Download e-book for iPad: Male Hypogonadism (Contemporary Endocrinology) by Stephen J. Winters, Ilpo T. Huhtaniemi

By Stephen J. Winters, Ilpo T. Huhtaniemi

This lucid interpretation of the newest clinical info on male reproductive endocrinology offers a radical knowing of the pathophysiology, scientific features, and coverings for issues that adversely impact testicular functionality. The authors specialize in the explicit reasons of gonadotropin deficiency and testicular failure coming up from issues of the mind and the testis and from gene defects and protracted disorder. extra chapters describe the endocrine mechanism for the decline of testicular functionality with getting older, summarize the information assisting the unfavorable effect of environmental pollution on testicular functionality, and talk about the testicular results of workout and weight problems.

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100. Kawakami S, Fujii Y, Okada Y, Winters SJ. Paracrine regulation of FSH by follistatin in folliculostellate cell-enriched primate pituitary cell cultures. Endocrinology 2002;143:2250–2258. 101. Kaiser UB, Chin WW. Regulation of follistatin messenger ribonucleic acid levels in the rat pituitary. J Clin Invest 1993;91:2523–2531. 102. Burger HG, Robertson DM. Editorial: inhibin in the male—progress at last. Endocrinology 1997;138:1361–1362. 103. McCullagh D. Dual endocrine activity of the testes.

Attisano L, Wrana JL. Signal transduction by members of the transforming growth factor-beta superfamily. Cytokine Growth Factor Rev 1996;7:327–339. 82. Kawabata M, Imamura T, Inoue H, et al. Intracellular signaling of the TGF-beta superfamily by Smad proteins. Ann N Y Acad Sci 1999;886:73–82. 83. Derynck R, Zhang Y, Feng XH. Smads: transcriptional activators of TGF-beta responses. Cell 1998;95:737–740. 84. Hoodless PA, Haerry T, Abdollah S, et al. MADR1, a MAD-related protein that functions in BMP2 signaling pathways.

The neonatal period is relatively brief, extending only through the first year of life (28,29). After the first year and continuing for a decade, Leydig cells are in a state of prepubertal quiescence. During this phase, well-differentiated Leydig cells are absent from the interstitial space. In their place are partially differentiated Leydig cells and primitive fibroblastic cells. At this stage, Leydig cells are dispersed in a loose connective tissue matrix and contain elongated nuclei with scarcely visible cytoplasm.

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