RESUMO
Signal transducer and activator of transcription (STAT) is a family of cytoplasmic transcription factors including seven proteins of STAT-1, -2, -3, -4, -5A, -5B and -6. The genes encoding the STAT family are located on are located on chromosome 2 (STAT1 and STAT4), chromosome 12 (STAT2 and STAT6) and chromosome 17 (STAT3, STAT5A and STAT5B). Among these seven proteins, STAT3 and STAT5 have the strongest correlation with tumor progression, and ionizing radiation can affect STAT3 level. Continuous activation of STAT3 can regulate a variety of functions, including cell proliferation, cell cycle progression, apoptosis, angiogenesis and immune escape. STAT3 is highly complex in its biological function and activator action. Therefore, it is of great significance to further study the biological function and signaling pathway of STAT3.
RESUMO
The skeletal muscle materials sectioned from 20 cases of patients were histologically examined, who had all died of Kerschen disease. In addition to the simple atrophy and the hyaline degeneration which are generally regarded as lesions often found by autopsy of Kerschen disease, special types of muscle damage and reparation were noticed and described in the musculus gastrocnemius in 6 cases out of them, namely the myofibrillar dissociation of the muscle fibers and the connective tissue growth extending from the periphery to the internal part of the individual muscle fiber. The dissociated and even the necrotic muscle fibers could be distinctly limited within the area of the foci, while beyond the edge of the foci muscle fibers still remained almost unchanged. In the case of reparation the mesenchymatous elements in some region displayed their active action of ground substance production on the surface of the damaged fibers. But it was more noteworthy that a rare phenomenon happened: connective tissue growth got increased from outside into inside of the individual muscle fibers and at the same time it substituted for the position of the lost muscular substance. Thus in the cross section of a single complete muscle fiber muscular mass and connective tissue including its blood capillaries did stand side by side with an obvious contrast after the staining. This evidence naturally leads to the suggestion that a process of sarcolemmolysis may occur and allow the continuity of the connective tissue between the exterior and interior of a single muscle fiber. The disbanding of myofibrils within focus can also be explained by lysis of the sarcolemma and of its invagination, the transverse tubule system. In fact, it has not to be suggested, but was virtually revealed in electron microscopy, that sarcolemma of the damaged muscle fiber was lost. In place of the lost myofibrils a filamentous network was produced, which contained perhaps collagen stainable with aniline blue in Mallory's trichrome methode used for light microscopy. Theory of metaplasia about the reparation after the skeletal muscle lesions is however not supported by our observations. Besides, no regular correlation can be established between these special pathological changes of skeletal muscle and the Kerschen disease.