It is still unclear whether Helicobacter pylori infection is associated with risk factors for coronary artery disease. The aim of this study was to determine whether eradication of H. pylori infection affects serum lipid levels and C-reactive protein (CRP) levels. Seventy-eight patients who had H. pylori antigen positivity in their stools were enrolled. Clarithromycin, 1 g/day, amoxicillin, 2 g/day, and omeprazole, 40 mg/day, were given for 14 days. Serum total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride (TG), and CRP were measured at baseline and 8 weeks after therapy. According to H. pylori stool antigen study after 8 weeks, individuals in whom H. pylori was eradicated were recruited as group A and those in whom H. pylori was not eradicated formed group B. Group A comprised 57 patients, and group B 21 patients. Patients in group A comprised 32 women and 25 men and their ages ranged from 35 to 59 years. Patients in group B included 13 women and 8 men, aged 32-61 years. No significant difference in LDL, TC, or TG serum levels were found between group A and group B. Although CRP and HDL serum levels were found to be the same before and after treatment in group B, CRP levels were found to decrease and HDL levels to increase significantly in group A (P < 0.05). We conclude that H. pylori infection may affect lipid metabolism in a way that could increase the risk of atherosclerosis. Thus H. pylori infection is an independent risk factor for coronary artery disease.

In this rat model study we evaluated whether pretreatment with simvastatin affects the severity of acute lung injury caused by intestinal ischemia-reperfusion (I/R). Twenty-four animals were randomly allocated to three equal groups (sham, control, simvastatin). The simvastatin group was pretreated with simvastatin 10 mg x kg(-1) x day(-1) for 3 days, whereas the other groups received placebo. The simvastatin and control groups underwent 60 min of superior mesenteric artery occlusion and 90 min of reperfusion. Compared with the simvastatin group, the control group exhibited significantly more severe intestinal I/R-induced acute lung injury, as indicated by lower Pao2 and oxygen saturation (P = 0.01 and P = 0.005, respectively) and higher mean values for neutrophil infiltration of the lungs (P = 0.003), total lung histopathologic injury score (P = 0.003), lung wet-to-dry weight ratio (P = 0.009), and lung-tissue malondialdehyde levels (P = 0.016). The control and simvastatin groups had similar serum levels and similar bronchoalveolar lavage fluid levels of cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-alpha) and P-selectin at all measurements, except for a significantly higher level of bronchoalveolar lavage fluid P-selectin in the control group (P = 0.006). Pretreatment with simvastatin reduces the severity of acute lung injury induced by intestinal I/R in rats.

This study aimed to clarify the local and systemic immune responses at different burn depths. Thirty female Sprague-Dawley rats were divided into three groups: full-thickness (F), partial-thickness (P), and Sham (S). Burns were induced on three separate areas on the dorsums of rats. Serum levels of interferon (IFN)-gamma; tumor necrosis factor-alpha; interleukin (IL)-1, IL-6, and IL-10 were measured once in controls and 1 hour after burn, 48 hours after burn, and 7 days after burn in F and P groups. Neutrophils, CD68-positive macrophages, HLA-DR-positive cells, and CD3-positive lymphocytes were graded semiquantitatively, and the wounds were examined once in shams and at 1 hour after burn, 48 hours after burn, and 7 days after burn in F and P groups. IL-6 levels were highest in F group, followed by P group 1 hour after burn. IFN-gamma levels were higher in the F group; IL-1 levels were higher in F and P groups at 1 hour after burn. Local accumulation of macrophages was similar in F and P groups. Lymphocytes were denser in P group at 1 hour after burn, and neutrophils were denser in F group at 7 days after burn. We suggest that early elevations of IL-6 and IFN-gamma prolong inflammation in full-thickness burns. Modulation of proinflammatory cytokines may improve burn wound treatment.

Treatment with activated protein C significantly improved hemodynamics after ischemia-reperfusion and reduced ischemia-reperfusion-induced myocardial apoptosis in rats.

No abstract