We present a new technological approach for in situ investigation of long-term impacts of elevated CO2 concentration (EC) on juvenile forests characterised by an intensive community level and canopy closure phase. Construction of the glass domes is based on the properties of earlier tested open-top chambers (OTCs). An air climatisation device together with an adjustable window system, that forms the shell cover of the domes, is able to keep the required [CO2] in both time and spatial scales with the relatively small consumption of supplied CO2. This is achieved by half-closing the windows on the windward side. We evidenced good coupling of treated trees to the atmosphere, including mutual interactions among trees. The semi-open design of the domes moderates the problems of strong wind, humidity, and temperature gradients associated with OTCs. The frequency distributions of the environmental variations within the domes indicate that: air temperature is maintained within the ambient range ±1.0 °C for ca. 80 % of the time, and changes in the relative air humidity vary from -15 to 0 % for ca. 82 % of the time. The most important chamber effect is associated with the penetration of solar irradiance, which is reduced by 26 % compared to the open condition outside the domes. The dimensions of the domes are 10×10 m in length and 7 m high in the central part. The experiment was done in three identical stands of twelve-year-old Norway spruce trees. The 56 trees are planted at two different spacings to estimate the impacts of stand spatial structure in relation to EC. and O. Urban ... [et al.].
Dyslipidemia and inflammation play an important role in the pathogenesis of cardiovascular and liver disease. Fenofibrate has a well-known efficacy to reduce cholesterol and triglycerides. Combination with statins can ameliorate hypolipidemic and anti-inflammatory effects of fibrates. In the current study, we tested the anti-inflammatory and metabolic effects of fenofibrate alone and incombination with rosuvastatin in a model of inflammation and metabolic syndrome, using spontaneously hypertensive
rats expressing the human C-reactive protein transgene (SHR-CRP transgenic rats). SHR-CRP rats treated with fenofibrate alone (100 mg/kg body weight) or in combination with rosuvastatin (20 mg/kg body weight) vs. SHR-CRP untreated controls showed increased levels of proinflammatory marker IL6, increased concentrations of ALT, AST and ALP, increased oxidative stress in the liver and necrotic changes of the liver. In addition, SHR-CRP rats treated with fenofibrate, or with fenofibrate combined with rosuvastatin vs. untreated controls, exhibited increased serum triglycerides and reduced HDL cholesterol, as well as reduced hepatic triglyceride, cholesterol and glycogen concentrations. These findings suggest that in the presence of high levels of human CRP, fenofibrate can induce liver damage even in combination with rosuvastatin. Accordingly, these results caution against the possible hepatotoxic effects of fenofibrate in patients with high levels of CRP.
Brown adipose tissue (BAT) plays an important role in lipid and glucose metabolism in rodents and possibly also in humans. Identification of genes responsible for BAT function would shed light on underlying pathophysiological mechanisms of metabolic disturbances. Recent linkage analysis in the BXH/HXB recombinant inbred (RI) strains, derived from Brown Norway (BN) and spontaneously hypertensive rats (SHR), identified two closely linked quantitative trait loci (QTL) associated with glucose oxidation and glucose incorporation into BAT lipids in the vicinity of Wars2 (tryptophanyl tRNA synthetase 2 (mitochondrial)) gene on chromosome 2. The SHR harbors L53F WARS2 protein variant that was associated with reduced angiogenesis and Wars2 thus represents a prominent positional candidate gene. In the current study, we validated this candidate as a quantitative trait gene (QTG) using transgenic rescue experiment. SHR-Wars2 transgenic rats with wild type Wars2 gene when compared to SHR, showed more efficient
mitochondrial proteosynthesis and increased mitochondrial respiration, which was associated with increased glucose oxidation and incorporation into BAT lipids, and with reduced weight of visceral fat. Correlation analyses in RI strains showed that increased activity of BAT was associated with amelioration of insulin resistance in muscle and white adipose tissue. In summary, these results demonstrate important role of Wars2 gene in regulating BAT function and consequently lipid and glucose metabolism.