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1.  Cystatin C and asymptomatic coronary artery disease in patients with metabolic syndrome and normal glomerular filtration rate 
All of the components of Metabolic syndrome (MetS) have been regarded as risk factors for coronary artery disease (CAD). Early detection of CAD in asymptomatic patients with MetS remains a challenge. Cystatin C,which has been proposed as a novel marker of renal dysfunction,is correlated with mortality in CAD, The purpose of the study was to evaluate whether cystatin C is a potential marker of asymptomatic CAD in MetS patients with normal kidney function.
A total of 211asymptomatic MetS patients without prior history of CAD patients were included in a cross-sectional study. Patients were divided into MetS with asymptomatic CAD (n = 136) and MetS without CAD (n = 75) groups according to coronary angiograph results. Serum cystatin C levels were measured using particle enhanced immunonephelometric assays. We first assessed whether there is an independent association of cystatin C with the presence and severity of asymptomatic CAD. Then, we investigated the association between cystatin C and other biochemical risk factors for atherosclerosis.
Serum cystatin C levels in patients with asymptomatic CAD were significantly higher than those without CAD (P = 0.004). A multiple logistic regression analysis demonstrated cystatin C was independently associated with the presence of asymptomatic CAD (OR = 1.326, 95%CI: 1.086-1.619). On receiver operating characteristics (ROC) analysis, the area under the curve (AUC) was 0.622 (95 % CI: 0543–0.701, P = 0.003), and cystatin C showed a moderate predictive value. Furthermore, cystatin C was independently correlated with Gensini score (standardized β = 0.183, P = 0.007), and serum cystatin C levels increased with the increasing of number of disease vessels (P = 0.005). In a multiple stepwise regression analysis, uric acid (UA)(P < 0.001), body mass index (BMI)(P = 0.002), triglyceride(TG)(P = 0.03), estimated glomerular filtration rate (eGFR)(P < 0.001), and fibrinogen(P = 0.001) were independently associated with cystatin C.
Serum cystatin C in our study was significantly associated with the presence and severity of asymptomatic CAD in MetS patients with normal kidney function, suggesting that cystatin C is probably more than a marker of glomerular filtration rate.
PMCID: PMC3473246  PMID: 22978689
Cystatin C; Gensini score; Metabolic syndrome; Asymptomatic coronary artery disease
2.  A high normal TSH level is associated with an atherogenic lipid profile in euthyroid non-smokers with newly diagnosed asymptomatic coronary heart disease 
Serum lipid profiles may be influenced by thyroid function, but the detailed mechanism remains unclear. Increasing evidence suggests that thyrotropin (TSH) may exert extra-thyroidal effects. The goal of this study was to evaluate the relationship between serum TSH levels and the lipid profiles in euthyroid non-smokers with newly diagnosed asymptomatic coronary heart disease (CHD).
This was a retrospective study of 406 euthyroid non-smokers (187 males and 219 females) with newly diagnosed asymptomatic CHD from 2004 to 2010 in Jinan, China. Lipid parameters and the levels of TSH, FT3, and FT4 were determined. Multiple linear regression analysis and Logistic regression analysis were used to assess the influence of TSH on the lipid profiles and the risks of dyslipidemia.
The TSH level, even within the normal range, was positively and linearly correlated with total cholesterol (TC), non-high density lipoprotein cholesterol (non-HDL-C) and triglycerides (TG) (Beta = 0.173, 0.181 and 0.103, respectively, P < 0.01 in all). With 1 mIU/L rise of TSH, the levels of TC, TG and non-HDL-C will increase by 1.010, 1.064, and 1.062 mmol/L, respectively. The odds ratio of hypercholesterolemia and hypertriglyceridemia with respect to the serum TSH level was 1.640 (95% CI 1.199-2.243, P = 0.002) and 1.349 (95% CI 1.054-1.726, P = 0.017), respectively.
TSH levels were correlated in a positive linear manner with the TC, non-HDL-C and TG levels in euthyroid non-smokers with newly diagnosed asymptomatic CHD. TSH in the upper limits of the reference range might exert adverse effects on lipid profiles and thus representing as a risk factor for hypercholesterolemia and hypertriglyceridemia in the context of CHD.
PMCID: PMC3331821  PMID: 22448646
TSH; Cholesterol; Triglyceride; Coronary heart disease
3.  Morpholinium 4-amino-5-meth­oxy-2-methyl­benzensulfonate 
In the crystal structure of the title compound, C4H10NO+·C8H10NO4S−, the components are linked by N—H⋯O hydrogen bonds, forming a centrosymmetric 2:2 aggregate. The aggregates are further connected by N—H⋯O hydrogen bonds between the anions, forming a double-tape structure along the a axis.
PMCID: PMC3051928  PMID: 21522385
4.  Influence of Ketotifen, Cromolyn Sodium, and Compound 48/80 on the survival rates after intestinal ischemia reperfusion injury in rats 
BMC Gastroenterology  2008;8:42.
Mast cells were associated with intestinal ischemia-reperfusion injury, the study was to observe the influence of Ketotifen, Cromolyn Sdium(CS), and Compound 48/80(CP) on the survival rates on the third day after intestinal ischemia-reperfusion injury in rats.
120 healthy Sprague-Dawley rats were randomly divided into 5 groups, Sham-operated group (group S), model group (group M), group K, group C and group CP. Intestinal damage was triggered by clamping the superior mesenteric artery for 75 minutes, group K, C, and CP were treated with kotifen 1 mg·kg-1, CS 50 mg·kg-1, and CP 0.75 mg·kg-1 i.v. at 5 min before reperfusion and once daily for three days following reperfusion respectively. Survival rate in each group was recorded during the three days after reperfusion. All the surviving rats were killed for determining the concentration of serum glutamic-oxaloacetic transaminase(AST), glutamic pyruvic transaminase(ALT), the ratio of AST compare ALT(S/L), total protein(TP), albumin(ALB), globulin(GLB), the ratio of ALB compare GLB(A/G), phosphocreatine kinase(CK), lactate dehydrogenase(LDH), urea nitrogen(BUN) and creatinine(CRE) at the 3rd day after reperfusion. And ultrastructure of IMMC, Chiu's score, lung histology, IMMC counts, the levels of TNF-α, IL-1β, IL-6 and IL-10 of the small intestine were detected at the same time.
Intestinal ischemia-reperfusion injury reduced the survival rate. The concentrations of TP, ALB and level of IL-10 in intestine in group M decreased significantly while the concentrations of S/L, LDH and the levels of IL-6 and TNF-α in intestine increased significantly compared with group S (P < 0.05). Treatment with Ketotifen and CS increased the survival rate compared with group M (P < 0.05), attenuated the down-regulation or up-regulation of the above index (P < 0.05). Treatment with CP decreased the survival rate on the 3rd day after reperfusion compared with group M(P < 0.05). Group K and C had better morphology in IMMC in the small intestine and in the lungs than in group M and CP, although the Chiu's score and IMMC counts remained the same in the five groups(P > 0.05).
Mast cell inhibition after ischemia prior to reperfusion and following reperfusion may decrease the multi-organ injury induced by intestine ischemia reperfusion, and increase the survival rates.
PMCID: PMC2564972  PMID: 18808687

Results 1-4 (4)