AimsWe used virtual histology-intravascular ultrasound (VH-IVUS) to evaluate the relation between coronary plaque characteristics and no-reflow in acute coronary syndrome (ACS) patients.Methods and resultsA total of 190 consecutive ACS patients were imaged using VH-IVUS and analysed retrospectively. Angiographic no-reflow was defined as TIMI flow grade 0, 1, and 2 after stenting. Virtual histology-intravascular ultrasound classified the colour-coded tissue into four major components: fibrotic, fibro-fatty, dense calcium, and necrotic core (NC). Thin-cap fibroatheroma (TCFA) was defined as focal, NC-rich (≥10% of the cross-sectional area) plaques being in contact with the lumen in a plaque burden ≥40%. Of the 190 patients studied at pre-stenting, no-reflow was observed in 24 patients (12.6%) at post-stenting. The absolute and %NC areas at the minimum lumen sites (1.6 ± 1.2 vs. 0.9 ± 0.8 mm2, P < 0.001, and 24.5 ± 14.3 vs. 16.1 ± 10.6%, P = 0.001, respectively) and the absolute and %NC volumes (30 ± 24 vs. 16 ± 17 mm3, P = 0.001, and 22 ± 11 vs. 14 ± 8%, P < 0.001, respectively) were significantly greater, and the presence of at least one TCFA and multiple TCFAs within culprit lesions (71 vs. 36%, P = 0.001, and 38 vs. 15%, P = 0.005, respectively) was significantly more common in the no-reflow group compared with the normal-reflow group. In the multivariable analysis, %NC volume was the only independent predictor of no-reflow (odds ratio = 1.126; 95% CI 1.045–1.214, P = 0.002).ConclusionIn ACS patients, post-stenting no-reflow is associated with plaque components defined by VH-IVUS analysis with larger NC and more TCFAs.

In this study, the amount of calcite precipitate resulting from microbially induced calcite precipitation (MICP) was estimated in order to determine the optimal conditions for precipitation. Two microbial species (Staphylococcus saprophyticus and Sporosarcina pasteurii) were tested by varying certain parameters such as (1) initial potential of hydrogen (pH) of urea-CaCl2 medium, (2) temperature during precipitation, and (3) the reaction duration. The pH values used for testing were 6, 7, 8, 9, and 10, the temperatures were 20, 30, 40, and 50 °C, and the reaction durations were 2, 3, and 4 days. Maximum calcite precipitation was observed at a pH of 7 and temperature of 30 °C. Most of the precipitation occurred within a reaction duration of 3 days. Under similar conditions, the amount of calcite precipitated by S. saprophyticus was estimated to be five times more than that by S. pasteurii. Both the species were sensitive to temperature; however, S. saprophyticus was less sensitive to pH and required a shorter reaction duration than S. pasteurii.

No abstract

No abstract

The protective effects of common dandelion leaf water extract (DLWE) were investigated by carbon tetrachloride (CCl4) induced hepatitis in Sprague-Dawley rats. The animals were divided into five groups: normal control, DLWE control, CCl4 control, and two DLWE groups (0.5 and 2 g/kg bw). After 1 week of administering corresponding vehicle or DLWE, a single dose of CCl4 (50% CCl4/olive oil; 0.5 mL/kg bw) was administered 24 h before killing in order to produce acute liver injury. The DLWE treatment significantly decreased CCl4-induced hepatic enzyme activities (AST, ALT and LDH) in a dose dependent manner. Also, the obstructed release of TG and cholesterol into the serum was repaired by DLWE administration. Hepatic lipid peroxidation was elevated while the GSH content and antioxidative enzyme activities were reduced in the liver as a result of CCl4 administration, which were counteracted by DLWE administration. Furthermore, the hepatocytotoxic effects of CCl4 were confirmed by significantly elevated Fas and TNF-α mRNA expression levels, but DLWE down-regulated these expressions to the levels of the normal control. Highly up-regulated cytochrome P450 2E1 was also lowered significantly in the DLWE groups. These results indicate that DLWE has a protective effect against CCl4-induced hepatic damage with at least part of its effect being attributable to the attenuation of oxidative stress and inflammatory processes resulting from cytochrome P450 activation by CCl4.