Relação entre autoavaliação vocal e dados da avaliação clínica em indivíduos disfônicos

OBJETIVO: associar os índices de autoavaliação vocal aos dados da avaliação clínica de indivíduos disfônicos. MÉTODOS: estudo observacional, analítico, retrospectivo. Foram analisados os prontuários de pacientes disfônicos atendidos em uma Clínica-Escola de Fonoaudiologia no período de 2007 a 2011. Foram levantados os dados referentes à autoavaliação vocal (índices de qualidade de vida em voz, desvantagem vocal e atribuição de nota referente ao impacto vocal), à anamnese (sexo, idade, profissão, tipo de queixa, tempo de queixa, tratamentos anteriores para a disfonia), à avaliação perceptivo-auditiva (qualidade vocal, grau de alteração, pitch, loudness, ressonância, articulação e coordenação pneumofonoarticulatória) e aos dados objetivos (tempos máximos fonatórios e relação s/z). Os dados foram tabulados e analisados estatisticamente. RESULTADOS: não houve diferença na comparação dos escores do protocolo de qualidade de vida em voz e índice de desvantagem vocal com as variáveis referentes a sexo, qualidade vocal, grau de alteração, pitch, ressonância, articulação, velocidade de fala e tipo de disfonia. Indivíduos que utilizam a voz profissionalmente e que já fizeram tratamentos anteriores para a disfonia apresentaram piores índices na autoavaliação vocal. Quanto à avaliação clínica, a incoordenação penumofonoarticulatória foi o único parâmetro que interferiu negativamente na autoavaliação. Não houve correlações entre os índices de autoavaliação vocal e as demais variáveis contínuas (idade, tempo de queixa, tempos máximos fonatórios e relação s/z). CONCLUSÃO: a autoavaliação vocal é uma impressão bastante subjetiva, e independe da maior parte dos dados coletados na avaliação clínica. Ser profissional da voz, já ter buscado outros tratamentos para a disfonia e apresentar incoordenação penumofonoarticulatória parece influenciar negativamente na autoavaliação do indivíduo acerca do impacto do distúrbio vocal em sua vida diária

Exploratory Data Analysis of Cell and Mitochondrial High-Fat, High-Sugar Toxicity on Human HepG2 Cells

Non-alcoholic steatohepatitis (NASH), one of the deleterious stages of non-alcoholic fatty liver disease, remains a significant cause of liver-related morbidity and mortality worldwide. In the current work, we used an exploratory data analysis to investigate time-dependent cellular and mitochondrial effects of different supra-physiological fatty acids (FA) overload strategies, in the presence or absence of fructose (F), on human hepatoma-derived HepG2 cells. We measured intracellular neutral lipid content and reactive oxygen species (ROS) levels, mitochondrial respiration and morphology, and caspases activity and cell death. FA-treatments induced a time-dependent increase in neutral lipid content, which was paralleled by an increase in ROS. Fructose, by itself, did not increase intracellular lipid content nor aggravated the effects of palmitic acid (PA) or free fatty acids mixture (FFA), although it led to an up-expression of hepatic fructokinase. Instead, F decreased mitochondrial phospholipid content, as well as OXPHOS subunits levels. Increased lipid accumulation and ROS in FA-treatments preceded mitochondrial dysfunction, comprising altered mitochondrial membrane potential (ΔΨm) and morphology, and decreased oxygen consumption rates, especially with PA. Consequently, supra-physiological PA alone or combined with F prompted the activation of caspase pathways leading to a time-dependent decrease in cell viability. Exploratory data analysis methods support this conclusion by clearly identifying the effects of FA treatments. In fact, unsupervised learning algorithms created homogeneous and cohesive clusters, with a clear separation between PA and FFA treated samples to identify a minimal subset of critical mitochondrial markers in order to attain a feasible model to predict cell death in NAFLD or for high throughput screening of possible therapeutic agents, with particular focus in measuring mitochondrial function

Exploratory Data Analysis of Cell and Mitochondrial High-Fat, High-Sugar Toxicity on Human HepG2 Cells

Non-alcoholic steatohepatitis (NASH), one of the deleterious stages of non-alcoholic fatty liver disease, remains a significant cause of liver-related morbidity and mortality worldwide. In the current work, we used an exploratory data analysis to investigate time-dependent cellular and mitochondrial effects of different supra-physiological fatty acids (FA) overload strategies, in the presence or absence of fructose (F), on human hepatoma-derived HepG2 cells. We measured intracellular neutral lipid content and reactive oxygen species (ROS) levels, mitochondrial respiration and morphology, and caspases activity and cell death. FA-treatments induced a time-dependent increase in neutral lipid content, which was paralleled by an increase in ROS. Fructose, by itself, did not increase intracellular lipid content nor aggravated the effects of palmitic acid (PA) or free fatty acids mixture (FFA), although it led to an up-expression of hepatic fructokinase. Instead, F decreased mitochondrial phospholipid content, as well as OXPHOS subunits levels. Increased lipid accumulation and ROS in FA-treatments preceded mitochondrial dysfunction, comprising altered mitochondrial membrane potential (ΔΨm) and morphology, and decreased oxygen consumption rates, especially with PA. Consequently, supra-physiological PA alone or combined with F prompted the activation of caspase pathways leading to a time-dependent decrease in cell viability. Exploratory data analysis methods support this conclusion by clearly identifying the effects of FA treatments. In fact, unsupervised learning algorithms created homogeneous and cohesive clusters, with a clear separation between PA and FFA treated samples to identify a minimal subset of critical mitochondrial markers in order to attain a feasible model to predict cell death in NAFLD or for high throughput screening of possible therapeutic agents, with particular focus in measuring mitochondrial function

Fighting Plasmodium chloroquine resistance with acetylenic chloroquine analogues

Malaria is among the tropical diseases that cause the most deaths in Africa. Around 500,000 malaria deaths are reported yearly among African children under the age of five. Chloroquine (CQ) is a low-cost antimalarial used worldwide for the treatment of Plasmodium vivax malaria. Due to resistance mechanisms, CQ is no longer effective against most malaria cases caused by P. falciparum. The World Health Organization recommends artemisinin combination therapies for P. falciparum malaria, but resistance is emerging in Southeast Asia and some parts of Africa. Therefore, new medicines for treating malaria are urgently needed. Previously, our group identified the 4-aminoquinoline DAQ, a CQ analog containing an acetylenic bond in its side chain, which overcomes CQ resistance in K1 P. falciparum strains. In this work, the antiplasmodial profile, drug-like properties, and pharmacokinetics of DAQ were further investigated. DAQ showed no cross-resistance against standard CQ-resistant strains (e.g., Dd2, IPC 4912, RF12) nor against P. falciparum and P. vivax isolates from patients in the Brazilian Amazon. Using drug pressure assays, DAQ showed a low propensity to generate resistance. DAQ showed considerable solubility but low metabolic stability. The main metabolite was identified as a mono N-deethylated derivative (DAQM), which also showed significant inhibitory activity against CQ-resistant P. falciparum strains. Our findings indicated that the presence of a triple bond in CQ-analogues may represent a low-cost opportunity to overcome known mechanisms of resistance in the malaria parasite

Núcleos de Ensino da Unesp: artigos 2014: volume 4: os processos de interação na escola e educação inclusiva

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq