An examination of health-related quality of life for individuals with HIV-infection.

With the improvements in morbidity and mortality as a result of new antiretroviral treatments, the examination of health related quality of life (HRQOL) has become an important consideration of client care. This study was a 15-month prospective examination of the underlying factor structure, test-retest reliability, and clinical utility of the widely used Medical Outcomes Study-HIV HRQOL instrument (MOS-HIV). Factor analysis of the MOS-HIV Physical Function, Role Function, Pain, Social Function, Overall Health, Fatigue, Cognitive Function, Health Distress, Quality of Life, and Mental Health dimensions resulted in mental health (MHS) and physical health (PHS) summary factors. Analysis of the individual MOS-HIV items generally revealed Physical Function, Overall Health, Cognitive Function, Health Distress, Mental Health, and Functional Status factors. MOS-HIV dimensions and factors typically had moderate to good test-retest reliability. Poor reliability coefficients generally occurred for dimensions that were only composed of 1 or 2 items. Multiple regression analyses were conducted to determine the impact of demographic, medical, depression, and neuropsychological variables on various HRQOL domains. Depression and medical symptom scores were the strongest predictors of HRQOL, with depression more highly related to mental health domains and medical symptoms more highly related to physical health domains. Neuropsychological variables, specifically psychomotor efficiency, were more likely to be related to physical function. Demographic and HIV status variables had less of an impact on HRQOL than depression and medical symptoms. The results of this analysis support the use of MHS and PHS scores and MOS-HIV item factors to convey HRQOL information. In addition, the results indicate that treatment of depressive and medical symptoms could result in a significant improvement in HRQOL.Dept. of Psychology. Paper copy at Leddy Library: Theses & Major Papers - Basement, West Bldg. / Call Number: Thesis2003 .Y36. Source: Dissertation Abstracts International, Volume: 64-08, Section: B, page: 4071. Adviser: Byron P. Rourke. Thesis (Ph.D.)--University of Windsor (Canada), 2003

Spectroscopic estimation of the photon number for superconducting Kerr parametric oscillators

Quantum annealing (QA) is a way to solve combinational optimization problems. Kerr nonlinear parametric oscillators (KPOs) are promising devices for implementing QA. When we solve the combinational optimization problems using KPOs, it is necessary to precisely control the photon number of the KPOs. Here, we propose a feasible method to estimate the photon number of the KPO. We consider coupling an ancillary qubit to the KPO and show that spectroscopic measurements on the ancillary qubit provide information on the photon number of the KPO

Influência do exercício físico na osteoporose em mulheres pós-menopausa : revisão de literatura

Orientadora: Ana Beatriz PacíficoMonografia (especialização) - Universidade Federal do Paraná, Setor de Ciências Biológicas, Curso de Especialização em Fisiologia do Exercício.Resumo : Introdução: O exercício físico auxilia na manutenção das atividades ósseas normais, com isso vem se mostrando uma alternativa interessante no tratamento da osteoporose. Objetivo: revisar na literatura os trabalhos que estudam a influência do exercício físico na osteoporose em mulheres pós-menopausa, e possíveis formas de melhorar a qualidade de vida das mulheres que possuem essa doença. Metodologia: A pesquisa foi realizada através de revisão da literatura, artigos publicados de 2000 a 2018, estudos experimentais e apenas da língua portuguesa e língua inglesa utilizando as seguintes bases de dados eletrônicas: Bireme e PubMed. A partir das buscas realizadas nas bases de dados (SciELO e Bireme) foram encontrados um total de 10 estudos experimentais. Desenvolvimento: Pode se analisar a partir dos dados apresentados na tabela que os exercícios relacionados a osteoporose no período de pós-climatério mais citados pela literatura científica são exercícios realizados em ambientes aquáticos, exercícios de caminhada e corrida e exercícios de força. As mulheres que realizaram alguns desses exercícios apresentaram evolução no que se refere a manutenção e/ou aumento da massa óssea, enquanto outros exercícios não se mostraram efetivos. Conclusão: Pode-se concluir que o exercício físico se mostra uma alternativa positiva na manutenção de mulheres pós-menopausa portadoras de osteoporose

PKC-Mediated ZYG1 Phosphorylation Induces Fusion of Myoblasts as well as of Dictyostelium Cells

We have previously demonstrated that a novel protein ZYG1 induces sexual cell fusion (zygote formation) of Dictyostelium cells. In the process of cell fusion, involvements of signal transduction pathways via Ca2+ and PKC (protein kinase C) have been suggested because zygote formation is greatly enhanced by PKC activators. In fact, there are several deduced sites phosphorylated by PKC in ZYG1 protein. Thereupon, we designed the present work to examine whether or not ZYG1 is actually phosphorylated by PKC and localized at the regions of cell-cell contacts where cell fusion occurs. These were ascertained, suggesting that ZYG1 might be the target protein for PKC. A humanized version of zyg1 cDNA (mzyg1) was introduced into myoblasts to know if ZYG1 is also effective in cell fusion of myoblasts. Quite interestingly, enforced expression of ZYG1 in myoblasts was found to induce markedly their cell fusion, thus strongly suggesting the existence of a common signaling pathway for cell fusion beyond the difference of species

Mechanism of Cancer Cell Death Induced by Hydrogen Discharged from Palladium Base Hydrogen Storage Alloy

The mechanism of cancer cell death induced by hydrogen discharged from Pd-5at.% Ni hydrogen storage alloy has been investigated. Cancer cell (HeLa: cervical cancer cell) death was observed in the limited region within ~ 3 mm from the sample. The measurement of surviving fraction of cells revealed that almost all the cancer cells in the well of 96-well multi plate, 6.2 mm in diameter were extinct (p < 0.01), while no detectable influence was observed in the normal cells. From the fluorescent imaging experiment, it was indicated that the cell death induced by discharged hydrogen was due to the "Apoptosis" and hydrogen peroxide was detected in both intracellular and extracellular regions. Furthermore, the generation of hydrogen radical and hydroxyl radical was observed in the ESR measurement. From the results obtained, the mechanism of cancer cell death is proposed.2013 International Conference on Materials Science and Chemical Engineering, MSCE 2013; ; 20 February 2013 ～ 21 February 201

Association of MUTYH Gln324His and APEX1 Asp148Glu with colorectal cancer and smoking in a Japanese population

This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

MYC-type transcription factors, MYC67 and MYC70, interact with ICE1 and negatively regulate cold tolerance in Arabidopsis

The expression of hundreds of genes is induced by low temperatures via a cold signaling pathway. ICE1, a MYC-type transcription factor, plays an important role in the induction of CBF3/DREB1A to control cold-responsive genes and cold tolerance. To elucidate other molecular factors, a yeast 2-hybrid screening was performed. Two MYC-type transcription factors, MYC67 and MYC70, were identified as ICE1-interacting proteins. The myc mutants were more tolerant to freezing temperatures than wild type. CBF3/DREB1A and other cold-responsive genes were up-regulated in the myc mutants. Overexpression of the MYC genes increased the cold sensitivity and down-regulated the expression of cold-responsive genes. The MYC proteins interacted with the cis-elements in the CBF3/DREB1A promoter, probably to interfere interaction between ICE1 and the cis-elements. Taken together, these results demonstrate that MYC67 and MYC70, ICE1 interactors, negatively regulate cold-responsive genes and cold tolerance

Mechanisms With Clinical Implications for Atrial Fibrillation–Associated Remodeling: Cathepsin K Expression, Regulation, and Therapeutic Target and Biomarker

Background: The cysteine protease cathepsin K (CatK) has been implicated in the pathogenesis of cardiovascular disease. We sought to determine the link between atrial fibrillation (AF) and plasma CatK levels and to investigate the expression of and therapeutic target for CatK in vivo and in vitro. Methods and Results: Plasma CatK and extracellular matrix protein peptides (intact procollagen type I of N‐terminal propeptide; carboxyl‐terminal telopeptide of type I collagen [ICTP]) were measured in 209 consecutive patients with AF (paroxysmal AF, 146; persistent AF, 63) and 112 control subjects. In addition, the regulation of CatK expression was investigated in vivo and vitro. Patients with AF had higher plasma CatK and ICTP levels than did control subjects. Patients with persistent AF had higher levels of plasma CatK and ICTP than did patients with paroxysmal AF. CatK was correlated with ICTP concentration and left atrial diameter in all subjects. In rabbits, superoxide production, CatK activity, fibrosis, and the levels of atrial tissue angiotensin II, angiotensin type 1 receptor, gp91phox, phospho‐p38 mitogen‐activated protein kinase, and CatK were greater in those with tachypacing‐induced AF than in controls, and these changes were reversed with angiotensin type 1 receptor antagonist. Olmesartan and mitogen‐activated protein kinase inhibitor decreased the CatK expression induced by angiotensin II in rat neonatal myocytes. Conclusions: These data indicated that increased plasma CatK levels are linked with the presence of AF. Angiotensin type 1 receptor antagonist appears to be effective in alleviating atrial fibrosis in a rabbit AF model, partly reducing angiotensin type 1 receptor‐p38mitogen‐activated protein kinase‐dependent and ‐independent CatK activation, thus preventing AF

Protein kinase C-δ signaling regulates glucagon secretion from pancreatic islets

Accumulating evidence supports the “glucagonocentric hypothesis”, in which antecedent α-cell failure and inhibition of glucagon secretion are responsible for diabetes progression. Protein kinase C (PKC) is involved in glucagon secretion from α-cells, although which PKC isozyme is involved and the mechanism underlying this PKC-regulated glucagon secretion remains unknown. Here, the involvement of PKCδ in the onset and progression of diabetes was elucidated. Immunofluorescence studies revealed that PKCδ was expressed and activated in α-cells of STZ-induced diabetic model mice. Phorbol 12-myristate 13-acetate (PMA) stimulation significantly augmented glucagon secretion from isolated islets. Pre-treatment with quercetin and rottlerin, PKCδ signaling inhibitors, significantly suppressed the PMA-induced elevation of glucagon secretion. While Go6976, a Ca2+ - dependent PKC selective inhibitor did not suppress glucagon secretion. Quercetin suppressed PMA-induced phosphorylation of Tyr311 of PKCδ in isolated islets. However, quercetin itself had no effect on either glucagon secretion or glucagon mRNA expression. Our data suggest that PKCδ signaling inhibitors suppressed glucagon secretion. Elucidation of detailed signaling pathways causing PKCδ activation in the onset and progression of diabetes followed by the augmentation of glucagon secretion could lead to the identification of novel therapeutic target molecules and the development of novel therapeutic drugs for diabetes