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Analyse:Iri

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[1.] Analyse:Iri/Fragment 005 01 - Diskussion
Bearbeitet: 21. March 2014, 17:43 Schumann
Erstellt: 5. December 2013, 17:40 (Graf Isolan)
Fragment, Gesichtet, Hedger und Hales 2005, Iri, SMWFragment, Schutzlevel, Verschleierung

Typus
Verschleierung
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Graf Isolan
Gesichtet
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Untersuchte Arbeit:
Seite: 5, Zeilen: 1ff (komplett)
Quelle: Hedger und Hales 2005
Seite(n): 1201, Zeilen: li.Sp. 3-33
[These cells remain in] intimate contact with their adjacent Sertoli cells at all times during the spermatogenetic process, with junctional and membrane specializations providing physical contact and communication and forming the so called “blood-testis barrier” (Cheng and Mruk, 2002).

The spermatogenic cells start out as mitotically dividing precursors called spermatogonia, sitting on the basal lamina (Fig. 1.1.2). At puberty these mitotically dividing cells enter into meiosis at regular intervals, moving from the periphery of the tubule to the luminal part and becoming primary and later secondary spermatocytes. Meiosis leads to chromosomal rearrangements leading to production of haploid round spermatids (early spermatids), that subsequently undergo structural differentiation to become mature or elongated spermatids (late spermatids). Once these cells are released by the Sertoli cell into the lumen of the tubule they are called spermatozoa and the fluid secreted by the Sertoli cells sweeps the released immotile spermatozoa to the rete testes.

Tight junctions between adjacent Sertoli cells and their associated membrane specializations form an intercellular barrier, which is completely impermeable for even small molecules (Whitehead, 1999, Cheng and Mruk, 2002). This blood-testis barrier separates the spermatogonia and early meiotic cells in the basal region of the seminiferous epithelium from the adluminal spermatocytes and spermatids. In this way a large majority of the developing germ cells are [sequestered behind a physical barrier and effectively isolated from the immune system.]


Cheng, C. Y. and Mruk, D. D. (2002) Physiol Rev, 82, 825-74.

Whitehead, S. S. N. S. A. (1999) Endocrinology, An Integrated Approach, BIOS Scientific Publishers Ltd.

These cells remain in intimate contact with their adjacent Sertoli cells at all times during the spermatogenetic process, with junctional and membrane specializations providing physical contact and communication (134,135). The spermatogenic cells start out as mitotically dividing precursors called spermatogonia sitting on the basal lamina. Commencing at the time of puberty, cohorts of these mitotically dividing cells begin to enter into meiosis at regular intervals, moving from the periphery of the tubule and becoming spermatocytes in the process. Meiosis is a lengthy procedure of chromosomal rearrangements leading to production of haploid round spermatids (see Chapter 18 for details). Once these cells are released by the Sertoli cell into the tubule lumen, they are called spermatozoa, and fluid secreted by the Sertoli cells sweeps the released spermatozoa toward the rete testes.

Occluding junctions between adjacent Sertoli cells and their associated membrane specializations form an intercellular barrier that is completely impermeable even to small molecules (42,134,135). This blood-testis barrier separates the spermatogonia and early meiotic cells in the basal region of the seminiferous epithelium from the adluminal spermatocytes and spermatids. In this way, a large majority of the developing germ cells are sequestered behind a physical barrier within a highly specialized environment, and effectively isolated from the immune system (Fig. 3).


42. Dym, M., and Fawcett, D. W. (1970). The blodd-testis barrier in the rat and the physiological compartmentation of the semineferous epithelium. Biol. Reprod. 3, 308-326.

134. Cheng, C. Y., and Mruk, D. D. (2002). Cell junction dynamics in the testis: Sertoli-germ cell interactions and male contraceptive development. Physiol Rev. 82, 825-874.

135. Pelletier, R. M. (2001). The tight junctions in the testis, epididymis and vas deferens. In Tight Junctions (2nd ed. M. Cereijido and J. Anderson, Eds.), pp. 599-628. CRC Press, Boca Raton, FL.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan) Schumann

[2.] Analyse:Iri/Fragment 012 25 - Diskussion
Bearbeitet: 21. March 2014, 17:49 Schumann
Erstellt: 5. December 2013, 18:13 (Graf Isolan)
Fragment, Gesichtet, Guazzone et al 2005, Iri, SMWFragment, Schutzlevel, Verschleierung

Typus
Verschleierung
Bearbeiter
Graf Isolan
Gesichtet
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Untersuchte Arbeit:
Seite: 12, Zeilen: 25-33
Quelle: Guazzone et al 2005
Seite(n): 603, Zeilen: li.Sp. 2-14
Acute or chronic inflammation of the male genital tract may result in alterations of spermatogenesis, steroidogenesis and fertility (Bohring and Krause, 2003). Chronic orchitis in men usually occurs as a consequence of different injuries induced by trauma or infectious agents. The interaction of immune cells with spermatic antigens is one of the pathogenic mechanisms involved in testis autoimmunity. Different models of experimental autoimmune orchitis (EAO) have been useful in understanding testicular cell interactions under pathological conditions. EAO has been induced in different species by active immunization with spermatic antigens, by adoptive T cell transfer or by [neonatal thymectomy (Tung and Teuscher, 1995).]

Bohring, C. and Krause, W. (2003) Hum Reprod, 18, 915-24.

Tung, K. and Teuscher, C. (1995) Hum Reprod Update, 1, 35-50.

Acute or chronic inflammation of the male genital tract may result in alterations of spermatogenesis, steroidogenesis and fertility (Hales et al. 1999). Orchitis in men usually occurs as a consequence of different injuries induced by trauma or physical or infectious agents. The interaction of immune cells with spermatic antigens is one of the pathogenic mechanisms involved in testis autoimmunity. Different models of experimental autoimmune orchitis (EAO) have been useful in understanding testicular cell interactions. EAO has been induced in different species by active immunization with spermatic antigens, by adoptive T cell transfer or by neonatal thymectomy (Itoh et al. 1992, Tung et al. 1994).

Hales DB, Diemer T & Hales KH 1999 Role of cytokines in testicular function. Endocrine 10 201–217.

Itoh M, Hiramine C, Mukasa A, Tokunaga Y, Fukui Y, Takeuchi Y & Hojo K 1992 Establishment of an experimental model of autoimmune epididymo-orchitis induced by the transfer of a T-cell line in mice. International Journal of Andrology 15 170–181.

Tung KSK, Taguchi O & Teuscher C 1994 Testicular and ovarian autoimmune diseases. In Guidebook to Animal Models for Autoimmune Diseases, pp 267–290. Eds IR Cohen & A Millers. New York: Academic Press.

Anmerkungen

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Sichter
(Graf Isolan) Schumann


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Quellen

Quelle Autor Titel Verlag Jahr Lit.-V. FN
Iri/Guazzone et al 2005 V.A Guazzone, B. Denduchis, L. Lustig Involvement of CD44 in leukocyte recruitment to the rat testis in experimental autoimmune orchitis 2005
Iri/Hedger und Hales 2005 M. P. Hedger, D. B. Hales Immunophysiology of the Male Reproductive Tract Elsevier/Academic Press 2006


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