1000 resultados para Angiotensina I - efeito de drogas
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2016
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2016
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2016
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2016
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2016
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O consumo e abuso do álcool já são considerados problemas de saúde pública, devido ao número elevado de dependentes e as repercussões que este padrão de consumo gera para o indivíduo, familiares e toda comunidade envolvida. dependência do álcool acomete cerca de 10 a 12% da população mundial. Mais alarmante que estes números, são os dados relacionados à morte pelo álcool, que é responsável por cerca de 60% dos acidentes de trânsito e aparece em 70% dos laudos por causas violentas. O projeto em questão propõe conhecer o perfil de consumo desta substância dentro de uma determinada comunidade, através da aplicação de um questionário padronizado, para então elaborar propostas de intervenções, com objetivo de diminuir o consumo do álcool, e consequentemente, os danos causados por ele. Os resultados confirmaram um padrão de consumo elevado, em que 5% dos entrevistados foram enquadrados na categoria dependente e 26% encontram-se na zona de uso nocivo, uso de risco e provável dependência.Todos os pacientes receberam as devidas orientações e, alguns deles, foram encaminhados a centros especializados em tratamento de álcool e drogas. Ficou evidente o quanto o consumo é elevado, desde que questionado, e o quanto este problema requer medidas emergenciais e eficazes.
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A realização do diagnóstico situacional do território da equipe Primavera I, permitiu identificar e definir os principais problemas enfrentados pela população nele encontrados. O problema de maior relevância selecionado para este trabalho foi o uso abusivo de benzodiazepínicos(BZD), estando parte significativa de usuários destes medicamentos sem assistência e cuidado, como a falta de consulta médica e acompanhamento da doença. Na tentativa de enfrentar o problema, foi elaborado um plano de ação. A insônia e a depressão são transtornos mentais comuns na prática clínica, principalmente na atenção primária. Os BDZ são drogas com atividade ansiolítica e seu uso indiscriminado é considerado um problema de saúde pública, representando elevada morbidade e dependência, sendo que na maioria dos casos está relacionado à utilização inadequada e com grande procura pelos pacientes em serviços de saúde. Identificados os nós críticos do problema, observou-se o uso irracional, falta de conhecimentos sobre os medicamentos, a prescrição inadequada, falta de capacitação suficiente dos profissionais do serviço de saúde para abordar o tema. Assim foi proposta esta intervenção visando o enfrentamento do problema, e que através da ajuda da participação da equipe multidisciplinar. Este projeto foi subsidiado por trabalhos científicos disponíveis em base de dados como: Biblioteca Virtual em Saúde, Biblioteca Virtual da Universidade Federal de Minas Gerais, SCIELO, dentre outros.
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Este estudo se propôs a identificar os fármacos prescritos na Odontologia geradores de riscos de interações medicamentosas com drogas que estão sendo empregadas para o controle de doenças sistêmicas comuns na senilidade. Foi realizada uma pesquisa bibliográfica na Literatura Latino-Americana e do Caribe em Ciências da Saúde - LILACs, Scientific Electronic Library Online - SCIELO e nos manuais do Ministério da Saúde e da Secretaria Estadual de Saúde associado à identificação das principais drogas usadas em tratamento de doenças comumente associadas à senilidade como a diabetes mellitus, a hipertensão arterial, a depressão, a artrite reumatóide e outras patologias. Várias drogas para controle de doenças sistêmicas predispõem o paciente a risco de interações medicamentosas. Como resultado da pesquisa constatou-se que o uso de antiinflamatórios não esteroidais (AINES) está relacionado à atenuação dos efeitos anti-hipertensivos inibidores de enzima conversora de angiotensina, betabloqueadores e diuréticos; potencialização dos efeitos adversos do Lítio, do efeito antiagregante plaquetário dos anticoagulantes e dos efeitos tóxicos do antimetabólico Metotrexato. O analgésico dipirona quando interage com cloropromazina, antipsicótico, causa aumento das reações adversas. Os antimicrobianos prescritos pelo odontólogo aumentam as concentrações sanguíneas por déficit na excreção renal do Lítio, digoxina, ansiolíticos (midazolan e triazolan), teofilina, anticoagulantes orais e Metotrexato. Novas drogas com novos espectros de ação são comercializadas a cada ano, criando sempre a necessidade de familiarização do profissional com a literatura clínica atual permitindo prevenir respostas iatrogênicas associadas com o uso de várias drogas ao mesmo tempo. Conclui-se que os profissionais odontólogos devem ter o conhecimento dos padrões do uso dos medicamentos e das prescrições para os idosos, visto que este conhecimento constitui uma medida importantíssima para se evitar interações medicamentosas na terapêutica farmacológica proposta.
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Snakebite is a neglected disease and serious health problem in Brazil, with most bites being caused by snakes of the genus Bothrops. Although serum therapy is the primary treatment for systemic envenomation, it is generally ineffective in neutralizing the local effects of these venoms. In this work, we examined the ability of 7,8,3'-trihydroxy-4'-methoxyisoflavone (TM), an isoflavone from Dipteryx alata, to neutralize the neurotoxicity (in mouse phrenic nerve-diaphragm preparations) and myotoxicity (assessed by light microscopy) of Bothrops jararacussu snake venom in vitro. The toxicity of TM was assessed using the Salmonella microsome assay (Ames test). Incubation with TM alone (200 μg/mL) did not alter the muscle twitch tension whereas incubation with venom (40 μg/mL) caused irreversible paralysis. Preincubation of TM (200 μg/mL) with venom attenuated the venom-induced neuromuscular blockade by 84% ± 5% (mean ± SEM; n = 4). The neuromuscular blockade caused by bothropstoxin-I (BthTX-I), the major myotoxic PLA2 of this venom, was also attenuated by TM. Histological analysis of diaphragm muscle incubated with TM showed that most fibers were preserved (only 9.2% ± 1.7% were damaged; n = 4) compared to venom alone (50.3% ± 5.4% of fibers damaged; n = 3), and preincubation of TM with venom significantly attenuated the venom-induced damage (only 17% ± 3.4% of fibers damaged; n = 3; p < 0.05 compared to venom alone). TM showed no mutagenicity in the Ames test using Salmonella strains TA98 and TA97a with (+S9) and without (-S9) metabolic activation. These findings indicate that TM is a potentially useful compound for antagonizing the neuromuscular effects (neurotoxicity and myotoxicity) of B. jararacussu venom.
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Assessment of central blood pressure (BP) has grown substantially over recent years because evidence has shown that central BP is more relevant to cardiovascular outcomes than peripheral BP. Thus, different classes of antihypertensive drugs have different effects on central BP despite similar reductions in brachial BP. The aim of this study was to investigate the effect of nebivolol, a β-blocker with vasodilator properties, on the biochemical and hemodynamic parameters of hypertensive patients. Experimental single cohort study conducted in the outpatient clinic of a university hospital. Twenty-six patients were recruited. All of them underwent biochemical and hemodynamic evaluation (BP, heart rate (HR), central BP and augmentation index) before and after 3 months of using nebivolol. 88.5% of the patients were male; their mean age was 49.7 ± 9.3 years and most of them were overweight (29.6 ± 3.1 kg/m2) with large abdominal waist (102.1 ± 7.2 cm). There were significant decreases in peripheral systolic BP (P = 0.0020), diastolic BP (P = 0.0049), HR (P < 0.0001) and central BP (129.9 ± 12.3 versus 122.3 ± 10.3 mmHg; P = 0.0083) after treatment, in comparison with the baseline values. There was no statistical difference in the augmentation index or in the biochemical parameters, from before to after the treatment. Nebivolol use seems to be associated with significant reduction of central BP in stage I hypertensive patients, in addition to reductions in brachial systolic and diastolic BP.
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Phase I trials use a small number of patients to define a maximum tolerated dose (MTD) and the safety of new agents. We compared data from phase I and registration trials to determine whether early trials predicted later safety and final dose. We searched the U.S. Food and Drug Administration (FDA) website for drugs approved in nonpediatric cancers (January 1990-October 2012). The recommended phase II dose (R2PD) and toxicities from phase I were compared with doses and safety in later trials. In 62 of 85 (73%) matched trials, the dose from the later trial was within 20% of the RP2D. In a multivariable analysis, phase I trials of targeted agents were less predictive of the final approved dose (OR, 0.2 for adopting ± 20% of the RP2D for targeted vs. other classes; P = 0.025). Of the 530 clinically relevant toxicities in later trials, 70% (n = 374) were described in phase I. A significant relationship (P = 0.0032) between increasing the number of patients in phase I (up to 60) and the ability to describe future clinically relevant toxicities was observed. Among 28,505 patients in later trials, the death rate that was related to drug was 1.41%. In conclusion, dosing based on phase I trials was associated with a low toxicity-related death rate in later trials. The ability to predict relevant toxicities correlates with the number of patients on the initial phase I trial. The final dose approved was within 20% of the RP2D in 73% of assessed trials.
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Pyrimidine-5'-nucleotidase type I (P5'NI) deficiency is an autosomal recessive condition that causes nonspherocytic hemolytic anemia, characterized by marked basophilic stippling and pyrimidine nucleotide accumulation in erythrocytes. We herein present two African descendant patients, father and daughter, with P5'N deficiency, both born from first cousins. Investigation of the promoter polymorphism of the uridine diphospho glucuronosyl transferase 1A (UGT1A) gene revealed that the father was homozygous for the allele (TA7) and the daughter heterozygous (TA6/TA7). P5'NI gene (NT5C3) gene sequencing revealed a further change in homozygosity at amino acid position 56 (p.R56G), located in a highly conserved region. Both patients developed gallstones; however the father, who had undergone surgery for the removal of stones, had extremely severe intrahepatic cholestasis and, liver biopsy revealed fibrosis and siderosis grade III, leading us to believe that the homozygosity of the UGT1A polymorphism was responsible for the more severe clinical features in the father. Moreover, our results show how the clinical expression of hemolytic anemia is influenced by epistatic factors and we describe a new mutation in the P5'N gene associated with enzyme deficiency, iron overload, and severe gallstone formation. To our knowledge, this is the first description of P5'N deficiency in South Americans.
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The aim of this work was to characterize the effects of partial inhibition of respiratory complex I by rotenone on H2O2 production by isolated rat brain mitochondria in different respiratory states. Flow cytometric analysis of membrane potential in isolated mitochondria indicated that rotenone leads to uniform respiratory inhibition when added to a suspension of mitochondria. When mitochondria were incubated in the presence of a low concentration of rotenone (10 nm) and NADH-linked substrates, oxygen consumption was reduced from 45.9 ± 1.0 to 26.4 ± 2.6 nmol O2 mg(-1) min(-1) and from 7.8 ± 0.3 to 6.3 ± 0.3 nmol O2 mg(-1) min(-1) in respiratory states 3 (ADP-stimulated respiration) and 4 (resting respiration), respectively. Under these conditions, mitochondrial H2O2 production was stimulated from 12.2 ± 1.1 to 21.0 ± 1.2 pmol H2O2 mg(-1) min(-1) and 56.5 ± 4.7 to 95.0 ± 11.1 pmol H2O2 mg(-1) min(-1) in respiratory states 3 and 4, respectively. Similar results were observed when comparing mitochondrial preparations enriched with synaptic or nonsynaptic mitochondria or when 1-methyl-4-phenylpyridinium ion (MPP(+)) was used as a respiratory complex I inhibitor. Rotenone-stimulated H2O2 production in respiratory states 3 and 4 was associated with a high reduction state of endogenous nicotinamide nucleotides. In succinate-supported mitochondrial respiration, where most of the mitochondrial H2O2 production relies on electron backflow from complex II to complex I, low rotenone concentrations inhibited H2O2 production. Rotenone had no effect on mitochondrial elimination of micromolar concentrations of H2O2. The present results support the conclusion that partial complex I inhibition may result in mitochondrial energy crisis and oxidative stress, the former being predominant under oxidative phosphorylation and the latter under resting respiration conditions.
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The 2005 National Institutes of Health (NIH) Consensus Conference proposed new criteria for diagnosing and scoring the severity of chronic graft-versus-host disease (GVHD). The 2014 NIH consensus maintains the framework of the prior consensus with further refinement based on new evidence. Revisions have been made to address areas of controversy or confusion, such as the overlap chronic GVHD subcategory and the distinction between active disease and past tissue damage. Diagnostic criteria for involvement of mouth, eyes, genitalia, and lungs have been revised. Categories of chronic GVHD should be defined in ways that indicate prognosis, guide treatment, and define eligibility for clinical trials. Revisions have been made to focus attention on the causes of organ-specific abnormalities. Attribution of organ-specific abnormalities to chronic GVHD has been addressed. This paradigm shift provides greater specificity and more accurately measures the global burden of disease attributed to GVHD, and it will facilitate biomarker association studies.