Marginal distributions in (2N)(\bf 2N)-dimensional phase space and the quantum (N+1)(\bf N+1) marginal theorem

We study the problem of constructing a probability density in 2N-dimensional phase space which reproduces a given collection of $n$ joint probability distributions as marginals. Only distributions authorized by quantum mechanics, i.e. depending on a (complete) commuting set of $N$ variables, are considered. A diagrammatic or graph theoretic formulation of the problem is developed. We then exactly determine the set of ``admissible'' data, i.e. those types of data for which the problem always admits solutions. This is done in the case where the joint distributions originate from quantum mechanics as well as in the case where this constraint is not imposed. In particular, it is shown that a necessary (but not sufficient) condition for the existence of solutions is $n\leq N+1$. When the data are admissible and the quantum constraint is not imposed, the general solution for the phase space density is determined explicitly. For admissible data of a quantum origin, the general solution is given in certain (but not all) cases. In the remaining cases, only a subset of solutions is obtained.Comment: 29 pages (Work supported by the Indo-French Centre for the Promotion of Advanced Research, Project Nb 1501-02). v2 to add a report-n

Joint Probabilities Reproducing Three EPR Experiments On Two Qubits

An eight parameter family of the most general nonnegative quadruple probabilities is constructed for EPR-Bohm-Aharonov experiments when only 3 pairs of analyser settings are used. It is a simultaneous representation of 3 Bohr-incompatible experimental configurations valid for arbitrary quantum states.Comment: Typo corrected in abstrac

Altered Prostasin (CAP1/Prss8) Expression Favors Inflammation and Tissue Remodeling in DSS-induced Colitis.

Inflammatory bowel diseases (IBD) including ulcerative colitis and Crohn's disease are diseases with impaired epithelial barrier function. We aimed to investigate whether mutated prostasin and thus, reduced colonic epithelial sodium channel activity predisposes to develop an experimentally dextran sodium sulfate (DSS)-induced colitis. Wildtype, heterozygous (fr/+), and homozygous (fr/fr) prostasin-mutant rats were treated 7 days with DSS followed by 7 days of recovery and analyzed with respect to histology, clinicopathological parameters, inflammatory marker mRNA transcript expression, and sodium transporter protein expression. In this study, a more detailed analysis on rat fr/fr colons revealed reduced numbers of crypt and goblet cells, and local angiodysplasia, as compared with heterozygous (fr/+) and wildtype littermates. Following 2% DSS treatment for 7 days followed by 7 days recovery, fr/fr animals lost body weight, and reached maximal diarrhea score and highest disease activity after only 3 days, and strongly increased cytokine levels. The histology score significantly increased in all groups, but fr/fr colons further displayed pronounced histological alterations with near absence of goblet cells, rearrangement of the lamina propria, and presence of neutrophils, eosinophils, and macrophages. Additionally, fr/fr colons showed ulcerations and edemas that were absent in fr/+ and wildtype littermates. Following recovery, fr/fr rats reached, although significantly delayed, near-normal diarrhea score and disease activity, but exhibited severe architectural remodeling, despite unchanged sodium transporter protein expression. In summary, our results demonstrate a protective role of colonic prostasin expression against experimental colitis, and thus represent a susceptibility gene in the development of inflammatory bowel disease

Exchange operator formalism for N-body spin models with near-neighbors interactions

We present a detailed analysis of the spin models with near-neighbors interactions constructed in our previous paper [Phys. Lett. B 605 (2005) 214] by a suitable generalization of the exchange operator formalism. We provide a complete description of a certain flag of finite-dimensional spaces of spin functions preserved by the Hamiltonian of each model. By explicitly diagonalizing the Hamiltonian in the latter spaces, we compute several infinite families of eigenfunctions of the above models in closed form in terms of generalized Laguerre and Jacobi polynomials.Comment: RevTeX, 31 pages, no figures; important additional conten

SLC2A9 (GLUT9) mediates urate reabsorption in the mouse kidney.

Uric acid (UA) is a metabolite of purine degradation and is involved in gout flairs and kidney stones formation. GLUT9 (SLC2A9) was previously shown to be a urate transporter in vitro. In vivo, humans carrying GLUT9 loss-of-function mutations have familial renal hypouricemia type 2, a condition characterized by hypouricemia, UA renal wasting associated with kidney stones, and an increased propensity to acute renal failure during strenuous exercise. Mice carrying a deletion of GLUT9 in the whole body are hyperuricemic and display a severe nephropathy due to intratubular uric acid precipitation. However, the precise role of GLUT9 in the kidney remains poorly characterized. We developed a mouse model in which GLUT9 was deleted specifically along the whole nephron in a tetracycline-inducible manner (subsequently called kidney-inducible KO or kiKO). The urate/creatinine ratio was increased as early as 4 days after induction of the KO and no GLUT9 protein was visible on kidney extracts. kiKO mice are morphologically identical to their wild-type littermates and had no spontaneous kidney stones. Twenty-four-hour urine collection revealed a major increase of urate urinary excretion rate and of the fractional excretion of urate, with no difference in urate concentration in the plasma. Polyuria was observed, but kiKO mice were still able to concentrate urine after water restriction. KiKO mice displayed lower blood pressure accompanied by an increased heart rate. Overall, these results indicate that GLUT9 is a crucial player in renal handling of urate in vivo and a putative target for uricosuric drugs

Infrared Fixed Point Structure in Minimal Supersymmetric Standard Model with Baryon and Lepton Number Violation

We study in detail the renomalization group evolution of Yukawa couplings and soft supersymmetry breaking trilinear couplings in the minimal supersymmetric standard model with baryon and lepton number violation. We obtain the exact solutions of these equations in a closed form, and then depict the infrared fixed point structure of the third generation Yukawa couplings and the highest generation baryon and lepton number violating couplings. Approximate analytical solutions for these Yukawa couplings and baryon and lepton number violating couplings, and the soft supersymmetry breaking couplings are obtained in terms of their initial values at the unification scale. We then numerically study the infrared fixed surfaces of the model, and illustrate the approach to the fixed points.Comment: 16 pages REVTeX, figures embedded as epsfigs, replaced with version to appear in Physical Review D, minor typographical errors eliminated and references reordered, figures correcte

On quaternary complex Hadamard matrices of small orders

One of the main goals of design theory is to classify, characterize and count various combinatorial objects with some prescribed properties. In most cases, however, one quickly encounters a combinatorial explosion and even if the complete enumeration of the objects is possible, there is no apparent way how to study them in details, store them efficiently, or generate a particular one rapidly. In this paper we propose a novel method to deal with these difficulties, and illustrate it by presenting the classification of quaternary complex Hadamard matrices up to order 8. The obtained matrices are members of only a handful of parametric families, and each inequivalent matrix, up to transposition, can be identified through its fingerprint.Comment: 7 page

Disrupting MLC1 and GlialCAM and ClC-2 interactions in leukodystrophy entails glial chloride channel dysfunction

Defects in the astrocytic membrane protein MLC1, the adhesion molecule GlialCAM or the chloride channel ClC-2 underlie human leukoencephalopathies. Whereas GlialCAM binds ClC-2 and MLC1, and modifies ClC-2 currents in vitro, no functional connections between MLC1 and ClC-2 are known. Here we investigate this by generating loss-of-function Glialcam and Mlc1 mouse models manifesting myelin vacuolization. We find that ClC-2 is unnecessary for MLC1 and GlialCAM localization in brain, whereas GlialCAM is important for targeting MLC1 and ClC-2 to specialized glial domains in vivo and for modifying ClC-2's biophysical properties specifically in oligodendrocytes (OLs), the cells chiefly affected by vacuolization. Unexpectedly, MLC1 is crucial for proper localization of GlialCAM and ClC-2, and for changing ClC-2 currents. Our data unmask an unforeseen functional relationship between MLC1 and ClC-2 in vivo, which is probably mediated by GlialCAM, and suggest that ClC-2 participates in the pathogenesis of megalencephalic leukoencephalopathy with subcortical cysts

Nonminimal Supersymmetric Standard Model with Baryon and Lepton Number Violation

We carry out a comprehensive analysis of the nonminimal supersymmetric standard model (NMSSM) with baryon and lepton number violation. We catalogue the baryon and lepton number violating dimension four and five operators of the model. We then study the renormalization group evolution and infrared stable fixed points of the Yukawa couplings and the soft supersymmetry breaking trilinear couplings of this model with baryon and lepton number (and R-parity) violation involving the heaviest generations. We show analytically that in the Yukawa sector of the NMSSM there is only one infrared stable fixed point. This corresponds to a non-trivial fixed point for the top-, bottom-quark Yukawa couplings and the $B$ violating coupling $\lambda_{233}''$, and a trivial one for all other couplings. All other possible fixed points are either unphysical or unstable in the infrared region. We also carry out an analysis of the renormalization group equations for the soft supersymmetry breaking trilinear couplings, and determine the corresponding fixed points for these couplings. We then study the quasi-fixed point behaviour, both of the third generation Yukawa couplings and the baryon number violating coupling, and those of the soft supersymmetry breaking trilinear couplings. From the analysis of the fixed point behaviour, we obtain upper and lower bounds on the baryon number violating coupling $\lambda_{233}''$, as well as on the soft supersymmetry breaking trilinear couplings. Our analysis shows that the infrared fixed point behavior of NMSSM with baryon and lepton number violation is similar to that of MSSM.Comment: 35 pages, Revtex, 6 eps fig

How can the Odderon be detected at RHIC and LHC

The Odderon remains an elusive object, 33 years after its invention. The Odderon is now a fundamental object in QCD and CGC and it has to be found experimentally if QCD and CGC are right. In the present paper, we show how to find it at RHIC and LHC. The most spectacular signature of the Odderon is the predicted difference between the differential cross-sections for proton-proton and antiproton-proton at high s and moderate t. The experiment can be done by using the STAR detector at RHIC and by combining these future data with the already present UA4/2 data. The Odderon could also be found by ATLAS exeperiment at LHC by performing a high-precision measurement of the real part of the hadron elastic scattering amplitude at small t.Comment: 14 pages, 16 figures, two typographical errors corrected and acknowledgments adde