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Objective To evaluate the preventive effect of a high loading dose of Rosuvastatin on contrast-induced nephropathy (CIN )after PCI in high-risk patients. Methods A total of 199 patients with diabetes mellitus and chronic kidney disease (CKD)(45< GFR<90 ml · min-1 · 1.73 m -2 )scheduled for PCI were included and randomized into two groups ,one group receiving a high loading dose of rosuvastatin(20 mg Rosuvastatin in 3 days before and after PCI ,Rosuvastatin Group-RG)and the other one (Control-Group-CG)receiving 10 mg/d Rosuvastatin.Serum samples were collected at baseline ,48 and 72 hours after PCI for testing of creatinine ,C-reactive protein (CRP ) , interleukin-6(IL-6) ,and malondialdehyde(MDA). Results Post-PCI levels of CRP ,IL-6 ,and MDA in the RG were significantly lower than in the CG [(10.44 ± 3.82 )mg/L vs. (12.62 ± 3.68) mg/L , (14.66 ± 3.61 )ng/L vs. (16.41 ± 4.73 )ng/L ,(7.2 ± 2.2) mmol/L vs. (8.6 ± 1.5) mmol/L ,P=0.000 ,0.004 ,and 0.000 ,respectively].The levels of creatinine after PCI in both groups were found to be higher than baseline levels ,while the increase in the RG was smaller than in the CG [(10 ± 10)μmol/L vs. (15 ± 15)μmol/L ,P=0.007]. The incidence of CIN in the RG was lower than in the CG (8.2％ vs.19.8％ ,χ2 = 5.573 ,P= 0.018). Conclusions High-dose Rosuvastatin treatment can reduce the incidence of CIN in high-risk patients undergoing PCI.
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Objective To investigate expression differences of neutrophil and mononuclear phagocyte related gene mRNAs among acute myocar-dial infarction (AMI), stable angina (SA) and control groups, and then discuss their expression characteristics in the stable angina pectoris (SAP) and AMI stages of coronary artery disease (CAD). Methods Whole Human Genome Oligo Microarrays were applied to assess the differential expression characteristics of neutrophil and mononuclear phagocyte related mRNAs in patients with AMI (n=20), SA (n=20) and controls (n=20). Results (1) Almost all colony-stimulating factors (CSF) and their receptors related mRNAs was up-regulated in AMI and SA groups compared with the control group, and the expression of granulocyte-macrophage colony stimulating factor receptor (GM-CSFR) and granulocyte colony stimulating factor receptor (G-CSFR) mRNAs in the AMI group was significantly up-regulated com-pared with the other two groups (P<0.01). (2) The expression of mRNAs related to monocyte chemoattractant protein-1 (MCP-1), CCR2 (MCP-1 receptor) and CXCR2 (IL-8 receptor) was significantly up-regulated (P<0.01) in AMI group compared with SA and control groups. IL-8 mRNA expression in the AMI group was clearly higher than the controls (P<0.05). (3) All mRNAs expression related to opsonic re-ceptors (IgG FcR and C3bR/C4bR) was significantly up-regulated in AMI group compared with SA and control group (P<0.01), and the SA group showed an upward trend compared with controls. (4) Most pattern recognition receptor (PRR)-related mRNAs expression was up-regulated in AMI group compared with SA and control groups. Most toll-like receptor (TLR) mRNAs expression was significantly up-regulated (P<0.01) than the SA and control groups;macrophage scavenger receptor (MSR) mRNA was significantly up-regulated in AMI group compared with the control group (P<0.01), and the SA group showed an upward trend compared with the controls. Conclusions The expression of most neutrophil and mononuclear-macrophage function related genes mRNAs was significantly up-regulated by stages during the progression of CAD, suggesting that the adhesive, chemotactic and phagocytic functions of neutrophil and mononuclear-ma-crophage were strengthened in the occurrence and development of coronary atherosclerosis and AMI. This also showed a stepped up-ward trend as the disease progressed.
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PubMed,Embase,Cochrane Library,and ISI web were searched without any limitations with regard to publication date or language,as well as the references of qualifying articles.All kinds of cohort studies comprising the risk of gastric cancer between diabetic patients and control subjects were included.We excluded studies that investigated only mortality but not incidence.25 studies met our criteria,and the qualities of these studies were evaluated using the Newcastle-Ottawa Quality Assessment Scale.Statistical analyses were carried out with STATA software version 12.0.A random-effects model meta-analysis showed an increased risk of gastric cancer in diabetic patients (RR =1.20,95 ％ CI 1.12-1.28).Subgroup analyses indicated that this result persisted in studies of both male(RR =1.15,95％ CI 1.02-1.29) and female (RR =1.29,95％ CI 1.09-1.53) subjects,in studies of European countries(RR =1.25,95％ CI 1.07-1.46) and Asia countries (RR =1.18,95％ CI 1.09-1.28).Compared with nondiabetics,the incidence of gastric cancer may be increased by approximately 20％ in diabetics.Thus diabetes may be an independent risk factor for gastric cancer.This effect tends to be more significant in type 1 and female patients.