Constraining Bosonic Supersymmetry from Higgs results and 8 TeV ATLAS multi-jets plus missing energy data

The collider phenomenology of models with Universal Extra Dimensions (UED) is surprisingly similar to that of supersymmetric (SUSY) scenarios. For each level-1 bosonic (fermionic) Kaluza-Klein (KK) state, there is a fermionic (bosonic) analog in SUSY and thus UED scenarios are often known as bosonic supersymmetry. The minimal version of UED (mUED) gives rise to a quasi-degenerate particle spectrum at each KK-level and thus, can not explain the enhanced Higgs to diphoton decay rate hinted by the ATLAS collaboration of the Large Hadron Collider (LHC) experiment. However, in the non-minimal version of the UED (nmUED) model, the enhanced Higgs to diphoton decay rate can be easily explained via the suitable choice of boundary localized kinetic (BLK) terms for higher dimensional fermions and gauge bosons. BLK terms remove the degeneracy in the KK mass spectrum and thus, pair production of level-1 quarks and gluons at the LHC gives rise to hard jets, leptons and large missing energy in the final state. These final states are studied in details by the ATLAS and CMS collaborations in the context of SUSY scenarios. We find that the absence of any significant deviation of the data from the Standard Model (SM) prediction puts a lower bound of about 2.1 TeV on equal mass excited quarks and gluons.Comment: 19 page

Collider Phenomenology with Split-UED

We investigate the collider implications of Split Universal Extra Dimensions. The non-vanishing fermion mass in the bulk, which is consistent with the KK-parity, largely modifies the phenomenology of Minimal Universal Exta Dimensions. We scrutinize the behavior of couplings and study the discovery reach of the Tevatron and the LHC for level-2 Kaluza-Klein modes in the dilepton channel, which would indicates the presence of the extra dimensions. Observation of large event rates for dilepton resonances can result from a nontrivial fermion mass profile along the extra dimensions, which, in turn, may corroborate extra dimensional explanation for the observation of the positron excess in cosmic rays.Comment: 23 pages, 15 figure

Retargeted adenoviruses for radiation-guided gene delivery

The combination of radiation with radiosensitizing gene delivery or oncolytic viruses promises to provide an advantage that could improve the therapeutic results for glioblastoma. X-rays can induce significant molecular changes in cancer cells. We isolated the GIRLRG peptide that binds to radiation-inducible 78 kDa glucose-regulated protein (GRP78), which is overexpressed on the plasma membranes of irradiated cancer cells and tumor-associated microvascular endothelial cells. The goal of our study was to improve tumor-specific adenovirus-mediated gene delivery by selectively targeting the adenovirus binding to this radiation-inducible protein. We employed an adenoviral fiber replacement approach to conduct a study of the targeting utility of GRP78-binding peptide. We have developed fiber-modified adenoviruses encoding the GRP78-binding peptide inserted into the fiber-fibritin. We have evaluated the reporter gene expression of fiber-modified adenoviruses in vitro using a panel of glioma cells and a human D54MG tumor xenograft model. The obtained results demonstrated that employment of the GRP78-binding peptide resulted in increased gene expression in irradiated tumors following infection with fiber-modified adenoviruses, compared with untreated tumor cells. These studies demonstrate the feasibility of adenoviral retargeting using the GRP78-binding peptide that selectively recognizes tumor cells responding to radiation treatment

Working Group Report: Heavy-Ion Physics and Quark-Gluon Plasma

This is the report of Heavy Ion Physics and Quark-Gluon Plasma at WHEPP-09 which was part of Working Group-4. Discussion and work on some aspects of Quark-Gluon Plasma believed to have created in heavy-ion collisions and in early universe are reported.Comment: 20 pages, 6 eps figures, Heavy-ion physics and QGP activity report in "IX Workshop on High Energy Physics Phenomenology (WHEPP-09)" held in Institute of Physics, Bhubaneswar, India, during January 3-14, 2006. To be published in PRAMANA - Journal of Physics (Indian Academy of Science

Seesaw Neutrino Signals at the Large Hadron Collider

We discuss the scenario with gauge singlet fermions (right-handed neutrinos) accessible at the energy of the Large Hadron Collider. The singlet fermions generate tiny neutrino masses via the seesaw mechanism and also have sizable couplings to the standard-model particles. We demonstrate that these two facts, which are naively not satisfied simultaneously, are reconciled in the five-dimensional framework in various fashions, which make the seesaw mechanism observable. The collider signal of tri-lepton final states with transverse missing energy is investigated for two explicit examples of the observable seesaw, taking account of three types of neutrino mass spectrum and the constraint from lepton flavor violation. We find by showing the significance of signal discovery that the collider experiment has a potential to find signals of extra dimensions and the origin of small neutrino masses.Comment: 27 pages, 4 figure

Hypoxia increases neutrophil-driven matrix destruction after exposure to Mycobacterium tuberculosis.

The importance of neutrophils in the pathology of tuberculosis (TB) has been recently established. We demonstrated that TB lesions in man are hypoxic, but how neutrophils in hypoxia influence lung tissue damage is unknown. We investigated the effect of hypoxia on neutrophil-derived enzymes and tissue destruction in TB. Human neutrophils were stimulated with M. tuberculosis (M.tb) or conditioned media from M.tb-infected monocytes (CoMTB). Neutrophil matrix metalloproteinase-8/-9 and elastase secretion were analysed by luminex array and gelatin zymography, gene expression by qPCR and cell viability by flow cytometry. Matrix destruction was investigated by confocal microscopy and functional assays and neutrophil extracellular traps (NETs) by fluorescence assay. In hypoxia, neutrophil MMP-8 secretion and gene expression were up-regulated by CoMTB. MMP-9 activity and neutrophil elastase (NE) secretion were also increased in hypoxia. Hypoxia inhibited NET formation and both neutrophil apoptosis and necrosis after direct stimulation by M.tb. Hypoxia increased TB-dependent neutrophil-mediated matrix destruction of Type I collagen, gelatin and elastin, the main structural proteins of the human lung. Dimethyloxalylglycin (DMOG), which stabilizes hypoxia-inducible factor-1α, increased neutrophil MMP-8 and -9 secretion. Hypoxia in our cellular model of TB up-regulated pathways that increase neutrophil secretion of MMPs that are implicated in matrix destruction

Bcl-2 protein family: Implications in vascular apoptosis and atherosclerosis

Apoptosis has been recognized as a central component in the pathogenesis of atherosclerosis, in addition to the other human pathologies such as cancer and diabetes. The pathophysiology of atherosclerosis is complex, involving both apoptosis and proliferation at different phases of its progression. Oxidative modification of lipids and inflammation differentially regulate the apoptotic and proliferative responses of vascular cells during progression of the atherosclerotic lesion. Bcl-2 proteins act as the major regulators of extrinsic and intrinsic apoptosis signalling pathways and more recently it has become evident that they mediate the apoptotic response of vascular cells in response to oxidation and inflammation either in a provocative or an inhibitory mode of action. Here we address Bcl-2 proteins as major therapeutic targets for the treatment of atherosclerosis and underscore the need for the novel preventive and therapeutic interventions against atherosclerosis, which should be designed in the light of molecular mechanisms regulating apoptosis of vascular cells in atherosclerotic lesions

Translational models for vascular cognitive impairment: a review including larger species.

BACKGROUND: Disease models are useful for prospective studies of pathology, identification of molecular and cellular mechanisms, pre-clinical testing of interventions, and validation of clinical biomarkers. Here, we review animal models relevant to vascular cognitive impairment (VCI). A synopsis of each model was initially presented by expert practitioners. Synopses were refined by the authors, and subsequently by the scientific committee of a recent conference (International Conference on Vascular Dementia 2015). Only peer-reviewed sources were cited. METHODS: We included models that mimic VCI-related brain lesions (white matter hypoperfusion injury, focal ischaemia, cerebral amyloid angiopathy) or reproduce VCI risk factors (old age, hypertension, hyperhomocysteinemia, high-salt/high-fat diet) or reproduce genetic causes of VCI (CADASIL-causing Notch3 mutations). CONCLUSIONS: We concluded that (1) translational models may reflect a VCI-relevant pathological process, while not fully replicating a human disease spectrum; (2) rodent models of VCI are limited by paucity of white matter; and (3) further translational models, and improved cognitive testing instruments, are required