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Clinical usefulness of intraductal ultrasonography for the management of acute biliary pancreatitis
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K.-C. Sung D.-C. Seo S.-J. Lee M.-Y. Lee S.H. Wild C.D. Byrne 《Nutrition, metabolism, and cardiovascular diseases : NMCD》2019,29(5):489-495
Background and aims
It is not known whether non alcoholic fatty liver disease (NAFLD) is a risk factor for diabetes in non obese, non centrally-obese subjects. Our aim was to investigate relationships between fatty liver, insulin resistance and a biomarker score for liver fibrosis with incident diabetes at follow up, in subjects who were neither obese nor centrally-obese.Methods and results
As many as 70,303 subjects with a body mass index (BMI) < 25 kg/m2 and without diabetes were followed up for a maximum of 7.9 years. At baseline, fatty liver was identified by liver ultrasound, insulin resistance (IR) by homeostatic model assessment of insulin resistance (HOMA-IR) ≥2.0, and central obesity by waist circumference (waist circumference ≥90 cm (men) and ≥85 cm (women). The Fibrosis-4 (FIB-4 score) was used to estimate extent of liver fibrosis. Cox proportional hazards models adjusted for confounders were used to estimate hazard ratios (aHRs) for incident diabetes. As many as 852 incident cases of diabetes occurred during follow up (median [IQR] 3.71 [2.03] years). Mean ± SD BMI was 22.8 ± 1.8 and 21.7 ± 2.0 kg/m2 in subjects with and without diabetes at follow up. In subjects without central obesity and with fatty liver, aHRs (95% CI) for incident diabetes at follow up were 2.17 (1.56, 3.03) for men, and 2.86 (1.50,5.46) for women. Similar aHRs for incident diabetes occurred with fatty liver, IR and the highest quartile of FIB-4 combined, in men; and there was a non significant trend toward increased risk in women.Conclusions
In normal weight, non-centrally obese subjects NAFLD is an independent risk factor for incident diabetes. 相似文献7.
Xiaoqing Guo Ji-Eun Seo Xilin Li Nan Mei 《Journal of toxicology and environmental health. Part B, Critical reviews》2020,23(1):27-50
ABSTRACTGenotoxic compounds may be detoxified to non-genotoxic metabolites while many pro-carcinogens require metabolic activation to exert their genotoxicity in vivo. Standard genotoxicity assays were developed and utilized for risk assessment for over 40 years. Most of these assays are conducted in metabolically incompetent rodent or human cell lines. Deficient in normal metabolism and relying on exogenous metabolic activation systems, the current in vitro genotoxicity assays often have yielded high false positive rates, which trigger unnecessary and costly in vivo studies. Metabolically active cells such as hepatocytes have been recognized as a promising cell model in predicting genotoxicity of carcinogens in vivo. In recent years, significant advances in tissue culture and biological technologies provided new opportunities for using hepatocytes in genetic toxicology. This review encompasses published studies (both in vitro and in vivo) using hepatocytes for genotoxicity assessment. Findings from both standard and newly developed genotoxicity assays are summarized. Various liver cell models used for genotoxicity assessment are described, including the potential application of advanced liver cell models such as 3D spheroids, organoids, and engineered hepatocytes. An integrated strategy, that includes the use of human-based cells with enhanced biological relevance and throughput, and applying the quantitative analysis of data, may provide an approach for future genotoxicity risk assessment. 相似文献
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目的:比较CT平扫与增强扫描对肝脾肾钝性损伤的诊断能力。方法:回顾性分析临床疑似钝性肝脾肾损伤,并经手术和临床观察证实的CT平扫和增强扫描的患者84例。结果:平扫确定的损伤:肝12例,脾25例,肾5例;平扫可疑损伤:肝22例,脾15例,肾5例。增强确定的损伤:肝32例,脾40例,肾12例(全肾梗塞1例,局限性梗塞3例);对比剂外溢(活动性出血)3例;无可疑损伤。平扫无异常而增强确定有损伤:肝10例,脾5例,肾2例。增强显示的损伤灶比平扫范围明显大、病灶多、界限清楚。结论:CT增强扫描显示肝脾肾损伤明显优于平扫,延时扫描有助于发现活动性出血,应常规增强扫描。 相似文献