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1.
Nihon Shokakibyo Gakkai Zasshi ; 119(11): 1036-1042, 2022.
Artigo em Japonês | MEDLINE | ID: mdl-36351623

RESUMO

A 23-year-old woman was presented with fever and epigastric pain. Contrast enhanced computed tomography revealed a 40mm mass in the lateral segment. Blood tests showed the elevation of WBC and CRP. With the diagnosis of liver abscess, the antibiotics were administered, and the clinical findings were promptly improved. One year later, she complained of the same symptoms, and the mass had increased to 50mm in diameter. Percutaneous liver biopsy led to the diagnosis of fibrolamellar hepatocellular carcinoma.


Assuntos
Carcinoma Hepatocelular , Abscesso Hepático , Neoplasias Hepáticas , Feminino , Humanos , Adulto Jovem , Adulto , Carcinoma Hepatocelular/diagnóstico por imagem , Neoplasias Hepáticas/diagnóstico por imagem , Neoplasias Hepáticas/patologia , Abscesso Hepático/diagnóstico por imagem , Tomografia Computadorizada por Raios X
2.
Arch Public Health ; 78: 101, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33088502

RESUMO

BACKGROUND: An elevated alanine aminotransferase (ALT) and a low aspartate aminotransferase (AST) to ALT ratio (AST/ALT ratio) suggest nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, increasing the risk of liver cirrhosis and hepatocellular carcinoma. In addition, eating quickly has been found to be associated with outcomes such as obesity. This study sought to investigate the relationship between eating quickly and an elevated ALT or a low AST/ALT ratio in Japanese middle-aged adults. METHODS: The present study included 283,073 adults aged 40-64 years who had annual health checkups in Japan from April 2013 to March 2014. The data of serum parameters and lifestyle factors, including eating speed, were analyzed. An elevated ALT was defined as > 40 U/L, and a low AST/ALT ratio was defined as < 1. Logistic regression analysis was performed to calculate the odds ratios (ORs) and the 95% confidence intervals (CIs) for an elevated ALT and a low AST/ALT ratio. RESULTS: Significantly increased ORs for an elevated ALT were observed in men (OR: 1.45, 95% CI: 1.41-1.49) and women (OR: 1.34, 95% CI: 1.25-1.43). Moreover, eating quickly significantly increased the ORs for a low AST/ALT ratio in men (OR: 1.53, 95% CI: 1.50-1.56) and women (OR: 1.36, 95% CI: 1.31-1.41). When the analysis was limited to those with ALT ≤40 U/L, eating quickly had significantly increased ORs for a low AST/ ALT ratio, regardless of sex. CONCLUSIONS: Eating quickly was significantly associated with an elevated ALT and a low AST/ALT ratio. In addition, eating quickly was significantly associated with a low AST/ALT ratio even for those without ALT elevation. This study suggested that modification of eating speed may contribute to reducing the risk for an elevated ALT and a low AST/ALT ratio.

3.
BMJ Open ; 9(6): e027752, 2019 06 21.
Artigo em Inglês | MEDLINE | ID: mdl-31230014

RESUMO

OBJECTIVES: Weight gain after 20 years of age is associated with chronic kidney disease (CKD). However, the impact of weight gain on CKD might differ by current obesity status. We investigated the association of the combination of weight gain after 20 years of age and current obesity with CKD among adults in Japan. DESIGN: A cross-sectional study. SETTING AND PARTICIPANTS: We analysed data from 94 822 adults aged 40-64 years who had an annual health check-up in Japan from April 2013 to March 2014. PRIMARY OUTCOME MEASURE: CKD was defined as an estimated glomerular filtration rate <60 mL/min/1.73 m2 and/or proteinuria. RESULTS: Both weight gain ≥10 kg after 20 years of age plus obesity (OR 2.21, 95% CI 2.07 to 2.36) and weight gain of ≥10 kg plus non-obesity (OR 1.31, 95% CI 1.21 to 1.42) significantly increased the OR for CKD when compared with weight gain <10 kg plus non-obesity in men. In women, weight gain ≥10 kg plus obesity (OR 2.04, 95% CI 1.84 to 2.25) and weight gain ≥10 kg plus non-obesity (OR 1.53, 95% CI 1.36 to 1.72) significantly increased the OR for CKD compared with weight gain <10 kg plus non-obesity. These results persisted even after adjustment for age, lifestyle factors, hypertension, dyslipidaemia and diabetes. CONCLUSIONS: Weight gain ≥10 kg after 20 years of age was significantly associated with CKD in both obese and non-obese subjects. Moreover, the influence of weight gain ≥10 kg plus obesity on CKD was greater than that of weight gain ≥10 kg plus non-obesity on CKD. The present study results suggest that it is important to consider weight gain after maturity in both obese and non-obese subjects to prevent CKD among Japanese middle-aged adults.


Assuntos
Obesidade/fisiopatologia , Insuficiência Renal Crônica/fisiopatologia , Aumento de Peso/fisiologia , Adulto , Estudos Transversais , Feminino , Taxa de Filtração Glomerular/fisiologia , Humanos , Japão/epidemiologia , Masculino , Pessoa de Meia-Idade , Obesidade/complicações , Obesidade/epidemiologia , Insuficiência Renal Crônica/complicações , Insuficiência Renal Crônica/epidemiologia
4.
J Med Invest ; 54(3-4): 255-60, 2007 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-17878674

RESUMO

Several specific locations in brain, including pyriform cortex and hypothalamus, are associated with regulation of food intake. Although lesions of these locations significantly alter food intake, their involvement in the selection of macronutrients is not well characterized. In this study, we examined distinct effects of anterior pyriform cortex (APC) and lateral hypothalamus (LH) lesions on protein intake in rats. The APC or LH of male adult rats were lesioned by treatment with kainic acid, and the rats were then given free access to two kinds of casein diets containing high (60%) and low (5%) protein. Total energy content of these diets was kept constant by changing the carbohydrate content. Following the APC lesions, body weight and food intake decreased, but returned to control levels on day 13 and day 4, respectively. APC lesions did not change the ratio of protein intake. In contrast, LH lesions disturbed body weight gain and the selection of a high protein diet for at least two weeks, although food intake returned to control levels by day 2. Our results suggest that LH, but not APC, may play an important role in the selection of protein intake in rats.


Assuntos
Ingestão de Alimentos/fisiologia , Região Hipotalâmica Lateral/fisiologia , Condutos Olfatórios/fisiologia , Animais , Proteínas Alimentares/administração & dosagem , Região Hipotalâmica Lateral/efeitos dos fármacos , Região Hipotalâmica Lateral/lesões , Ácido Caínico/toxicidade , Masculino , Condutos Olfatórios/efeitos dos fármacos , Condutos Olfatórios/lesões , Ratos , Ratos Sprague-Dawley
5.
Mol Pharmacol ; 70(6): 1916-24, 2006 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-16985185

RESUMO

Ginseng root is one of the most popular herbs throughout the world and is believed to be a panacea and to promote longevity. It has been used as a medicine to protect against cardiac ischemia, a major cause of death in the West. We have previously demonstrated that ginsenoside Re, a main phytosterol of Panax ginseng, inhibits Ca(2+) accumulation in mitochondria during cardiac ischemia/reperfusion, which is attributable to nitric oxide (NO)-induced Ca(2+) channel inhibition and K(+) channel activation in cardiac myocytes. In this study, we provide compelling evidence that ginsenoside Re activates endothelial NO synthase (eNOS) to release NO, resulting in activation of the slowly activating delayed rectifier K(+) current. The eNOS activation occurs via a nongenomic pathway of each of androgen receptor, estrogen receptor-alpha, and progesterone receptor, in which c-Src, phosphoinositide 3-kinase, Akt, and eNOS are sequentially activated. However, ginsenoside Re does not stimulate proliferation of androgen-responsive LNCaP cells and estrogen-responsive MCF-7 cells, implying that ginsenoside Re does not activate a genomic pathway of sex hormone receptors. Fluorescence resonance energy transfer experiments with a probe, SCCoR (single cell coactivator recruitment), indicate that the lack of genomic action is attributable to failure of coactivator recruitment. Thus, ginsenoside Re acts as a specific agonist for the nongenomic pathway of sex steroid receptors, and NO released from activated eNOS underlies cardiac K(+) channel activation and protection against ischemia-reperfusion injury.


Assuntos
Ginsenosídeos/farmacologia , Coração/efeitos dos fármacos , Panax/química , Canais de Potássio/agonistas , Animais , Células Cultivadas , Ativação Enzimática , Receptor alfa de Estrogênio/efeitos dos fármacos , Feminino , Transferência Ressonante de Energia de Fluorescência , Cobaias , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo III/metabolismo , Fosforilação , Proteínas Proto-Oncogênicas c-akt/metabolismo , Receptores Androgênicos/efeitos dos fármacos , Receptores de Progesterona/efeitos dos fármacos
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