABP content was also noted 10 and 30 days after the drug treatment. These observations suggest that Sertoli cell functions were affected by cisplatinum treatment. The effects of cisplatinum upon Sertoli cells were further demonstrated by the dose-dependent suppression of the production of ABP, lactate, and estradiol in cultured Sertoli cells. In addition, cisplatinum administration resulted in a reversible decrease in pituitary weights and an irreversible decrease in seminal vesicle weights. These results further demonstrate the toxic effects of cisplatinum upon various aspects of the male reproductive system.