We conclude that only S-100B in severe traumatic brain injury has consistently demonstrated the ability to predict injury and outcome in adults. The number of studies with protein degradation products is insufficient especially in the pediatric care. Cohort studies with well-defined end points and further neuroproteomic search for biomarkers in mild injury should be triggered. After critically reviewing the study designs, we found that large homogenous patient populations, consistent injury, and outcome measures prospectively determined cutoff values, and a combined use of different predictors should be considered in future studies.
It is generally believed that the apparent diffusion coefficient (ADC) changes measured by diffusion-weighted imaging (DWI) in brain pathologies are related to alterations in the water compartments. The aim of this study was to elucidate the role of compartmentalization in DWI via biexponential analysis of the signal decay due to diffusion. DWI experiments were performed on mouse brain over an extended range of b-values (up to 10000 mm -2 s) under intact, global ischemic, and cold-injury conditions. DWI was additionally applied to centrifuged human erythrocyte samples with a negligible extracellular space. Biexponential signal decay was found to occur in the cortex of the intact mouse brain. During global ischemia, in addition to a drop in the ADC in both components, a shift from the volume fraction of the rapidly diffusing component to the slowly diffusing one was observed. In cold injury, the biexponential signal decay was still present despite the electron-microscopically validated disintegration of the membranes. The biexponential function was also applicable for fitting of the data obtained on erythrocyte samples Diffusion-weighted imaging (DWI) and measurements of the apparent diffusion coefficient (ADC) play important roles in clinical diagnosis. Alterations in the ADC of water occur in many pathological conditions, such as stroke (1,2), diffuse axonal injury (3), tumors (4), and epilepsy (5). Nevertheless, despite the widespread use of DWI, the underlying mechanisms that cause these changes in ADC are still unclear. Many theories have been put forward to explain the phenomenon, including: 1) water shifts from the extracellular space to the more viscous intracellular space (2,6,7); 2) a loss of cytoplasmic streaming and/or an increased intracellular viscosity results in a drop in ADC (8,9); 3) the extracellular space becomes more tortuous during such a water shift (10 -12); and 4) water goes through a transition from a sol state to a gel state (13).It is clear that, with exception of the latter theory, the physiological compartments appear to be involved. Van Zijl et al. (14) reported evidence suggesting that complete separation of the intra-and extracellular spaces in cell cultures was feasible by means of DW spectroscopy. However, the work of Niendorf et al. (15) on rat brain indicated that the correspondence between the water populations determined in vivo by localized DW spectroscopy and the extra-and intracellular compartments is not straightforward. Nevertheless, several studies involving experimental models (15-17) have indicated that the changes in these volume fractions, as assessed by NMR, follow the alterations in the water compartments in the brain. It becomes more difficult to understand the diffusion properties of water molecules in nervous tissue when the b-value range is extended over 10000 mm -2 s, where more than two exponentially decaying components can be determined (18).The results of the above-cited studies indicate that the origin of the water signal and the multiexponential funct...
The anti-tumor response of human invariant NKT (NKT) cells is well established. A novel T cell subset, mucosal-associated invariant T (MAIT) cells, possesses similar regulatory properties to NKT cells in autoimmune models and disease. Here, we examined the clonality of four T cell subsets expressing invariant alphaTCR, including Valpha7.2-Jalpha33 of MAIT cells, in 19 kidney and brain tumors. The MAIT clonotype was identified and co-expressed with NKT clonotype in half of the tumors. In contrast, two other invariant T cell clonotypes (Valpha4 and Valpha19) were not present in tumors. Such tumors also expressed Vbeta2 and Vbeta13, the restricted TCRbeta chain of MAIT cells and the antigen-presenting molecule MR1. A high percentage of infiltrating T cells was CD8+ and expressed HLA-DR suggesting activation. Although the MAIT alphaTCR was identified in both peripheral CD56+ and CD56- subsets, infiltrating lymphocytes were CD56 negative. The clonal presence of MAIT cells in tumors correlated with the expression of pro-inflammatory cytokines but no IL-4, IL-5 and IL-10, suggesting that a pro-inflammatory subset of human MAIT cells may exist. Our data imply that a CD56- subset of MAIT cells may participate in tumor immune responses similarly to NKT cells.
The presence of m3AChR(213-228) antibodies is a common feature in pSS. Although it is significantly more common in pSS than in the comparison groups, anti-m3AChR(213-228) positivity is not exclusive to pSS.
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