Moscow Institute of Physics and Technology

About: Moscow Institute of Physics and Technology is a education organization based out in Dolgoprudnyy, Russia. It is known for research contribution in the topics: Laser & Large Hadron Collider. The organization has 8594 authors who have published 16968 publications receiving 246551 citations. The organization is also known as: MIPT & Moscow Institute of Physics and Technology (State University).

Search for pair production of up-type vector-like quarks and for four-top-quark events in final states with multiple b-jets with the ATLAS detector

Abstract: A search for pair production of up-type vector-like quarks (T) with a significant branching ratio into a top quark and either a Standard Model Higgs boson or a Z boson is presented. The same analys ...

Physics potentials with the second Hyper-Kamiokande detector in Korea

Abstract: We have conducted sensitivity studies on an alternative configuration of the Hyper-Kamiokande experiment by locating the 2nd Hyper-Kamiokande detector in Korea at $\sim$1100$-\ $1300 km baseline. Having two detectors at different baselines improves sensitivity to leptonic CP violation, neutrino mass ordering as well as nonstandard neutrino interactions. There are several candidate sites in Korea with greater than 1 km high mountains ranged at an 1$-$3 degree off-axis angle. Thanks to larger overburden of the candidate sites in Korea, low energy physics, such as solar and supernova neutrino physics as well as dark matter search, is expected to be improved. In this paper sensitivity studies on the CP violation phase and neutrino mass ordering are performed using current T2K systematic uncertainties in most cases. We plan to improve our sensitivity studies in the near future with better estimation of our systematic uncertainties.

The Role of Oxidative Stress in Diabetic Neuropathy: Generation of Free Radical Species in the Glycation Reaction and Gene Polymorphisms Encoding Antioxidant Enzymes to Genetic Susceptibility to Diabetic Neuropathy in Population of Type I Diabetic Patients

Abstract: Diabetic neuropathy (DN) represents the main cause of morbidity and mortality among diabetic patients. Clinical data support the conclusion that the severity of DN is related to the frequency and duration of hyperglycemic periods. The presented experimental and clinical evidences propose that changes in cellular function resulting in oxidative stress act as a leading factor in the development and progression of DN. Hyperglycemia- and dyslipidemia-driven oxidative stress is a major contributor, enhanced by advanced glycation end product (AGE) formation and polyol pathway activation. There are several polymorphous pathways that lead to oxidative stress in the peripheral nervous system in chronic hyperglycemia. This article demonstrates the origin of oxidative stress derived from glycation reactions and genetic variations within the antioxidant genes which could be implicated in the pathogenesis of DN. In the diabetic state, unchecked superoxide accumulation and resultant increases in polyol pathway activity, AGEs accumulation, protein kinase C activity, and hexosamine flux trigger a feed-forward system of progressive cellular dysfunction. In nerve, this confluence of metabolic and vascular disturbances leads to impaired neural function and loss of neurotrophic support, and over the long term, can mediate apoptosis of neurons and Schwann cells, the glial cells of the peripheral nervous system. In this article, we consider AGE-mediated reactive oxygen species (ROS) generation as a pathogenesis factor in the development of DN. It is likely that oxidative modification of proteins and other biomolecules might be the consequence of local generation of superoxide on the interaction of the residues of L-lysine (and probably other amino acids) with α-ketoaldehydes. This phenomenon of non-enzymatic superoxide generation might be an element of autocatalytic intensification of pathophysiological action of carbonyl stress. Glyoxal and methylglyoxal formed during metabolic pathway are detoxified by the glyoxalase system with reduced glutathione as co-factor. The concentration of reduced glutathione may be decreased by oxidative stress and by decreased in situ glutathione reductase activity in diabetes mellitus. Genetic variations within the antioxidant genes therefore could be implicated in the pathogenesis of DN. In this work, the supporting data about the association between the -262T > C polymorphism of the catalase (CAT) gene and DN were shown. The -262TT genotype of the CAT gene was significantly associated with higher erythrocyte catalase activity in blood of DN patients compared to the -262CC genotype (17.8 ± 2.7 × 10(4) IU/g Hb vs. 13.5 ± 3.2 × 10(4) IU/g Hb, P = 0.0022). The role of these factors in the development of diabetic complications and the prospective prevention of DN by supplementation in formulations of transglycating imidazole-containing peptide-based antioxidants (non-hydrolyzed carnosine, carcinine, n-acetylcarcinine) scavenging ROS in the glycation reaction, modifying the activity of enzymic and non-enzymic antioxidant defenses that participate in metabolic processes with ability of controlling at transcriptional levels the differential expression of several genes encoding antioxidant enzymes inherent to DN in Type I Diabetic patients, now deserve investigation.

Search for top-squark pair production in final states with one lepton, jets, and missing transverse momentum using 36 fb−1 of s√=13 TeV pp collision data with the ATLAS detector

Abstract: The results of a search for the direct pair production of top squarks, the supersymmetric partner of the top quark, in final states with one isolated electron or muon, several energetic jets, and missing transverse momentum are reported. The analysis also targets spin-0 mediator models, where the mediator decays into a pair of dark-matter particles and is produced in association with a pair of top quarks. The search uses data from proton-proton collisions delivered by the Large Hadron Collider in 2015 and 2016 at a centre-of-mass energy of $ \sqrt{s}=13 $ TeV and recorded by the ATLAS detector, corresponding to an integrated luminosity of 36 fb$^{−1}$. A wide range of signal scenarios with different mass-splittings between the top squark, the lightest neutralino and possible intermediate supersymmetric particles are considered, including cases where the W bosons or the top quarks produced in the decay chain are off-shell. No significant excess over the Standard Model prediction is observed. The null results are used to set exclusion limits at 95% confidence level in several supersymmetry benchmark models. For pair-produced top-squarks decaying into top quarks, top-squark masses up to 940 GeV are excluded. Stringent exclusion limits are also derived for all other considered top-squark decay scenarios. For the spin-0 mediator models, upper limits are set on the visible cross-section.

Search for anomalous production of prompt same-sign lepton pairs and pair-produced doubly charged Higgs bosons with s =8 TeV pp collisions using the ATLAS detector

Abstract: A low-background inclusive search for new physics in events with same-sign dileptons is presented The search uses proton-proton collisions corresponding to 203 fb−1 of integrated luminosity taken in 2012 at a centre-of-mass energy of 8 TeV with the ATLAS detector at the LHC Pairs of isolated leptons with the same electric charge and large transverse momenta of the type e±e±, e±μ±, and μ±μ± are selected and their invariant mass distribution is examined No excess of events above the expected level of Standard Model background is found The results are used to set upper limits on the cross-sections for processes beyond the Standard Model Limits are placed as a function of the dilepton invariant mass within a fiducial region corresponding to the signal event selection criteria Exclusion limits are also derived for a specific model of doubly charged Higgs boson production