FOOD DISTRIBUTION CHANGES FROM A JAPANESE PERSPECTIVE

Agribusiness,

Householder transformations and optimal linear combinations

Several theorems related to the Householder transformation and separability criteria are proven. Orthogonal transformations, topology, divergence, mathematical matrices, and group theory are discussed

Delamination growth in composite materials

The Double Cantilever Beam (DCB) and the End Notched Flexure (ENF) specimens are employed to characterize MODE I and MODE II interlaminar fracture resistance of graphite/epoxy (CYCOM 982) and graphite/PEEK (APC2) composites. Sizing of test specimen geometries to achieve crack growth in the linear elastic regime is presented. Data reduction schemes based upon beam theory are derived for the ENF specimen and include the effects of shear deformation and friction between crack surfaces on compliance, C, and strain energy release rate, G sub II. Finite element (FE) analyses of the ENF geometry including the contact problem with friction are presented to assess the accuracy of beam theory expressions for C and G sub II. Virtual crack closure techniques verify that the ENF specimen is a pure Mode II test. Beam theory expressions are shown to be conservative by 20 to 40 percent for typical unidirectional test specimen geometries. A FE parametric study investigating the influence of delamination length and depth, span, thickness and material properties on G sub II is presented. Mode I and II interlaminar fracture test results are presented. Important experimental parameters are isolated, such as precracking techniques, rate effects, and nonlinear load-deflection response. It is found that subcritical crack growth and inelastic materials behavior, responsible for the observed nonlinearities, are highly rate-dependent phenomena with high rates generally leading to linear elastic response

Delamination growth in composite materials

Research related to growth of an imbedded through-width delamination (ITWD) in a compression loaded composite structural element is presented. Composites with widely different interlaminar fracture resistance were examined, viz., graphite/epoxy (CYCOM 982) and graphite/PEEK (APC-2). The initial part of the program consisted of characterizing the material in tension, compression and shear mainly to obtain consistent material properties for analysis, but also as a check of the processing method developed for the thermoplastic APC-2 material. The characterization of the delamination growth in the ITWD specimen, which for the unidirectional case is essentially a mixed Mode 1 and 2 geometry, requires verified mixed-mode growth criteria for the two materials involved. For this purpose the main emphasis during this part of the investigation was on Mode 1 and 2 fracture specimens, namely the Double Cantilever Beam (DCB) and End Notched Flexure (ENF) specimens

Combination schemes for turning point prediction

We propose new forecast combination schemes for predicting turning points of business cycles. The combination schemes deal with the forecasting performance of a given set of models and possibly providing better turning point predictions. We consider turning point predictions generated by autoregressive (AR) and Markov-Switching AR models, which are commonly used for business cycle analysis. In order to account for parameter uncertainty we consider a Bayesian approach to both estimation and prediction and compare, in terms of statistical accuracy, the individual models and the combined turning point predictions for the United States and Euro area business cycles

Fibrin Facilitates Both Innate and T Cell-Mediated Defense against Yersinia pestis

The gram-negative bacterium Yersinia pestis causes plague, a rapidly progressing and often fatal disease. The formation of fibrin at sites of Y. pestis infection supports innate host defense against plague, perhaps by providing a non-diffusible spatial cue that promotes the accumulation of inflammatory cells expressing fibrin-binding integrins. This report demonstrates that fibrin is an essential component of T cell-mediated defense against plague but can be dispensable for antibody-mediated defense. Genetic or pharmacologic depletion of fibrin abrogated innate and T cell-mediated defense in mice challenged intranasally with Y. pestis. The fibrin-deficient mice displayed reduced survival, increased bacterial burden, and exacerbated hemorrhagic pathology. They also showed fewer neutrophils within infected lung tissue and reduced neutrophil viability at sites of liver infection. Depletion of neutrophils from wild type mice weakened T cell-mediated defense against plague. The data suggest that T cells combat plague in conjunction with neutrophils, which require help from fibrin in order to withstand Y. pestis encounters and effectively clear bacteria

A comprehensive study on the role of the Yersinia pestis virulence markers in an animal model of pneumonic plague

We determined the role of Yersinia pestis virulence markers in an animal model of pneumonic plague. Eleven strains of Y. pestis were characterized using PCR assays to detect the presence of known virulence genes both encoded by the three plasmids as well as chromosomal markers. The virulence of all Y. pestis strains was compared in a mouse model for pneumonic plague. The presence of all known virulence genes correlated completely with virulence in the Balb/c mouse model. Strains which lacked HmsF initially exhibited visible signs of disease whereas all other strains (except wild-type strains) did not exhibit any disease signs. Forty-eight hours post-infection, mice which had received HmsF– strains regained body mass and were able to control infection; those infected with strains possessing a full complement of virulence genes suffered from fatal disease. The bacterial loads observed in the lung and other tissues reflected the observed clinical signs as did the cytokine changes measured in these animals. We can conclude that all known virulence genes are required for the establishment of pneumonic plague in mammalian animal models, the role of HmsF being of particular importance in disease progression

Association between variations in the TLR4 gene and incident type 2 diabetes is modified by the ratio of total cholesterol to HDL-cholesterol

<p>Abstract</p> <p>Background</p> <p>Toll-like receptor 4 (TLR4), the signaling receptor for lipopolysaccharides, is an important member of the innate immunity system. Since several studies have suggested that type 2 diabetes might be associated with changes in the innate immune response, we sought to investigate the association between genetic variants in the <it>TLR4 </it>gene and incident type 2 diabetes.</p> <p>Methods</p> <p>A case-cohort study was conducted in initially healthy, middle-aged subjects from the MONICA/KORA Augsburg studies including 498 individuals with incident type 2 diabetes and 1,569 non-cases. Seven SNPs were systematically selected in the <it>TLR4 </it>gene and haplotypes were reconstructed.</p> <p>Results</p> <p>The effect of <it>TLR4 </it>SNPs on incident type 2 diabetes was modified by the ratio of total cholesterol to high-density lipoprotein cholesterol (TC/HDL-C). In men, four out of seven <it>TLR4 </it>variants showed significant interaction with TC/HDL-C after correction for multiple testing (p < 0.01). The influence of the minor alleles of those variants on the incidence of type 2 diabetes was observed particularly for male patients with high values of TC/HDL-C. Consistent with these findings, haplotype-based analyses also revealed that the effect of two haplotypes on incident type 2 diabetes was modified by TC/HDL-C in men (p < 10^-3). However, none of the investigated variants or haplotypes was associated with type 2 diabetes in main effect models without assessment of effect modifications.</p> <p>Conclusion</p> <p>We conclude that minor alleles of several <it>TLR4 </it>variants, although not directly associated with type 2 diabetes might increase the risk for type 2 diabetes in subjects with high TC/HDL-C. Additionally, our results confirm previous studies reporting sex-related dissimilarities in the development of type 2 diabetes.</p