Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.59 (MIP)
 4,906 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies applying the minimal group paradigm to analyze social discrimination processes have been analyzing for the most part the behavior of individuals. The present experiment extends the minimal group paradigm to the group level. The aim of the present study was to compare the decisions made by real groups (N = 3 persons) with those made by single persons. The analysis of the total points given to the in- or the outgroup as well as the strategy MIP + MDI on F revealed that groups are significantly more biased towards the ingroup than individuals. On the other hand, individuals use the strategy F on MIP + MDI significantly more than groups and thus show a greater amount of fairness. These conclusions are qualified by a new method of identifying dominant strategies which shows that the dominant strategy used by individuals and groups is fairness. A theoretical explanation of the results is offered based on social identity theory, the groupthink model and self-awareness theory.
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PMID:[Real groups in the minimal group paradigm; does the group context work as corrective or catalysing agent for social discrimination?]. 1168 45

Prior studies and the efficacy of immunotherapies provide evidence that inflammation is mechanistic in pathogenesis of Duchenne muscular dystrophy. To identify putative pro-inflammatory mechanisms, we evaluated chemokine gene/protein expression patterns in skeletal muscle of mdx mice. By DNA microarray, reverse transcription-polymerase chain reaction, quantitative polymerase chain reaction, and immunoblotting, convergent evidence established the induction of six distinct CC class chemokine ligands in adult MDX: CCL2/MCP-1, CCL5/RANTES, CCL6/mu C10, CCL7/MCP-3, CCL8/MCP-2, and CCL9/MIP-1gamma. CCL receptors, CCR2, CCR1, and CCR5, also showed increased expression in mdx muscle. CCL2 and CCL6 were localized to both monocular cells and muscle fibers, suggesting that dystrophic muscle may contribute toward chemotaxis. Temporal patterns of CCL2 and CCL6 showed early induction and maintained expression in mdx limb muscle. These data raise the possibility that chemokine signaling pathways coordinate a spatially and temporally discrete immune response that may contribute toward muscular dystrophy. The chemokine pro-inflammatory pathways described here in mdx may represent new targets for treatment of Duchenne muscular dystrophy.
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PMID:Persistent over-expression of specific CC class chemokines correlates with macrophage and T-cell recruitment in mdx skeletal muscle. 1260 4