Doadores de sangue envelhescentes e idosos: prevalência e reações adversas / Aging and elderly blood donors: prevalence and adverse reactions / Envejecimiento y donantes de sangre elderly: prevalencia y reacciones adversas

Verificou-se a prevalência e reações adversas às doações de sangue em doadores envelhescentes e idosos. Estudo retrospectivo, com dados do sistema informatizado de Hemocentro em Brasília. Do total de 55636 doadores, 6,3% eram envelhescentes; e 0,8%, idosos. Houve menor prevalência de reações adversas nos idosos, sem diferença significativa. Quanto à intensidade das reações, foram leves nos idosos, leves e moderados nos envelhescentes, também sem diferença significativa.

Prevalence and adverse reactions to blood donations were found in aging and elderly donors. Retrospective study with data from the computerized system of Hemocenter in Brasília. Of the 55636 donors, 6.3% were aging and 0.8% elderly. There was a lower prevalence of adverse reactions in the elderly, with no significant difference. Regarding the intensity of the reactions, they were mild in the elderly, mild and moderate in the aging, also without significant difference.

La prevalencia y las reacciones adversas a las donaciones de sangre se encontraron en donantes envejecimiento y ancianos. Estudio retrospectivo con datos del sistema computarizado de Hemocentro en Brasilia. De los 55636 donantes, 6.3% estaban envejeciendo y 0.8% ancianos. Hubo una menor prevalencia de reacciones adversas en los ancianos, sin diferencias significativas. En cuanto a la intensidad de las reacciones, fueron leves en los ancianos, leves y moderados en el envejecimiento, también sin diferencias significativas.

Hypertonic Saline Solution Reduces Microcirculatory Dysfunction and Inflammation in a Rat Model of Brain Death.

BACKGROUND: Brain death (BD) induces hemodynamic instability with microcirculatory hypoperfusion, leading to increased organ inflammation and dysfunction. This study investigated the effects of 7.5% hypertonic saline solution (HSS) on mesenteric microcirculatory dysfunction and inflammation in a rat model of BD. METHODS: Male Wistar rats were anesthetized and mechanically ventilated. BD was induced by rapidly inflating an intracranial balloon catheter. The rats were randomly divided into: SH, sham-operated rats subjected to trepanation; NS, rats treated with NaCl 0.9%, 4 mL/kg immediately after BD; T1, rats treated with HSS (NaCl 7.5%, 4 mL/kg) immediately or 60 min after BD, T60. All groups were analyzed 180 min after the start of the experiment. RESULTS: Rats in BD groups presented with a similar hypertensive peak, followed by hypotension. Proportion of perfused small vessels was decreased in the NS group (46%) compared with the SH group (74%, P = 0.0039). HSS restored the proportion of perfused vessels (T1 = 71%, P = 0.0018). The anti-endothelial nitric oxide synthase (eNOS) protein expression significantly increased in rats given HSS (T1, and T60, P = 0.0002). Similar results were observed regarding endothelin-1 (P < 0.0001). Increased numbers of rolling (P = 0.0015) and migrated (P = 0.0063) leukocytes were observed in the NS group compared with the SH group. Rats given HSS demonstrated an overall reduction in leukocyte-endothelial interactions. The ICAM-1 levels increased in the NS group compared with the SH group, and decreased in the HSS-treated groups (P = 0.0002). CONCLUSIONS: HSS may improve the density of mesenteric perfused small vessels due to its effects on eNOS and endothelin-1 protein expression, and reduces inflammation by decreasing leukocyte adhesion and migration in a rat model of BD.

The impact of interleukin-13 receptor expressions in cell migration of astrocytomas / O impacto da expressão dos receptores de interleucina-13 na migração celular em astrocitomas

INTRODUCTION: Astrocytomas are common brain tumors. Increased expression levels of Interleukin-13 Receptor α2 (IL-13RA2) have been reported in astrocytomas. The Interleukin-13 signaling pathway may be associated with cell migration when binding to Interleukin-13 Receptor α1. OBJECTIVE: To investigate Interleukin-13 Receptor α1 (IL-13RA1) and IL13RA2 expression levels in human diffusely infiltrative astrocytomas and test the involvement of Interleukin-13 levels in cell migration in two glioblastoma cell lines. METHODS: IL13RA expression levels were accessed by quantitative real time PCR in 128 samples of astrocytomas and 18 samples of non-neoplastic brain tissues from temporal lobe epilepsy surgery. The impact of IL-13 levels (10 and 20 ng/mL) on cell migration was analyzed by the wound assay in U87MG and A172 cells. RESULTS: Glioblastoma presented higher IL13RA1 and IL13RA2 expression levels compared to lower grades astrocytomas and to non-neoplastic cases. U87MG and A172 cells presented higher expression levels of IL-13RA1 vs. IL-13RA2. A significant difference in migration rate was observed in A172 cells treated with 10 ng/mL of IL-13 vs. control: treated cells presented slower migration than non-treated cells. U87MG cells treated with IL-13 20ng/mL presented slower migration than non-treated cells. This indicates that the IL13Rα1 signaling pathway was not activated, indeed inhibited by the decoy IL-13Rα2, slowing cell migration. This impact occurred with a lesser concentration of IL-13 on the A172 than on the U87MG cell line, because A172 cells have a higher IL-13RA2/A1 ratio. CONCLUSION: The present results suggest IL-13 receptors as possible targets to decrease tumor cell migration.

INTRODUÇÃO Astrocitomas são os tumores cerebrais mais frequentes. Nestes tumores foi observada maior expressão do receptor de Interleucina-13 α2 (IL13RA2). A cascata de sinalização da Interleucina-13 pode estar associada com a migração celular, após sua ligação com o receptor de Interleucina-13 α1 (IL13Rα1). OBJETIVO: Investigar os níveis de expressão dos receptores de Interleucina-13 (IL13RA1 e IL13RA2) em astrocitomas difusamente infiltrativos e avaliar o envolvimento da Interleucina-13 na migração celular de duas linhagens de glioblastoma. MÉTODOS: A expressão dos receptores IL13RA foi analisada por PCR em tempo real, em 128 amostras de astrocitomas e 18 amostras de tecido cerebral não neoplásico, provenientes de cirurgia de epilepsia do lobo temporal. E o impacto da quantidade de IL-13 (10ng/ml e 20ng/ml) em ensaio de migração celular. RESULTADOS: As amostras de Glioblastoma apresentaram maior expressão de IL13RA1 and IL13RA2 comparados com astrocitomas de baixo grau e os casos não-neoplásicos. Nas células U87MG e A172 foi observado maior nível de expressão de IL-13RA1 do que IL-13RA2. Uma diferença significativa na taxa de migração foi obtida em células A172 tratadas com 10 ng/mL comparadas com o controle: as células tratadas apresentaram menor migração que as células não tratadas. As células U87MG tratadas com 20ng/mL de IL-13 apresentaram menor migração celular que as células não tratadas. A diferença na migração celular indica que o caminho de sinalização de IL13Rα1 não foi ativado e foi inibido pelo IL-13Rα2, diminuindo a migração celular. Esse impacto ocorreu com uma concentração menor de IL-13 nas células A172 ao contrário da U87MG, porque as células A172 possuem uma razão IL-13RA2/A1 maior. CONCLUSÃO: os resultados sugerem que os receptores de IL-13 podem ser utilizados como possíveis alvos para a diminuição da migração celular tumoral.

Avaliação do risco para desenvolvimento de úlceras por pressão em pacientes críticos / Risk assessment for development of pressure ulcers in critical patients / Evaluación del riesgo para el desarrollo de úlceras por presión en pacientes críticos

Objetivo: avaliar o risco para desenvolvimento ou evolução de úlceras por pressão em pacientes críticos através da escala de Braden. Método: estudo descritivo, com abordagem quantitativa, realizada na Unidade de Terapia Intensiva de um hospital universitário. Foram coletados dados nos prontuários de 51 pacientes no período de fevereiro a abril de 2013. A análise estatística foi avaliada pelo teste de Mann-Whitney. O projeto de pesquisa foi aprovado pelo Comitê de Ética em Pesquisa, CAAE nº 26122213.4.0000.5208. Resultados: foi encontrado nos pacientes um risco moderado ao desenvolvimento de úlceras por pressão; verificou-se a associação de risco elevado na escala de Braden e utilização de noradrenalina, ventilação mecânica invasiva e pontuações baixas na escala de Glasgow. Conclusão: verificou-se o risco moderado ao desenvolvimento de úlceras por pressão e uma associação de risco elevado nos pacientes em uso terapêutico de noradrenalina, ventilação mecânica invasiva, monitorizações invasivas e baixos escores na escala de Glasgow.(AU)

Objective: to evaluate the risk for development or progression of pressure ulcers in critically ill patients through the Braden Scale. Method: a descriptive study with a quantitative approach, performed in the Intensive Care Unit of a university hospital. Data were collected from 51 patients´ medical records in February to April 2013. The statistical analysis was assessed by the Mann-Whitney test. The research project was approved by the Ethics Committee in Research, CAAE number 26122213.4.0000.5208. Results: a moderate risk to the development of pressure ulcers was found in patients; there was a high-risk association in Braden Scale and use of noradrenaline, invasive mechanical ventilation and low scores in Glasgow Scale. Conclusion: there was a moderate risk to the development of pressure ulcers and a high-risk association in patients with therapeutic use of norepinephrine, invasive mechanical ventilation, invasive monitoring and low scores on the Glasgow Scale.(AU)

Objetivo: evaluar el riesgo para desarrollo o evolución de úlceras por presión en pacientes críticos a través de la Escala de Braden. Método: estudio descriptivo, con enfoque cuantitativo, realizado en la Unidad de Terapia Intensiva de un hospital universitario. Fueron recogidos datos en los registros de 51 pacientes en el período de febrero a abril de 2013. El análisis estadístico fue evaluado por el test de Mann-Whitney. El proyecto de investigación fue aprobado por el Comité de Ética en Investigación, CAAE n. 26122213.4.0000.5208. Resultados: fue encontrado en los pacientes un riesgo moderado al desarrollo de úlceras por presión; se verificó asociación riesgo elevado en la Escala de Braden y uso de Noradrenalina, ventilación mecánica invasiva y puntuaciones bajas en la Escala de Glasgow. Conclusión: se verificó riesgo moderado al desarrollo de úlceras por presión y una asociación de riesgo elevado en los pacientes en uso terapéutico de noradrenalina, ventilación mecánica invasiva, monitorizaciones invasivas y baja puntuación en la Escala de Glasgow.(AU)

Lipoprotein (a): structure, pathophysiology and clinical implications.

The chemical structure of lipoprotein (a) is similar to that of LDL, from which it differs due to the presence of apolipoprotein (a) bound to apo B100 via one disulfide bridge. Lipoprotein (a) is synthesized in the liver and its plasma concentration, which can be determined by use of monoclonal antibody-based methods, ranges from < 1 mg to > 1,000 mg/dL. Lipoprotein (a) levels over 20-30 mg/dL are associated with a two-fold risk of developing coronary artery disease. Usually, black subjects have higher lipoprotein (a) levels that, differently from Caucasians and Orientals, are not related to coronary artery disease. However, the risk of black subjects must be considered. Sex and age have little influence on lipoprotein (a) levels. Lipoprotein (a) homology with plasminogen might lead to interference with the fibrinolytic cascade, accounting for an atherogenic mechanism of that lipoprotein. Nevertheless, direct deposition of lipoprotein (a) on arterial wall is also a possible mechanism, lipoprotein (a) being more prone to oxidation than LDL. Most prospective studies have confirmed lipoprotein (a) as a predisposing factor to atherosclerosis. Statin treatment does not lower lipoprotein (a) levels, differently from niacin and ezetimibe, which tend to reduce lipoprotein (a), although confirmation of ezetimibe effects is pending. The reduction in lipoprotein (a) concentrations has not been demonstrated to reduce the risk for coronary artery disease. Whenever higher lipoprotein (a) concentrations are found, and in the absence of more effective and well-tolerated drugs, a more strict and vigorous control of the other coronary artery disease risk factors should be sought.

Lipoprotein (a): Structure, Pathophysiology and Clinical Implications / Lipoproteína (a): Estrutura, Metabolismo, Fisiopatologia e Implicações Clínicas

The chemical structure of lipoprotein (a) is similar to that of LDL, from which it differs due to the presence of apolipoprotein (a) bound to apo B100 via one disulfide bridge. Lipoprotein (a) is synthesized in the liver and its plasma concentration, which can be determined by use of monoclonal antibody-based methods, ranges from < 1 mg to > 1,000 mg/dL. Lipoprotein (a) levels over 20-30 mg/dL are associated with a two-fold risk of developing coronary artery disease. Usually, black subjects have higher lipoprotein (a) levels that, differently from Caucasians and Orientals, are not related to coronary artery disease. However, the risk of black subjects must be considered. Sex and age have little influence on lipoprotein (a) levels. Lipoprotein (a) homology with plasminogen might lead to interference with the fibrinolytic cascade, accounting for an atherogenic mechanism of that lipoprotein. Nevertheless, direct deposition of lipoprotein (a) on arterial wall is also a possible mechanism, lipoprotein (a) being more prone to oxidation than LDL. Most prospective studies have confirmed lipoprotein (a) as a predisposing factor to atherosclerosis. Statin treatment does not lower lipoprotein (a) levels, differently from niacin and ezetimibe, which tend to reduce lipoprotein (a), although confirmation of ezetimibe effects is pending. The reduction in lipoprotein (a) concentrations has not been demonstrated to reduce the risk for coronary artery disease. Whenever higher lipoprotein (a) concentrations are found, and in the absence of more effective and well-tolerated drugs, a more strict and vigorous control of the other coronary artery disease risk factors should be sought.

A partícula de lipoproteína (a) apresenta estrutura semelhante à da LDL, diferenciando-se pela presença da apolipoproteína (a) ligada por uma ponte dissulfeto à apolipoproteína B. Sua síntese ocorre no fígado e sua concentração plasmática varia de < 1 mg a > 1.000 mg/dL, podendo ser dosada de rotina em laboratório clínico por método baseado em anticorpos monoclonais. Acima de 20 a 30 mg/dL o risco de desenvolvimento de doença cardiovascular aumenta em cerca de duas vezes, o que não é válido para os afrodescendentes, que já apresentam normalmente níveis mais altos dessa lipoproteína, do que caucasianos e orientais. Entretanto, o risco para indivíduos negros também deve ser levado em conta. Gênero e idade exercem pouca influência na concentração de lipoproteína (a). A homologia com o plasminogênio, que interfere na cascata fibrinolítica, pode ser um mecanismo da aterogenicidade da lipoproteína (a). Entretanto, a deposição direta na parede da artéria também é um dos mecanismos possíveis, sendo a lipoprotrína (a) mais oxidável do que a LDL. De forma geral estudos prospectivos confirmam a lipoproteína (a) como fator predisponente à aterosclerose. O uso de estatinas não interfere no nível da lipoproteína (a), diferentemente da niacina e da ezetimiba, que promovem sua diminuição, embora essa última dependa de confirmação. Não está demonstrado que a redução de lipoproteína (a) resulte em diminuição de risco de doença arterial coronária. Diante de concentrações mais elevadas de lipoproteína (a) e na falta de medicações mais efetivas e de boa tolerabilidade, deve-se, pelo menos, procurar controlar, de forma mais rigorosa, os outros fatores de risco de doença arterial coronária.