Objective: To investigate and establish the related factors of non-invasive score model for prediction of non-alcoholic fatty liver disease in chronic hepatitis B patients with normal or mildly elevated alanine aminotransferase (ALT). Methods: A total of 128 cases with chronic hepatitis B who had undergone liver biopsy were included. According to the presence or absence of hepatocyte steatosis on the pathological results of liver biopsy, they were divided into a fatty infiltration and a non-fatty infiltration group. Patients' demographic characteristics, laboratory test indexes, and pathological test results were collected. Univariate and multivariate logistic regression analysis combined with clinical screening variables were used to establish a predictive model. The prediction efficiency of the new model was evaluated by the receiver operating curve, and the difference between the accuracy of the new model and ultrasound in the diagnosis of fatty liver was compared by Delong's-test. Result: Multivariate regression analysis showed that serum triglyceride, serum uric acid and platelets were highly correlated with intrahepatic steatosis (P<0.05). The regression equation triglyceride-uric acid-platelet (TUP)-1=-8.195+0.011×uric acid+1.439×triglyceride+0.012×platelet count was established by combining the above variables. Tthe equation TUP-2=-7.527+0.010×uric acid+1.309×triglyceride+0.012×platelet count+1.397×fatty liver (ultrasound) was established (yes=1; no=0) after incorporating the results of abdominal ultrasound. The diagnostic value of TUP-1 and TUP-2 models for fatty liver was better than that of ultrasound alone and there was no statistically significant difference in diagnostic value between TUP-1 and TUP-2 models (Z=1.453, P=0.146). Conclusion: Compared with abdominal ultrasonography alone, the new model is more effective in diagnosing fatty liver and has good application value.

Osteoporosis and cardiovascular diseases often coexist in the same elderly individuals. Does this suggest some potential correlation between the two diseases? Low bone mass and change of bone biomarker are associated with a higher risk of carotid and cardiac calcification plaques. Bone mineral density (BMD) and bone metabolism marker may contribute to the progression of carotid and cardiac arterial calcifications. The aim of this study was to investigate whether low bone mass and the change of bone biomarker are associated with the prevalence of calcified atherosclerotic plaque in elderly Chinese. We conducted a five-year prospective study. BMD was measured by dual-energy X-ray absorptiometry scanning. Carotid and cardiac computed tomography angiography (CTA) was conducted using a 64-multidetector row scanner to assess carotid and cardiac arterial plaque at baseline and during follow-up. Of 1571 community residents over 60 years of age, 184 (11.7%) subjects developed carotid calcified plaque, 510 (32.5%) subjects developed cardiac calcified plaque and 97 (6.2%) subjects developed co-existence calcified plaques in carotid and cardiac arteries. After adjustment for age and all relevant confounders, Q1, Q2 quartile of BMD, and osteoprotegerin (OPG), osteocalcin (OC), and C-terminal cross-linked telopeptide of type I collagen (CTX) were associated with increased risk of calcified plaques. This study suggested that lower BMD and change of bone metabolism biomarker were associated with a higher risk of carotid and cardiac calcified plaque development.

The mitochondrial cytochrome c oxidase (CO) gene sequence was determined on a patient with Alzheimer’s disease (AD). Compared to the standard Cambridge sequence to identify base changes,two missense mutations were found in the patient with AD. The mutations were a G to T transition at np 8206 and an A to T transition at np 8224. The np 8206 mutation changed a Met to an Ile and np 8224 mutation changed a Leu to a Phe. The normal bases and the mutations of mitochondrial DNA (mtDNA) coexist in the patient. Further studies will be required to demonstrate the role of the point mutations of mitochondrial DNA in the pathogenisis of Alzheimer’s disease.