RESUMO
Fatigue-related traffic accidents and fatalities have been extensively studied by scholars globally.Specialized vehicles,due to their unique mission profiles,are more likely to cause driving-related fatigue and serious consequences.This paper reviews the current research of fatigue driving by using an inductive analysis method to summarize the mechanisms,risk factors,and monitoring methods.This paper also offers a vision of priorities and methodologies for research in the future.It is recommended that the mechanisms of driving fatigue be explored at the molecular biological level and that fatigue monitoring systems be made more feasible via the combined application of non-intrusive monitoring in order to reduce the toll on life and property taken by driving fatigue.
RESUMO
The gene expression of both the mouse plasmocytoma (SP2/0) and the hybrid cells crossed with rat nucleated erythroblasts were detected by in situ hybridization technique using the probes of mouse ?-globin gene and 7 oncogenes (v-Ki-ras, v-H-ras, v-sis, erb-B, v-abl, v-fos, c-myc). After plasmic amplification, DNA was isolated by alkali lysis, purified and recovered, the DNA containing gene fragments were labelled with ~(32)P to become high activity ~(32)P-cDNA probes through nick translation, and the labelled probes were used to detect the gene transcripts in cellular level. The results indicated that: (1) no mouse ?-globin gene transcripts could be detected in the cytoplasm of SP2/0 cells, as well as in hybrid cells within 72 hours after cell fusion, but transcript signals could be observed in hybrid cells from 4th to 26th passages. (2) Active expression of multioncogenes in SP2/0 cells was demonstrated, all the 7 oneogenes tested, except v-sis, were expressed more strongly. On the other hand, the expression of oncogenes in hybrid cells was found to be dramatically decreased, among them, the oncogenes of c-myc and Ki-ras been suppressed completely. After long term of passages (26th subcultures), the expression of c-myc and Ki-ras was still lower than that of SP2/o ceils although in some cases other oncogenes increased in their expression levels. These results confirmed that the multistep carcinogenesis involved multi-oncogenes expression and that the decancerization of tumor cells may be due to the suppression of multi-oncogenes activity as well as to activate the expression of differentiation genes.
RESUMO
The present study reported the observations with light and electronic micros copy on hybrid cells crossed between rat intermediate or late erythroblasts and mouse SP2/0 plasmocytoma cells. In a short period after fusion, the cell size and the ratio of nuclear heterochromatin in hybrid cells appeared to be increased, but the number of nucleoli, as well as the number of microvilli, finger-like processes, and nuclear cytoplasmic ratio were decreased. Swelling mitochondria, pycnotic nuclei and/or process of enucleation also could be seen in some hybrid cells. The subcul tured hybrid cells were characterized with less microvilli and cellular surface membrane processes, and showing marked changes in nuclear size, as well as the appearance of cytoplasmic vesicles and dense granules in some cells. The observations mentioned above provide morphological and ultrastructural evidences for the regulation of malignant phenotype of hybrid cell model we reported previously. The possible relationship between the deeancerization and the morphological changes of hybrid cell nucleus, cytoplasm and cell surface were briefly discussed.