RESUMO
BACKGROUND: Treatment effectiveness holds considerable importance in the association between service quality and satisfaction in medical service studies. While complementary and alternative medicine (CAM) use grows more prominent, comprehensive evaluations of the quality of medical service at CAM-oriented hospitals are scarce. This study assesses the quality of medical services provided at a CAM-oriented hospital of Korean medicine using the service encounter system approach and analyzes the influence of treatment effectiveness on patient loyalty. METHODS: A survey study using one-on-one interviews was conducted using a cross-sectional design in outpatients visiting one of fifteen Korean medicine facilities located throughout Korea. A total of 880 surveys were completed from June to July, 2014, and 728 surveys were included in the final analysis after excluding incomplete or incorrect questionnaires. The reliability and validity of the surveys was confirmed using Cronbach's alpha coefficient and confirmatory factor analysis, and a structural equation modeling analysis was performed to verify causality and association between factors (quality of medical service, treatment effectiveness, patient satisfaction, and intent to revisit). RESULTS: The measured factors of physician performance and quality of service procedures had a positive effect on treatment effectiveness. The impression of the facilities and environment directly impacted satisfaction rates for interpersonal-based medical service encounters, while treatment effectiveness positively affected satisfaction regarding quality of medical service. However, treatment effectiveness had a more significant effect on satisfaction compared to facilities and environment, and it indirectly affected satisfaction and directly influenced intent to revisit. Treatment effectiveness and satisfaction both positively influenced intent to revisit. CONCLUSIONS: The importance of treatment effectiveness should be recognized when examining quality of medical services, and we hope that these findings may contribute to future studies.
Assuntos
Terapias Complementares/psicologia , Pacientes Ambulatoriais/psicologia , Satisfação do Paciente , Qualidade da Assistência à Saúde , Adulto , Estudos Transversais , Feminino , Hospitais , Humanos , Masculino , República da Coreia , Resultado do Tratamento , Recursos HumanosRESUMO
Chronic administration to rats of mood-stabilizers that are effective against mania in bipolar disorder, is reported to downregulate markers of the brain arachidonic acid cascade. We hypothesized that chronic administration of lamotrigine, which is used to treat depression and rapid cycling in bipolar disorder, might do so as well. Male CDF rats were administered a therapeutically relevant dose of lamotrigine (10 mg/kg) or vehicle intragastrically once daily for 42 days. Protein levels of isoforms of phospholipase A(2) (PLA(2)) and of cyclooxygenase (COX), and the mRNA level of COX-2, were quantified in the frontal cortex using immunoblotting and RT-PCR, respectively. Compared to vehicle-treated rats, chronic lamotrigine significantly decreased frontal cortex protein and mRNA levels of COX-2 without altering protein levels of the PLA(2) isoforms. Consistent with the hypothesis, lamotrigine and other mood-stabilizers have a common downregulatory action on COX-2 expression in rat brain, which may account in part for their efficacy in bipolar disorder.
Assuntos
Ciclo-Oxigenase 2/metabolismo , Regulação para Baixo/efeitos dos fármacos , Lobo Frontal/efeitos dos fármacos , RNA Mensageiro/genética , Triazinas/farmacologia , Animais , Western Blotting , Ciclo-Oxigenase 2/genética , Lobo Frontal/enzimologia , Lamotrigina , Masculino , Ratos , Ratos Endogâmicos F344 , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Triazinas/administração & dosagemRESUMO
OBJECTIVES: Valproic acid (VPA) is used to treat bipolar disorder, but its mechanism of action is not clear. VPA shares many cellular and molecular targets with lithium, including reducing arachidonic acid turnover in rat brain phospholipids and cyclooxygenase-2 (COX-2) protein level and activity in rat brain. METHODS: We examined the effect of chronic VPA administration (200 mg/kg body weight for 30 days) to produce therapeutically relevant plasma concentrations, on transcription factors (NF-kappaB, AP-1, AP-2, C/EBP, CREB, and ETS) that are known to regulate the COX-2 gene. RESULTS: Chronic VPA significantly increased AP-1 DNA binding activity and decreased NF-kappaB DNA binding activity, p50 subunit protein and mRNA expression of COX-2 in frontal cortex compared with untreated control rats. It did not alter AP-2, C/EBP, ETS or CREB DNA binding activity. CONCLUSIONS: VPA downregulates NF-kappaB DNA binding activity, likely by decreasing the p50 protein levels. This effect may explain its downregulation of COX-2 mRNA. The decrease in NF-kappaB activity by chronic VPA may affect other NF-kappaB-regulated genes and may be related to VPA's action in bipolar disorder. Chronic VPA may decrease the reported increased brain NF-kappaB components in bipolar patients.
Assuntos
Ciclo-Oxigenase 2/genética , Ciclo-Oxigenase 2/metabolismo , Proteínas de Ligação a DNA/efeitos dos fármacos , Proteínas de Ligação a DNA/genética , Regulação para Baixo/efeitos dos fármacos , Lobo Frontal/efeitos dos fármacos , Lobo Frontal/metabolismo , NF-kappa B/efeitos dos fármacos , NF-kappa B/genética , RNA Mensageiro/efeitos dos fármacos , RNA Mensageiro/genética , Ácido Valproico/farmacologia , Animais , Sequência de Bases , Sítios de Ligação , Western Blotting , Modelos Animais de Doenças , Esquema de Medicação , Masculino , Dados de Sequência Molecular , Ratos , Ratos Endogâmicos F344 , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Ácido Valproico/administração & dosagemRESUMO
Excessive N-methyl-D-aspartate (NMDA) signaling is thought to contribute to bipolar disorder symptoms. Lithium and carbamazepine, effective against bipolar mania, are reported in rats to reduce brain transcription of an arachidonic acid selective calcium-dependent cytosolic phospholipase A(2) (cPLA(2)), as well as expression of one of its transcription factors, activator protein (AP)-2. In this study, we determined if chronic administration of NMDA (25 mg/kg i.p.) to rats would increase brain cPLA(2) and AP-2 expression, as these antimanic drugs are known to down-regulate excessive NMDA signaling. Administration of a daily subconvulsive dose of NMDA to rats for 21 days decreased frontal cortex NMDA receptor (NR)-1 and NR-3A subunits and increased cPLA(2) activity, phosphorylation, protein, and mRNA levels. The activity and protein levels of secretory phospholipase A(2) or calcium-independent phospholipase A(2) were not changed significantly. Chronic NMDA also increased the DNA-binding activity of AP-2 and the protein levels of its alpha and beta subunits. These changes were absent following acute (3 h earlier) NMDA administration. The changes, opposite to those found following chronic lithium or carbamazepine, are consistent with up-regulated arachidonic acid release due to excessive NR signaling and may be a contributing factor to bipolar mania.
Assuntos
Ácido Araquidônico/metabolismo , Transtorno Bipolar/metabolismo , Lobo Frontal/metabolismo , Fosfolipases A/metabolismo , Receptores de N-Metil-D-Aspartato/metabolismo , Fator de Transcrição AP-2/metabolismo , Animais , Antimaníacos/farmacologia , Transtorno Bipolar/tratamento farmacológico , Transtorno Bipolar/fisiopatologia , Proteínas de Ligação a DNA/efeitos dos fármacos , Proteínas de Ligação a DNA/metabolismo , Esquema de Medicação , Agonistas de Aminoácidos Excitatórios/farmacologia , Lobo Frontal/efeitos dos fármacos , Lobo Frontal/fisiopatologia , Fosfolipases A2 do Grupo IV , Masculino , N-Metilaspartato/farmacologia , Fosfolipases A/efeitos dos fármacos , Fosfolipases A/genética , Fosfolipases A2 , Fosforilação , Subunidades Proteicas/efeitos dos fármacos , Subunidades Proteicas/metabolismo , RNA Mensageiro/efeitos dos fármacos , RNA Mensageiro/metabolismo , Ratos , Ratos Endogâmicos F344 , Receptores de N-Metil-D-Aspartato/efeitos dos fármacos , Frações Subcelulares , Fator de Transcrição AP-2/efeitos dos fármacos , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/fisiologiaRESUMO
BACKGROUND: G-protein receptor kinases (GRKs) are a family of serine/threonine kinases involved in the homologous desensitization of agonist activated G-protein coupled receptors (GPCRs). G-protein coupled receptor supersensitivity, possibly as a result of decreased GRK, has been suggested in affective disorders. METHODS: We used immunobloting to determine if chronic, therapeutically relevant doses of lithium (Li+), carbamazepine (CBZ), and valproate (VPA), would increase GRK2/3 protein levels in rat frontal cortex. RESULTS: Chronic Li+ (24%) and CBZ (44%) significantly increased GRK3 in the membrane but not cytosol fractions. Chronic VPA had no effect on GRK3. G-protein receptor kinase 2 protein levels were unchanged by all treatments. The GRK3 membrane to cytosol ratio was increased significantly in Li+ and CBZ treated rats. CONCLUSIONS: These results show that chronically administered Li+ and CBZ, but not VPA, increase the translocation of GRK3 from cytosol to membrane, possibly correcting supersensitivity of GPCRs in bipolar disorder.
Assuntos
Anticonvulsivantes/farmacologia , Antimaníacos/farmacologia , Carbamazepina/farmacologia , Lobo Frontal/efeitos dos fármacos , Cloreto de Lítio/farmacologia , Membranas Sinápticas/efeitos dos fármacos , Ácido Valproico/farmacologia , Quinases de Receptores Adrenérgicos beta/metabolismo , Animais , Western Blotting , Citosol/efeitos dos fármacos , Quinase 2 de Receptor Acoplado a Proteína G , Quinase 3 de Receptor Acoplado a Proteína G , Masculino , Ratos , Ratos Endogâmicos F344RESUMO
This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of author Stanley Rapoport, with approval from Biological Psychiatry Editor, John H. Krystal, MD. The National Institutes of Health has found that Dr. Jagadeesh S. Rao engaged in research misconduct by falsifying data in Figures 1, 3, and 5 of the aforementioned manuscript. No other authors were implicated in the data falsification
Assuntos
Anticonvulsivantes/farmacologia , Antimaníacos/farmacologia , Carbamazepina/farmacologia , Lobo Frontal/efeitos dos fármacos , Fator de Transcrição AP-2/metabolismo , Fatores de Transcrição/metabolismo , Animais , Ácido Araquidônico/metabolismo , Transtorno Bipolar/genética , Transtorno Bipolar/fisiopatologia , Regulação para Baixo/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Masculino , Fosfolipases A/genética , Fosfolipases A/metabolismo , Fosfolipases A2 , Ratos , Ratos Endogâmicos , Fator de Transcrição AP-2/genética , Fatores de Transcrição/genéticaRESUMO
RATIONALE: Fluoxetine is used to treat unipolar depression and is thought to act by increasing the concentration of serotonin (5-HT) in the synaptic cleft, leading to increased serotonin signaling. The 5-HT(2A/2C) receptor subtypes are coupled to a phospholipase A(2) (PLA(2)). We hypothesized that chronic fluoxetine would increase the brain activity of PLA(2) and the turnover rate of arachidonic acid (AA) in phospholipids of the unanesthetized rat. MATERIALS AND METHODS: To test this hypothesis, rats were administered fluoxetine (10 mg/kg) or vehicle intraperitoneally daily for 21 days. In the unanesthetized rat, [1-(14)C]AA was infused intravenously and arterial blood plasma was sampled until the animal was killed at 5 min and its brain was subjected to chemical, radiotracer, or enzyme analysis. RESULTS: Using equations from our fatty acid model, we found that chronic fluoxetine compared with vehicle increased the turnover rate of AA within several brain phospholipids by 75-86%. The activity and protein levels of brain cytosolic PLA(2) (cPLA(2)) but not of secretory or calcium-independent PLA(2) were increased in rats administered fluoxetine. In a separate group of animals that received chronic fluoxetine followed by a 3-day saline washout, the turnover of AA and activity and protein levels of cPLA(2) were not significantly different from controls. The protein levels of cyclooxygenases 1 and 2 as well as the concentration of prostaglandin E(2) in rats chronically administered fluoxetine did not differ significantly from controls. CONCLUSION: The results support the hypothesis that fluoxetine increases the cPLA(2)-mediated turnover of AA within brain phospholipids.