Search

TC25G alloy was heat treated at 950 °C/3 h, AC + 580 °C/6 h, AC and the bimodal structure with primary α phase + β transition structure was obtained. The creep properties of the alloy were tested in 550–600 °C/150–250 MPa. The results show that the precipitations of silicide and α2 phase is accompanied by the creep process. α2 phase plays a dispersion strengthening role in both the primary and steady-state creep stages. However, in the accelerated creep stage, the mechanism of α2 phase and dislocation changes from cutting mechanism to bypassing mechanism, and the strengthening effect is weakened. Silicide inhibits grain boundary slip mainly in the primary creep stage, and inhibits dislocation slip in the steady-state and accelerated creep stages. At 550 °C, n = 1.6 and Q = 280–371 kJ/mol (150–250 MPa) indicate that the creep of the alloy is a self-diffusion process, and the creep deformation is mainly controlled by dislocation slip. At 570–600 °C, n = 3.2 indicates that the dislocation climb controls the creep deformation. Meanwhile, compared with Q = 274 kJ/mol at low stress (150 MPa), Q = 365 kJ/mol at the high stress (200–250 MPa) indicates that the second phase precipitation enhancement is enhanced. [ABSTRACT FROM AUTHOR]

Previously, we demonstrated that β1,4galactosyltransferase (gal-T1) reversibly segregates from α2,6sialyltransferase (ST6Gal) to swollen vesicles after monensin treatment of the cells. To further explore this phenomenon, we investigated the response to monensin of various Golgi proteins. Within 30 min of monensin treatment, gal-T1 moved from the Golgi apparatus, as defined by localization of giantin, to swollen vesicles whereas ST6Gal, α2,3(N)sialyltransferase, mannosidase II, and N-acetylgalactosaminyltransferase 2 remained associated with the Golgi apparatus. Stably transfected CHO cells exhibited a similar phenomenon of monensin-induced displacement of recombinant gal-T1 to swollen vesicles while recombinant ST6Gal remained colocalized with endogenously expressed giantin. Gal-T1 and the cation-insensitive mannose 6-phosphate receptor colocalized in swollen vesicles as observed at both light and electron microscopic levels. When monensin was replaced by chloroquine, gal-T1 remained arrested in swollen vesicles. Brefeldin A treatment known to cause relocation of Golgi-associated gal-T1 to the endoplasmic reticulum had no effect on gal-T1 trapped in swollen vesicles. This evidence suggests that monensin blocks gal-T1 trafficking in post-Golgi structures and argues against swelling of gal-T1-containing trans Golgi cisternae as previously assumed. [ABSTRACT FROM AUTHOR]

The case of a 70-year-old patient with an epithelial mesothelioma is presented. The patient suffered from dyspnea due to a right-sided recurrent hemorrhagic effusion. Cytological analysis of the effusion revealed marked lymphocytosis and tumor cells, some of them multinucleated with prominent nucleoli. Open lung biopsy revealed nodular thickening of the diaphragmatic, visceral, and parietal pleura; histological examination of biopsies detected intravascular growth of tumor cells. Immunocytochemical characterization of cultured tumor cells and the biopsy specimens showed positive staining to vimentin and cytokeratin, but negative reaction with antibodies against epithelial membrane associated antigen, leukocyte common antigen, van Willebrand factor, and neurofilament. Hence, the tumor was classified as malignant mesothelioma. In vitro, interferon-α2 produced a dose-dependent inhibition of proliferation in the cultured mesothelioma cells. Two weeks after initiation of interferon-α2 treatment the patient improved and the pleural effusion vanished. [ABSTRACT FROM AUTHOR]