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You searched for +publisher:"Universidade Estadual de Campinas" +contributor:("Passarelli, Marisa"). Showing records 1 – 3 of 3 total matches.

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Universidade Estadual de Campinas

1. Malaguti, Carina, 1981-. Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice.

Degree: 2012, Universidade Estadual de Campinas

Abstract: Reactive oxygen species (ROS) have been extensively associated with a large variety of human metabolic diseases including type 1 diabetes auto-immune (T1D A). The destruction of islet beta cells in T1DA is associated with cellular oxidative stress and with the mitochondrial pathway of cell death. The aim of this study was to determine whether oxidative stress and mitochondrial dysfunction are present in T1DA experimental model NOD (non obese diabetic mouse) and if they are related to the stages of the development of the disease. The experiments were done in liver and soleus muscles biopsies, isolated liver mitochondria, spleen and circulating lymphocytes, bone marrow stem cells and isolated pancreatic islets from NOD and control Balb/c mice. NOD mice were studied at 3 stages: non-diabetic (glycemia < 100 mg/dL, 4-6 weeks of age), pre-diabetic (glycemia range 100-150 mg/dL, 7-10 weeks of age) and diabetic (glycemia > 250 mg/dL, 14-25 weeks of age) and compared to age matched Balb/c mice. Mitochondria respiration rates (oxygen consumption) measured at phosphorylating and resting states in liver and soleus biopsies and in isolated liver mitochondria were similar in NOD at the three stages of the disease as compared to age matched Balb/c mice. However, NOD isolated liver mitochondrial were shown to be more susceptible to calcium induced mitochondrial permeability transition (MPT), as determined by calcium induced cyclosporine A sensitive swelling and by decreased calcium retention capacity. This higher MPT susceptibility was observed in all 3 stages of the development of diabetes. Hydrogen peroxide production (Amplex red) was higher in isolated liver mitochondria from non-diabetic NOD, but unaltered in pre-diabetic and diabetic NOD mice. The oxidation of H2DCF by intact cells was significantly increased in NOD lymphocytes and stem cells in non-, pre- and diabetic stages as compared to controls. In addition, we observed higher rates of H2DCF oxidation in pancreatic islets from non-diabetic NOD mice. These results suggest that the oxidative stress precedes the establishment of diabetes and may be the cause of mitochondrial dysfunction that is involved in beta cell death. We propose that oxidative stress is a key event in the pathogenesis of T1DA and may be a potential target for interventions Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Vercesi, Anibal Eugenio, 1946- (advisor), Oliveira, Helena Coutinho Franco de, 1958- (coadvisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Fisiopatologia Médica (nameofprogram), Passarelli, Marisa (committee member), Silveira, Leonardo dos Reis (committee member), Boschiero, Antonio Carlos (committee member), Pavin, Elizabeth João (committee member).

Subjects/Keywords: Diabetes mellitus tipo 1; Mitocôndria; Consumo de oxigênio; Espécies de oxigênio reativas; Type 1 diabetes; Mitochondria; Oxygen consumption; Reactive oxygen species

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APA (6th Edition):

Malaguti, Carina, 1. (2012). Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Malaguti, Carina, 1981-. “Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice.” 2012. Thesis, Universidade Estadual de Campinas. Accessed October 24, 2020. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Malaguti, Carina, 1981-. “Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice.” 2012. Web. 24 Oct 2020.

Vancouver:

Malaguti, Carina 1. Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2012. [cited 2020 Oct 24]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Malaguti, Carina 1. Estresse oxidativo e susceptibilidade à transição de permeabilidade mitocondrial precedem o apareceimento do diabetes autoimune em camundongos nod: Oxidative stress susceptibility to permeability transition precede the onset of autoimmune diabetes in nod mice. [Thesis]. Universidade Estadual de Campinas; 2012. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/311455

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

2. Virginio, Vitor Wilson de Moura, 1989-. HDL 3B e 3C reduzem a lesão de isquemia e reperfusão e preservam a função sistólica do ventrículo esquerdo após infarto do miocárdio por mecanismo mediado pelo óxido nítrico   : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  .

Degree: 2019, Universidade Estadual de Campinas

Abstract: The pandemic of ischemic heart disease mainly manifested in the form of myocardial infarction (MI) is associated with a high mortality and morbidity rate in the world population. During MI, even with rapid intervention to restore coronary flow, about half the size of the remaining lesion is due to ischemia and reperfusion (I/R) injury. Several therapeutic strategies have been studied to reduce the damage caused by I/R injury, however, no effective therapy has been demonstrated. Based on the cardioprotective effects of high-density lipoprotein (HDL) particles such as anti-inflammatory, antioxidant, antiapoptotic activity, as well as its important regulation on vascular homeostasis, make HDL a potential candidate for attenuation I/R injury. HDL particles can be divided into five subclasses: 2B and 2A (larger and rich in lipids), 3A, 3B and 3C (smaller and rich in proteins). However, it is not clear until now which HDL subclass would yield the most benefits in the I/R injury. The aim of this study was to evaluate which HDL subclass could result in greater protection after MI, in relation to infarct size, left ventricular (LV) systolic function, and coronary flow. Similarly, we sought to evaluate the role of nitric oxide (NO) synthesis, as well as to explore the cell pathways directly involved in the protection triggered by HDL/NO and mitochondrial protection. The present hypothesis was verified with total and subclass HDL samples isolated from 15 healthy volunteers (26 ± 5 years old). HDL was tested in an I/R model in hearts isolated from Wistar rats perfused in the Langendorff system. The hearts were submitted to 35 minutes of ischemia and 90 minutes of regional myocardial reperfusion. The HDL was infused at very first minutes of reperfusion. The same approach was tested in vitro separately on endothelial and cardiomyocytes cells in the hypoxia-reoxygenation scenario. NO biosynthesis was evaluated ex vivo and in vitro by chemiluminescence, and cardioprotection pathways were evidenced by immunoblotting. Mitochondrial respiration was characterized by the rate of oxygen uptake Our results demonstrated that total HDL was able to decrease -24% (p<0.01) infarct size and improve systolic function during reperfusion. We found that the smallest HDL, subclasses 3C and 3B, were more efficient in reducing infarct size (-30%, p<0.001; -25%, p<0.01, respectively) and increasing viability of cardiomyocytes (three times; p=0.023) in the hypoxia-reoxygenation scenario. HDL 3C and 3B also improved LV systolic function during reperfusion and reduced coronary resistance compared to control and other subclasses. In addition, we have shown that NO plays a key role in cardioprotection after ischemia and that the HDL 3C and 3B were the most effective phenotypes in stimulating increased NO bioavailability in coronary effluent (240%, p<0.0001 and 204%, p<0.0001), in the extracellular environment of human coronary endothelial cells (330%, p<0.0001) and cardiomyocytes (390%, p<0.0001). In endothelial cells, this NO increase by… Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Sposito, Andrei Carvalho, 1967- (advisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Clínica Médica (nameofprogram), Velloso, Licio Augusto (committee member), Rached, Fabiana Hanna (committee member), Passarelli, Marisa (committee member), Oliveira, Rodrigo Bueno de (committee member).

Subjects/Keywords: Lipoproteinas HDL; Infarto do miocárdio; Cardioproteção; Isquemia miocárdica; Reperfusão miocárdica; Óxido nítrico; Respiração mitocondrial; Lipoproteins, HDL; Myocardial infarction; Cardioprotection; Myocardial ischemia; Myocardial reperfusion; Nitric oxide; Mitochondrial respiration

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Virginio, Vitor Wilson de Moura, 1. (2019). HDL 3B e 3C reduzem a lesão de isquemia e reperfusão e preservam a função sistólica do ventrículo esquerdo após infarto do miocárdio por mecanismo mediado pelo óxido nítrico   : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  . (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/335311

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Virginio, Vitor Wilson de Moura, 1989-. “HDL 3B e 3C reduzem a lesão de isquemia e reperfusão e preservam a função sistólica do ventrículo esquerdo após infarto do miocárdio por mecanismo mediado pelo óxido nítrico   : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  .” 2019. Thesis, Universidade Estadual de Campinas. Accessed October 24, 2020. http://repositorio.unicamp.br/jspui/handle/REPOSIP/335311.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Virginio, Vitor Wilson de Moura, 1989-. “HDL 3B e 3C reduzem a lesão de isquemia e reperfusão e preservam a função sistólica do ventrículo esquerdo após infarto do miocárdio por mecanismo mediado pelo óxido nítrico   : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  .” 2019. Web. 24 Oct 2020.

Vancouver:

Virginio, Vitor Wilson de Moura 1. HDL 3B e 3C reduzem a lesão de isquemia e reperfusão e preservam a função sistólica do ventrículo esquerdo após infarto do miocárdio por mecanismo mediado pelo óxido nítrico   : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  . [Internet] [Thesis]. Universidade Estadual de Campinas; 2019. [cited 2020 Oct 24]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/335311.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Virginio, Vitor Wilson de Moura 1. HDL 3B e 3C reduzem a lesão de isquemia e reperfusão e preservam a função sistólica do ventrículo esquerdo após infarto do miocárdio por mecanismo mediado pelo óxido nítrico   : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  : HDL 3B and 3C reduce ischemia and reperfusion injury and preserve the systolic function of the left ventricle after myocardial infarction by a mechanism dependent on nitric oxide  . [Thesis]. Universidade Estadual de Campinas; 2019. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/335311

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Universidade Estadual de Campinas

3. Kaplan, Denise Beheregaray. Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose.

Degree: 2004, Universidade Estadual de Campinas

Abstract: There is an inverse association between the concentration of high density lipoprotein (HDL) and the risk of a coronary arterial disease (CAD). One ofthe HDL anti-atherogenic properties is its participation in the reverse cholesterol transport (RCT). The cholesteryl ester transfer protein (CETP) facilitates the cholesteryl esters (CE) and triglycerides (TAG) exchange between HDL and others lipoproteins, increasing the cholesterol content of apoB lipoproteins. Mutations and polymorphisms of the CETP gene were detected in several populations, especially among Asiatic. In spite of a lower activity of the CETP and an increase of the HDL-C leveI in hyperalphalipoproteinemia (HALP), there are some doubts in regard to the prevalence ofthe cardiovascular disease (CVD) in these population groups. The aim of this work was to evaluate the prevalence of HALP and its relationship to the presence ofmutations and polymorphisms ofthe CETP gene, in a Brazilian population, and its relation with the arteriosclerosis.We determined lipid, lipoproteins, metabolic plasmatic parameters and markers of CVD, in a population of 291 to 294 HALP individuaIs (HDL-C 2: 68mg/dl) and 139 controls (HDL-C < 68mg/dl). The prevalence of the mutations Int14A and D442G, and the polymorphisms TaqIB and 1405V, was investigated by molecular methods. The presence of atherosclerosis in those patients with mutations and polymorphisms and in controls, was evaluated by clínical analyzes and measurements of the arterial intima-media thickness (IMT) by ultrasound method was performed. HDL-C was 1.5 higher in the HALP when compared to controls. A very low prevalence equal to 0.7% was found for D442G mutations, lower than in the Asiatic and Japanese population, and 4% for Int14A mutations, higher than the one described in the Caucasians. On HALP, the activities of lipoprotein lipase (LPL) and phospholipid transfer protein (PLTP) were higher and activities of CETP and hepatic lipase (HL) were lower than in controls. The seven mutants presented similar tendencies. The homozygous Int14A, showed indetectable activity of CETP and a reduction of HL, besides very high values of HDL-C. The BIB2 TaqIB genotype presented a :&equencyequal to 45%, and the IV I405V to 49%. Comparing all genotypes, B2B2 TaqIB presented higher IMT, lower autoantibodies against oxidized low density lipoprotein (LDLox) and lower CETP activity. The II I405V showed a highest CETP activity and a lowest HDL-C value. The lipoproteins, lipids and apolipoproteins were equal among all genotypes, as well as activities of LPL, HL and PLTP. The HALP phenotype was characterized by lower CETP and HL activities and higher LPL and PLTP activities when compared with controls but with no association with mutations or polymorphisms studied. It is possible that the low :&equencyof CETP mutations made impossible this statistic association. Perhaps other mutations, like in HL gene, could explain this phenotype. The HALP mutants did not show a difference in c1inical atherosc1erosis and IMT as compared with… Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Faria, Eliana Cotta de, 1950- (advisor), Oliveira, Helena Coutinho Franco de, 1958- (coadvisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Ciências Médicas (nameofprogram), Hirata, Mario (committee member), Passarelli, Marisa (committee member), Assumpção, Ligia Vera Montali da (committee member), Castilho, Lucia Nassi (committee member).

Subjects/Keywords: Proteinas de transporte; Genética; Aterosclerose

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Kaplan, D. B. (2004). Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Kaplan, Denise Beheregaray. “Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose.” 2004. Thesis, Universidade Estadual de Campinas. Accessed October 24, 2020. http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Kaplan, Denise Beheregaray. “Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose.” 2004. Web. 24 Oct 2020.

Vancouver:

Kaplan DB. Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose. [Internet] [Thesis]. Universidade Estadual de Campinas; 2004. [cited 2020 Oct 24]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kaplan DB. Genetica da proteina de transferencia dos esteres de colesterol (CETP) na hiperalfalipoproteinemia e sua relação com a aterosclerose. [Thesis]. Universidade Estadual de Campinas; 2004. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/313572

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

.