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3.
Rev. clín. esp. (Ed. impr.) ; 216(2): 92-98, mar. 2016. tab
Artigo em Espanhol | IBECS | ID: ibc-149836

RESUMO

La proporción de pacientes diabéticos hospitalizados por ictus ha ido aumentando en los últimos años, alcanzando en la actualidad casi un tercio de todos los ictus. Además, prácticamente la mitad de los enfermos con ictus agudo pueden presentar hiperglucemia en las primeras horas del evento. A pesar de que la hiperglucemia en la fase aguda del ictus se asocia a un peor pronóstico, su tratamiento es en la actualidad motivo de controversia. No existen evidencias de que la administración de insulina por vía intravenosa en estos pacientes proporcione beneficios en la evolución del ictus. Nuevos estudios en desarrollo, como el estudio Stroke Hyperglycemia Insulin Network Effort (SHINE), posiblemente contribuyan a aclarar el papel del control intensivo de la glucemia durante la fase aguda del ictus. Finalmente, los pacientes que han presentado un ictus deberían ser sometidos a un cribado de diabetes (AU)


The proportion of diabetic patients who are hospitalised for stroke has been increasing in recent years, currently reaching almost a third of all cases of stroke. In addition, about half of patients with acute stroke present hyperglycaemia in the first hours of the stroke. Although hyperglycaemia in the acute phase of stroke is associated with a poor prognosis, its treatment is currently a topic of debate. There is no evidence that the adminstration of intravenous insulin to these patients offers benefits in terms of the evolution of the stroke. New studies in development, such as the SHINE study (Stroke Hyperglycemia Insulin Network Effort), may contribute to clarifying the role of intensive control of glycaemia during the acute phase of the stroke (AU)


Assuntos
Humanos , Masculino , Feminino , Hiperglicemia/sangue , Hiperglicemia/genética , Acidente Vascular Cerebral/congênito , Acidente Vascular Cerebral/patologia , Diabetes Mellitus/sangue , Diabetes Mellitus/patologia , Proteólise , Lipólise/genética , Ensaios Clínicos Controlados Aleatórios como Assunto/métodos , Hiperglicemia/complicações , Hiperglicemia/metabolismo , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/metabolismo , Diabetes Mellitus/classificação , Diabetes Mellitus/metabolismo , Lipólise/fisiologia , Ensaios Clínicos Controlados Aleatórios como Assunto
4.
Arch. bronconeumol. (Ed. impr.) ; 50(2): 73-77, feb. 2014. ilus
Artigo em Espanhol | IBECS | ID: ibc-129148

RESUMO

Es probable que la disfunción de los músculos respiratorios, principalmente del diafragma, constituya una pieza clave dentro de los mecanismos fisiopatológicos que conducen a la dificultad del destete de la ventilación mecánica. La limitada movilidad del paciente crítico -y en especial del diafragma- cuando se requiere soporte prolongado con ventilación mecánica favorece el inicio temprano de la disfunción muscular respiratoria, la cual puede originarse también o hacerse mayor en presencia de factores frecuentes en el paciente críticamente enfermo, tales como sepsis, desnutrición, edad avanzada, duración y modo ventilatorio, uso de algunos medicamentos como glucocorticoides y bloqueadores neuromusculares. En esta revisión haremos énfasis en este origen multicausal, en el que la alteración del metabolismo de las proteínas es un mecanismo común involucrado, de acuerdo con los hallazgos reportados en diferentes modelos. El entendimiento de esta multicausalidad integrada por un mismo mecanismo fisiopatológico podría favorecer el manejo y la monitorización de los pacientes sometidos a ventilación mecánica


Respiratory muscle dysfunction, particularly of the diaphragm, may play a key role in the pathophysiological mechanisms that lead to difficulty in weaning patients from mechanical ventilation. The limited mobility of critically ill patients, and of the diaphragm in particular when prolonged mechanical ventilation support is required, promotes the early onset of respiratory muscle dysfunction, but this can also be caused or exacerbated by other factors that are common in these patients, such as sepsis, malnutrition, advanced age, duration and type of ventilation, and use of certain medications, such as steroids and neuromuscular blocking agents. In this review we will study in depth this multicausal origin, in which a common mechanism is altered protein metabolism, according to the findings reported in various models. The understanding of this multicausality produced by the same pathophysiological mechanism could facilitate the management and monitoring of patients undergoing mechanical ventilation


Assuntos
Humanos , Insuficiência Respiratória/fisiopatologia , Músculos Respiratórios/fisiopatologia , Respiração Artificial , Estado Terminal , Desmame do Respirador , Sepse/complicações , Proteólise , Desnutrição Proteico-Calórica/complicações , Monitorização Fisiológica
5.
J. physiol. biochem ; 68(4): 683-690, dic. 2012.
Artigo em Inglês | IBECS | ID: ibc-122316

RESUMO

Caveolin-3 (cav-3), which is involved in the regulation of signal transduction and vesicular trafficking, could interact with activin receptor IIB to inhibit myostatin (MSTN) activity and may therefore play a role in muscle development and hypertrophy. MSTN is a member of the transforming growth factor-â family, identified as a negative regulator of skeletal muscle mass. The expression of MSTN is fiber-type specific and the greatest amount of MSTN is present in fiber, which is composed of myosin heavy chain (MHC) type IIb. MSTN acts through the activin receptor IIB to activate smad2/3 which leads to an increase in gene transcription involved in muscle atrophy. Muscle hypertrophy is a consequence of two mechanisms: (1) the inhibition of proteolysis such as the calcium-dependent proteolytic system calpains and calpastatin and (2) an increase in protein synthesis through theAkt/mTOR/p70s6K pathway. In order to determine which of the two processes predominates in inhibition of MSTN activity in a cav-3 context, we transfected a C2C12 cell line with plasmids containing mstn or cav-3 wild genes. The results reported in this study demonstrate that inhibition of MSTN activity by overexpression of cav-3 induces an activation of protein synthesis rather than an inhibition of proteolysis through the calcium proteolytic system. The inhibition of phosphorylation of smad-3 due to overexpression of cav-3 causes an increase in the phosphorylation of the ribosomal protein S6, promoting the synthesis of MHC type II, probably through activation of Akt/mTOR/p70s6K. These data highlight the role of protein synthesis as the predominant mechanism in muscle hypertrophy observed when the expression of MSTN is altered and confirm the value of studying the physiological role of MSTN in the growing processes of skeletal muscle (AU)


Assuntos
Animais , Ratos , Caveolina 3/farmacocinética , Proteólise , Mioblastos , Miostatina/farmacocinética , Distrofias Musculares/fisiopatologia , Músculo Esquelético/crescimento & desenvolvimento
6.
J. physiol. biochem ; 66(4): 311-319, dic. 2010.
Artigo em Inglês | IBECS | ID: ibc-122818

RESUMO

No disponible


Beta-Hydroxy-beta-methylbutyrate (HMB) is a leucine metabolite that may have a positive effect in protein catabolic conditions. Therefore, we hypothesized that HMB treatment could attenuate the sepsis-induced protein catabolic state. The aims of our study were to elucidate the effect of HMB in healthy and septic animals and to evaluate the differences in the action of HMB in different muscle types. Intact and septic (5 mg endotoxin/kg i.p.) rats were administered with HMB (0.5 g/kg/day) or saline. After 24 h, extensor digitorum longus (EDL) and soleus (SOL) muscles were isolated and used for determination of total and myofibrillar proteolysis, protein synthesis, leucine oxidation, activity ofcathepsins B and L, chymotrypsin-like activity, and expression of á-subunits of proteasome. Our results indicate that the catabolic state induced by the endotoxin treatment was caused both by increase in protein breakdown (due to activation of proteasome system) and by attenuation of protein synthesis. The EDL (muscle composed of white, fast-twitch fibers) was more susceptible to these changes than the SOL (muscle composed of red, slow-twitch fibers). The HMB treatment had no effect in healthy animals but counteracted the changes in septic animals. The action of HMB was mediated by attenuation of proteasome activity and protein breakdown, not by stimulation of protein synthesis. More pronounced effect of the HMB treatment on myofibrillar proteolysis was observed in the SOL (AU)


Assuntos
Animais , Ratos , Ácido 3-Hidroxibutírico/farmacocinética , Sepse/tratamento farmacológico , Complexo de Endopeptidases do Proteassoma , Substâncias Protetoras/farmacocinética , Modelos Animais de Doenças , Proteólise , Estudos de Casos e Controles
7.
Rev. esp. cardiol. (Ed. impr.) ; 62(6): 677-688, jun. 2009. ilus, mapas
Artigo em Espanhol | IBECS | ID: ibc-123760

RESUMO

Las enfermedades cardiovasculares son la primera causa de muerte en el mundo occidental. El proceso patológico que subyace a ellas es un engrosamiento de la pared arterial debido a la formación de placas ateroscleróticas, las cuales se complican frecuentemente con un trombo y pueden dar lugar a síndrome coronario agudo o accidente cerebrovascular. Uno de los mayores retos de la medicina cardiovascular es encontrar la manera de predecir el riesgo de un sujeto de sufrir un evento trombótico agudo. En las últimas décadas, hay un gran interés en la búsqueda de biomarcadores diagnósticos y pronósticos que puedan ser identificados en sangre. Entre ellos, la proteína C reactiva es la más conocida. Otros, como el ligando de CD40 soluble, pueden predecir eventos cardiovasculares. En cambio, hasta el momento no hay un biomarcador aceptado en la práctica clínica. Actualmente, existen diversas técnicas de alto rendimiento como la proteómica, que permite la detección de múltiples biomarcadores potenciales. Estas aproximaciones pueden identificar en un futuro próximo nuevos biomarcadores que, junto con las técnicas de imagen, pueden ayudar a mejorar la predicción de eventos vasculares agudos (AU)


Cardiovascular disease is the principal cause of death in developed countries. The underlying pathological process is arterial wall thickening due to the formation of atherosclerotic plaque, which is frequently complicated by thrombus, thereby giving rise to the possibility of acute coronary syndrome or stroke. One of the major challenges in cardiovascular medicine is to find a way of predicting the risk that an individual will suffer an acute thrombotic event. During the last few decades, there has been considerable interest in finding diagnostic and prognostic biomarkers that can be detected in blood. Of these, C-reactive (..) (AU)


Assuntos
Humanos , Aterosclerose/fisiopatologia , Doenças Cardiovasculares/fisiopatologia , Biomarcadores/análise , Proteômica/métodos , Fatores de Risco , Risco Ajustado/métodos , Mediadores da Inflamação/análise , Inflamação/fisiopatologia , Estresse Oxidativo , Proteólise
8.
Rev. esp. cardiol. (Ed. impr.) ; 53(supl.1): 14-18, 2000.
Artigo em Espanhol | IBECS | ID: ibc-134984

RESUMO

La recuperación tardía de la función después de períodos breves de isquemia se conoce como aturdimiento. El aturdimiento miocárdico y la insuficiencia cardíaca parecerían, a primera vista, tener muy poco en común aparte de la disfunción contráctil obvia que se produce en los dos casos. En este artículo se describen estudios que aportan luz sobre los mecanismos subyacentes de estas dos formas de disfunción contráctil, y que revelan similitudes fundamentales inesperadas (AU)


The delayed recovery of function after brief episodes of ischemia is known as stunning. Myocardial stunning and heart failure would, at first glance, appear to have little in common other than the obvious contractile dysfunction in both settings. Here I describe studies which shed new light on the underlying mechanisms of these two forms of contractile dysfunction, revealing unexpected fundamental similarities (AU)


Assuntos
Humanos , Insuficiência Cardíaca/fisiopatologia , Miocárdio Atordoado/fisiopatologia , Isquemia Miocárdica/fisiopatologia , Eletrofisiologia Cardíaca/métodos , Acoplamento Excitação-Contração/fisiologia , Proteólise , Troponina/análise , Contração Miocárdica/fisiologia
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