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  • Wiley-Blackwell  (3)
  • Singapore :Springer Singapore Pte. Limited,  (1)
Publikationsart
Verlag/Herausgeber
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Erscheinungszeitraum
  • 1
    Online-Ressource
    Online-Ressource
    Singapore :Springer Singapore Pte. Limited,
    Schlagwort(e): Animal Physiology. ; Electronic books.
    Materialart: Online-Ressource
    Seiten: 1 online resource (497 pages)
    Ausgabe: 1st ed.
    ISBN: 9789811040177
    DDC: 571.1
    Sprache: Englisch
    Anmerkung: Intro -- Preface -- About the Editors -- Contents -- Contributors -- Abbreviations -- Part I: Understanding Spermatogenesis and Male Fertility -- 1: Overview of the Male Reproductive System -- 1.1 Origin of the Reproductive Organs -- 1.2 Anatomy and Physiology of the Male Reproductive System -- 1.2.1 Scrotum -- 1.2.2 Testes -- 1.2.2.1 Leydig Cells -- 1.2.2.2 Sertoli Cells -- 1.2.2.3 Blood-Testis Barrier -- 1.2.2.4 Germ Cells -- 1.2.2.5 Spermatogenesis -- 1.3 Testosterone -- 1.4 Sperm Transport -- 1.4.1 Epididymis -- 1.4.2 Duct System -- 1.5 Seminal Vesicle -- 1.6 Prostate Gland -- 1.7 Bulbourethral Gland -- 1.8 Urethra -- 1.9 Penis -- 1.10 Structure of Human Mature Sperm -- References -- 2: Embryonic Development of the Testis -- 2.1 Introduction -- 2.2 Overview of the Development of the Testes -- 2.3 Formation of the Primitive Gonads -- 2.4 Cell Lineages -- 2.4.1 Primordial Germ Cells -- 2.4.2 Somatic Cell Lineages in the Male Testis -- 2.4.2.1 Sertoli Cells -- 2.4.2.2 Leydig Cells -- 2.4.2.3 Peritubular Cells -- 2.5 Testicular Descent -- 2.6 Perinatal Events in Testicular Maturation -- 2.7 Cryptorchidism: The Failure of Testicular Descent -- 2.8 Testicular Descent: Associated Disorders -- References -- 3: HPG Axis: The Central Regulator of Spermatogenesis and Male Fertility -- 3.1 Introduction -- 3.2 The Hypothalamic-Pituitary-Gonadal Axis -- 3.3 GnRH Neurons: Origin and Development -- 3.4 Role of FSH and LH in Spermatogenesis -- 3.5 FSH and LH in Human Male Infertility -- 3.6 Endocrine Disruptors: Modulators of the HPG Axis -- 3.7 Melatonin and HPG Axis in Reproductive Health -- References -- 4: Sperm Maturation in Epididymis -- 4.1 Introduction -- 4.2 Epididymal Morphology -- 4.3 Epididymis: The Site of Sperm Maturation -- 4.4 Epididymal Transcriptome and Proteome -- 4.5 Epididymal Secretome. , 4.6 Maturational Changes in Sperm During Epididymal Transit -- 4.7 Development of Motility Potential in Sperm During Epididymal Transit -- References -- 5: Sperm Capacitation: The Obligate Requirement for Male Fertility -- 5.1 Introduction -- 5.2 What Is Sperm Capacitation? -- 5.3 Hallmarks of Capacitation -- 5.3.1 Hyperactivation -- 5.3.2 Acrosome Reaction -- 5.3.3 Protein Tyrosine Phosphorylation -- 5.4 Diagnosis and Prognosis of Male Infertility/Fertility: Importance of Capacitation-Based Sperm Function Tests -- 5.4.1 Monitoring Hyperactivation (HA) -- 5.4.2 Monitoring Acrosome Reaction (AR) -- 5.4.3 Monitoring Tyrosine Phosphorylation (pY) -- 5.5 From Bench to Clinics: Male Fertility Biomarkers and ARTs -- References -- 6: Genomic Landscape of Human Y Chromosome and Male Infertility -- 6.1 Introduction -- 6.2 Y Chromosome and the Azoospermia Factor Region (AZF) -- 6.2.1 AZFa -- 6.2.2 AZFb -- 6.2.3 AZFc -- 6.3 Sex-Determining Region Y (SRY) -- 6.4 Y Chromosome Has Significance Beyond Sex Determination and Spermatogenesis -- 6.5 Oncogenic Role of Y Chromosome -- 6.6 Gene Conversions -- 6.7 Y Chromosome: Evolution and Degeneration -- 6.8 Y Chromosome: Regulation of Autosomal Gene Expression -- 6.9 Future Prospects -- References -- 7: Seminal Decline in Semen Quality in Humans Over the Last 80 years -- 7.1 Introduction -- 7.2 Hallmark Studies Describing a Decline Over the Past 80 years -- 7.3 Factors Alleged for Deteriorating Semen Quality -- 7.4 Discussion and Future Directions -- References -- Part II: Causes of Male Infertility -- 8: Syndromic Forms of Male Infertility -- 8.1 Introduction -- 8.2 Syndromes with Chromosomal Aneuploidy -- 8.2.1 Klinefelter's Syndrome (47,XXY) -- 8.2.2 Jacob's Syndrome (47,XYY) -- 8.3 Syndromes with Gene Mutations -- 8.3.1 Kallmann Syndrome. , 8.3.2 Androgen Insensitivity Syndrome (AIS) -- 8.3.3 Noonan Syndrome -- 8.3.4 Cystic Fibrosis -- 8.4 Rare Syndromes of Male Infertility -- 8.4.1 Myotonic Dystrophy 1 -- 8.4.2 Primary Ciliary Dyskinesia -- 8.4.3 Kearns-Sayre Syndrome -- 8.4.4 Aarskog-Scott Syndrome -- 8.4.5 Persistent Müllerian Duct Syndrome -- 8.4.6 Prader-Willi Syndrome -- 8.4.7 Deafness Infertility Syndrome -- References -- 9: Cystic Fibrosis, CFTR Gene, and Male Infertility -- 9.1 Introduction -- 9.2 Pathogenesis -- 9.3 Epidemiology -- 9.4 Diagnosis -- 9.5 Fertility in Men Having CF -- 9.6 CFTR-Related Disorders Associated with Male Infertility -- 9.6.1 Congenital Bilateral Absence of the Vas Deferens (CBAVD) -- 9.6.2 CBAVD Having Renal Anomalies (CBAVD-URA) -- 9.6.3 Congenital Unilateral Absence of the Vas Deferens (CUAVD) -- 9.6.4 Ejaculatory Duct Obstruction -- 9.7 Infertility Management in CBAVD -- 9.7.1 Assisted Reproduction -- 9.7.2 Genetic Counseling -- 9.7.3 Sperm Collection Techniques -- 9.7.3.1 Percutaneous Epididymal Sperm Aspiration (PESA) -- 9.7.3.2 Microsurgical Epididymal Sperm Aspiration (MESA) -- 9.8 Our Experience -- 9.8.1 CFTR Gene Variants in Isolated CBAVD in Indian Population -- 9.8.2 CBAVD-URA -- 9.9 Future Perspectives -- References -- 10: Oxidative Stress and Male Infertility -- 10.1 Introduction -- 10.2 Significance of ROS in Sperm Function -- 10.3 Sources of ROS in Semen -- 10.4 Oxidative Stress: Potential Origins -- 10.5 Oxidative Stress: A Major Contributor to the Disease Pathology -- 10.6 Oxidative Stress and Declining Semen Quality -- 10.7 Oxidative Stress Correlates with Erectile Dysfunction -- 10.8 Oxidative Stress: Clinical Perspectives and Laboratory Assessment -- 10.9 Management of Oxidative Stress-Induced Male Infertility -- 10.9.1 Antioxidants -- 10.9.2 Other Therapies -- References. , 11: Obesity, Spermatogenesis, and Male Infertility -- 11.1 Introduction -- 11.2 Obesity and Reproduction -- 11.3 Obesity Compromises Testosterone Production -- 11.4 Obesity Disturbs Testosterone: Estrogen Ratio -- 11.5 Obesity Disturbs Scrotal Thermal Regulation -- 11.6 Obesity Increases DNA Damage -- 11.7 Obesity Leads to Transgenerational Epigenetic Effects -- 11.8 microRNAs (miRNAs), Obesity, and Male Infertility -- 11.9 Obesity Correlates with Erectile Dysfunction -- 11.10 Obesity, Adipokines, and Male Infertility -- 11.11 Impact of Childhood Obesity on Puberty -- 11.12 Effect of Maternal Obesity on Fetal Health -- 11.13 Obesity and Quality of Sexual Life -- 11.14 Animal Studies on Obesity and Fertility -- 11.15 Management of Obesity-Related Infertility -- References -- 12: Sexually Transmitted Infections and Male Infertility: Old Enigma, New Insights -- 12.1 Introduction -- 12.2 STD Pathogens: Locus of Infection and Resultant Pathology in the Male Urogenital Tract -- 12.2.1 Urethritis -- 12.2.2 Epididymitis and Orchitis -- 12.2.3 Prostatitis -- 12.2.4 Vesiculitis -- 12.3 Bacterial Infections and Male Infertility -- 12.3.1 Neisseria gonorrhoeae -- 12.3.2 Chlamydia trachomatis -- 12.3.3 Treponema pallidum -- 12.3.4 Mycoplasma Species -- 12.3.5 Ureaplasma Species -- 12.4 Viral Infections and Associated Male Infertility -- 12.4.1 Human Papillomavirus -- 12.4.2 Human Cytomegalovirus -- 12.4.3 Human Immunodeficiency Virus -- 12.4.4 Herpes Simplex Virus -- 12.4.5 Hepatitis B Virus (HBV) -- 12.4.6 Hepatitis C Virus or HCV -- 12.5 Protozoan Infections and Male Infertility -- 12.5.1 Trichomonas vaginalis -- References -- 13: Cytogenetic Factors in Male Infertility -- 13.1 Introduction -- 13.2 SRY Gene Translocation on X Chromosome or Autosomes -- 13.3 Somatic Chromosome Aneuploidies -- 13.3.1 47,XXY. , 13.3.2 47,XYY -- 13.4 Meiotic Abnormalities and Sperm Aneuploidies -- 13.5 Chromosomal Translocations and Inversions -- 13.6 The Interchromosomal Effects -- 13.7 Sperm Aneuploidies and Adverse Reproductive Outcomes -- 13.8 Advances in Human Molecular Cytogenetics: From Chromosomes to SNPs -- 13.8.1 Multiplex-Fluorescence In Situ Hybridization (M-FISH) and Spectral Karyotyping (SKY) -- 13.8.2 Combining Binary and Ratio Labelling (COBRA-FISH) -- 13.8.3 Array-Based CGH -- 13.8.4 Single-Nucleotide Polymorphism Array (SNP Array) -- 13.8.5 Next-Generation Sequencing (NGS) -- References -- 14: Autosomal Genes in Male Infertility -- 14.1 Introduction -- 14.2 Genes in Gonadal Development and Fertility: Establishing Fertility -- 14.3 Autosomal Pathways in Spermatogenesis -- 14.3.1 Infertility and Apoptosis: Eliminating the Unfit -- 14.3.1.1 Intrinsic Pathway -- 14.3.1.2 Extrinsic Pathway -- 14.3.2 DNA Damage, Replication and Repair Pathways: Keeping It Correct -- 14.3.3 Hormonal/Endocrine Pathways -- 14.4 Standalone Drivers from the Autosomal Store -- References -- 15: Sex Chromosomal Genes in Male Infertility -- 15.1 Introduction -- 15.2 Y Deletions Are Common in Infertility -- 15.3 Screening of Y deletions -- 15.4 Classical Deletions/Microdeletions -- 15.5 Partial Deletions -- 15.5.1 gr/gr Is a Risk Factor for Male Infertility -- 15.5.2 b2/b3 May Increase Risk in Some Ethnic Groups -- 15.6 Y Haplotypes -- 15.6.1 Terminology and Nomenclature of Y Haplotypes -- 15.6.2 Y Haplotypes and Male Infertility -- 15.7 Genes on the X Chromosome -- 15.8 X-Linked Testis-Specific or Testis-Enriched Genes -- 15.9 Mutation Analysis of Human X-Linked and Testis-­Enriched Genes -- 15.9.1 A-Kinase Anchor Protein 4 (AKAP4) -- 15.9.2 Fetal and Adult Expressed 1 (FATE1) -- 15.9.3 TATA Box Binding Protein-Associated Factor 7 Like (TAF7L). , 15.9.4 Ubiquitin-Specific Peptidase 26 (USP26).
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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
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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
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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
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