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BACKGROUND: Abnormal lipid metabolism is one of the risk factors in patients with ischemic cerebral disorders, and is correlated with the changes of lecithin cholesterol acyltransferase activity.OBJECTIVE: To observe the relationship between the changes of lecithin cholesterol acyltransferase activity and lipid content in red blood cell membrane.DESIGN: A case-control study(experimental group with control as standard level).SETTING: Department of clinical laboratory, emergency room and department of neurology of a hospital affiliated to a medical college of a university.PARTICIPANTS: Totally 105 inpatients and outpatients with cerebrovascular diseases were selected from the Department of Neurology, Affiliated Hospital of Medical College of Qingdao University, from March 2002 to December 2003. They accorded with the Diagnostic Criteria set at the Second National Conference on Cerebrovascular Diseases. A total of 42 patients with cerebral arteriosclerosis and 63 patients with cerebral infarction were selected as patients group consisting of 67 males and 38 females. Another 65 healthy people receiving physical examination in the hospital, 36 males and 29 females, were selected as control group.METHODS: Venous blood of 8 mL was drawn from the participants on an empty stomach. We assayed the activity of lecithin cholesterol acyltransferase,high density lipoprotein cholesterol, low density lipoprotein cholesterol,apolipoprotein A1 and apolipoprotein B. Red blood cell membrane cholesterol was determined by phthalyl aldehyde-acetometry and red blood cell membrane phospholipid was determined by chemical quantitative analysis.MAIN OUTCOME MEASURES: Changes of lecithin cholesterol acyltransferase activity and lipid content in red blood cell membrane in patients group and control group.RESULTS: According to intention analysis, all the 105 patients in patients group and 65 patients in control group entered the results analysis. Activity of lecithin cholesterol acyltransferase: Activity changes in cerebral arteriosclerosis group and cerebral infarction group were obvious lower than those in control group[(2.14±0.72) kat/L, (2.06±0.80) kat/L, and(2.61± 0. 74) kat/L, P ＜ 0.01 ] . Level of high density lipoprotein cholesterol and apolipoprotein A1: The level in cerebral arteriosclerosis group and cerebral infarction group was obvious lower than that in control group[ (1.32±0.33) mmol/L, (1.37±0.33) g/L, (1.28±0.33) mmol/L; (1.27±0.31) g/L, (1.60±0.43) mmol/L, (1.60±0.43) g/L, t=2.72 to 5.01, P ＜ 0.01 ]. Content of low density lipoprotein cholesterol and red blood cell membrane-cholesterol: The content in cerebral arteriosclerosis group and cerebral infarction group was obvious higher than that in control group [ (2.94 ± 0. 82) mmol/L, (0.63 ±0.05) mmol/g, (3.02 ±0.79) mmol/L;(0.60 ±0.07) mmol/g, (2.56 ±0. 58) mmol/L, (0.57 ±0.05) mmol/g, P ＜ 0. 01 ] . Moreover, the activity of lecithin cholesterol acyltransferase was positively correlated with high density lipoprotein cholesterol and apolipoprotein A1(r=0.247, P ＜0.05; r=0.303, P ＜0.01), but was negatively correlated with low density lipoprotein cholesterol and red blood cell membrane cholesterol(r= -0.212, P ＜0.05;r= -0.346, P ＜0.01).CONCLUSION: In patients with ischemic cerebral disorders, the major change of plasma lipid is the decrease of lecithin cholesterol acyltransferase,but it is not secondary to cerebral infarction. The activity of lecithin cholesterol acyltransferase is positively correlated with high density lipoprotein cholesterol and apolipoprotein A1, but is negatively correlated with low density lipoprotein cholesterol and red blood cell membrane cholesterol.
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Objective To study the fecel-oral and blood transfusion of TT virus. Methods Paired feces and serum samples from 6 patients with type B and/or C hepatitis were tested for TTV DNA and its titers by PCR with seminested primers.Genotypes were determined after their sequences were compared with the original N22 and TA278 clone.Results TTV DNA was detected in sera from all patients,while it was detected in feces from 3 patients,including 2 with high viral titers in serum.The detection of fecal TTV DNA was dependent on the viral titers in serum.TTV isolates in 3 pairs of feces and serum had identical sequence of 222 base pairs.Their genotypes were 1a,1b and 2,respectively.Conclusion The excretion of TTV into feces indicates that TTV would be transmitted not only parenterally but also nonparenterally by a fecal-oral route.