RESUMO
Objective To investigate the capability of empathy for pain in bipolar disorder (BD). Methods Thirty-two patients with BD (16, 8 and 8 in depressed, manic and remitted phases, respectively) and 32 healthy controls matched for age, gender and education were recruited. Empathy for pain paradigm were used. Subjects were required to judge whether the person in the picture felt painful and rate pain degree regarding to painful and neutral pictures. Accuracy, reaction time and ratings of pain degree were used as indicators of empathy for pain. Chinese version of Interpersonal Reactivity Index (IRI-C) were used to measure empathy. Results Compared to controls, accuracy of painful pictures was significantly lower in patients [(0.74±0.16) vs.(0.83±0.10), P<0.05]. Reaction time for both painful [(903.84±167.49) ms vs. (765.06±108.21) ms] and neutral [(880.44 ± 190.36) ms vs. (750.31 ± 103.15)ms] pictures were significantly longer in patients (P<0.05). Pa?tients showed lower scores in factors of perspective taking [(9.20±5.43) vs. (12.43±4.13)], fantasy [(11.85±4.57) vs. (15.50± 5.56)] and empathy concern [(14.59±5.35) vs. (17.63±3.37)] in IRI-C (P<0.05). Accuracy of painful pictures was positively correlated with scores in fantasy (r=0.37, P=0.04) and reaction time was positively correlated with duration of disease in pa?tients (r=0.64, P<0.01). Conclusion Bipolar disorder has deficit in the capability of empathy for pain.
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Patients with ER/HER2-positive breast cancer have a poor prognosis and are less responsive to selective estrogen receptor modulators; this is presumably due to the crosstalk between ER and HER2. Fatty acid synthase (FASN) is essential for the survival and maintenance of the malignant phenotype of breast cancer cells. An intimate relationship exists between FASN, ER and HER2. We hypothesized that FASN may be the downstream effector underlying ER/HER2 crosstalk through the PI3K/AKT/mTOR pathway in ER/HER2-positive breast cancer. The present study implicated the PI3K/AKT/mTOR pathway in the regulation of FASN expression in ER/HER2-positive breast cancer cells and demonstrated that rapamycin, an mTOR inhibitor, inhibited FASN expression. Cerulenin, a FASN inhibitor, synergized with rapamycin to induce apoptosis and inhibit cell migration and tumorigenesis in ER/HER2-positive breast cancer cells. Our findings suggest that inhibiting the mTOR-FASN axis is a promising new strategy for treating ER/HER2-positive breast cancer.
Assuntos
Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/patologia , Sinergismo Farmacológico , Receptor alfa de Estrogênio/metabolismo , Ácido Graxo Sintase Tipo I/antagonistas & inibidores , Receptor ErbB-2/metabolismo , Sirolimo/farmacologia , Animais , Apoptose/efeitos dos fármacos , Western Blotting , Neoplasias da Mama/enzimologia , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Cerulenina/farmacologia , Receptor alfa de Estrogênio/genética , Ácido Graxo Sintase Tipo I/genética , Ácido Graxo Sintase Tipo I/metabolismo , Feminino , Técnica Indireta de Fluorescência para Anticorpo , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Camundongos , Camundongos Nus , Inibidores de Proteínas Quinases/farmacologia , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Receptor ErbB-2/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Células Tumorais Cultivadas , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
Lung cancer has the highest morbidity and mortality of any malignant tumor. To improve efficacy and reduce toxicity in patients with advanced non-small cell lung cancer (NSCLC), it is important to integrate traditional and conventional medicine. Two hundred and forty patients with advanced NSCLC were randomized to tetrandrine plus GP or GP only. We infused gemcitabine on days 1 and 8; cisplatin on day 1. The tetrandrine group received continuous i.v. infusion for 10 days, with treatment repeated every 21 days. After 2 consecutive treatment cycles, we used RECIST criteria to evaluate short-term efficacy. Quality of life (QOL) was assessed according to Karnofsky score (KPS) and body weight change. We used NCI CTC 3.0 to evaluate treatment toxicity. The short-term objective response rate was 36.1% in the tetrandrine group and 24.3% in the controls (P=0.057). The short-term disease control rate was 63.9% in the tetrandrine group and 52.3% in the controls (P=0.081). The 1-year survival rates were 45.7% and 31.3%, respectively (P=0.059). KPS scores improved by 49.1% and 32.4%, respectively (P=0.012). Body weight increased by 28.7% in the tetrandrine group and 16.2% in the controls (P=0.027). The incidence of grade 2-4 leukopenia, thrombocytopenia, nausea, and vomiting in the tetrandrine group was 38.0%, 19.4%, 46.3%, and 16.7%, respectively; the control group figures were 53.2%, 34.2%, 63.0% and 27.9% (P<0.05). Tetrandrine may improve short-term efficacy and survival in patients with advanced NSCLC. Tetrandrine may also mitigate adverse reactions to chemotherapy and improve QOL for patients with NSCLC.
