CLINICAL CHEMISTRY RESEARCH -- Contents -- Preface -- Phytoestrogens: Biochemical Aspects and Biological Activities -- Abstract -- Introduction -- Signal Transduction by Estrogens -- General Aspects -- Receptor Structure and Function -- Phytoestrogens: Biology, Structure,Distribution and Metabolism -- Isoflavones -- Lignans -- Coumestans -- Prenylflavonoids -- Stillbenes -- Effects on Human Health -- Cancer -- Breast Cancer -- Prostate Cancer -- Menopause -- Osteoporosis -- Cardiovascular Disease -- Inhibition of Angiogenesis -- Reproductive Actions -- Female Reproductive System -- Male Reproductive System -- Developmental Actions -- Neurobehavioral Actions -- Renal Disease -- Anti-Viral Activity -- Phytoestrogen Toxicity -- Conclusion -- References -- (Q)SAR and Clinical Chemistry ofCamptothecin Analogues -- Abstract -- 1. Introduction -- 2. Structure-Activity Relationships (SAR) -- 2.1. Modification in the A Ring -- 2.2. Modification in the B Ring -- 2.3. Modification in the A/B Ring -- 2.4. Modification in the C Ring -- 2.5. Modification in the D Ring -- 2.6. Modification in the E Ring -- 3. Quantitative Structure-Activity Relationships (QSAR) -- 3.1. QSAR for the Inhibition of DNA Topoisomerase I -- Inhibition of DNA topo I by 7-X-9-Y-10-Z-camptothecins (XXVII) [108] -- Inhibition of DNA topo I by 7-X-9-Y-10,11-methylenedioxycamptothecins(XXVIII) [108] -- Inhibition of DNA topo I by X-camptothecins (XXIX) [110] -- Inhibition of DNA topo I by 10-X-camptothecins (XXX) [111] -- 3.2. QSAR for the Inhibition of Various Cancer Cells -- Cytotoxicities (pIC50) of 7-oxyiminomethyl derivatives of camptothecin i.e. 7-X-camptothecins (XXXI) to H460 human NSCLS cell line [114] -- Inhibition of HL-60 (human promyelocytic leukemic) cells by 7-silylcamptothecin derivatives with variable substitution at C-10 position i.e.7-X-10-Y-camptothecins (XXXII) [114].

Cytotoxic activities (IC50) of 20-S-camptothecin alkanoic esters (XXXIII) onBRE-MCF-7 cells (a breast cancer cell line) [114] -- Inhibition of SKOV-3 human ovarian cancer cells by camptothecin derivatives(XXXIV) [115] -- Cytotoxic activities (IC50) of camptothecin derivatives (XXXV) against H460human NSCLC cell line [53] -- 4. Clinical Chemistry -- 5. Conclusions -- References -- Application of Lanthanide(Ln = Eu & Tb) Nanoparticles in Biologyand Medicine -- Abstract -- 1. Introduction -- 2. General Properties of Lanthanides(Brief Description) -- 3. Biomedical Nanotechnology:Definition and Application -- 4. Development of LanthanideCompounds (Background) -- 5. Application of Lanthanide Salt andChelates in Biologgy and Medicine -- 5.1. Forensic Applications -- 5.2. Detection of DNA Hybridization and Protein Expression -- 5.3. Heparin Determination -- 5.4. Staining the Nucleolus of Cells -- 6. Lanthanide (Eu & Tb) Nanorods/Nanoparticlesin Nanobiotechnology -- 6.1. Synthesis -- 6.1.1. Chemical Methods -- 6.1.2. Physical Methods -- 6.2. Characterization of LanthanideNanorods/Nanoparticles -- 7. Application of Lnpo4.H2o (Ln = Eu, Tb)Nanorods in Cell Biology -- 7.1. Synthesis of Lnpo4.H2O Nanords -- 7.2. Advantage of Microwave Heating -- 7.3. Characterization of Lnpo4.H2O Nanords -- 7.4. Fluorescence Spectroscopy of HUVEC and 786-O cells treated withLnPO4.H2O Nanords -- 7.5. Internalization of Lnpo4.H2O Nanorods in HUVEC and 786-O Cells -- 7.6. Confocal Microscopy of HUVEC and 786-O Cells Treated withLnpo4·H2O -- 7.8. In Vitro Toxicity (Cell viability test, Cell Proliferation and Apoptosisassay) -- 8. Europium Oxide Nanoparticles in anImmunoassay for Atrazine -- 9. Angiogenesis By Euiii(Oh)3 Nanorods -- 9.1. Synthesis, Characterization and Internalization of Euiii(OH)3 Nanorods -- 9.2. Cell Viablity, Apoptosis Assay and [3H]Thymidine Incorporation Assay.

9.3. Mapkinase Phosphorylation -- 9.5. Chick Chorioallantoic Membrane (CAM) Assay (In Vivo Model) -- 9.6. Plausible Mechanism for Nanorods Induced Angiogenesis -- 10. Therapeutic Application Lanthanide Nanoparticles -- 11. Conclusion -- 12. Abbreviations -- Acknowledgement -- References -- Identification and Analysis of EffectiveComponents in Animal BiofluidsFollowing Administration ofNatural Medicines -- Abstract -- 1. Introduction -- 2. The Natural Medicine Sample Preparation -- 2.1. The Pure Natural Compounds -- 2.2. The Crude Natural Medicine Extracts -- 3. The Proper Experimental Animals and DrugAdministration -- 4. Medicated Biofluids Collection and Disposal -- 4.1. Medicated Biofluids Collection -- 4.1.1. The Blood Collection -- 4.1.2. The Urine Collection -- 4.2. Medicated Biofluids Disposal -- 4.2.1. Removal of Proteins by Precipitators or Denaturants -- 4.2.2. Removal of Proteins by Organic Solvents Extraction -- 4.2.3. Removal of Proteins by Solid Phase Extraction (SPE) -- 4.2.4. The Pure Compounds Isolated from Biofluids -- 5. Analysis of Medicated Biofluids -- 5.1 Analysis of Pure Compounds -- 5.1.1 Qualitative Identification -- 5.1.1.1 Qualitative Identification by the Standard Sample Compounds -- 5.1.1.2 Qualitative Identification by HPLC-Msn -- 5.1.1.3 Qualitative Identification by Spectrums -- 5.1.2 Quantitative Determination -- 5.2 Analysis of Crude Natural Medicine Extracts -- 5.2.1 Qualitative Identification -- 5.2.1.1 Qualitative Identification by the Standard Sample Compound -- 5.2.1.2 Qualitative Identification by HPLC-Msn -- 5.2.2 Quantitative Determination -- 6. Conclusion -- References -- Frontiers of Molecular Technologiesin Noninvasive Prenatal Diagnosis -- Introduction -- Results in Real-Time -- Girl or Boy? -- Being Selective to be Specific -- Size Matters -- All about Mass -- Back to Real-Time in Digital -- References.

Polymeric Nanoparticles as CarrierSystems: How Does the Material andSurface Charge Affect Cellular Uptake? -- Abstract -- 1. Introduction -- 2. Polystyrene Nanoparticles -- 2.1. Synthesis and Characterization -- 2.2. In Vitro Cellular Uptake of Polystyrene-Based Nanoparticles -- 2.3. In Vitro Cellular Uptake of Polystyrene-Based Nanoparticles in thePresence of Inhibitors[32]. -- 2.3.1. Effect of Temperature -- 2.3.2. Effect of Dynamin -- 2.3.3. Effect of F-Actin and Microtubules -- 2.3.4 Effect of the Clathrin Pathway and Contribution of Micropinocytosis -- 2.3.5 Lipid Raft-Associated Proteins are involved in Particle Uptake -- 3. Polyester Nanoparticles[26] -- 3.1. Synthesis and Characterization -- 3.2. In Vitro Cellular Uptake of Polyester Nanoparticles -- 4. Conclusion -- Acknowledgments -- 5. References -- The Role of 1, 25 Dihydroxy-Vitamin D3in Immunity to Infectious Disease. -- Abstract -- 1. Introduction -- 2. 1,25 Dihydroxy Cholecalciferol asRegulator of Cell Mediated Immunity -- 2.1. Regulation of Monocyte Function -- 2.2. Regulation of T-Cell Mediated Immunity -- 2.3. Regulation of B-Cell Mediated Immunity by 1,25 DihydroxyCholecalciferol -- 3. Vitamin D Deficiency and Susceptibility toActive Tuberculosis -- 3.1. Background -- 3.2. In Vitro Studies -- 3.2.1. Changes in Cytokine Production to Mycobacterium Tuberculosis inResponse to Vitamin D. -- 3.2.2. Induction of Antimicrobial Peptides by Vitamin D. -- 3.2.3. Role of Free Radicals in Calcitriol Induced Antimycobacterial ImmuneDefence -- 3.3. Data from Animal Models of Tuberculosis -- 3.4. Epidemiological Data in Humans -- 3.4.1. Vitamin D Levels in Patients with Mycobacterium TuberculosisInfection. -- 3.4.2. Vitamin D Receptor Gene Polymorphisms -- 3.5. Treatment of Tuberculosis with Vitamin D -- 3.6. Directions for Future Research.

4. Influence of 1,25 Dihydroxy Cholecalciferol onHuman Immunodeficiency Virus -1 multiplication -- 4.1. In Vitro Studies -- 4.2. Data from Studies in Humans -- 4.2.1. HIV-1 Infection and Vitamin D Status -- 4.2.2. Vitamin D Receptor Polymorphisms -- 4.3. Directions for Future Research -- 5. Role Of 1,25 Dihydroxy Cholecalciferolin other Infections -- 5.1. Animal Models -- 5.2. Studies in Humans -- 5.2.1. Association of Vitamin D Levels with Frequency and Severity ofRespiratory Tract Infections -- 5.2.2. Vitamin D receptor polymorphisms -- 5.2.2.1. Viral Bronchiolitis -- 5.2.2.2. Extrapulmonary Infections -- 6. Conclusion -- References -- Generation and Analysis of Disease-Specific Mouse Models by ClinicalChemical Screening -- Abstract -- Introduction -- Standardized Clinical ChemicalAnalysis of the Mouse -- Experimental Procedures -- Standardization -- Outcome of the Analysis -- Clinical Chemical Phenotypingto Define Novel Mouse Models -- Generation of Novel Mouse Models by Phenotype-Driven ENU Mouse Mutagenesis Projects -- Clinical Chemical Screening in ENU Projects -- ENU-Induced Mouse Models for SelectedDisorders by Clinical Chemical Screen of theMunich ENU Project -- Plasma Cholesterol as Screening Parameter -- Plasma Glucose as Screening Parameter -- Plasma Urea as Screening Parameter -- Conclusion -- Acknowledgments -- References -- Gene Therapy of Congenital Diseases:Applications, Problems and Prospects -- Abstract -- Introduction -- 1. Development and Advancement of GeneTherapy of Congenital Diseases Sortedby Target Organ/Tissue/Cell/Virus -- 1.1. Respiratory Epithelia -- 1.2. Muscle -- 1.3. Myocardial Tissue -- 1.4. Liver -- 1.5. Kidney -- 1.6. CD34+ Periphery Blood Stem Cells, Lymphocytes and CD34+ Cells -- 1.7. Multiple Target Cells -- 1.8. Viruses -- 2. Development of Vectors in Gene Therapy ofCongenital Diseases -- 2.1. Viral Vectors.

2.2. Nonviral Vectors.