Evidence-based guideline of the diagnosis and treatment in the nonalcoholic fatty liver disease was formulated by Chinese Medical Association of fatty liver disease and alcoholic liver disease in order to simplify medical decision making and to help physicians make good decisions about NAFLD,which was published in 2006.Compared with some international guidelines or recommendations,Chinese guideline is more wide and complete for diagnosis and therapy of NAFLD.Meanwhile,there is significant difference in evaluation and treatment between these guidelines.

Objective To evaluate the prevalence of hepatic steatosis in patients with chronic hepatitis B (CHB) and the impact of hepatic steatosis on the progress of fibrosis. Methods Five hundred and sixty two untreated CHB patients (405 males and 157 females) with an average age of 31.3 underwent liver biopsy from January to August 2007. On the day of liver biopsy, a questionnaire was completed and a blood sample was obtained for laboratory analysis. The degree of liver steatosis, necroinflammation and fibrosis was assessed; demographic information and clinical data including age, gender, body mass index (BMI), history of diabetes mellitus, hypertension, dyslipidemia, and HBeAg status, HBV DNA viral load were documented. Results In 562 patients, 102 (18. 2% ) had steatosis. Multivariate analysis demonstrated that liver steatosis was associated with the levels of TG, APO-B, UA, FSG, and higher BMI; and the progress of fibrosis was associated with high degree of hepatic steatosis and necroinflammation, age over 35 years, HBV DNA > 103 copies/L, high BMI and GGT. Conclusions The results show that obesity and dyslipidemia in CHB patients are associated with the hepatic steatosis, and the latter seems to be an important determinant for fibrosis.

Amyloid Neuropathies, Familial ; genetics ; Cardiomyopathies ; Humans ; Mutation

Objective: To establish an autoregressive moving average model for the prediction of tuberculosis cases in students of Shanxi Province, and to provide scientific basic for the prevention and treatment of pulmonary tuerculosis among students. Methods: A optimized ARIMA model was set up based on reported monthly data of TB in students from January 2010 to September 2019 in Shanxi Province by SAS 9.3 software, and the incidence trend in the next two years was predicted. Results: The average reported rate of active TB in students of Shanxi Province was 23.52 per 100 000 from 2010 to 2019,showing an overall downward trend(χ2=999 980.46，P<0.01). The optimal model was SARIMA(0，1，1)(0，1，1)12,SBC=982.16. The fitted equation was (1-0.63B) (1-B12)Yt=(1-0.61B12)εt. The mean relative error was 19.35%,and the predicted incidence trend was consistent with the previous years,and the peak was from March to May. Conclusion Substantial progress has been made in student TB prevention of Shanxi Province. The ARIMA product season model is suitable for forecasting the TB incidence in students,so as to provide scientific guidance for its early prevention and control.

Insulin resistance has been regarded as a hallmark of diabetes heart disease (DHD). Numerous studies have shown that insulin resistance can affect blood circulation and myocardium, which indirectly cause cardiac hypertrophy and ventricular remodeling, participating in the pathogenesis of DHD. Meanwhile, hyperinsulinemia, hyperglycemia, and hyperlipidemia associated with insulin resistance can directly impair the metabolism and function of the heart. Targeting insulin resistance is a potential therapeutic strategy for the prevention of DHD. Currently, the role of insulin resistance in the pathogenic development of DHD is still under active research, as the pathological roles involved are complex and not yet fully understood, and the related therapeutic approaches are not well developed. In this review, we describe insulin resistance and add recent advances in the major pathological and physiological changes and underlying mechanisms by which insulin resistance leads to myocardial remodeling and dysfunction in the diabetic heart, including exosomal dysfunction, ferroptosis, and epigenetic factors. In addition, we discuss potential therapeutic approaches to improve insulin resistance and accelerate the development of cardiovascular protection drugs.

Insulin resistance has been regarded as a hallmark of diabetes heart disease (DHD). Numerous studies have shown that insulin resistance can affect blood circulation and myocardium, which indirectly cause cardiac hypertrophy and ventricular remodeling, participating in the pathogenesis of DHD. Meanwhile, hyperinsulinemia, hyperglycemia, and hyperlipidemia associated with insulin resistance can directly impair the metabolism and function of the heart. Targeting insulin resistance is a potential therapeutic strategy for the prevention of DHD. Currently, the role of insulin resistance in the pathogenic development of DHD is still under active research, as the pathological roles involved are complex and not yet fully understood, and the related therapeutic approaches are not well developed. In this review, we describe insulin resistance and add recent advances in the major pathological and physiological changes and underlying mechanisms by which insulin resistance leads to myocardial remodeling and dysfunction in the diabetic heart, including exosomal dysfunction, ferroptosis, and epigenetic factors. In addition, we discuss potential therapeutic approaches to improve insulin resistance and accelerate the development of cardiovascular protection drugs.

Insulin resistance has been regarded as a hallmark of diabetes heart disease (DHD). Numerous studies have shown that insulin resistance can affect blood circulation and myocardium, which indirectly cause cardiac hypertrophy and ventricular remodeling, participating in the pathogenesis of DHD. Meanwhile, hyperinsulinemia, hyperglycemia, and hyperlipidemia associated with insulin resistance can directly impair the metabolism and function of the heart. Targeting insulin resistance is a potential therapeutic strategy for the prevention of DHD. Currently, the role of insulin resistance in the pathogenic development of DHD is still under active research, as the pathological roles involved are complex and not yet fully understood, and the related therapeutic approaches are not well developed. In this review, we describe insulin resistance and add recent advances in the major pathological and physiological changes and underlying mechanisms by which insulin resistance leads to myocardial remodeling and dysfunction in the diabetic heart, including exosomal dysfunction, ferroptosis, and epigenetic factors. In addition, we discuss potential therapeutic approaches to improve insulin resistance and accelerate the development of cardiovascular protection drugs.

Objective:To investigate the apoptotic induction effects of homoharringtonine (HHT) combined with imatinib (STI571) on human chronic myeloid leukemia (CML) KU812 cells. Methods:KU812 cells were treated with HHT or/and STI571. Total cell numbers were counted by using hemocytometer. Apoptotic cells were determined by using fluorescence microscope and FACS after staining with AO-EB and PI respectively. The cleavage of poly ADP-ribose polymerase (PARP) and the expression of anti-apoptotic proteins were determined by Western blot. Results:HHT could prompt the apoptotic induction of imatinib in KU812 cells, which was in a time and dose dependent manner. Apoptosis induced by HHT and imatinib was correlated with the down-regulation of Bcl-XL and the cleavage of PARP. Conclusion:HHT prompt apoptotic induction of imatinb in KU812 cells and the combination of HHT with imatinib will provide a more effective strategy for the clinical treatment of CML.

Objective To explore the regulatory effects of cucumin onoxidation and antioxidation in non-alcoholic steatohepatitis (NASH ) .Methods Fifty-six clean male rats were randomly divided into 7 groups by random numbers table .Eight rats in normal control group were fed by normal diet for 12 weeks .Twenty-four rats in model group were fed by choline dificinet (CD) diet and randomly sacrificedat week 4 ,8 and 12 with 8 rats each time point .Twenty-four rats incucumin treatment group were given cucumin at high (500 mg/[kg · d]) ,medium (100 mg/[kg · d]) and low (50 mg/[kg · d]) dosages with 8 rats each dosage from week 5 of CD diet for 8 weeks ,and the rats were sacrificed at week 12 .The liver tissues were reserved for pathology test and detections of thiobarbituric acid reactive substances (TBARS) ,glutathione (GSH) ,the activities of superoxide dismutase (SOD) ,manganese superoxide dismutase (MnSOD) ,glutathione peroxidase (GPx) ,and levels of triglyceride (TG) and total cholesterol (TC) .The measurement data with normal distribution were analyzed using t test ,and the data with non-normal distribution were analyzed using rank sum Z test .Results The liver of rats presented with the performance of NASH when fed with CD diet for 4 weeks ,and presented with early fibrosis after 8 weeks of CD diet ,even progressed to cirrhosis after 12 weeks of CD diet .The NAS scores of medium and high dose curcumin treatment groups were 6 .50 (5 .25 ,7 .00) and 6 .00 (5 .00 ,6 .75) ,respectively ,which were both lower than that model group at week 12 (8 .00 [7 .00 ,8 .00])(Z=2 .441 and 2 .728 ,respectively , both P< 0 .01) ,while fibrosis stages at week 12 were not significantly different compared with model group (Z=0 .795 and 1 .807 ,respectively ,both P> 0 .05) .TG and TC levels in liver tissues of rats in low ,medium and high doses treatment group were not significantly different compared with model group at week 12(TG :t=0 .54 ,1 .18 and 1 .66 ,respectively ;TC :t=0 .11 ,0 .59 and 0 .62 ,respectively ;all P>0 .05) .The GSH contentin liver of rats in high dose group was (1185 .82+204 .01) mg/g ,which was significantly different from that in model group at week 12 (735 .29 + 35 .08) (t=4 .97 ,P<0 .01) .The TBARS contents in the liver of the middle and high doses curcumin treatment group were significantly different from that of model group at week 12 (t=7 .58 and 11 .62 ,respectively ,both P< 0 .01) .The SOD activities in liver of rats in low ,medium and high doses curcumin treatment group were statistically different from that in model group (t=4 .17 ,4 .32 and 6 .10 ,respectively ,all P<0 .01) .MnSOD activity in liver of rats in high dose group was significantly different from model group at week 12 (t=8 .42 ,P<0 .01) .The live GPx contents in low ,medium and high doses curcumin treatment group were all not significantly different from that in model group at week 12 (t=0 .27 ,0 .21 and 0 .60 ,respectively ,all P>0 .05) .Conclusions CD diet in SD rats could induce hepatic lipid deposition in liver ,and cause liver antioxidative system disorders ,GSH exhaustion ,and decreases of SOD and GPx activities .Curcumin treatment could improve liver NAS score of NASH rats ,and might play a protective role by upregulating the SOD activity and increasing liver GSH content .But curcumin has no effects on liver GPx activity and fat deposition in liver of NASH rats .

OBJECTIVETo evaluate the controlled attenuation parameter (CAP) assessment of fatty liver and choose a cut-off value of hepatic steatosis more than 5%.

METHODSConsecutive patients, 18 years or older, who had undergone percutaneous liver biopsy and CAP measurement were recruited from five liver healthcare centers in China. All enrollees were categorized as hepatic steatosis grade S0 (<5%) or S1 (5%). An M-probe equipped FibroScan 502 was used to capture CAP values. Receiver operating characteristic (ROC) curves were plotted, and the areas under (AU) the curves were calculated to determine the diagnostic efficacy. The CAP cut-off values at the optimal thresholds were defined by maximum Youden indices; sensitivity and specificity were also calculated.

RESULTSA total of 332 patients were enrolled in the study, including 67 patients with non-alcoholic fatty liver disease (NAFLD) and 265 with chronic hepatitis B (CHB) viru: infection. The median age (inter quartile range, IQR) of the study cohort was 39.0 (32.0-50.5) years-old. There were 46 males (68.7%) in the NAFLD group, with a median age of 37.0 (28.0-45.0) years-old, and 182 males (68.7%) in the CHB group; the differences between the two groups in median age and male: female ratio did not reach statistical significance. Multivariate linear regression analysis identified steatosis grade and body mass index (BMI) as independently associated with CAP. The median (IQR) CAP values among patients with S0 and S1 grade steatosis were 215.0 (190.0-241.0) dB/m and 294.0 (255.0-325.5) dB/m (P<0.001), respectively. For all patients, when BMI was <25 kg/m2, the ability of the AUROC of the CAP to discriminate hepatic steatosis more than or equal to 5% was 0.853, and the optimal cut-off value was 244.5 dB/m; however, when BMI≥25 kg/m2, the AUROC was 0.835 and the optimal cut-off value 269.5 dB/m.

CONCLUSIONCAP can identify hepatic steatosis more than or equal to 5% and is applicable for the diagnosis of fatty liver if it is adjusted for BMI.

Adult ; Area Under Curve ; Bile ; Biopsy ; Body Mass Index ; China ; Fatty Liver ; Female ; Hepatitis B, Chronic ; Humans ; Linear Models ; Male ; Middle Aged ; Multivariate Analysis ; ROC Curve ; Tissue Extracts