Chiral Analysis of Quenched Baryon Masses

We extend to quenched QCD an earlier investigation of the chiral structure of the masses of the nucleon and the delta in lattice simulations of full QCD. Even after including the meson-loop self-energies which give rise to the leading and next-to-leading non-analytic behaviour (and hence the most rapid variation in the region of light quark mass), we find surprisingly little curvature in the quenched case. Replacing these meson-loop self-energies by the corresponding terms in full QCD yields a remarkable level of agreement with the results of the full QCD simulations. This comparison leads to a very good understanding of the origins of the mass splitting between these baryons.Comment: 23 pages, 6 figure

Quark contributions to baryon magnetic moments in full, quenched, and partially quenched QCD

The chiral nonanalytic behavior of quark-flavor contributions to the magnetic moments of octet baryons is determined in full, quenched and partially quenched QCD, using an intuitive and efficient diagrammatic formulation of quenched and partially quenched chiral perturbation theory. The technique provides a separation of quark-sector magnetic-moment contributions into direct sea-quark loop, valence-quark, indirect sea-quark loop and quenched valence contributions, the latter being the conventional view of the quenched approximation. Both meson and baryon mass violations of SU(3)-flavor symmetry are accounted for. Following a comprehensive examination of the individual quark-sector contributions to octet baryon magnetic moments, numerous opportunities to observe and test the underlying structure of baryons and the nature of chiral nonanalytic behavior in QCD and its quenched variants are discussed. In particular, the valence u-quark contribution to the proton magnetic moment provides the optimal opportunity to directly view nonanalytic behavior associated with the meson cloud of full QCD and the quenched meson cloud of quenched QCD. The u quark in Σ+ provides the best opportunity to display the artifacts of the quenched approximation.Derek B. Leinwebe

Non-invasive diagnosis of infarct artery patency after acute myocardial infarction by use of serial plasma troponin T concentrations: importance of measurement of peak levels

Objective-To confirm the validity of a previously described method for assessment of infarct artery patency involving serial measurements of creatine kinase activity by use of troponin T concentration as an independent plasma marker. Design-Streptokinase (1.5 x 10(6) units) was given intravenously to 60 patients within 6 h of onset of prolonged chest pain and ST segment elevation, and blood was taken for measurement of troponin T concentration at baseline and at 1, 2, 3, 4, 8, 12, 16, 20, and 24 h after starting treatment. Coronary arteriography was performed at 2 6 (SD 0 3) h. Plasma troponin T concentration was assessed by two methods: (1) as the absolute rise between 0 and 3 h; and (2) as the proportion of the total rise (from baseline to peak) over the same period. Accuracy for prediction of infarct artery patency, assessed by receiver operating characteristic curves, was compared for both methods of assessment using troponin T and was in turn compared with previously reported results on the same patients using serial measurements of creatine kinase activity. Results-Sufficient values for prediction of patency using troponin T were available in 53 patients. A rise in troponin T between 0 and 3 h to greater than or equal to 9% of peak concentration predicted angiographic patency with sensitivity of 94% and specificity of 100%. By contrast, at the optimum cutoff for absolute rate of rise (0.5 mu g/1/h) sensitivity was only 66% and specificity 86%. Comparable figures for creatine kinase were 92% and 91% (greater than or equal to 20% of peak by 3 h) and 62% and 78% (150 IU/1/h). Receiver operating curves confirmed better predictive accuracy for proportions over absolute rates of rise for both markers (P < 0.01). Conclusions-For accurate diagnosis of infarct artery patency using plasma markers it is necessary to express the rate of rise as a proportion of the peak level. Analysed in this way, both creatine kinase and troponin T are suitable for use in randomised trials of new thrombolytic or adjuvant drugs

Independent and combined effects of airway remodelling and allergy on airway responsiveness

Airway remodelling and allergic inflammation are key features of airway hyperresponsiveness (AHR) in asthma; however, their interrelationships are unclear. The present study investigated the separate and combined effects of increased airway smooth muscle (ASM) layer thickness and allergy on AHR. We integrated a protocol of ovalbumin (OVA)-induced allergy into a non-inflammatory mouse model of ASM remodelling induced by conditional and airway-specific expression of transforming growth factor-a (TGF-a) in early growth response-1 (Egr-1)-deficient transgenic mice, which produced thickening of the ASM layer following ingestion of doxycycline. Mice were sensitised to OVA and assigned to one of four treatment groups: Allergy - normal chow diet and OVA challenge, Remodelling - doxycycline in chow and saline challenge, Allergy and Remodelling - doxycycline in chow and OVA challenge, and Control - normal chow diet and saline challenge. Airway responsiveness to methacholine (MCh) and histology were assessed. Compared with the Control group, airway responsiveness to MCh was increased in the Allergy group, independent of changes in wall structure, whereas airway responsiveness in the Remodelling group was increased independent of exposure to aeroallergen. The combined effects of allergy and remodelling on airway responsiveness were greater than either of them alone. There was a positive relationship between the thickness of the ASM layer with airway responsiveness, which was shifted upward in the presence of allergy. These findings support allergy and airway remodelling as independent causes of variable and excessive airway narrowing