Application of 'Optimised' Perturbation Theory to Determination of alpha_s(M_Z^2) from Hadronic Event Shape Observables in e+e- Annihilation

We have applied so-called `optimised' perturbation theory to resolve the renormalisation-scale (mu) ambiguity of exact O(alpha_s^2) QCD calculations of event shape observables in e+e- --> hadrons. We fitted the optimised predictions for 15 observables to hadronic Z0 decay data from the SLD experiment to determine alpha_s(M_Z^2). Comparing with results using the physical scale mu = M_Z we found no reduction in the scatter among alpha_s(M_Z^2) values from the 15 observables, implying that the O(alpha_s^2) predictions with optimised scales are numerically no closer to the exact all-orders results than those with the physical scale.Comment: 19 pages for text plus 4 pages for figures which were tar'ed, gzip'ed, uuencoded and put as one package. Original text is in PS format and original figures are in EPS forma

Circulating Mycobacterium tuberculosis DosR latency antigen-specific, polyfunctional, regulatory IL10(+) Th17 CD4 T-cells differentiate latent from active tuberculosis

Immunogenetics and cellular immunology of bacterial infectious disease

Effects of the Private-Label Invasion in Food Industries

Using supermarket scanner data, we test a variety of hypotheses from trade journals about the invasion of private-label food products. According to conventional industry wisdom, name-brand firms defended their brands against new private-label products by lowering their prices, engaging in additional promotional activities, and increasingly differentiating their products. Our empirical evidence is inconsistent with these beliefs. Copyright 2002, Oxford University Press.

HIV Skews a Balanced Mtb-Specific Th17 Response in Latent Tuberculosis Subjects to a Pro-inflammatory Profile Independent of Viral Load

HIV infection predisposes latent tuberculosis-infected (LTBI) subjects to active TB. This study is designed to determine whether HIV infection of LTBI subjects compromises the balanced Mycobacterium tuberculosis (Mtb)-specific T helper 17 (Th17) response of recognized importance in anti-TB immunity. Comparative analysis of Mtb- and cytomegalovirus (CMV)-specific CD4(+) T cell responses demonstrates a marked dampening of the Mtb-specific CD4(+) T cell effectors and polyfunctional cells while preserving CMV-specific response. Additionally, HIV skews the Mtb-specific Th17 response in chronic HIV-infected LTBI progressors, but not long-term non-progressors (LTNPs), with preservation of pro-inflammatory interferon (IFN)-gamma(+)/interleukin-17(+) (IL-17(+)) and significant loss of anti-inflammatory IL-10(+)/IL-17(+) effectors that is restored by anti-retroviral therapy (ART). HIV-driven impairment of Mtb-specific response cannot be attributed to preferential infection as cell-associated HIV DNA and HIV RNA reveal equivalent viral burden in CD4(+) T cells from different antigen specificities. We therefore propose that beyond HIV-induced loss of Mtb-specific CD4(+) T cells, the associated dysregulation of Mtb-specific T cell homeostasis can potentially enhance the onset of TB in LTBI subjects.Immunogenetics and cellular immunology of bacterial infectious disease

HIV Skews a balanced Mtb-specific Th17 response in latent tuberculosis subjects to a pro-inflammatory profile independent of viral load

HIV infection predisposes latent tuberculosis-infected (LTBI) subjects to active TB. This study is designed to determine whether HIV infection of LTBI subjects compromises the balanced Mycobacterium tuberculosis (Mtb)-specific T helper 17 (Th17) response of recognized importance in anti-TB immunity. Comparative analysis of Mtb- and cytomegalovirus (CMV)-specific CD4(+) T cell responses demonstrates a marked dampening of the Mtb-specific CD4(+) T cell effectors and polyfunctional cells while preserving CMV-specific response. Additionally, HIV skews the Mtb-specific Th17 response in chronic HIV-infected LTBI progressors, but not long-term non-progressors (LTNPs), with preservation of pro-inflammatory interferon (IFN)-gamma(+)/interleukin-17(+) (IL-17(+)) and significant loss of anti-inflammatory IL-10(+)/IL-17(+) effectors that is restored by anti-retroviral therapy (ART). HIV-driven impairment of Mtb-specific response cannot be attributed to preferential infection as cell-associated HIV DNA and HIV RNA reveal equivalent viral burden in CD4(+) T cells from different antigen specificities. We therefore propose that beyond HIV-induced loss of Mtb-specific CD4(+) T cells, the associated dysregulation of Mtb-specific T cell homeostasis can potentially enhance the onset of TB in LTBI subjects