The Bath metrology index as assessed by a trained and an untrained rater in patients with spondylarthropathy: a study of intra- and inter-rater agreements.

The Bath ankylosing spondylitis metrology index (BASMI; range 0-10) has gained widespread use in daily clinical practice as an objective measure of spinal stiffness not only in patients with ankylosing spondylitis (AS) but also in patients with other spondylarthropathies (SpA). We examined intra-rater and inter-rater reproducibility of BASMI scoring in 30 Danish patients with SpA (median age 40 years, range 22-56 years) fulfilling the European Spondylarthropathy Study Group criteria, 25 of them satisfying the modified New York Criteria for AS. Measurements were performed twice on two different days (median interval 7 days, range 4-11) by a trained physiotherapist (PT) and by an untrained nurse who had undergone a single 1-h training session with the PT. The median BASMI score obtained by the PT on the two test days was 3.5 (range 1-8) and 3.0 (range 1-8), respectively (NS). Test-retest BASMI scores from the PT were significantly correlated (r(s) = 0.95, p < 0.0001). The 95% likely range for the difference between a patient's BASMI scores from two tests was +/-1.4 corresponding to a minimal detectable difference of +/-2 in the individual patient as the scale consists of intervals of 1. Similar results were achieved by the nurse. BASMI scores obtained by the two raters were significantly inter-correlated (r(s) = 0.95, p < 0.0001). The mean difference between paired BASMI scores obtained by the nurse and the PT on test day 1 was -0.2 with a minimal detectable difference of +/-2. A similar result was found using data from test day 2. In conclusion, a change in BASMI less than 2 may be due solely to expected random measurement error. A single 1-h training session allowed an untrained nurse to obtain BASMI results almost identical to those of an experienced PT.

Activation of the extracellular signal-regulated protein kinase cascade in the hippocampal CA1 region in a rat model of global cerebral ischemic preconditioning.

A short period of sublethal preconditioning ischemia (3 min) followed by two days of reperfusion provides almost complete protection against ischemic cell death induced by a second (9 min) lethal ischemic episode. Here, we have investigated the extracellular signal-regulated protein kinase kinase and extracellular signal-regulated protein kinase, two kinases known to activate gene transcription and to be of importance for cell survival, after sublethal preconditioning ischemia in the rat hippocampal CA1 region. The activation levels of these two kinases were also studied after a second ischemic episode both in preconditioned and nonconditioned brains. An increased phosphorylation of the extracellular signal-regulated protein kinase kinase was found in neuronal cell bodies, particularly in the nucleus, 30 min, 4 h and two days of reperfusion after preconditioning ischemia. Two days after preconditioning ischemia both extracellular signal-regulated protein kinase kinase and extracellular signal-regulated protein kinase were markedly phosphorylated. During the early reperfusion period (30 min) after the second ischemic insult the phosphorylation levels of these two kinases were increased in both nonconditioned and preconditioned brains. In the late reperfusion time (one day), the phosphorylation levels of the extracellular signal-regulated protein kinase kinase and extracellular signal-regulated protein kinase were decreased in preconditioned brains, but remained elevated in nonconditioned brains. We conclude that phosphorylation of the extracellular signal-regulated protein kinase kinase and extracellular signal-regulated protein kinase after sublethal ischemia correlates with the neuroprotection induced by preconditioning, possibly by transcriptional activation of neuroprotective genes. Also, preconditioning enhances normalization of the disturbed cell signaling through the extracellular signal-regulated protein kinase cascade induced by lethal ischemia.

Characterization of subpopulations of T-cell receptor intermediate (TCRint) T cells.

CD1-autoreactive T cells of two types have been demonstrated among T cells expressing the T-cell receptor (TCR) alphabeta at intermediate levels (TCRint cells). One type constitutes a major fraction of the natural killer (NK)1.1+ TCRint population in C57BL/6 (B6) mice and carries a restricted TCR composed of an alpha-chain with an invariant Valpha14-J281 rearrangement, and a beta-chain using Vbeta8. 2, 7 or 2. The second type utilises a variety of TCR and was derived from CD4+ cells in mice lacking MHC class II. To increase our understanding of the two different CD1-reactive subsets, we have investigated and compared the populations of origin: NK1.1+ and NK1. 1- TCRint subsets from MHC class II-deficient mice and CD4+NK1.1+ T cells from B6 mice. The three TCRint populations shared a phenotype indicating previous activation, and contained low frequencies of cells expressing NK receptors of the Ly49 family. In contrast to control CD4+ cells, the three TCRint subsets produced high amounts of interleukin (IL)-4 and interferon (IFN)-gamma after activation. Importantly, no IL-10 could be detected in either TCRint population, implying a distinct function for these cells, different from those of conventional CD8+ and CD4+ cells, including the typical T-helper 2 (Th2) cell. Analysis of TCR expression indicated that the proportion of cells using the semi-invariant Valpha14/Vbeta8.2-type TCR was lower in NK1.1+ cells from MHC class II-negative mice than in CD4+NK1.1+ B6 cells. Further, usage of the Valpha14-J281 rearrangement was also demonstrated among NK1.1- TCRint cells.