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排序方式: 共有6165条查询结果,搜索用时 312 毫秒
51.
Susumu Yoshikawa Jitsuo Kiji Junji Furukawa 《Macromolecular chemistry and physics.》1977,178(4):1077-1087
The dimerization of 1-alkynes by rhodium(I) complexes in the presence of phosphorus ligands is described. The products are linear and branched dimers, the ratio of which is correlated with the electronic parameters, vCO of Ni(CO)3L, of the ligands L, but no simple correlation is apparent between their steric parameter and the selectivity. Electron-donating ligands promote the formation of the linear dimer. The substituents of the 1-alkynes also affect the distribution of linear and branched dimers. Electron-donating substituents prefer linear isomer to branched one. The reactivity of the substituted 1-alkynes (R? C?C? H) increased with substituent R in the order 相似文献
52.
53.
T Furukawa 《Rinsho byori. The Japanese journal of clinical pathology》1991,39(10):1044-1048
The medical advancements, during the 20th century symbolize the industrialization of medical technologies, i.e., many clinical tests are carried out by the highly advanced automated machines. Also, the concept of intelligent processing of clinical diagnosis seems to have been established in the practice. However, it may be an illusion caused from the term artificial intelligence (AI) which attracts the attention of not only specialists of computer science but also clinicians. The essential nature of AI, especially of expert consultation systems is the same as the existing theories, such as Bayes' theorem, Boolean algebra, multivariate statistical analysis, and Fussy theorem, i.e., the evaluation of a weighted sum of multiple parameters. The weak point of these theories is the lack of time parameter. Therefore, the models using a time parameter including physiological simulation, dynamics model, Weibull model and Markov process are important to realize the revolution of clinical diagnosis from the standpoint of intelligent science and technology. 相似文献
54.
Toru Furukawa Rumi Fujisaki Yoshitaro Yoshida Naomi Kanai Makoto Sunamura Tadayoshi Abe Kazunori Takeda Seiki Matsuno Akira Horii 《Modern pathology》2005,18(8):1034-1042
DUSP6/MKP-3 is identified as a candidate tumor suppressor gene for pancreatic cancer. The aim of this study was to elucidate the roles of DUSP6 in the pancreatic carcinogenesis through the pancreatic intraepithelial neoplasia and/or intraductal papillary-mucinous neoplasms, both of which are considered to be precursor lesions of invasive carcinoma of the pancreas, by comparing with involvements of other major tumor suppressive pathways. Expressions of DUSP6, CDKN2A, TP53, and SMAD4 were investigated by immunohistochemistry in a total of 206 lesions of dysplastic ductal precursors and carcinomas retrieved from 52 pancreata with invasive ductal carcinomas and 51 of those with intraductal papillary-mucinous neoplasms. The intensity of staining was evaluated in lesions at different atypical grades and statistically compared among them. Mutations of KRAS2 were analyzed by methods of the allele-specific oligonucleotide hybridization and nucleotide sequencing. In pancreata with invasive ductal carcinomas, expressions of DUSP6 were abrogated exclusively in the invasive carcinoma cells in contrast to its fairly preserved expressions in pancreatic intraepithelial neoplasia. In pancreata with intraductal papillary-mucinous neoplasms, abrogated expressions of DUSP6 were observed in a relatively small fraction of intraductal adenoma/borderlines and intraductal carcinomas. Most of the intraductal adenoma/borderline lesions with abrogation of DUSP6 harbored mutations of KRAS2. None of the molecules was associated with each other in any grade of lesions. Morphological variations of papillae of the intraductal papillary-mucinous neoplasms were evaluated and analyzed for their associations with abrogations of the molecules, which resulted in finding of no significant associations. Our results suggest that the abrogation of DUSP6 is associated exclusively with progression from pancreatic intraepithelial neoplasia to the invasive ductal carcinoma while it is potentially associated with initiation of intraductal papillary-mucinous neoplasms with mutated KRAS2, which is independent of other major tumor suppressive pathways in both types of neoplasms. 相似文献
55.
Prediction of sensitivity of advanced non-small cell lung cancers to gefitinib (Iressa, ZD1839) 总被引:7,自引:0,他引:7
Kakiuchi S Daigo Y Ishikawa N Furukawa C Tsunoda T Yano S Nakagawa K Tsuruo T Kohno N Fukuoka M Sone S Nakamura Y 《Human molecular genetics》2004,13(24):3029-3043
Gefitinib (Iressa, ZD1839), an inhibitor of epidermal growth factor receptor-tyrosine kinase, has shown potent anti-tumor effects and improved symptoms and quality-of-life of a subset of patients with advanced non-small cell lung cancer (NSCLC). However, a large portion of the patients showed no effect to this agent. To establish a method to predict the response of NSCLC patients to gefitinib, we used a genome-wide cDNA microarray to analyze 33 biopsy samples of advanced NSCLC from patients who had been treated with an identical protocol of second to seventh line gefitinib monotherapy. We identified 51 genes whose expression differed significantly between seven responders and 10 non-responders to the drug. We selected the 12 genes that showed the most significant differences to establish a numerical scoring system (GRS, gefitinib response score), for predicting response to gefitinib treatment. The GRS system clearly separated the two groups without any overlap, and accurately predicted responses to the drug in 16 additional NSCLC cases. The system was further validated by the semi-quantitative RT-PCR, immunohistochemistry and ELISA for serological test. Moreover, we proved that the anti-apoptotic activity of amphiregulin, a protein that was significantly over-expressed in non-responders but undetectable in responders, leads to resistance of NSCLC cells to gefitinib in vitro. Our results suggested that sensitivity of a given NSCLC to gefitinib can be predicted according to expression levels of a defined set of genes that may biologically affect drug sensitivity and survival of lung cancer cells. Our scoring system might eventually lead to achievement of personalized therapy for NSCLC patients. 相似文献
56.
When 2-vinyl-1,3-dioxolane was treated at low temperature (?78 or ?130°C.) with cationic catalysts, oily or semi-solid polymer was produced. The result of alkaline hydrolysis showed that the polymeric product contained ester units whose amount was about 2 to 15 mole-% of the total units. The remaining part of the polymer consisted of units containing the dioxolane ring. In the alkaline alcoholysis of the polymer with ethanol ethyl δ-hydroxyvalerate was formed. These findings indicate that in the low temperature cationic polymerization of 2-vinyl-1,3-dioxolane the ester unit, ? O(CH2)4CO? , is formed in addition to the unit of vinyl polymerization. A mechanism for the formation of the ester unit has been proposed, in which the process of hydride-shift is followed by ring-opening of the resulting carbonium ion species of dioxolane. 相似文献
57.
Ayres FM Narita M Takahashi M Alldawi L Liu A Osman Y Abe T Yano T Sakaue M Toba K Furukawa T Aizawa Y 《Immunological investigations》2003,32(4):219-227
Dendritic cells (DCs) are potent antigen presenting cells and possess a direct anti-tumor cytotoxic ability. Nevertheless, the mechanism of anti-tumor cytotoxicity by DCs and the methods for its evaluation are not fully elucidated. In order to clarify this mechanism of cytotoxicity, we examined the ability of DCs 1) to suppress [3H] thymidine (3H-TdR) uptake by tumor cells; 2) to induce cytolysis on 51Cr-labeled tumor cells; 3) and to induce DNA fragmentation on 3H-TdR labeled tumor cells (JAM test). Cytolysis and DNA fragmentation are markers of necrotic and apoptotic mechanisms of cytotoxicity in vitro, respectively. DCs inhibited approximately 38.6% to 54.8% of the growth of B4D6, NB4, U937, and Daudi cells as evaluated by the uptake of 3H-TdR. However no cytolysis was verified by 51Cr-release assay. On the other hand, cytotoxicity rates found using the JAM test ranged from 3 to 81% depending on the cell line and the effector to target cell ratio. The discrepancy of cytotoxicity between 51Cr-release assay and the JAM test may be due to the phagocytosis of apoptotic tumor cells or the absorption of released 51Cr by DCs surrounding the target cells. In conclusion, the JAM test was more sensitive than the 4-h and the 10-h 51Cr-release assay to investigate cytotoxicity mediated by DCs toward hematopoietic tumor cell lines in vitro. 相似文献
58.
Ma Q Kobayashi M Sugiura M Ozaki N Nishio K Shiraishi Y Furukawa K Furukawa K Sugiura Y 《Archives of histology and cytology》2003,66(1):37-44
Gangliosides, a family of glycosphingolipids that contain sialic acid, are abundant on the neuronal cell membranes, but their precise functions in the central nervous system remain largely undefined. In a previous study of GalNAc-T(-/-) mice engineered to lack beta1,4-N-acetylgalactos-aminyltransferase (GM2/GD2 synthase) to abolish any, complex gangliosides, we observed the reduction of nerve conduction velocity but did not find any obvious morphological change in the brain. In the present study, we observed morphological changes in the nerve fiber tracts of the spinal cord in these mice. In GalNAc-T(-/-) mice, the number of degenerated axons was markedly increased in the dorsal funiculus, tract of Lissauer, and dorsolateral funiculus of the cervical segment of the spinal cord as well as the dorsal funiculus and tract of Lissauer of the lumbar segment of the spinal cord. There were also increased numbers of unmyelinated fibers in GalNAc-T(-/-) mice. Loosened myelin sheaths and myelin sheaths separated from axons by wide spaces were also observed in GalNAc-T(-/-) mice. These results provide a morphological basis for the previously observed reduction in the nerve conduction velocity and suggest that complex gangliosides are essential for the maintenance of myelin and the integrity of nerve fibers of the spinal cord. 相似文献
59.
Reduction of voltage-dependent magnesium block of N-methyl-D-aspartate receptor-mediated current by in vivo axonal injury 总被引:2,自引:0,他引:2
The post-traumatic change of the voltage-dependent Mg(2+) block of N-methyl-D-aspartate response was investigated using nystatin perforated patch recording mode under the voltage-clamp condition. Motor neurons of the dorsal motor nucleus of vagus nerve were freshly dissociated from rat brain at 2h to 10 days after receiving axonal crush injuries in vivo at the neck. The reduction of voltage-dependent Mg(2+) block of N-methyl-D-aspartate response became evident at more than 12h after the injury, sustained for at least five days and recovered within 10 days. Other characteristics examined such as reversal potentials, the Hill coefficient and EC(50) of N-methyl-D-aspartate-induced current were not affected by axonal injury. The Mg(2+) block of N-methyl-D-aspartate response was not affected at all by local application of colchicine onto the vagal axon in in vivo condition, suggesting that axonal injury, but not the blockade of the axonal flow, is responsible for the change of the sensitivity of N-methyl-D-aspartate response to extracellular Mg(2+). In addition, the reduction of Mg(2+) block by the nerve injury persisted regardless of the presence of protein kinase C modulators, such as 10(-6)M chelerythrine and 10(-7)M calphostin C. Therefore alteration of protein kinase C activity after axonal injury is not responsible for the maintenance of the reduced Mg(2+) block.These findings suggest that injured neurons acquire immature characteristics of plasticity with respect to the sensitivity of N-methyl-D-aspartate receptors to extracellular Mg(2+) or a long-term increase in the susceptibility to Ca(2+) excitotoxicity. 相似文献
60.
T Yamane T Inoue Y Furukawa Y Yasui K Ota Y Nakao H Ohira K Tanaka T Hasuike M Hirai 《Rinsho byori. The Japanese journal of clinical pathology》1991,39(12):1347-1350
CD56 antigen (detected by NKH-1) is distributed on NK cells, monocytes, and ectodermal neural cells. In this study, the blasts of 29.2% of 27 patients with acute nonlymphocytic leukemia (ANLL) expressed CD56 antigen, but not CD16, CD2, or CD3 antigen. Leukemic cells isolated from 3 patients with CD56-positive ANLL did not have NK activity. There were no significant differences between CD56-positive and CD56-negative ANLL in CD13-positive cases, CD33-positive cases, and HLA-DR-positive cases. These results suggest that CD56-positive ANLL could be so-called mixed-lineage leukemia (lymphoid-associated antigen in ANLL). 相似文献