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1.
Neuropsychiatr ; 29(2): 84-7, 2015.
Artigo em Alemão | MEDLINE | ID: mdl-25917541

RESUMO

BACKGROUND: The integration of psychiatric departments in general hospitals lead to an increasing demand of psychiatric consultation, which often overstrains personnel resources of short staffed psychiatric services. To provide consulting service, as it is demanded by guidelines, a multidisciplinary consulting team could be a possible solution. METHODS: A retrospective descriptive analysis of all consultations made by the psychosocial consultation and liaison service at the general hospital Wels-Grieskirchen in the years 2012 and 2013. RESULTS: There was an increase in referrals overall of 22 % from 2012 to 2013. The largest increase was observed in the group of psychiatrists, who carried out 33.1 % of all consultations. Most consultations, 39.5 %, were done by the group of clinical psychologists, partly substituting medical attendance. Taking together both occupational groups, the expected number of consultations of at least 3 % of all admissions could be achieved. CONCLUSION: A multidisciplinary consulting team consisting of psychiatrists, psychologists, psychosomatic physicians and social workers staffed with 5.11-6.79 full-time personnel is able to provide psychosocial consultation service at a quantitative level required by international guidelines.


Assuntos
Comportamento Cooperativo , Hospitais Gerais/economia , Comunicação Interdisciplinar , Transtornos Mentais/economia , Equipe de Assistência ao Paciente/economia , Psiquiatria/economia , Encaminhamento e Consulta/economia , Centros de Atenção Terciária/economia , Áustria , Análise Custo-Benefício/economia , Recursos em Saúde/economia , Humanos , Transtornos Mentais/diagnóstico , Transtornos Mentais/terapia , Psicologia Clínica/economia
2.
J Am Coll Cardiol ; 63(15): 1569-79, 2014 Apr 22.
Artigo em Inglês | MEDLINE | ID: mdl-24315909

RESUMO

OBJECTIVES: This study sought to explore whether subclinical alterations of sarcoplasmic reticulum (SR) Ca(2+) release through cardiac ryanodine receptors (RyR2) aggravate cardiac remodeling in mice carrying a human RyR2(R4496C+/-) gain-of-function mutation in response to pressure overload. BACKGROUND: RyR2 dysfunction causes increased diastolic SR Ca(2+) release associated with arrhythmias and contractile dysfunction in inherited and acquired cardiac diseases, such as catecholaminergic polymorphic ventricular tachycardia and heart failure (HF). METHODS: Functional and structural properties of wild-type and catecholaminergic polymorphic ventricular tachycardia-associated RyR2(R4496C+/-) hearts were characterized under conditions of pressure overload induced by transverse aortic constriction (TAC). RESULTS: Wild-type and RyR2(R4496C+/-) hearts had comparable structural and functional properties at baseline. After TAC, RyR2(R4496C+/-) hearts responded with eccentric hypertrophy, substantial fibrosis, ventricular dilation, and reduced fractional shortening, ultimately resulting in overt HF. RyR2(R4496C+/-)-TAC cardiomyocytes showed increased incidence of spontaneous SR Ca(2+) release events, reduced Ca(2+) transient peak amplitude, and SR Ca(2+) content as well as reduced SR Ca(2+)-ATPase 2a and increased Na(+)/Ca(2+)-exchanger protein expression. HF phenotype in RyR2(R4496C+/-)-TAC mice was associated with increased mortality due to pump failure but not tachyarrhythmic events. RyR2-stabilizer K201 markedly reduced Ca(2+) spark frequency in RyR2(R4496C+/-)-TAC cardiomyocytes. Mini-osmotic pump infusion of K201 prevented deleterious remodeling and improved survival in RyR2(R4496C+/-)-TAC mice. CONCLUSIONS: The combination of subclinical congenital alteration of SR Ca(2+) release and pressure overload promoted eccentric remodeling and HF death in RyR2(R4496C+/-) mice, and pharmacological RyR2 stabilization prevented this deleterious interaction. These findings suggest potential clinical relevance for patients with acquired or inherited gain-of-function of RyR2-mediated SR Ca(2+) release.


Assuntos
Sinalização do Cálcio/genética , DNA/genética , Insuficiência Cardíaca/genética , Miócitos Cardíacos/metabolismo , Canal de Liberação de Cálcio do Receptor de Rianodina/genética , Retículo Sarcoplasmático/metabolismo , Remodelação Ventricular/genética , Animais , Análise Mutacional de DNA , Modelos Animais de Doenças , Progressão da Doença , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/fisiopatologia , Camundongos , Camundongos Knockout , Mutação , Miócitos Cardíacos/patologia , Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo , Pressão Ventricular
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