Quantization and renormalization of the manifest left-right symmetric model of electroweak interactions

Quantization and renormalization of the left-right symmetric model is the main purpose of the paper. First the model at tree level with a Higgs sector containing one bidoublet and two triplets is precisely discussed. Then the canonical quantization and Faddeev-Popov Lagrangian are carried out ('t Hooft gauge). The BRST symmetry is discussed. Subsequently the on mass shell renormalization is performed and, as a test of consistency, the renormalization of the ZNiNj vertex is analyzed.Comment: 74 pages, 65 Postscript figures, submitted to Annals of Physic

Higgs Sector of the Minimal Left-Right Symmetric Model

We perform an exhaustive analysis of the most general Higgs sector of the minimal left-right symmetric model (MLRM). We find that the CP properties of the vacuum state are connected to the Higgs spectrum: if CP is broken spontaneously, the MLRM does not approach the Standard Model in the limit of a decoupling left-right symmetry breaking scale. Depending on the size of the CP phases scenarios with extra non-decoupling flavor-violating doublet Higgses or very light SU(2) triplet Higgses emerge, both of which are ruled out by phenomenology. For zero CP phases the non-standard Higgses decouple only if a very unnatural fine-tuning condition is fulfilled. We also discuss generalizations to a non-minimal Higgs sector.Comment: brief discussion of non-minimal Higgs sectors added, journal versio

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

Tauopathic Changes in the Striatum of A53T α-Synuclein Mutant Mouse Model of Parkinson's Disease

Tauopathic pathways lead to degenerative changes in Alzheimer's disease and there is evidence that they are also involved in the neurodegenerative pathology of Parkinson's disease [PD]. We have examined tauopathic changes in striatum of the α-synuclein (α-Syn) A53T mutant mouse. Elevated levels of α-Syn were observed in striatum of the adult A53T α-Syn mice. This was accompanied by increases in hyperphosphorylated Tau [p-Tau], phosphorylated at Ser202, Ser262 and Ser396/404, which are the same toxic sites also seen in Alzheimer's disease. There was an increase in active p-GSK-3β, hyperphosphorylated at Tyr216, a major and primary kinase known to phosphorylate Tau at multiple sites. The sites of hyperphosphorylation of Tau in the A53T mutant mice were similar to those seen in post-mortem striata from PD patients, attesting to their pathophysiological relevance. Increases in p-Tau were not due to alterations on protein phosphatases in either A53T mice or in human PD, suggesting lack of involvement of these proteins in tauopathy. Extraction of striata with Triton X-100 showed large increases in oligomeric forms of α-Syn suggesting that α-Syn had formed aggregates the mutant mice. In addition, increased levels of p-GSK-3β and pSer396/404 were also found associated with aggregated α-Syn. Differential solubilization to measure protein binding to cytoskeletal proteins demonstrated that p-Tau in the A53T mutant mouse were unbound to cytoskeletal proteins, consistent with dissociation of p-Tau from the microtubules upon hyperphosphorylation. Interestingly, α-Syn remained tightly bound to the cytoskeleton, while p-GSK-3β was seen in the cytoskeleton-free fractions. Immunohistochemical studies showed that α-Syn, pSer396/404 Tau and p-GSK-3β co-localized with one another and was aggregated and accumulated into large inclusion bodies, leading to cell death of Substantia nigral neurons. Together, these data demonstrate an elevated state of tauopathy in striata of the A53T α-Syn mutant mice, suggesting that tauopathy is a common feature of synucleinopathies

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

Epileptiform Activity in Alcohol Dependent Patients and Possibilities of Its Indirect Measurement

Background: Alcohol dependence during withdrawal and also in abstinent period in many cases is related to reduced inhibitory functions and kindling that may appear in the form of psychosensory symptoms similar to temporal lobe epilepsy frequently in conditions of normal EEG and without seizures. Because temporal lobe epileptic activity tend to spread between hemispheres, it is possible to suppose that measures reflecting interhemispheric information transfer such as electrodermal activity (EDA) might be related to the psychosensory symptoms. Methods and Findings: We have performed measurement of bilateral EDA, psychosensory symptoms (LSCL-33) and alcohol craving (ACQ) in 34 alcohol dependent patients and 32 healthy controls. The results in alcohol dependent patients show that during rest conditions the psychosensory symptoms (LSCL-33) are related to EDA transinformation (PTI) between left and right EDA records (Spearman r = 0.44, p,0.01). Conclusions: The result may present potentially useful clinical finding suggesting a possibility to indirectly assess epileptiform changes in alcohol dependent patients

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.

Xirp Proteins Mark Injured Skeletal Muscle in Zebrafish

Myocellular regeneration in vertebrates involves the proliferation of activated progenitor or dedifferentiated myogenic cells that have the potential to replenish lost tissue. In comparison little is known about cellular repair mechanisms within myocellular tissue in response to small injuries caused by biomechanical or cellular stress. Using a microarray analysis for genes upregulated upon myocellular injury, we identified zebrafish Xin-actin-binding repeat-containing protein1 (Xirp1) as a marker for wounded skeletal muscle cells. By combining laser-induced micro-injury with proliferation analyses, we found that Xirp1 and Xirp2a localize to nascent myofibrils within wounded skeletal muscle cells and that the repair of injuries does not involve cell proliferation or Pax7+ cells. Through the use of Xirp1 and Xirp2a as markers, myocellular injury can now be detected, even though functional studies indicate that these proteins are not essential in this process. Previous work in chicken has implicated Xirps in cardiac looping morphogenesis. However, we found that zebrafish cardiac morphogenesis is normal in the absence of Xirp expression, and animals deficient for cardiac Xirp expression are adult viable. Although the functional involvement of Xirps in developmental and repair processes currently remains enigmatic, our findings demonstrate that skeletal muscle harbours a rapid, cell-proliferation-independent response to injury which has now become accessible to detailed molecular and cellular characterizations