Climatology of Ultraviolet Budgets using Earth Observation (CUBEO): mapping UV from the perspective of risk assessments : final report

No RIVM report number in publicationThe use of satellite data to construct ground level UV-radiation maps offers a unique opportunity to investigate geographical and temporal variability of ground level UV-radiation levels related to atmospheric changes, like ozone depletion or cloud changes. The calculation of long term yearly UV-doses in combination with dose-effect models for UV-related effects, like skin cancer, further enhances the application of UV-maps as a powerful tool to support environmental assessments. This report describes the results obtained in the CUBEO-project: a Climatology of Ultraviolet Budgets using Earth Observation. The project aimed at the development and validation of UV-mapping methods that can be applied in environmental assessments. The results indicated that the satellite derived cloud correction provides accurate and representative results if the ground albedo is low. The comparison with ground based UV-measurements at different sites in Europe shows an agreement for the yearly UV-dose within 10%. An indication of the long term stability of the UV-mapping methods is obtained by means of a systematic comparison of UV-doses derived from ground based ozone and cloud data and doses derived from satellite observations over a period of nearly 20 years. The European maps of changes in UV-budgets at the ground and associated excess skin cancer risks have been reported in national and international state of the environment reports published by the National Institute of Public Health and the Environment (RIVM) and/or the European Environmental Agency (EEA). These state of the environment reports contribute to the provision of information necessary for framing and implementing sound and effective environmental policies. This investigation has been performed by order and for the account of BCRS, EU and RIVM, within the framework of the projects CUBEO and MAUVE.Beleidscommissie Remote Sensing (BCRS

Woody plant communities of isolated Afromontane cloud forests in Taita Hills, Kenya

In the Taita Hills in southern Kenya, remnants of the original Afromontane forest vegetation are restricted to isolated mountain peaks. To assess the level of degradation and the need for forest restoration, we examined how forest plant communities and their indicator species vary between and within remnant patches of cloud forest. We used ordinal abundance data to compare plant communities in eight forest fragments. We also analyzed data on the diversity and abundance of trees in 57 0.1 ha plots to compare tree communities within and between the largest two of these fragments, Ngangao (120 ha) and Mbololo (220 ha). The extant vegetation of the Taita Hills at landscape scale consists of secondary moist montane to intermediate montane forest. There was a high species dissimilarity between fragments (69%). Variation in species composition coincided with an abiotic gradient related to elevation. At plot level, secondary successional species and species of forest edges were most abundant and most frequent. Inferred clusters of plots almost entirely coincided with the two forest fragments. Indicator species associated with forest margins and gaps were more frequent in the smaller of the two forest fragments, while indicators for the larger fragment were more typical for less disturbed moist forest. Abiotic site variability but also different levels of disturbance determine site-specific variants of the montane forest. Conservation efforts should not only focus on maintaining forest quantity (size), but also on forest quality (species composition). Late-successional rainforest species are underrepresented in the woody plant communities of the Taita Hills and assisting restoration of viable populations of cloud forest climax tree species is urgently needed

Problems of methodological determination of the place of financial and budgetary control in the system of state financial control

The relevance of this report due to the presence of problems in the field of budgetary control at all levels of the Russian budget system, which leads to numerous cases of misuse and inefficient use of budget funds and other public property, overestimation of the cost of purchased goods, works and services for state and municipal needs, the use of other corruption schemes in the budget mechanism

Enterocyte Shedding and Epithelial Lining Repair Following Ischemia of the Human Small Intestine Attenuate Inflammation

BACKGROUND: Recently, we observed that small-intestinal ischemia and reperfusion was found to entail a rapid loss of apoptotic and necrotic cells. This study was conducted to investigate whether the observed shedding of ischemically damaged epithelial cells affects IR induced inflammation in the human small gut. METHODS AND FINDINGS: Using a newly developed IR model of the human small intestine, the inflammatory response was studied on cellular, protein and mRNA level. Thirty patients were consecutively included. Part of the jejunum was subjected to 30 minutes of ischemia and variable reperfusion periods (mean reperfusion time 120 (+/-11) minutes). Ethical approval and informed consent were obtained. Increased plasma intestinal fatty acid binding protein (I-FABP) levels indicated loss in epithelial cell integrity in response to ischemia and reperfusion (p<0.001 vs healthy). HIF-1alpha gene expression doubled (p = 0.02) and C3 gene expression increased 4-fold (p = 0.01) over the course of IR. Gut barrier failure, assessed as LPS concentration in small bowel venous effluent blood, was not observed (p = 0.18). Additionally, mRNA expression of HO-1, IL-6, IL-8 did not alter. No increased expression of endothelial adhesion molecules, TNFalpha release, increased numbers of inflammatory cells (p = 0.71) or complement activation, assessed as activated C3 (p = 0.14), were detected in the reperfused tissue. CONCLUSIONS: In the human small intestine, thirty minutes of ischemia followed by up to 4 hours of reperfusion, does not seem to lead to an explicit inflammatory response. This may be explained by a unique mechanism of shedding of damaged enterocytes, reported for the first time by our group

Summary of the cloud chemistry modeling intercomparison: Photochemical box model simulation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94892/1/jgrd10037.pd

Особенности дуговой сварки вертикальных швов резервуара

Цель работы – расчет режимов сварки и выбор сварочных материалов для получения равнопрочного коррозионностойкого соединения. Сложность изготовления стенок резервуара состоит в том, что резервуар РВС предназначен работать в агрессивной среде и должен выдерживать большое давление и нагрузку на свои основные части. При выборе стали необходимо руководствоваться основными её характеристиками - минимальным пределом текучести, толщиной проката и ударной вязкости.The aim of this work is the calculation of the modes of welding and selection of welding materials to obtain a durable corrosion-resistant connection

CD55 Deficiency Protects against Atherosclerosis in ApoE-Deficient Mice via C3a Modulation of Lipid Metabolism

Atherosclerosis, the leading cause of death in the Western world, is driven by chronic inflammation within the artery wall. Elements of the complement cascade are implicated in the pathogenesis, because complement proteins and their activation products are found in the atherosclerotic plaque. We examined the role of CD55, a membrane inhibitor of the complement component 3 (C3) convertase, which converts C3 into C3a and C3b, in atherosclerosis. CD55-deficient (CD55−/−) mice were crossed onto the atherosclerosis-prone apolipoprotein E (apoE)-deficient (apoE−/−) background. High fat–fed male apoE−/−/CD55−/− mice were strongly protected from developing atherosclerosis compared with apoE−/− controls. Lipid profiling showed significantly lower levels of triglycerides, nonesterified fatty acids, and cholesterol in apoE−/−/CD55−/− mice than that in controls after high-fat feeding, whereas body fat in apoE−/−/CD55−/− mice content was increased. Plasma levels of C3 fell, whereas concentrations of C3adesArg (alias acylation stimulating protein; ASP), produced by serum carboxypeptidase N–mediated desargination of C3a, increased in nonfasted high fat–fed apoE−/−/CD55−/− mice, indicating complement activation. Thus, complement dysregulation in the absence of CD55 provoked increased C3adesArg production that, in turn, caused altered lipid handling, resulting in atheroprotection and increased adiposity. Interventions that target complement activation in adipose tissue should be explored as lipid-decreasing strategies

Platelet-Associated CD40/CD154 Mediates Remote Tissue Damage after Mesenteric Ischemia/Reperfusion Injury

Several innate and adaptive immune cell types participate in ischemia/reperfusion induced tissue injury. Amongst them, platelets have received little attention as contributors in the process of tissue damage after ischemia reperfusion (I/R) injury. It is currently unknown whether platelets participate through the immunologically important molecules including, CD40 and when activated, CD154 (CD40L), in the pathogenesis of I/R injury. We hypothesized that constitutive expression of CD40 and activation-induced expression of CD154 on platelets mediate local mesenteric and remote lung tissue damage after I/R injury. Wild type (WT; C57BL/6J), CD40 and CD154 deficient mice underwent mesenteric ischemia for 30 minutes followed by reperfusion for 3 hours. WT mice subjected to mesenteric I/R injury displayed both local intestinal and remote lung damage. In contrast, there was significantly less intestinal damage and no remote lung injury in CD40 and CD154 deficient mice when compared to WT mice. Platelet-depleted WT mice transfused with platelets from CD40 or CD154 deficient mice failed to reconstitute remote lung damage. In contrast, when CD40 or CD154 deficient mice were transfused with WT platelets lung tissue damage was re-established. Together, these findings suggest that multiple mechanisms are involved in local and remote tissue injury and also identify platelet-expressed CD40 and/or CD154 as mediators of remote tissue damage