0.05). No significant association between Q/R 192 genotype and blood lipids was found.Conclusion The polymorphism of PON-1 Q/R 192 gene is not associated with CI.

Objective To investigate the therapeutic effect of enteral nutrition in patients with severe traumatic brain injury (sTBI) by nasogastric tube and nasointestinal tube.Methods A retrospective case control study was made on 64 patients with sTBI hospitalized from October 2013 to December 2015.The patients were assigned to nasogastric tube group (n=32) and nasointestinal tube group (n=32) according to the random number table, and the same nutrient solution was given to all patients.Eighteen male and 14 female patients aged (37.8±8.7)years were identified in nasogastric tube group, and the Glasgow coma score (GCS) was (4.7±1.3)points.Twenty males and 14 females aged (39.7±6.5)years were identified in nasointestinal tube group, and the GCS was (4.1±1.2)points.Triceps skinfold thickness, body mass index, hemoglobin, level of serum albumin and level of prealbumin were measured and compared between groups before and after operation.Incidence of complications was recorded as well.Results All the above-mentioned indexes of the two groups did not differ significantly before the therapy (P>0.05), but showed significant differences 7 and 15 days after therapy (P<0.05).Incidence of complications in nasointestinal tube group (17 lung infection, nine gastrointestinal bleeding, 11 electrolyte imbalance) was lower than that in nasogastric tube group (seven lung infection, two gastrointestinal bleeding, one reflux esophagitis, four electrolyte imbalance) (P<0.05).Conclusion Nasointestinal tube enteral nutrition is better than nasogastric tube enteral nutrition in improving nutritional status and reducing complications in patients with sTBI.

Objective To explore the relationship between plasma protein Z level and severity of coronary atherosclerosis in patients with coronary heart disease,and analyze the clinical value of plasma protein Z detection.Methods Eighty-five patients who undertaken coronary arteriography were selected,and the patients were divided into coronary heart disease group (63 patients) and control group (22 patients)according to coronary arteriography results.The patients in coronary heart disease group were divided into three groups according to the Gensini score:A group (≤30 scores),B group (31-60 scores) and C group (＞ 60 scores).All patients' plasma was collected and stored at-80 ℃ until examined,and the plasma PZ level was detected by enzyme-linked immunosorbent assay method.Results The plasma protein Z level in coronary heart disease group was significantly lower than that in control group [(721.82 ± 289.53) μ g/L vs.(1 077.80 ± 338.12) μ g/L],and there was statistical difference (P＜ 0.05).The plasma protein Z level in A group,B group and C group was (856.09 ± 312.53),(665.27 ± 267.15) and (643.04 ±248.39) μg/L,respectively.The plasma protein Z level in B group and C group was significantly lower than that in A group,and there was statistical difference (P ＜ 0.05),but there was not statistical difference between C group and B group (P ＞ 0.05).There was negative correlation between the plasma Z level and Gensini score (r =-0.300,P =0.017).In coronary heart disease group,the plasma Z level in patients with smoking was significantly lower than that in patients without smoking [(687.83 ± 249.94) μ g/L vs.(844.29 ± 454.71) μ g/L,and there was statistical difference (P ＜ 0.05).There was negative correlation between the plasma Z level,age and hypersensitive C reactive protein (r =-0.349,-0.339,P ＜ 0.05).Conclusions Plasma protein Z level in patients with coronary heart disease is significantly decreased,and the plasma protein Z level has negative correlation with the severity of coronary atherosclerosis.Smoking can induce the decrease of plasma protein Z level,and the decrease of protein Z level maybe a predictor for coronary heart disease.

Background Liver X receptors (LXRs) are members of the nuclear hormone receptor superfamily which involve in energy metabolism of intracellular cholesterol and glucose regulation.Objective To investigate the effect of Liver X receptors (LXRs) agonists on the hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ) in the murine HL-1 cardiomyocytes in vitro.Methods Hypertrophy in murine HL-1 cardiomyocytes was induced by Ang Ⅱ and treated with LXRs agonist T0901317 (1 ?mol/L).Immunofluorescent staining was carried out to identify the HL-1 cells.The surface area of HL-1 cells was analyzed by using NIH Image J software.The synthetic rate of protein in HL-1 cells was detected by {}3H leucine incorporation.The mRNA level of atrial natriuretic peptide (ANP) was measured by quantitative realtime PCR.Results HL-1 cells hypertrophy induced by Ang Ⅱ were manifested by the increases in surface area,mRNA expression of ANP,and {}3H leucine incorporation(control group vs Ang Ⅱ group:cell surface:1.00?0.16 vs 2.00?0.21,ANP mRNA:1.00?0.02 vs 1.58?0.27,{}3H leucine incorporation:1.00?0.03 vs 1.44?0.07,respectively,all P

OBJECTIVETo explore the relationship of apolipoprotein E (ApoE) genotype with hypertriglyceridemia-associated recurrent acute pancreatitis.

METHODSTaking the fasting serum triglyceride (TG) level > or = 2.3 mmol/L as hypertriglyceridemia, ApoE genotypes in 115 patients with hypertriglyceridemia-associated recurrent acute pancreatitis were assessed by polymerase chain reaction. According to the fasting serum TG level, all patients were divided into 3 groups: TG mild elevation group (2.3 mmol/L < or = TG < 5.5 mmol/L, Group A), TG moderate elevation group (5.5 mmol/L < or = TG < 11.3 mmol/L, Group B), and TG severe elevation group (TG > or = 11.3 mmol/L, Group C).

RESULTSGroup C had significantly fewer patients with biliary tract disease, improper diet and heavy alcohol consumption, and significantly more patients with passed history of moderate-severe hypertriglyceridemia than Group A and B (P < 0.05). The proportion of patients with E3/4, E3/2, E2/4 and E2/2 genotypes and gene frequency for epsilon 2 and epsilon 4 alleles are significantly higher in Group C than in Group A and B(P < 0.05). Group B had significantly more patients with E3/2 genotype and higher gene frequency for epsilon 2 allele than Group A (P < 0.05).

CONCLUSIONSApo epsilon 2 and epsilon 4 alleles are closely related to moderate-severe hypertriglyceridemia-associated recurrent acute pancreatitis.

Acute Disease ; Adolescent ; Adult ; Alleles ; Apolipoproteins E ; genetics ; Female ; Gene Frequency ; Genotype ; Humans ; Hypertriglyceridemia ; complications ; Male ; Middle Aged ; Pancreatitis ; complications ; genetics ; Recurrence

OBJECTIVETo investigate the role of liver X receptors (LXRs) on endothelin-1 (ET-1) induced murine HL-1 cardiomyocytes hypertrophy.

METHODSCultured murine HL-1 cardiomyocytes were divided into four experiment groups: (1) CONTROL GROUP:treated with DMSO; (2) T0901317 group:treated with LXRs agonist T0901317 (1 µmol/L); (3) ET-1 group:treated with ET-1 (1 nmol/L); (4) T0901317 + ET-1 group:treated with T0901317 (1 µmol/L) for 8 hours, then treated with ET-1 (1 nmol/L). Twenty-four hours later, immunofluorescent staining was performed on HL-1 cells, the surface area of HL-1 cells was analyzed with NIH Image J software, and the synthetic rate of protein in HL-1 cells was detected by (3)H-leucine incorporation. The mRNA level of atrial natriuretic peptide (ANP) and β-myosin heavy chain (β-MyHC) was measured by quantitative realtime PCR. The effect of T0901317 on mRNA expression of ANP was also detected after LXRs gene silencing.

RESULTSThe surface area of HL-1 cells, mRNA expression of ANP and β-MyHC, and (3)H-leucine incorporation in ET-1 group were 2.00 ± 0.29, 1.98 ± 0.47, 2.13 ± 0.39 and 1.79 ± 0.17, respectively, which were significantly higher than those of control group (1.00 ± 0.26, 1.00 ± 0.21, 1.00 ± 0.31 and 1.00 ± 0.03, respectively, all P < 0.05). Compared with ET-1 group, the surface area of HL-1 cells, mRNA expression of ANP and β-MyHC, and (3)H-leucine incorporation were significantly decreased in T0901317 + ET-1 group (1.24 ± 0.25, 1.19 ± 0.21, 1.48 ± 0.27 and 1.15 ± 0.11, respectively, all P < 0.05). After inhibition of LXRα/β expression in HL-1 cardiomyocytes using the specific siRNAs, the mRNA expression of ANP in T0901317 + ET-1 group was 1.78 ± 0.05, which was similar as that in ET-1 group (1.94 ± 0.17, P > 0.05).

CONCLUSIONT0901317, an agonist of LXRs, could inhibit ET-1 induced cardiac hypertrophy in vitro, and LXR ligand-mediated inhibition on ANP mRNA expression by T0901317 is receptor dependent.

Animals ; Cardiomegaly ; metabolism ; Cell Line ; Endothelin-1 ; metabolism ; Hydrocarbons, Fluorinated ; pharmacology ; Liver X Receptors ; Mice ; Myocytes, Cardiac ; drug effects ; metabolism ; Orphan Nuclear Receptors ; agonists ; metabolism ; Signal Transduction ; drug effects ; Sulfonamides ; pharmacology

OBJECTIVETo measure the effect of atorvastatin on COX-2 expression in monocytes in patients with acute myocardial infarction (AMI).

METHODSForty patients with AMI (AMI group) and 18 patients with stable coronary heart disease (control group) were enrolled, and patients with AMI were randomly given routine therapy (n = 20) and routine therapy plus atorvastatin (20 mg/day, n = 20) for a week. Peripheral blood monocytes for each participant including patients with AMI were isolated and cultured for 24 hours. During the culture, monocytes in patients with pretreatment AMI were incubated with celecoxib in different concentration (0, 0.1, 1 and 10 micromol/L). COX-2 mRNA expression in monocytes was measured by reverse transcription polymerase chain reaction (RT-PCR); concentrations of interleukin-6 (IL-6) in supernatant from monocytes and plasma hs-CRP levels were measured by using enzyme-linked immunosorbent assay (ELISA).

RESULTSCOX-2 expression in monocytes in patients with AMI (0.92 +/- 0.13) was significantly higher than that in the control subjects (0.19 +/- 0.08), and decreased by 66% after atorvastatin (compared with that on routine therapy, P < 0.05); IL-6 secretions of monocytes in the AMI group (204.8 +/- 45.6 ng/L) increased dramatically compared with those in the control group (40.9 +/- 1.2 ng/L, P < 0.05), and reduced dramatically by 58% when incubated with 10 micromol/L celecoxib (P < 0.05) in a concentration-dependent manner; plasma levels of CRP in the AMI group (43.3 +/- 14.9 mg/L) significantly increased compared with those in the control group (1.7 +/- 0.8 mg/L), and reduced by 62% after atorvastatin (compared with those in the routine therapy group, P < 0.05). COX-2 expression in monocytes in the AMI group was positively correlated with both secretions of IL-6 and plasma level of CRP (r = 0.636 and 0.662, respectively, both P < 0.05).

CONCLUSIONSThere is an inflammatory activation in peripheral blood monocytes in patients with early AMI, and the monocytes-derived COX-2 may play an important role in promoting early inflammatory process. Atorvastatin may decrease COX-2 expression in peripheral blood monocytes in patients with AMI and cyclooxygenase-dependent pathway might be correlated with the anti-inflammation mechanism of statin.

Aged ; Atorvastatin Calcium ; Cyclooxygenase 2 ; metabolism ; Female ; Heptanoic Acids ; therapeutic use ; Humans ; Inflammation ; Interleukin-6 ; metabolism ; Leukocytes, Mononuclear ; drug effects ; metabolism ; Male ; Middle Aged ; Myocardial Infarction ; drug therapy ; metabolism ; Pyrroles ; therapeutic use ; RNA, Messenger ; genetics

OBJECTIVETo investigate the relationship between apolipoprotein E (ApoE) gene polymorphism and serum lipid profile.

METHODSPolymerase chain reaction-restricted fragments length polymorphism (PCR-RFLP) was used to determine ApoE genotype on 1452 subjects including 1101 cases with cardio cerebrovascular disease including 379 cases with cerebral infarction, 313 cases with cerebral hemorrhage, 257 cases with coronary heart disease, and 152 cases with other types and on 351 healthy controls.

RESULTSAfter adjusting for age, sex and BMI, the subjects with ApoE4 carriers had significantly higher levels of total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C) and ApoB than those with ApoE2 carriers and ApoE3/3 (P < 0.05), and higher level of triglyceride(TG) than those with ApoE3/3 (P < 0.05), while the subjects with ApoE2 carriers had significantly higher levels of high density lipoprotein-cholesterol (HDL-C) than those with ApoE4 (P < 0.05). The effects of ApoE polymorphism exhibited similarity in different sex and age of subjects. Linear regression analysis showed that unlike ApoE3/3, the HDL-C level in ApoE2 carriers tend upward with age (beta = 0.178, P = 0.015), significantly higher than ApoE4 carriers and ApoE3/3 in the cohort of 65-74 years (P < 0.05). The level of TC and TG in ApoE4 carriers had a tendency of downward with age (p = -0.179, P = 0.009; beta = -0.147, P = 0.032).

CONCLUSIONApoE gene polymorphism affected profile of blood lipids and the effects were found in different sex and age. The degrees of effects related to ApoE2 carriers and ApoE4 carriers to blood lipid level seemed to be related to age.

Adult ; Age Factors ; Aged ; Aged, 80 and over ; Apolipoproteins E ; genetics ; Case-Control Studies ; Female ; Genotype ; Humans ; Lipids ; blood ; Male ; Middle Aged ; Polymorphism, Genetic ; Sex Factors ; Young Adult

Objective To observe the effects of triptolide on drebrin and cofilin expression in the hippocampus of rats with Alzheim-er's disease (AD). Methods Sixty male Sprague-Dawley rats were equally divided into control group, model group and triptolide-treated group with 20 cases in each group. The AD model was established with unilateral injection of beta amyloid 1-40 (Aβ1- 40) into hippocampus in rats. The control group was established with unilateral injection of normal saline with the same volume into hippocampus in rats. The triptolide-treated group was administered triptolide intraperi-toneally, 0.4 mg/kg, once a day, for 15 days after modeling. Spine density of hippocampal neurons was assayed by Golgi staining. Drebrin and cofilin expression of hippocampal neurons was assayed by immunohistochemical staining and reverse transcription polymerase chain reaction (RT-PCR). Results The spine density of hippocampal neurons was higher in the triptolide-treated group than in the model group (P<0.05). The average optical density of drebrin was higher in the triptolide-treated group than in the the model group (P<0.01), while the cell number and average optical density of cofilin were lower (P<0.05). The drebrin mRNA expression was higher in the triptolide-treated group than in the model group (P<0.05), and the cofilin mRNA expression was lower (P<0.01). Conclusion Triptolide may delay the degeneration of dendritic spines in hippocampal neurons of AD rats by regulating the expression of drebrin and cofilin.

Objective To investigate the relationship between the Apolipoprotein(Apo)A5-1131T>C polymorphism and strokes.Methods Polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP)and polyacrylamide gel eletrophoresis(PAGE)wefe used to analyze the genotypic polymorphism in 327 patients with stroke(including 194 cerebral infarction patients and 133 cerebral hemorrhage patients)and 311 healthy controls.The levels of serum lipids profiles were also measuredby enzymatic methods. Results The frequency of the-1131C allele in cerebral infarction patients was significantly higher than that of the control group(44.1% vs 32.3%,P<0.05),but there was not statisticai difference between cerebral hemorrhage patients and controls on the-1131C allele frequeney(35.4%vs 32.3%,P>0.05).Compared with the noncamers,the C carriers also had a higher triglyceride(TG)levels in stroke group[(1.45±0.77)vs(1.69±1.06)mmol/L,P<0.05],but the total cholesterol(TC),high density lipoprotein cholesterol(HDL-C)and low density lipoprotein cholesterol (LDL-C)levels did not show statistical differences in various genotypes(P>0.05).Unadjusted Logistic regression analysis indicated that TC+CC genotype of A5-1131T>C was significantly associated with the presence of cerebral infarction,but not with hemorrhage stroke.Logistic regression analysis adjustedfor BMI,presence of hypertension or diabetes and HDL-C levels revealed that TC+CC genotype was an independent risk factor for cerebralinfarction(OR=1.932,95%CI:1.057-3.532,P=0.032). Conclusion The ApoA5-1131C allele frequency of the patients with cerebral infarction is significantly higher than controls.ApoA5-1131T>C polymorphism has a significant influence on serum TG levels.The ApoA5-1131T>C variant is associated with an increased susceptibility for ischemic stroke.