Effets des erreurs dans les coefficients structuraux d’un modèle intersectoriel « rectangulaire ». Une approche de type Monte-Carlo

The most simple rectangular input-output models use two rectangular matrices: R a market coefficient matrix, A* a production coefficient matrix. A given exogenous demand Xo determines the sectorial activity levels X* = [I — RA*]-1Xo. We assume that A* is random with expectation A. We study the distribution of the "error" X* — X with X = [I — RA]-1Xo.(1) For the statistically independent elements of A*, we analytically prove that X < EX*.(2) In the more realistic case of statistically dependent elements of A*.(a) One submatrix of A* with T non zero elements is chosen. The probabilistic model which generates the T coefficients is as follows: a* = (1 — μ)a + μ(S/n) b* où a* is the vector of the T random elements, a is the expectation of a* whose components are observed values of a real input-output model, S is the sum of components of a, μ is a parameter between zero and one, b* is a multinomial random vector with T components and parameters n, number of drawings during an experiment, and a/S, the corresponding probabilities.We control the variability of a* through μ and n. For a given experiment, we get a realisation of A* and we compute X*. K independent experiments allow us to estimate the expectation and the variance-covariance matrix of X*, simultaneous confidence intervals for the expectation of the components of X*, and also a few global measures of errors on X*.The Canadian model for 1961 (16 productive sectors, 40 commodities), is tested with that model.The main result is: the relative errors, measured according to the variation coefficients, are greatly reduced when we pass from the "errors" on a* to the corresponding "errors" on X*.(b) The same random model is also simultaneously applied to 2 or 3 sub-matrices of A*

Overexpression of CD97 in Intestinal Epithelial Cells of Transgenic Mice Attenuates Colitis by Strengthening Adherens Junctions

The adhesion G-protein-coupled receptor CD97 is present in normal colonic enterocytes but overexpressed in colorectal carcinoma. To investigate the function of CD97 in colorectal carcinogenesis, transgenic Tg(villin-CD97) mice overexpressing CD97 in enterocytes were generated and subjected to azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colitis-associated tumorigenesis. Unexpectedly, we found a CD97 cDNA copy number-dependent reduction of DSS-induced colitis in Tg compared to wild-type (WT) mice that was confirmed by applying a simple DSS protocol. Ultrastructural analysis revealed that overexpression of CD97 strengthened lateral cell-cell contacts between enterocytes, which, in contrast, were weakened in CD97 knockout (Ko) mice. Transepithelial resistance was not altered in Tg and Ko mice, indicating that tight junctions were not affected. In Tg murine and normal human colonic enterocytes as well as in colorectal cell lines CD97 was localized preferentially in E-cadherin-based adherens junctions. CD97 overexpression upregulated membrane-bound but not cytoplasmic or nuclear β-catenin and reduced phospho-β-catenin, labeled for degradation. This was associated with inactivation of glycogen synthase kinase-3β (GSK-3β) and activation of Akt. In summary, CD97 increases the structural integrity of enterocytic adherens junctions by increasing and stabilizing junctional β-catenin, thereby regulating intestinal epithelial strength and attenuating experimental colitis

Identification of a Sudden Cardiac Death Susceptibility Locus at 2q24.2 through Genome-Wide Association in European Ancestry Individuals

Sudden cardiac death (SCD) continues to be one of the leading causes of mortality worldwide, with an annual incidence estimated at 250,000–300,000 in the United States and with the vast majority occurring in the setting of coronary disease. We performed a genome-wide association meta-analysis in 1,283 SCD cases and >20,000 control individuals of European ancestry from 5 studies, with follow-up genotyping in up to 3,119 SCD cases and 11,146 controls from 11 European ancestry studies, and identify the BAZ2B locus as associated with SCD (P = 1.8×10−10). The risk allele, while ancestral, has a frequency of ∼1.4%, suggesting strong negative selection and increases risk for SCD by 1.92–fold per allele (95% CI 1.57–2.34). We also tested the role of 49 SNPs previously implicated in modulating electrocardiographic traits (QRS, QT, and RR intervals). Consistent with epidemiological studies showing increased risk of SCD with prolonged QRS/QT intervals, the interval-prolonging alleles are in aggregate associated with increased risk for SCD (P = 0.006)

Effets des erreurs dans les coefficients structuraux d’un modèle intersectoriel « rectangulaire ». Une approche de type Monte-Carlo

The most simple rectangular input-output models use two rectangular matrices: R a market coefficient matrix, A* a production coefficient matrix. A given exogenous demand Xo determines the sectorial activity levels X* = [I — RA*]-1Xo. We assume that A* is random with expectation A. We study the distribution of the "error" X* — X with X = [I — RA]-1Xo.

Disseminated infection caused by Sparganum proliferum in an AIDS patient.

International audienc

Genetic variation in myosin IXB is associated with ulcerative colitis.

BACKGROUND & AIMS: Common germline genetic variation in the 3' region of myosin IXB (MYO9B) has been associated recently with susceptibility to celiac disease, with a hypothesis that MYO9B variants might influence intestinal permeability. These findings suggested the current study investigating a possible further role for MYO9B variation in inflammatory bowel disease. METHODS: Eight single-nucleotide polymorphisms (SNPs) were selected to tag common haplotypes from the 35-kb 3' region of MYO9B. These included the strongest celiac disease-associated variants reported in a Dutch cohort. These SNPs were studied in 3 independently collected and genotyped case-control cohorts of European descent (UK, Dutch, and Canadian/Italian), comprising in total 2717 inflammatory bowel disease patients (1197 with Crohn's disease, 1520 with ulcerative colitis) and 4440 controls. RESULTS: Common variation in MYO9B was associated with susceptibility to inflammatory bowel disease in all 3 cohorts examined (most associated SNP, rs1545620; meta-analysis P = 1.9 x 10(-6); odds ratio, 1.2), with the same alleles showing association as reported for celiac disease. CONCLUSIONS: MYO9B genetic variants predispose to inflammatory bowel disease. Interestingly, rs1545620 is a nonsynonymous variant leading to an amino acid change (Ala1011Ser) in the third calmodulin binding IQ domain of MYO9B. Unlike previous variants (in other genes) reported to predispose to inflammatory bowel disease, the association at MYO9B was considerably stronger with ulcerative colitis, although weaker association with Crohn's disease also was observed. These data imply shared causal mechanisms underlying intestinal inflammatory diseases