95 research outputs found
Plasma chemical purification of flue gases using pulsed electron beams
The article presents the study of the pulsed electron beam propagation in oxygen and nitrogen. The researches were performed using the TEA-500 pulsed electron accelerator and drift tube. Parameters of the TEA-500 pulsed electron accelerator are as follows: the electron energy (varies) is 200-450 keV, the beam current is 10 kA, the half-amplitude current pulse duration is 60 ns, the pulse repetition rate is up to 10 Hz (in the pulse burst). The accelerator is equipped with the necessary means of diagnostics of the beam parameters: particle energy, current and current density, the total energy transferred by the beam. The drift tube includes a chamber consisting of two sections of reverse current shunts located along the entire length of the drift tube. The following precursors used N2 and O2. The specified types of gases were chosen as they are among the main components of the flue gases, whose treatment has been widely reported recently
Genomic correlates of glatiramer acetate adverse cardiovascular effects lead to a novel locus mediating coronary risk
Glatiramer acetate is used therapeutically in multiple sclerosis but also known for adverse effects including elevated coronary artery disease (CAD) risk. The mechanisms underlying the cardiovascular side effects of the medication are unclear. Here, we made use of the chromosomal variation in the genes that are known to be affected by glatiramer treatment. Focusing on genes and gene products reported by drug-gene interaction database to interact with glatiramer acetate we explored a large meta-analysis on CAD genome-wide association studies aiming firstly, to investigate whether variants in these genes also affect cardiovascular risk and secondly, to identify new CAD risk genes. We traced association signals in a 200-kb region around genomic positions of genes interacting with glatiramer in up to 60 801 CAD cases and 123 504 controls. We validated the identified association in additional 21 934 CAD cases and 76 087 controls. We identified three new CAD risk alleles within the TGFB1 region on chromosome 19 that independently affect CAD risk. The lead SNP rs12459996 was genome-wide significantly associated with CAD in the extended meta-analysis (odds ratio 1.09, p = 1.58×10-12). The other two SNPs at the locus were not in linkage disequilibrium with the lead SNP and by a conditional analysis showed p-values of 4.05 × 10-10 and 2.21 × 10-6. Thus, studying genes reported to interact with glatiramer acetate we identified genetic variants that concordantly with the drug increase the risk of CAD. Of these, TGFB1 displayed signal for association. Indeed, the gene has been associated with CAD previously in both in vivo and in vitro studies. Here we establish genome-wide significant association with CAD in large human samples.This work was supported by grants from the Fondation Leducq (CADgenomics: Understanding CAD Genes, 12CVD02), the German Federal Ministry of Education and Research (BMBF) within the framework of the e:Med research and funding concept (e:AtheroSysMed, grant 01ZX1313A-2014 and SysInflame, grant 01ZX1306A), and the European Union Seventh Framework Programme FP7/2007-2013 under grant agreement no HEALTH-F2-2013-601456 (CVgenes-at-target). Further grants were received from the DFG as part of the Sonderforschungsbereich CRC 1123 (B2). T.K. was supported by a DZHK Rotation Grant. I.B. was supported by the Deutsche Forschungsgemeinschaft (DFG) cluster of excellence ‘Inflammation at Interfaces’. F.W.A. is supported by a Dekker scholarship-Junior Staff Member 2014T001 - Netherlands Heart Foundation and UCL Hospitals NIHR Biomedical Research Centre
New genetic loci link adipose and insulin biology to body fat distribution.
Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms
Computational Model Study of the Experimentally Suggested Mechanism for Nitrogenase
The mechanism for
N2 activation in the E4 state of nitrogenase
was investigated by model calculations. In
the experimentally suggested mechanism, the E4 state is
obtained after four reductions to the ground state. In a recent theoretical
study, results for a different mechanism have been found in excellent
agreement with available Electron Paramagnetic Resonance (EPR) experiments
for E4. The two hydrides in E4 leave as H2 concertedly with the binding of N2. The mechanism
suggested differs from the experimentally suggested one by a requirement
for four activation steps prior to catalysis. In the present study,
the experimentally suggested mechanism is studied using the same methods
as those used in the previous study on the theoretical mechanism.
The computed results make it very unlikely that a structure obtained
after four reductions from the ground state has two hydrides, and
the experimentally suggested mechanism does therefore not agree with
the EPR experiments for E4. Another structure with only
one hydride is here suggested to be the one that has been observed
to bind N2 after only four reductions of the ground state
Substrate Water Exchange for the Oxygen Evolving Complex in PSII in the S<sub>1</sub>, S<sub>2</sub>, and S<sub>3</sub> States
Detailed
mechanisms for substrate water exchange in the oxygen
evolving complex in photosystem II have been determined with DFT methods
for large models. Existing interpretations of the experimental water
exchange results have been quite different. By many groups, these
results have been the main argument against the water oxidation mechanism
suggested by DFT, in which the oxygen molecule is formed between a
bridging oxo and an oxyl radical ligand in the center of the OEC.
That mechanism is otherwise in line with most experiments. The problem
has been that the mechanism requires a rather fast exchange of a bridging
oxo ligand, which is not a common finding for smaller Mn-containing
model systems. However, other groups have actually favored a substrate
derived oxo ligand partly based on the same experiments. In the present
study, three S-states have been studied, and the rates have been well
reproduced by the calculations. The surprising experimental finding
that water exchange in S<sub>1</sub> is slower than the one in S<sub>2</sub> is reproduced and explained. The key to this rate difference
is the ease by which one of the manganese centers (<b>Mn3</b>) is reduced. This reduction has to occur to release the substrate
water from <b>Mn3</b>. The similar rate of the slow exchange
in S<sub>2</sub> and S<sub>3</sub> has been rationalized on the basis
of earlier experiments combined with the present calculations. The
results strongly support the previous DFT-suggested water oxidation
mechanism
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