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

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

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

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

Search for R-parity violating supersymmetry via the LLE couplings lambda_{121}, lambda_{122} or lambda_{133} in ppbar collisions at sqrt(s)=1.96 TeV

A search for gaugino pair production with a trilepton signature in the framework of R-parity violating supersymmetry via the couplings lambda_121, lambda_122, or lambda_133 is presented. The data, corresponding to an integrated luminosity of L~360/pb, were collected from April 2002 to August 2004 with the D0 detector at the Fermilab Tevatron Collider, at a center-of-mass energy of sqrt(s)=1.96 TeV. This analysis considers final states with three charged leptons with the flavor combinations eel, mumul, and eetau (l=e or mu). No evidence for supersymmetry is found and limits at the 95% confidence level are set on the gaugino pair production cross section and lower bounds on the masses of the lightest neutralino and chargino are derived in two supersymmetric models.Comment: 9 pages, 4 figures (fig2 includes 3 subfigures

Search for W' boson production in the W'->tb decay channel

We present a search for the production of a new heavy gauge boson W' that decays to a top quark and a bottom quark. We have analyzed 230 pb^{-1} of data collected with the Dzero detector at the Fermilab Tevatron collider at a center-of-mass energy of 1.96 TeV. No significant excess of events above the standard model expectation is found in any region of the final state invariant mass distribution. We set upper limits on the production cross section of W' bosons times branching ratio to top quarks at the 95% confidence level for several different W' boson masses. We exclude masses between 200 GeV and 610 GeV for a W' boson with standard-model-like couplings, between 200 GeV and 630 GeV for a W' boson with right-handed couplings that is allowed to decay to both leptons and quarks, and between 200 GeV and 670 GeV for a W' boson with right-handed couplings that is only allowed to decay to quarks.Comment: 9 pages, 6 figures, accepted by Phys. Lett.

Measurement of the Bs0B^{0}_{s} Lifetime Using Semileptonic Decays

We report a measurement of the $B^0_{s}$ lifetime in the semileptonic decay channel $B^0_{s}\to D^-_s \mu^{+}\nu X$ (and its charge conjugate), using approximately 0.4 fb$^{-1}$ of data collected with the D0 detector during 2002 -- 2004. We have reconstructed 5176 $D^-_s \mu^{+}$ signal events, where the $D_s^-$ is identified via the decay $D_s^-\to \phi\pi^-$, followed by $\phi\to K^+ K^-$. Using these events, we have measured the $B^0_s$ lifetime to be $\tau(B^0_{s}) = 1.398 \pm 0.044$ $({stat}) ^{+0.028}_{-0.025}$ $({syst}) {ps}$. This is the most precise measurement of the $B_s^0$ lifetime to date.Comment: To appear in Phys. Rev. Lett., 7 pages, 2 figure

Measurement of the Lifetime Difference in the B_s^0 System

We present a study of the decay B_s^0 -> J/psi phi We obtain the CP-odd fraction in the final state at time zero, R_perp = 0.16 +/- 0.10 (stat) +/- 0.02 (syst), the average lifetime of the (B_s, B_sbar) system, tau (B_s^0) =1.39^{+0.13}_{-0.16} (stat) ^{+0.01}_{-0.02} (syst) ps, and the relative width difference between the heavy and light mass eigenstates, Delta Gamma/Gamma = (Gamma_L - Gamma_H)/Gamma =0.24^{+0.28}_{-0.38} (stat) ^{+0.03}_{-0.04} (syst). With the additional constraint from the world average of the B_s^0$lifetime measurements using semileptonic decays, we find tau (B_s^0)= 1.39 +/- 0.06 ~ps and Delta Gamma/\Gamma = 0.25^{+0.14}_{-0.15}. For the ratio of the B_s^0 and B^0 lifetimes we obtain tau(B_s^0)/tau(B^0)} = 0.91 +/- 0.09 (stat) +/- 0.003 (syst).Comment: submitted to Phys. Rev. Lett. FERMILAB-PUB-05-324-

Measurement of Semileptonic Branching Fractions of B Mesons to Narrow D** States

Using the data accumulated in 2002-2004 with the DO detector in proton-antiproton collisions at the Fermilab Tevatron collider with centre-of-mass energy 1.96 TeV, the branching fractions of the decays B -> \bar{D}_1^0(2420) \mu^+ \nu_\mu X and B -> \bar{D}_2^{*0}(2460) \mu^+ \nu_\mu X and their ratio have been measured: BR(\bar{b}->B) \cdot BR(B-> \bar{D}_1^0 \mu^+ \nu_\mu X) \cdot BR(\bar{D}_1^0 -> D*- pi+) = (0.087+-0.007(stat)+-0.014(syst))%; BR(\bar{b}->B)\cdot BR(B->D_2^{*0} \mu^+ \nu_\mu X) \cdot BR(\bar{D}_2^{*0} -> D*- \pi^+) = (0.035+-0.007(stat)+-0.008(syst))%; and (BR(B -> \bar{D}_2^{*0} \mu^+ \nu_\mu X)BR(D2*0->D*- pi+)) / (BR(B -> \bar{D}_1^{0} \mu^+ \nu_\mu X)\cdot BR(\bar{D}_1^{0}->D*- \pi^+)) = 0.39+-0.09(stat)+-0.12(syst), where the charge conjugated states are always implied.Comment: submitted to Phys. Rev. Let