Two-Time Correlation Functions: Stochastic and Conventional Quantum Mechanics

An investigation of two-time correlation functions is reported within the framework of (i) Stochastic Quantum Mechanics and (ii) conventional Heisenberg-Schr\"odinger Quantum Mechanics. The spectral functions associated with the two-time electric dipole correlation functions are worked out in detail for the case of the hydrogen atom. While the single time averages are identical for stochastic and conventional quantum mechanics, differences arise in the two approaches for multiple time correlation functions.Comment: Version published by the Eur. Phys. J. B. Few references added. Minor typos correcte

Search for techniparticles at D0 Run II

Technicolor theory (TC) accomplishes the necessary electroweak symmetry breaking responsible for the mass of the elementary particles. TC postulates the existence of a new SU(N{sub TC}) gauge theory. Like QCD the exchange of gauge bosons causes the existence of a non-vanishing chiral condensate which dynamically breaks the SU(N{sub TC}){sub L} x SU(N{sub TC}){sub R} symmetry. This gives rise to N{sub TC}{sup 2}-1 Nambu-Goldstone Bosons. Three of these Goldstone Bosons become the longitudinal components of the W{sup {+-}} and Z which therefore acquire mass; the remaining ones are new particles (technihadrons) that can be produced at the high energy colliders and detected. The Technicolor Straw Man Model (TCSM) is a version of the dynamical symmetry breaking with a large number of technifermions and a relative low value of their masses. One of the processes predicted by the TCSM is q{bar q} {yields} V{sub T} {yields} W{pi}{sub T}, where V{sub T} is the Technicolor equivalent of the QCD vector meson and {pi}{sub T} is the equivalent of the pion. W is the electroweak gauge boson of the Standard Model. This dissertation describes the search for W{pi}{sub T} with the D0 detector, a multi-purpose particle detector located at one of the collision points of the Tevatron accelerator situated in Batavia, IL. The final state considered for this thesis is a W boson that decays to electron and neutrino plus a {pi}{sub T} that decays into b{bar c} or b{bar b}, depending on the charge of the initial technivector meson produced. In the D0 detector this process will appear as a narrow cluster of energy deposits in the electromagnetic calorimeter with an associated track reconstructed in the tracking detector. The undetected neutrino from the decay of the W boson will be seen as missing momentum. The fragmentation of the quarks from the decay of the {pi}{sub T} will produce two jets of collimated particles. Events where a b-quark is produced are selected by requesting at least one jet to be associated with a secondary vertex of interaction produced by the decay of B-meson (b-tagging). In the absence of an excess over the Standard Model prediction for the final state considered in this analysis, we compute a 95% Confidence Level upper limit on the techniparticle production cross section for the V{sub T} mass range: 190 GeV/c{sup 2} {le} m(V{sub T} ) {le} 220 GeV/c{sup 2}

Hyperhomocysteinemia as a Risk Factor and Potential Nutraceutical Target for Certain Pathologies

Hyperhomocysteinemia is recognized as a risk factor for several diseases, including cardiovascular and neurological conditions. Homocysteine (HCys) is a key metabolite involved in the biosynthesis and metabolism of methionine (Met), which plays a pivotal role in the physiological cell's life cycle. The biochemistry of Met is finely regulated by several enzymes that control HCys concentration. Indeed, balanced activity among the enzymes is essential for the cell's well-being, while its malfunction could raise HCys concentration which can lead to the onset of several pathological conditions. The HCys concentration increase seems to be caused mainly by the widely diffused polymorphisms of several enzymes. Nowadays, a blood test can easily detect elevated concentrations of HCys, referred to as Hyperhomocysteinemia (HHCys). Prolonged exposure to this condition can lead to the onset of cardiovascular disease and can lead to the development of atherosclerosis, stroke, inflammatory syndromes like osteoporosis and rheumatism, as well as neuronal pathologies including Alzheimer's and Parkinson's diseases. In this review, we analyzed the literature of several pathological conditions in which the molecular pathways of HHCys are involved. Interestingly, several observations indicate that the calibrated assumption of correct doses of vitamins such as folic acid, vitamin B6, vitamin B12, and betaine may control HHCys-related conditions

Classical Vs Quantum Probability in Sequential Measurements

We demonstrate in this paper that the probabilities for sequential measurements have features very different from those of single-time measurements. First, they cannot be modelled by a classical stochastic process. Second, they are contextual, namely they depend strongly on the specific measurement scheme through which they are determined. We construct Positive-Operator-Valued measures (POVM) that provide such probabilities. For observables with continuous spectrum, the constructed POVMs depend strongly on the resolution of the measurement device, a conclusion that persists even if we consider a quantum mechanical measurement device or the presence of an environment. We then examine the same issues in alternative interpretations of quantum theory. We first show that multi-time probabilities cannot be naturally defined in terms of a frequency operator. We next prove that local hidden variable theories cannot reproduce the predictions of quantum theory for sequential measurements, even when the degrees of freedom of the measuring apparatus are taken into account. Bohmian mechanics, however, does not fall in this category. We finally examine an alternative proposal that sequential measurements can be modelled by a process that does not satisfy the Kolmogorov axioms of probability. This removes contextuality without introducing non-locality, but implies that the empirical probabilities cannot be always defined (the event frequencies do not converge). We argue that the predictions of this hypothesis are not ruled out by existing experimental results (examining in particular the "which way" experiments); they are, however, distinguishable in principle.Comment: 56 pages, latex; revised and restructured. Version to appear in Found. Phy

Inflammation subverts hippocampal synaptic plasticity in experimental multiple sclerosis

Abnormal use-dependent synaptic plasticity is universally accepted as the main physiological correlate of memory deficits in neurodegenerative disorders. It is unclear whether synaptic plasticity deficits take place during neuroinflammatory diseases, such as multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). In EAE mice, we found significant alterations of synaptic plasticity rules in the hippocampus. When compared to control mice, in fact, hippocampal long-term potentiation (LTP) induction was favored over long-term depression (LTD) in EAE, as shown by a significant rightward shift in the frequency-synaptic response function. Notably, LTP induction was also enhanced in hippocampal slices from control mice following interleukin-1β (IL-1β) perfusion, and both EAE and IL-1β inhibited GABAergic spontaneous inhibitory postsynaptic currents (sIPSC) without affecting glutamatergic transmission and AMPA/NMDA ratio. EAE was also associated with selective loss of GABAergic interneurons and with reduced gamma-frequency oscillations in the CA1 region of the hippocampus. Finally, we provided evidence that microglial activation in the EAE hippocampus was associated with IL-1β expression, and hippocampal slices from control mice incubated with activated microglia displayed alterations of GABAergic transmission similar to those seen in EAE brains, through a mechanism dependent on enhanced IL-1β signaling. These data may yield novel insights into the basis of cognitive deficits in EAE and possibly of MS

Experimental tests of hidden variable theories from dBB to Stochastic Electrodynamics

In this paper we present some of our experimental results on testing hidden variable theories, which range from Bell inequalities measurements to a conclusive test of stochastic electrodynamics

TOpic: rare and special cases, the real "Strange cases"

Introduction: The bladder hernia represents approximately 1-3% of all inguinal hernias, where patients aged more than 50 years have a higher incidence (10%). Many factors contribute to the development of a bladder hernia, including the presence of a urinary outlet obstruction causing chronic bladder distention, the loss of bladder tone, pericystitis, the perivesical bladder fat protrusion and the obesity

RIM1α SUMOylation is required for fast synaptic vesicle exocytosis

The rapid, activity-dependent quantal presynaptic release of neurotransmitter is vital for brain function. The complex process of vesicle priming, fusion, and retrieval is very precisely controlled and requires thespatiotemporal coordination of multiple protein-protein interactions. Here, we show that posttranslational modification of the active zone protein Rab3-interacting molecule 1α (RIM1α) by the small ubiquitin-like modifier 1 (SUMO-1) functions as a molecular switch to direct these interactions and isessential for fast synaptic vesicle exocytosis. RIM1α SUMOylation at lysine residue K502 facilitatesthe clustering of CaV2.1 calcium channels andenhances the Ca2+ influx necessary for vesicular release, whereas non-SUMOylated RIM1α participates in the docking/priming of synaptic vesicles and maintenance of active zone structure. These results demonstrate that SUMOylation of RIM1α is a key determinant of rapid, synchronous neurotransmitter release, and the SUMO-mediated "switching" of RIM1α between binding proteins provides insight into the mechanisms underpinning synaptic function and dysfunction

Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release

Activation of c-Jun N-terminal kinase (JNK) signaling pathway is a critical step for neuronal death occurring in several neurological conditions. JNKs can be activated via receptor tyrosine kinases, cytokine receptors, G-protein coupled receptors and ligand-gated ion channels, including the NMDA glutamate receptors. While JNK has been generally associated with postsynaptic NMDA receptors, its presynaptic role remains largely unexplored. Here, by means of biochemical, morphological and functional approaches, we demonstrate that JNK and its scaffold protein JIP1 are also expressed at the presynaptic level and that the NMDA-evoked glutamate release is controlled by presynaptic JNK-JIP1 interaction. Moreover, using knockout mice for single JNK isoforms, we proved that JNK2 is the essential isoform in mediating this presynaptic event. Overall the present findings unveil a novel JNK2 localization and function, which is likely to play a role in different physiological and pathological conditions

NH2-truncated human tau induces deregulated mitophagy in neurons by aberrant recruitment of Parkin and UCHL-1: implications in Alzheimer's disease.

Disarrangement in functions and quality control of mitochondria at synapses are early events in Alzheimer's disease (AD) pathobiology. We reported that a 20-22 kDa NH2-tau fragment mapping between 26 and 230 amino acids of the longest human tau isoform (aka NH2htau): (i) is detectable in cellular and animal AD models, as well in synaptic mitochondria and cerebrospinal fluids (CSF) from human AD subjects; (ii) is neurotoxic in primary hippocampal neurons; (iii) compromises the mitochondrial biology both directly, by inhibiting the ANT-1-dependent ADP/ATP exchange, and indirectly, by impairing their selective autophagic clearance (mitophagy). Here, we show that the extensive Parkin-dependent turnover of mitochondria occurring in NH2htau-expressing post-mitotic neurons plays a pro-death role and that UCHL-1, the cytosolic Ubiquitin-C-terminal hydrolase L1 which directs the physiological remodeling of synapses by controlling ubiquitin homeostasis, critically contributes to mitochondrial and synaptic failure in this in vitro AD model. Pharmacological or genetic suppression of improper mitophagy, either by inhibition of mitochondrial targeting to autophagosomes or by shRNA-mediated silencing of Parkin or UCHL-1 gene expression, restores synaptic and mitochondrial content providing partial but significant protection against the NH2htau-induced neuronal death. Moreover, in mitochondria from human AD synapses, the endogenous NH2htau is stably associated with Parkin and with UCHL-1. Taken together, our studies show a causative link between the excessive mitochondrial turnover and the NH2htau-induced in vitro neuronal death, suggesting that pathogenetic tau truncation may contribute to synaptic deterioration in AD by aberrant recruitment of Parkin and UCHL-1 to mitochondria making them more prone to detrimental autophagic clearance