Made available in DSpace on 2014-06-11T19:33:23Z (GMT). No. of bitstreams: 0 Previous issue date: 2003-06-02Bitstream added on 2014-06-13T19:23:16Z : No. of bitstreams: 1 araujo_am_dr_arafo.pdf: 327250 bytes, checksum: f1b666ee0bb9d92663feec590f32d1e9 (MD5) / O propósito desse estudo foi avaliar os efeitos transversais nos maxilares e o crescimento mandibular ântero-posterior após terapia com aparelho ortopédico funcional. A amostra foi composta por 25 pacientes (15 do gênero masculino e 10 do gênero feminino) com má oclusão de Classe II e idade variando entre 6.9 e 11.2 anos. Os pacientes foram aleatoriamente divididos em dois grupos, grupo controle (n=11) e grupo experimental (n=14) e acompanhados longitudinalmente por 12 meses. O tratamento foi exclusivamente executado com o aparelho bionator de Balters por um período de 12 meses. O método de sobreposição, com auxílio de implantes metálicos, foi realizado na avaliação das alterações esqueléticas transversais dos maxilares, crescimento condilar e remodelação óssea da mandíbula. Os resultados mostraram que os pacientes sem tratamento exibiram um aumento significante, em largura, entre os implantes maxilares posteriores, mas a diferença entre os implantes anteriores e mandibulares não foi estatisticamente significante. A distância entre os implantes posteriores, no sentido transversal, aumentaram significantemente para os dois grupos, com o grupo bionator mostrando um aumento significativo maior do que o grupo controle. O grupo bionator também mostrou uma maior expansão entre os implantes localizado na mandíbula, porém essa diferença não foi estatisticamente significante. Com relação ao crescimento condilar, os resultados mostraram um redirecionamento do crescimento (mais posterior), e semelhante quantidade de crescimento para os dois grupos. O tratamento com o aparelho bionator produziu um crescimento e remodelação óssea maior do que o esperado nas regiões condilar e goniana da mandíbula. Sobreposição na base do crânio mostrou um deslocamento anterior da mandíbula e uma pequena ou quase ausente rotação anterior... . / The purpose of this study was to describe transverse skeletal base adaptations and mandibular growth associated with bionator therapy. The sample included 25 patients (15 males and 10 females) between 6.9 and 11.2 years of age with Class II division 1 malocclusion. The patients were randomly allocated to either a control (n=11) or treatment (n=14) group. Treatment consisted of a bionator only, and the patients were following longitudinally for approximately 12 months. Using metallic implants for superimposition, transverse skeletal base adaptations, condylar growth and mandibular remodeling changes were evaluated. The results showed that untreated Class II controls exhibit significant increases between posterior maxillary implants, but no significant changes between the anterior maxillary or mandibular implants. While posterior maxillary implants increased significantly in both groups, the treated group showed significantly greater width increases than the control group. The treated group also showed greater increases between mandibular implants, but the differences were not statistically significant. Condylar growth in perspective, the results showed significant changes in the direction (more posterior) but not in the amount of overall amount of condylar growth. The bionator appliance produced greater than expected posterior drift of landmarks in the condylar and gonial regions. Cranial base superimposition showed greater than expected anterior mandibular displacement, but little or no true mandibular forward rotation with bionator therapy. In conclusion, the bionator appliance alone produces transverse skeletal adaptations, condylar growth redirection and remodeling changes associated with mandibular rotation and displacement.

Optimal induction of coronary thrombolysis depends in part upon the nature of the specific plasminogen activator used. The two general classes of plasminogen activators available clinically differ in a fundamental respect delineated by the term, clot selectivity. Clot selective agents are less prone to induce plasminemia and consequent occult activation of the coagulation cascade than are non-selective agents. However, under clinical conditions, all plasminogen activators result in some activation of the cascade with consequent generation of thrombin. Accordingly, optimal therapy requires the use of conjunctive anticoagulation to preclude the deleterious effects of rebound generation of thrombin, which has been well documented biochemically. The potential value of antiplatelet agents that can attenuate the positive feedback loop between activation of platelets and markedly amplified generation of thrombin in the setting of coronary thrombolysis is under active exploration. With appropriate monitoring of the efficacy of such agents in vivo it should be possible to enhance even further the benefits that can be conferred by pharmacologically induced coronary thrombolysis.

No description available.

Thesis (Ph. D.)--University of Virginia, 2008. / Title from title page. Includes bibliographical references. Also available online through Digital Dissertations.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 3 uppsatser.

Caseinolytic protease (ClpP) is a cylindrical protease forming the core of protein degradation machinery in eubacteria. ClpP is tightly regulated and is non-functional without a member of the Clp-ATPases. A new class of antibiotics, termed ADEPs, bind to ClpP and allow for activation without the Clp-ATPases; leading to cell death. A more efficient synthetic route to the ADEPs utilizing solid-phase peptide synthesis was investigated. A linear peptide was synthesized, however attempts to close the depsipeptidic macrocycle via macrolactonization failed. Further attempts of assembling a branched depsipeptide for ring closure via a macrolactamization resulted in products that were not stable to cleavage conditions. A group of molecules termed Activators of Self-Compartmentalizing Proteases (ACP) were identified through a screen for activity towards ClpP. Compound ACP1 was synthesized along with twelve analogs and their activity towards ClpP evaluated. The project resulted in a compound with a higher activity than its natural product counterpart.

Glycosaminoglycans (GAGs) are complex biopolymers that play important roles in inflammation, coagulation, angiogenesis, cell adhesion and viral invasion by interacting with several different proteins.1,2 Structurally, GAGs are built up of several different sulfated disaccharide units.3 Specific GAG sequences that uniquely recognize their cognate proteins exist. Such specificity typically arises from the binding of unique sulfation patterns on the linear GAG chain to highly electropositive protein domains. Thus, these highly charged, sulfated biopolymers potentially represent a new class of therapeutics. Yet, the major stumbling block to the development to these agents is their extremely complicated and tedious chemical synthesis. We hypothesized that replacing the saccharide skeleton with an equivalent non-saccharide and readily synthesized organic skeleton would usher in an era of new, GAG-based therapeutics. This challenge has been addressed on two fronts, computational design and chemical synthesis, by focusing on the heparin pentasaccharide-antithrombin system that represents an exhaustively studied model GAG-protein system. With respect to chemical synthesis, a microwave-based synthetic procedure that can rapidly introduce multiple sulfate groups on a poly-hydroxyl substrate within minutes was developed.4 Using this method, the synthesis of a previously designed activator (IAS5), which otherwise proved to be problematic, was successfully completed. Biochemical screening of IAS5 and its analogs revealed that these molecules could activate antithrombin up to 30-fold in comparison to the 300-fold activation by the heparin pentasaccharide. In an effort to develop more potent antithrombin activators, a new method to predict high affinity GAG sequences for a given GAG-binding protein based on combinatorial virtual-library screening was developed.5 This combinatorial virtual-library screening method was applied to a library of 24,576 non-saccharide, sulfated molecules that were created using the structure of IAS5 as a template. Thirty seven‘hits’ that had common structural features were identified from this study. Interestingly, all these ‘hits’ bind to antithrombin similarly and orient the 4 negative charges identical to the corresponding groups in the heparin pentasaccharide. The synthesis of selected targets is currently in progress and several synthetic steps have already been optimized.

by Ray, Kit Ng. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (leaves 112-121). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgments --- p.iv / Abbreviations --- p.x / List of Figures --- p.xii / List of Tables --- p.xiv / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Hepatitis B Virus (HBV) --- p.1 / Chapter 1.2 --- Hepatitis B Virus X Protein (HBx) --- p.5 / Chapter 1.2.1 --- The Genomic Structure of HBx --- p.5 / Chapter 1.2.2 --- The HBx Protein Structure --- p.6 / Chapter 1.2.3 --- Subcellular Localization of HBx --- p.7 / Chapter 1.2.4 --- Possible Functions of HBx --- p.8 / Chapter 1.3 --- Etiology of Hepatocellular Carcinoma (HCC) --- p.12 / Chapter 1.4 --- Relationship between HCC and HBx --- p.13 / Chapter 1.5 --- Aims of Study --- p.14 / Chapter 1.6 --- The Basis of Tet-On System --- p.15 / Chapter 1.7 --- The Basis of DNA Microarray --- p.18 / Chapter 1.8 --- The Basis of Two-Dimensional Electrophoresis --- p.20 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- Construction of a Tet-On HBx Expressing Cell Model --- p.22 / Chapter 2.1.1 --- Cloning of HBx Gene into pTRE2 Vector --- p.22 / Chapter 2.1.1.1 --- PCR of HBx Gene --- p.22 / Chapter 2.1.1.2 --- Purification of the PCR Product --- p.23 / Chapter 2.1.1.3 --- Restriction Enzyme Digestion --- p.23 / Chapter 2.1.1.4 --- Ligation of HBx into pTRE Vector --- p.24 / Chapter 2.1.1.5 --- Transformation of the Ligation Product into Competent Cells --- p.24 / Chapter 2.1.2 --- Preparation of the Plasmid DNA --- p.24 / Chapter 2.1.2.1 --- DNA Sequencing of the Cloned Plasmid DNA --- p.25 / Chapter 2.1.3 --- Cell Culture of AML12 Cell Line --- p.26 / Chapter 2.1.4 --- Transfection of pTet-On Vector into AML12 Cells --- p.26 / Chapter 2.1.5 --- Selection of the Transfected AML12 Cells by G418 --- p.27 / Chapter 2.1.6 --- Single Clone Isolation --- p.27 / Chapter 2.1.6.1 --- Luciferase Assay for Selection of Highly Inducible Clones --- p.28 / Chapter 2.1.7 --- Second Transfection of pTRE-HBx Plasmid --- p.28 / Chapter 2.1.8 --- Selection of the Transfected Cells by Hygromycin --- p.29 / Chapter 2.1.9 --- Second Single Clone Isolation --- p.29 / Chapter 2.1.10 --- Total RNA Isolation --- p.29 / Chapter 2.1.11 --- DNase I Digestion --- p.30 / Chapter 2.1.12 --- First-Strand cDNA Synthesis --- p.31 / Chapter 2.1.13 --- RT-PCR of HBx Gene --- p.31 / Chapter 2.1.14 --- Northern Blotting --- p.32 / Chapter 2.1.15 --- Preparation of the Probe --- p.33 / Chapter 2.1.16 --- Northern Blot Hybridization --- p.33 / Chapter 2.1.17 --- 3H-Thymidine Incorporation Assay --- p.34 / Chapter 2.1.18 --- Analysis of Cell Cycle by Flow Cytometry --- p.35 / Chapter 2.2 --- Microarray Analysis of Differential Gene Expression upon HBx Induction --- p.35 / Chapter 2.2.1 --- Sample Preparation for Microarray Analysis --- p.35 / Chapter 2.2.2 --- Probe Labelling --- p.36 / Chapter 2.2.3 --- Microarray Hybridization --- p.37 / Chapter 2.2.4 --- RT-PCR of the Candidate Genes --- p.38 / Chapter 2.2.5 --- Northern Blot Analysis of the Candidate Genes --- p.39 / Chapter 2.3 --- Two-Dimensional (2D) Gel Electrophoretic Analysis --- p.40 / Chapter 2.3.1 --- Protein Sample Preparation for 2D Gel Electrophoresis --- p.40 / Chapter 2.3.2 --- First-Dimension Isoelectric Focusing (IEF) --- p.40 / Chapter 2.3.3 --- Second-Dimension SDS-PAGE --- p.41 / Chapter 2.3.4 --- Silver Stain of 2D Gel --- p.42 / Chapter 2.3.5 --- Mass Spectroscopic Analysis --- p.43 / Chapter 2.4 --- Subcellular Localization of HBx --- p.44 / Chapter 2.4.1 --- Cloning of HBx into Green Fluorescent Protein (GFP) Expression Vector --- p.44 / Chapter 2.4.2 --- Transfection of GFP-HBx --- p.44 / Chapter 2.4.3 --- Propidium Iodide (PI) Staining --- p.45 / Chapter 2.4.4 --- Mitochondria Staining --- p.45 / Chapter 2.4.5 --- Subcellular Localization Study using Epi-Fluorescent Microscopy --- p.45 / Chapter 2.5 --- Analysis of Mitochondrial Transmembrane Potential --- p.46 / Chapter Chapter 3 --- Results / Chapter 3.1 --- Construction of Tet-On AML12 Cell Line of HBx Gene --- p.47 / Chapter 3.2 --- Characterization of the HBx-Expressing Cell Model --- p.53 / Chapter 3.2.1 --- 3H-Thymidine Proliferation Assay --- p.53 / Chapter 3.2.2 --- Cell Cycle Analysis --- p.55 / Chapter 3.3 --- Microarray Analysis of Differential Gene Expression Pattern upon HBx Induction --- p.57 / Chapter 3.4 --- Northern Blot Analysis and RT-PCR of the Candidate Genes --- p.65 / Chapter 3.5 --- Differential Protein Expression Pattern under HBx Induction --- p.70 / Chapter 3.6 --- Subcellular Localization of HBx --- p.77 / Chapter 3.7 --- Analysis of Mitochondrial Transmembrane Potential --- p.83 / Chapter Chapter 4 --- Discussion / Chapter 4.1 --- Conditional HBx-Expressing Cell Model --- p.84 / Chapter 4.2 --- The Effects of HBx in Clone X18 --- p.86 / Chapter 4.2.1 --- Proliferative Effect of HBx --- p.86 / Chapter 4.2.2 --- Deregulation of G2/M Checkpoint by HBx --- p.86 / Chapter 4.3 --- Early Differential Gene Expression due to HBx Induction --- p.88 / Chapter 4.4 --- The Relationship of the Potential Candidate Genes and Cancer Development --- p.90 / Chapter 4.5 --- The Protein Expression Pattern due to HBx Induction --- p.93 / Chapter 4.6 --- The Subcellular Localization of HBx --- p.96 / Chapter 4.7 --- The Possible Involvement of HBx in Mitochondrial Transmembrane Potential --- p.98 / Chapter 4.8 --- Conclusions --- p.101 / Chapter 4.9 --- Future Prospects --- p.104 / Appendix --- p.107 / References --- p.112

Cheng Sze-Lok Alfred. / "March 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 175-211). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

"June 2003." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (p. 162-187). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.