Linear Collider Test of a Neutrinoless Double Beta Decay Mechanism in left-right Symmetric Theories

There are various diagrams leading to neutrinoless double beta decay in left-right symmetric theories based on the gauge group SU(2)_L x SU(2)_R. All can in principle be tested at a linear collider running in electron-electron mode. We argue that the so-called lambda-diagram is the most promising one. Taking the current limit on this diagram from double beta decay experiments, we evaluate the relevant cross section e e to W_L W_R, where W_L is the Standard Model W-boson and W_R the one from SU(2)_R. It is observable if the life-time of double beta decay and the mass of the W_R are close to current limits. Beam polarization effects and the high-energy behaviour of the cross section are also analyzed.Comment: 17 pages, 6 figures. v2: minor changes, references added, to be published in EPJ

Left-right symmetry at LHC and precise 1-loop low energy data

Despite many tests, even the Minimal Manifest Left-Right Symmetric Model (MLRSM) has never been ultimately confirmed or falsified. LHC gives a new possibility to test directly the most conservative version of left-right symmetric models at so far not reachable energy scales. If we take into account precise limits on the model which come from low energy processes, like the muon decay, possible LHC signals are strongly limited through the correlations of parameters among heavy neutrinos, heavy gauge bosons and heavy Higgs particles. To illustrate the situation in the context of LHC, we consider the "golden" process $pp \to e^+ N$. For instance, in a case of degenerate heavy neutrinos and heavy Higgs masses at 15 TeV (in agreement with FCNC bounds) we get $\sigma(pp \to e^+ N)>10$ fb at $\sqrt{s}=14$ TeV which is consistent with muon decay data for a very limited $W_2$ masses in the range (3008 GeV, 3040 GeV). Without restrictions coming from the muon data, $W_2$ masses would be in the range (1.0 TeV, 3.5 TeV). Influence of heavy Higgs particles themselves on the considered LHC process is negligible (the same is true for the light, SM neutral Higgs scalar analog). In the paper decay modes of the right-handed heavy gauge bosons and heavy neutrinos are also discussed. Both scenarios with typical see-saw light-heavy neutrino mixings and the mixings which are independent of heavy neutrino masses are considered. In the second case heavy neutrino decays to the heavy charged gauge bosons not necessarily dominate over decay modes which include only light, SM-like particles.Comment: 16 pages, 10 figs, KL-KS and new ATLAS limits taken into accoun

Left-right symmetry in 5D and neutrino mass in TeV scale gravity models

We construct a left-right symmetric model based on the gauge group $SU(2)_L\times SU(2)_R\times U(1)_{B-L}$ in five dimensions where both the gauge bosons and fermions reside in all five dimensions. The orbifold boundary conditions are used not only to break the gauge symmetry down to $SU(2)_L\times U(1)_Y\times U(1)_{Y'}$ but also to ``project'' the right handed neutrino out of the zero mode part of the spectrum, providing a new way to understand the small neutrino masses without adding (singlet) bulk neutrinos. This formulation of the left-right model has also two new features: (i) it avoids most existing phenomenological bounds on the scale of the right handed $W_R$ boson allowing for the possibility that the right handed gauge bosons could have masses under a TeV, and (ii) it predicts a stable lepton with mass of order of the inverse radius of the fifth dimension.Comment: 20 pages; some new materials and references adde

Role of Esrrg in the Fibrate-Mediated Regulation of Lipid Metabolism Genes in Human ApoA-I Transgenic Mice

We have used a new ApoA-I transgenic mouse model to identify by global gene expression profiling, candidate genes that affect lipid and lipoprotein metabolism in response to fenofibrate treatment. Multilevel bioinformatical analysis and stringent selection criteria (2-fold change, 0% false discovery rate) identified 267 significantly changed genes involved in several molecular pathways. The fenofibrate-treated group did not have significantly altered levels of hepatic human APOA-I mRNA and plasma ApoA-I compared with the control group. However, the treatment increased cholesterol levels to 1.95-fold mainly due to the increase in high-density lipoprotein (HDL) cholesterol. The observed changes in HDL are associated with the upregulation of genes involved in phospholipid biosynthesis and lipid hydrolysis, as well as phospholipid transfer protein. Significant upregulation was observed in genes involved in fatty acid transport and β-oxidation, but not in those of fatty acid and cholesterol biosynthesis, Krebs cycle and gluconeogenesis. Fenofibrate changed significantly the expression of seven transcription factors. The estrogen receptor-related gamma gene was upregulated 2.36-fold and had a significant positive correlation with genes of lipid and lipoprotein metabolism and mitochondrial functions, indicating an important role of this orphan receptor in mediating the fenofibrate-induced activation of a specific subset of its target genes.National Institutes of Health (HL48739 and HL68216); European Union (LSHM-CT-2006-0376331, LSHG-CT-2006-037277); the Biomedical Research Foundation of the Academy of Athens; the Hellenic Cardiological Society; the John F Kostopoulos Foundatio

Influence of the left-handed part of the neutrino mass matrix on the lepton number violating e-e- -> W-W- process

Influence of the neutrino mass submatrix $M_L$ on the e-e- -> W-W- process is discussed. Taking into account various possible CP signatures of heavy neutrinos it is shown that, in some cases, nonzero $M_L$ substantially changes predictions for maximum possible values of the e-e- -> W-W- cross section. A direct role of the $\omega^2$ parameter (coming from neutrinoless double beta decay) is clarified. The consequences of doubly charged Higgs particles $\delta^{--}$ with resonances even far away from energies of the future linear lepton collider ($\sqrt{s}=0.5-1$ TeV) are studied.Comment: revtex, epsfig, 5 figures, 9 pages. To appear in Phys.Rev.

Kinin B1 Receptor Enhances the Oxidative Stress in a Rat Model of Insulin Resistance: Outcome in Hypertension, Allodynia and Metabolic Complications

BACKGROUND: Kinin B(1) receptor (B(1)R) is induced by the oxidative stress in models of diabetes mellitus. This study aims at determining whether B(1)R activation could perpetuate the oxidative stress which leads to diabetic complications. METHODS AND FINDINGS: Young Sprague-Dawley rats were fed with 10% D-Glucose or tap water (controls) for 8-12 weeks. A selective B(1)R antagonist (SSR240612) was administered acutely (3-30 mg/kg) or daily for a period of 7 days (10 mg/kg) and the impact was measured on systolic blood pressure, allodynia, protein and/or mRNA B(1)R expression, aortic superoxide anion (O(2)(*-)) production and expression of superoxide dismutase (MnSOD) and catalase. SSR240612 reduced dose-dependently (3-30 mg/kg) high blood pressure in 12-week glucose-fed rats, but had no effect in controls. Eight-week glucose-fed rats exhibited insulin resistance (HOMA index), hypertension, tactile and cold allodynia and significant increases of plasma levels of glucose and insulin. This was associated with higher aortic levels of O(2)(*-), NADPH oxidase activity, MnSOD and catalase expression. All these abnormalities including B(1)R overexpression (spinal cord, aorta, liver and gastrocnemius muscle) were normalized by the prolonged treatment with SSR240612. The production of O(2)(*-) in the aorta of glucose-fed rats was also measured in the presence and absence of inhibitors (10-100 microM) of NADPH oxidase (apocynin), xanthine oxidase (allopurinol) or nitric oxide synthase (L-NAME) with and without Sar[D-Phe(8)]des-Arg(9)-BK (20 microM; B(1)R agonist). Data show that the greater aortic O(2)(*-) production induced by the B(1)R agonist was blocked only by apocynin. CONCLUSIONS: Activation of kinin B(1)R increased O(2)(*-) through the activation of NADPH oxidase in the vasculature. Prolonged blockade of B(1)R restored cardiovascular, sensory and metabolic abnormalities by reducing oxidative stress and B(1)R gene expression in this model

Evaluating the relationship between amyloid-β and α-synuclein phosphorylated at Ser129 in dementia with Lewy bodies and Parkinson’s disease

INTRODUCTION: Lewy body and Alzheimer-type pathologies often co-exist. Several studies suggest a synergistic relationship between amyloid-β (Aβ) and α-synuclein (α-syn) accumulation. We have explored the relationship between Aβ accumulation and the phosphorylation of α-syn at serine-129 (pSer129 α-syn), in post-mortem human brain tissue and in SH-SY5Y neuroblastoma cells transfected to overexpress human α-syn. METHODS: We measured levels of Aβ40, Aβ42, α-syn and pSer129 α-syn by sandwich enzyme-linked immunosorbent assay, in soluble and insoluble fractions of midfrontal, cingulate and parahippocampal cortex and thalamus, from cases of Parkinson’s disease (PD) with (PDD; n = 12) and without dementia (PDND; n = 23), dementia with Lewy bodies (DLB; n = 10) and age-matched controls (n = 17). We also examined the relationship of these measurements to cognitive decline, as measured by time-to-dementia and the mini-mental state examination (MMSE) score in the PD patients, and to Braak tangle stage. RESULTS: In most brain regions, the concentration of insoluble pSer129 α-syn correlated positively, and soluble pSer129 α-syn negatively, with the levels of soluble and insoluble Aβ. Insoluble pSer129 α-syn also correlated positively with Braak stage. In most regions, the levels of insoluble and soluble Aβ and the proportion of insoluble α-syn that was phosphorylated at Ser129 were significantly higher in the PD and DLB groups than the controls, and higher in the PDD and DLB groups than the PDND brains. In PD, the MMSE score correlated negatively with the level of insoluble pSer129 α-syn. Exposure of SH-SY5Y cells to aggregated Aβ42 significantly increased the proportion of α-syn that was phosphorylated at Ser129 (aggregated Aβ40 exposure had a smaller, non-significant effect). CONCLUSIONS: Together, these data show that the concentration of pSer129 α-syn in brain tissue homogenates is directly related to the level of Aβ and Braak tangle stage, and predicts cognitive status in Lewy body diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13195-014-0077-y) contains supplementary material, which is available to authorized users