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  • Wiley-Blackwell  (3)
  • Milton :Taylor & Francis Group,  (1)
  • 1
    Online-Ressource
    Online-Ressource
    Milton :Taylor & Francis Group,
    Schlagwort(e): Spermatogenesis. ; Electronic books.
    Beschreibung / Inhaltsverzeichnis: Spermatogenesis involves the coordination of a number of signaling pathways, which culminate into production of sperm. Its failure results in male factor infertility, which can be due to hormonal, environmental, genetic or other unknown factors. This book inludes chapters on most of the signaling pathways known to contribute to spermatogenesis.
    Materialart: Online-Ressource
    Seiten: 1 online resource (199 pages)
    Ausgabe: 1st ed.
    ISBN: 9780429520952
    DDC: 612.61
    Sprache: Englisch
    Anmerkung: Cover -- Half Title -- Title Page -- Copyright Page -- Dedication -- Contents -- Foreword -- Preface -- Editor -- Contributors -- 1. Primordial germ cells: Origin, migration and testicular development -- 1.1 Introduction -- 1.2 Origin of primordial germ cells -- 1.2.1 Molecular mechanisms during the origin of PGCs -- 1.3 Migration of PGCs -- 1.3.1 Molecular mechanisms during PGC migration -- 1.3.2 Migration stoppage of PGCs -- 1.4 Gonad and testicular development -- 1.4.1 Sertoli cell specification and expansion -- 1.4.2 Testis cord formation and compartmentalization -- 1.4.3 Formation of seminiferous tubules from testis cord by elongation -- 1.5 Conclusion and future directions -- Acknowledgments -- References -- 2. DNA methylation, imprinting and gene regulation in germ cells -- 2.1 Introduction -- 2.2 Dynamics of DNA methylation during PGC development -- 2.3 Mechanism and factors of DNA methylation erasure -- 2.4 Mechanism and factors of DNA methylation establishment -- 2.5 DNA methylation and histone modifications -- 2.6 Conclusion and future directions -- Acknowledgments -- References -- 3. Testicular stem cells, spermatogenesis and infertility -- 3.1 Introduction -- 3.2 Development of male germline cells -- 3.3 Testicular stem cells -- 3.3.1 As model for spermatogonial multiplication and stem cell renewal -- 3.3.2 Fragmentation model -- 3.3.3 Hierarchical model -- 3.4 Our views -- 3.4.1 Pluripotent very small embryonic-like stem cells (VSELs) are the most primitive stem cells in adult mammalian testis -- 3.4.2 Protocols to detect VSELs in testicular tissue -- 3.4.3 Pluripotent VSELs in adult testes undergo asymmetrical cell divisions -- 3.4.4 Pluripotent VSELs provide an alternate premise to explain testicular germ cell tumors -- 3.5 Discussion and future directions -- Acknowledgments -- References. , 4. Testicular germ cell apoptosis and spermatogenesis -- 4.1 Introduction -- 4.1.1 Proliferative phase of spermatogonia -- 4.1.2 Entry of spermatogenic cells into meiosis -- 4.1.3 Spermiogenesis and attainment of the motility appendage -- 4.1.4 Spermatogenic wave -- 4.2 Germ cell apoptosis -- 4.2.1 Pathways of apoptosis in testis -- 4.2.2 Fas/FasL system: Central regulator of testicular germ cell population -- 4.2.3 Activation of caspase-9 via the intrinsic pathway -- 4.2.4 P53 and spermatogenic cell apoptosis -- 4.3 Executioner caspases -- 4.4 Apoptosis of germ cells caused by hormonal, temperature and chemical insult -- 4.4.1 Hormonal variations -- 4.4.2 Heat stress -- 4.5 Testicular toxicants and germ cell apoptosis -- 4.6 Conclusion -- References -- 5. Hormonal regulation of spermatogenesis -- 5.1 Introduction -- 5.2 Spermatogenesis: An overview -- 5.3 Germ cell regeneration and death -- 5.4 Hypothalamic-pituitary-gonadal axis -- 5.5 Endocrine regulation of spermatogenesis -- 5.5.1 Follicle-stimulating hormone -- 5.5.2 Luteinizing hormone -- 5.5.3 Prolactin -- 5.5.4 Inhibin, activin and follistatin -- 5.5.5 Sex steroids -- 5.5.6 Metabolic hormones and growth factors -- 5.5.7 Other hormones -- 5.6 Sertoli cell interaction with Leydig and peritubular myoid cells -- 5.7 Role of hormones in spermiogenesis and spermiation -- 5.8 Conclusion -- References -- 6. GH-IGF1 axis in spermatogenesis and male fertility -- 6.1 Introduction -- 6.2 Growth hormone and male reproductive system -- 6.2.1 Effects on development -- 6.2.2 Effects on steroidogenesis -- 6.2.3 Effects on spermatogenesis -- 6.2.4 Other functions and mechanisms of regulation -- 6.3 Effects of altered growth hormone secretion on male fertility -- 6.4 Therapeutic use of growth hormone for male infertility -- 6.5 Conclusions -- References. , 7. Retinoic acid signaling in spermatogenesis and male (in)fertility -- 7.1 Introduction -- 7.2 Vitamin A and retinoids -- 7.2.1 Retinoid metabolism -- 7.2.2 Tissue targeting and retinoic acid signaling -- 7.3 Effects of RA on spermatogenesis -- 7.3.1 Evidence of retinoid acid effects in spermatogenesis -- 7.3.2 Expression of retinoids and retinoid receptors in the mammalian testis -- 7.3.3 RA signaling pathways in male germ cells and spermatogenesis -- 7.3.4 Influence of RA on sperm metabolism and oxidative stress -- 7.4 Abnormal RA signaling and human male infertility -- 7.5 Concluding remarks -- References -- 8. Testosterone signaling in spermatogenesis, male fertility and infertility -- 8.1 Introduction -- 8.2 Testosterone production and regulation of the steroidogenic pathway -- 8.3 Classical and nonclassical testosterone signaling -- 8.3.1 Classical testosterone signaling -- 8.3.2 Nonclassical testosterone signaling -- 8.4 Estrogen signaling and testosterone -- 8.5 Regulation of testosterone signaling by melatonin -- 8.6 Melatonin and human fertility -- 8.7 Aberrant testosterone signaling and male infertility -- 8.8 Testosterone therapy for azoospermic men -- 8.9 Conclusion and future directions -- References -- 9. Wnt signaling in spermatogenesis and male infertility -- 9.1 Introduction -- 9.2 Canonical Wnt signaling pathway -- 9.2.1 Wnt/Receptor interactions -- 9.2.2 Signal relay in the cytoplasm -- 9.2.3 Nuclear activity of ß-catenin -- 9.3 Wnt signaling in testis determination and development -- 9.4 Wnt signaling in male germ cell proliferation and maturation -- 9.5 Role of Wnt signaling in development and maintenance of Sertoli cells -- 9.6 Deregulated Wnt signaling and testicular tumor -- 9.7 Wnt signaling in male fertility -- 9.8 Conclusion and future directions -- References -- 10. MAPK signaling in spermatogenesis and male infertility. , 10.1 Introduction -- 10.2 Mitogen-activated protein kinases: An overview -- 10.3 Junction dynamics in spermatogenesis and its regulation -- 10.3.1 MAPK-ERK1/2 signaling in junction dynamics -- 10.3.2 MAPK-p38 in junction dynamics -- 10.3.3 JNK in junction dynamics -- 10.4 MAPK role in germ cell apoptosis -- 10.5 MAPKs in male infertility -- 10.6 Conclusion and future directions -- References -- 11. TGF-ß signaling in testicular development, spermatogenesis, and infertility -- 11.1 Introduction -- 11.2 Components of TGF-ß signaling cascade -- 11.2.1 Ligands -- 11.2.2 Receptors -- 11.2.3 SMAD proteins -- 11.3 Knockout mouse studies -- 11.4 TGF-ß superfamily action in testis -- 11.4.1 TGF-ß signaling -- 11.4.2 Activin signaling -- 11.4.3 Glial cell-derived neurotrophic factor signaling -- 11.4.4 Müllerian inhibiting substance signaling -- 11.4.5 Bone morphogenetic protein signaling -- 11.5 Reproductive disorders associated with aberrant TGF-ß signaling -- 11.5.1 Testicular cancer -- 11.5.2 Disrupted spermatogenesis -- 11.5.3 Leydig cell hyperplasia -- 11.5.4 Sertoli cell-only syndrome (germ cell aplasia) -- 11.5.5 Persistent Müllerian duct syndrome -- 11.6 TGF-ß cross talk with other pathways -- 11.7 Conclusion and future directions -- Acknowledgments -- References -- 12. Notch signaling in spermatogenesis and male (in)fertility -- 12.1 Introduction -- 12.2 Notch signaling: General concepts -- 12.3 How crucial is Notch signaling for spermatogenetic events? -- 12.4 Spermatogenesis in Caenorhabditis elegans and Notch signaling -- 12.5 Cross talk between Notch and other pathways in regulating spermatogenesis in C. elegans -- 12.6 Spermatogenesis in Drosophila melanogaster -- 12.7 Cross talk between Notch and other pathways in D. melanogaster -- 12.8 Spermatogenesis in Mus musculus -- 12.9 Cross talk between Notch and other pathways. , 12.10 Male infertility due to dysregulation of Notch signaling -- 12.11 Concluding remarks and future perspective -- Acknowledgments -- References -- 13. Hedgehog signaling in spermatogenesis and male fertility -- 13.1 Introduction -- 13.2 Hedgehog molecules -- 13.3 Hedgehog signaling in mammals -- 13.4 Hedgehog signaling in spermatogonial stem cell proliferation and differentiation -- 13.5 Indirect hedgehog signaling in SSCs -- 13.6 Direct hedgehog signaling in SSCs -- 13.7 Hedgehog signaling in spermatogenesis -- 13.7.1 Desert hedgehog -- 13.7.2 Sonic hedgehog (Shh) -- 13.7.3 Indian hedgehog -- 13.8 Conclusion -- References -- 14. mTOR signaling in spermatogenesis and male infertility -- 14.1 Introduction -- 14.2 mTOR-signaling pathway and mTOR complexes -- 14.3 Role of mTOR signaling in spermatogenesis -- 14.3.1 mTOR signaling in spermatogonial proliferation and Sertoli cell polarity -- 14.3.2 Role of mTOR signaling in blood-testes barrier -- 14.4 Clinical evidence of the role of mTOR in male fertility -- 14.5 Conclusion -- References -- 15. JAK-STAT pathway: Testicular development, spermatogenesis and fertility -- 15.1 Introduction -- 15.2 Model organisms for studying the JAK-STAT pathway -- 15.3 Components of the JAK-STAT pathway -- 15.3.1 Ligand molecules -- 15.3.2 Receptors -- 15.3.3 Janus kinases -- 15.3.4 Signal transducer for activation of transcription -- 15.3.5 Regulators of the JAK-STAT pathway -- 15.4 JAK-STAT signaling in gonad development -- 15.4.1 Germline sexual development in Drosophila melanogaster -- 15.5 JAK-STAT pathway and spermatogenesis -- 15.5.1 Drosophila testis stem cell niche -- 15.5.2 Intercellular communications -- 15.5.3 Role of JAK-STAT in maintenance of stem cell niche -- 15.5.4 Integration of signaling pathways for stem cell maintenance -- 15.6 JAK-STAT pathway in human sperm capacitation. , 15.7 JAK-STAT pathway in sperm motility.
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  • 2
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    X-Ray Spectrometry 17 (1988), S. 99-101 
    ISSN: 0049-8246
    Schlagwort(e): Chemistry ; Analytical Chemistry and Spectroscopy
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Physik
    Notizen: A method has been devised to test the correctness of relationships for computing L shell vacancies in radionuclides following electron capture and internal conversions. The average L shell fluorescence yields in eleven elements have been derived from a comparison of computed vacancies and measured subshell intensities. The validity of the relationships derived earlier is confirmed.
    Zusätzliches Material: 2 Tab.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Publikationsdatum: 2012-06-13
    Beschreibung: BACKGROUND Benign prostatic hyperplasia (BPH) is an age related non-malignant disease diagnosed as lower urinary tract symptoms and prostatic enlargement. Null genotypes in drug detoxification glutathione- S -transferase genes/enzymes, such as GSTT1 and GSTM1 have been reported to increase risk of several cancers including prostate. Meta-analysis on PC also suggested significant impact of GSTM1 null genotype but not that of GSTT1 ; however, BPH data have not been subjected to meta-analysis. METHODS We investigated GSTT1 and GSTM1 genotypes in 429 subjects which included 244 BPH, 51 prostate cancer (PC) patients, and 134 control subjects to find if null genotype in any of the two genes increased the risk of BPH/PC. We also performed a quantitative meta-analysis on 888 BPH cases and 793 controls for GSTM1 and on 890 BPH cases and 793 controls for GSTT1 to assess overall consensus about the impact of null genotypes on BPH risk. RESULTS We did not find any significant difference in the distribution of genotypes of either of the two genes between BPH/PC cases and controls; however, double deletion ( GSTM1 null +  GSTT1 null) increased BPH risk, significantly. Upon meta-analysis, null genotype of GSTM1 but not that of GSTT1 appeared to strongly affect BPH risk. CONCLUSIONS In our population, null genotypes of either GSTM1 or GSTT1 do not appear to affect BPH risk; however, the double deletion was significantly associated with BPH. Meta-analysis suggested significant influence of GSTM1 null genotype but not that of GSTT1 on BPH risk. Prostate © 2012 Wiley Periodicals, Inc.
    Print ISSN: 0270-4137
    Digitale ISSN: 1097-0045
    Thema: Medizin
    Publiziert von Wiley-Blackwell
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Publikationsdatum: 2015-11-25
    Beschreibung: Estrogen Receptor-β (ER-β), a tumor-suppressor in prostate cancer, is epigenetically repressed by hypermethylation of its promoter. DNA-methyltransferases (DNMTs), which catalyze the transfer of methyl-groups to CpG islands of gene promoters, are overactive in cancers and can be inhibited by DNMT-inhibitors to re-express the tumor suppressors. The FDA-approved nucleoside DNMT-inhibitors like 5-Azacytidine and 5-Aza-deoxycytidine carry notable concerns due to their off-target toxicity, therefore non-nucleoside DNMT inhibitors are desirable for prolonged epigenetic therapy. Disulfiram (DSF), an antabuse drug, inhibits DNMT and prevents proliferation of cells in prostate and other cancers, plausibly through the re-expression of tumor suppressors like ER-β. To increase the DNMT-inhibitory activity of DSF, its chemical scaffold was optimized and compound-339 was discovered as a doubly potent DSF-derivative with similar off-target toxicity. It potently and selectively inhibited cell proliferation of prostate cancer (PC3/DU145) cells in comparison to normal (non-cancer) cells by promoting cell-cycle arrest and apoptosis, accompanied with inhibition of total DNMT activity, and re-expression of ER-β (mRNA/protein). Bisulfite-sequencing of ER-β promoter revealed that compound-339 demethylated CpG sites more efficaciously than DSF, restoring near-normal methylation status of ER-β promoter. Compound-339 docked on to the MTase domain of DNMT1 with half the energy of DSF. In xenograft mice-model, the tumor volume regressed by 24% and 50% after treatment with DSF and compound-339, respectively, with increase in ER-β expression. Apparently both compounds inhibit prostate cancer cell proliferation by re-expressing the epigenetically repressed tumor-suppressor ER-β through inhibition of DNMT activity. Compound-339 presents a new lead for further study as an anti-prostate cancer agent. © 2015 Wiley Periodicals, Inc.
    Print ISSN: 0899-1987
    Digitale ISSN: 1098-2744
    Thema: Medizin
    Publiziert von Wiley-Blackwell
    Standort Signatur Einschränkungen Verfügbarkeit
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