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51.
52.
Yabuki T Togami I Kitagawa T Sasai N Tsushima T Shirasaki Y Hiraki Y 《Acta medica Okayama》2003,57(4):179-186
The purpose of this study was to compare the MR characteristics of renal cell carcinomas against histologic findings and to assess the correlations among signal intensity, tumor enhancement, and pathologic findings. Fifty-four patients (56 lesions) were examined by MR imaging and then underwent partial or radical nephrectomy. The pathologic diagnosis of all lesions was renal cell carcinoma. All MR examinations were performed as dynamic studies using the same 1.5-T scanner. MR characteristics were compared against pathologic findings after resection, and the correlations among signal intensity, tumor enhancement, and pathologic findings were then assessed. A significant correlation was observed between tumor grade and tumor enhancement, with G3 lesions tending to show little enhancement. Regardless of the histologic classification, G3 tumors were found to contain highly heterotypic cancer cells and very few vessels by histopathologic examination. No significant correlations were noted between the other MR characteristics and pathologic findings. Renal cell carcinomas showing little enhancement tend to be highly malignant lesions based on the pathologic findings. Special consideration is required for these tumors with regard to the selection of surgical intervention and follow-up observation. 相似文献
53.
Takako Iwata Toshiakir Kamei Fumiya Uchino Hiromichi Mimaya Takayuki Yanagaki Hirofumi Etoh 《Pathology international》1978,28(2):193-203
Senile aortic amyloidosis in 224 autopsy cases over 40 years was investigated comparing cardiac and pancreatic amyloidosis in them. A total of 176 cases of aortic amyloidosis was found for an average incidence of 79%. Under the 5th decade the incidence was 51% and it rose sharply with age and reached 95% in over the 8th decade. The incidence of cardiac amyloidosis also increased with age, but it was always higher in the aorta. Aortic and cardiac amyloid were both positive in the DMAB method for tryptophan. The major part exposed to amyloidosis in the aorta was the media. The medial amyloid consisted of numerous minute deposits and had no relation to atherosclerosis. Some comments about the pathogenesis of senile amyloidosis were also mentioned. 相似文献
54.
Histogenesis of the duodenum, especially changes in the epithelium in relation to temporal occlusion and re-canalization of
the lumen, was investigated by light microscopy together with morphometric analysis, as well as by scanning and transmission
electron microscopy of 133 externally normal human embryos ranging from Carnegie stage 12 to 23. A series of morphogenetic
events passed the duodenum in a cranio-caudal (proximo-distal) wave like fashion during the period examined. They included:
(1) a decrease in the caliber and area of the lumen, (2) ’occlusion’ of the lumen, (3) vacuole formation, (4) ’re-canalization’
and villi formation. The only exemption to this rule was that, in the upper part of the duodenum, the lumen was not obliterated
in the embryos examined. Morphometric analyses revealed that both the area of the epithelium and the number of epithelial
cells decreased during the ’occlusion’ phase. This result suggests that, unlike the classical view, epithelial cell proliferation
does not play an important role in occluding the lumen, but the predominant morphogenetic event during this phase is convergence
of the epithelial cells to elongate the duodenum. Apoptosis, contrary to some classical views, decreased during the ’re-canalization’
phase, and it appeared to be involved in the formation of the small lumens in the epithelial ’plug’ and in villi formation,
but not in enlarging the secondary lumens. The secondary small lumens in the occluded lumen were frequently formed near the
border between the central ’plug’ and peripheral basal cells on the basement membrane. This and other findings of concentric
differentiation in both the epithelial and mesenchymal layers suggested a possible control mechanism by the epithelium-mesenchymal
interaction on human duodenal morphogenesis and histogenesis. The present electron microscopic observations also provided
details on the mechanisms involved in the enlargement of the secondary lumen and differentiation of villi. The implications
of these findings to duodenal anomalies are also discussed.
Accepted: 12 November 2001 相似文献
55.
Metal ions induce bone-resorbing cytokine production through the redox pathway in synoviocytes and bone marrow macrophages 总被引:6,自引:0,他引:6
Niki Y Matsumoto H Suda Y Otani T Fujikawa K Toyama Y Hisamori N Nozue A 《Biomaterials》2003,24(8):1447-1457
To evaluate the biological reactions to metal ions potentially released from prosthetic implants, we examined the ability of metal ions to produce bone-resorbing cytokines and the underlying mechanism using synoviocytes and bone marrow (BM) macrophages. The cells were incubated with NiCl(2), CoCl(2), CrCl(3) or Fe(2)(SO(4))(3) at optimal concentrations, which are detectable in joint fluid following total joint arthroplasty. The production of interleukin-1beta, interleukin-6 and tumor necrosis factor-alpha were enhanced by all metal ions tested as determined by enzyme-linked immunosorbent assay. From the results of electrophoresis mobility shift assay, all metal ions enhanced the DNA-binding activity of nuclear factor kappaB (NF-kappaB), and p50-p65 heterodimers and p50 homodimers were the major subunits. These effects of the metal ions were considerably blocked by pyrrolidine dithiocarbamate (PDTC) known as a radical scavenger. An electron spin resonance study clearly demonstrated the ability of metal ions to generate activated oxygen species (AOS), especially hydroxyl radicals (*OH), which accounts for PDTC-blockade of metal ion-induced NF-kappaB activation and subsequent cytokine production. Taken together, our data raised the possibility that small amounts of metal ions released from prosthetic implants activate synoviocytes and BM macrophages through the AOS-mediated process (i.e. the redox pathway), and contribute to the initiation of osteolysis at the bone-implant interface. 相似文献
56.
The aim of this study was to examine if adhesion molecules had relation with degeneration and regeneration processes of mammalian vestibular epithelia. The distribution of E-cadherin and beta-catenin was immunohistochemically examined in normal and aminoglycoside-treated utricles of mice. E-cadherin and beta-catenin linearly expressed between epithelial cells in normal specimens. Aminoglycoside injury resulted in temporal alteration in distribution of these molecules with induction of apoptosis in hair cells. Degradation of both molecules was widely observed in vestibular epithelia, while some supporting cells exhibited accumulation of beta-catenin. After completion of induction of apoptosis, expression of these adhesion molecules was normal in distribution. These findings suggest that the E-cadherin-beta-catenin complex plays roles in degeneration and subsequent repair processes in vestibular epithelia affected by aminoglycosides. 相似文献
57.
Anca Ram Qiuhe Cao Paul E. Keck Harrison G. Pope Koichi Otani Gerard Addonizio Susan L. McElroy Sunao Kaneko Michaela Redlichova Elliot S. Gershon Pablo V. Gejman 《American journal of medical genetics. Part A》1995,60(3):228-230
Dysfunction of the dopaminergic system has been suggested as a pathogenic mechanism in neuroleptic malignant syndrome. Therefore, we examined the complete coding sequences of the dopamine D2 receptor (DRD2) gene for structural abnormalities in 12 patients with a history of NMS, including two cases of familial NMS. Mutational analysis was performed by denaturing gradient gel electrophoresis (DGGE), a highly sensitive technique for detecting sequence differences. We found in one patient with a history of NMS a nucleotide substitution at codon 310 (CCG→TCG) of exon 7 of the DRD2 gene which predicts the replacement of proline to serine in the third cytoplasmic loop of the receptor, a part of the receptor that interacts with G-proteins. A larger series of patients with NMS needs to be investigated to establish whether this allele is associated with an increased susceptibility to NMS. © 1995 Wiley-Liss, Inc. 相似文献
58.
Role of p27Kip1 and Cyclin-Dependent Kinase 2 in the Proliferation of Non-Small Cell Lung Cancer 总被引:12,自引:0,他引:12
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Hidetada Kawana Jun-ichi Tamaru Tomoaki Tanaka Aizan Hirai Yasushi Saito Masatoshi Kitagawa Atsuo Mikata Kenichi Harigaya Takayuki Kuriyama 《The American journal of pathology》1998,153(2):505-513
The cell cycle is governed by a family of cyclin-dependent kinases (Cdks). Cdk2 forms a functional complex with cyclin E and plays a pivotal role in the regulation of G1/S transition. Cdk2 activity is negatively regulated by interactions with inhibitors. p27Kip1, one of the most potent inhibitors of Cdk2, was recently identified as a powerful negative prognostic marker in non-small cell lung cancer as well as in colorectal and breast cancer. In the present study, the expression of p27 and Ki-67 antigen in nonneoplastic and cancerous lung tissues was determined by immunohistochemistry. After establishing that the antibody-measured p27 labeling index was a good reflection of the level of p27 expression measured by Western blotting, we show that p27 labeling index is decreased in cancerous lung tissues, compared with nonneoplastic lung tissues, and exhibits a significant inverse relation to the proliferation marker Ki-67 antigen, detected with monoclonal antibody MIB-1. Consistent with these data, all cancerous lung tissues showed enhanced degradation activity of p27 compared with nonneoplastic lung tissues and, in addition, increased levels of the phosphorylated form of Cdk2, as determined with Western blot analysis. The H1 histone kinase activity associated with Cdk2 was also increased in non-small cell lung cancers. Statistical analysis showed that proliferative activity as measured by MIB-1 labeling index was highly correlated with Cdk2 activity (r = 0.767, P < 0.0015). These results suggest that p27 and Cdk2 may play an important role in the proliferation of non-small cell cancer. 相似文献
59.
Stimulation of nonspecific resistance to infection induced by muramyl dipeptide analogs substituted in the gamma-carboxyl group and evaluation of N alpha-muramyl dipeptide-N epsilon-stearoyllysine. 总被引:1,自引:5,他引:1
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Stimulation of resistance to infection induced by the analogs of muramyl dipeptide (MDP) having substituted functions in the gamma-carboxyl group of D-isoglutamyl residue was examined in experimental Escherichia coli infections in mice. An MDP analog which is an efficient strengthener of resistance to infection, N alpha-MDP-N epsilon-stearoyllysine [MDP-Lys(L18)], was selected through the comparative assessment of a number of compounds in three categories: (i) gamma-alkylamides, (ii) gamma-esters, and (iii) N alpha-MDP-N epsilon-acyllysine derivatives. Furthermore, the antiinfectious activity of MDP-Lys(L18) was evaluated bacteriologically in comparison with that of MDP. The effect of MDP-Lys(L18) on the susceptibility of mice to infections with various species of microorganisms was studied. Protective activity was greatest against E. coli and staphylococcal infections, considerable against Pseudomonas and Candida infections, and least against Klebsiella infection. The effects of bacterial inoculum size and MDP treatment timing, dose, and route of administration on protective activity were studied. The efficacy of MDP-Lys(L18) in protection tests was demonstrated for all administration routes, even the oral. Its high potency was confirmed by the smaller influence of inoculum size and particularly small value of the minimum dosage required for inducing protective activity. A decrease in bacterial survival was observed in the blood and organs of mice treated with the analog and infected with E. coli. The following two useful effects were obtained: the synergistic effect of glycopeptide and chemotherapeutic agents and the stimulation of resistance to infection in animals immunocompromised by cyclophosphamide treatment. 相似文献
60.
Molecular cloning and complete nucleotide sequence of the genome of Japanese encephalitis virus Beijing-1 strain 总被引:5,自引:0,他引:5
Hiroshi Hashimoto Akio Nomoto Koji Watanabe Takayuki Mori Toshiyuki Takezawa Chikara Aizawa Tsutomu Takegami Keiichi Hiramatsu 《Virus genes》1988,1(3):305-317
The genomic RNA of the Japanese encephalitis virus (JEV) Beijing-1 strain was reversely transcribed and the synthesized cDNA was molecularly cloned. Six continuous cDNA clones that cover the entire virus genome were established and sequenced to determine the complete nucleotide sequence of the JEV RNA. The precise genomic size was estimated as 10,965 bases long. With flanking 95 bases at the 5 and 583 bases at the 3 non-coding regions, one long open reading frame (ORF) was revealed encoding a virus polyprotein with 3,429 amino acid residues. Because of sequence homologies observed between JEV and other flaviviruses, the genome organization of JEV appears to be identical with other flaviviruses. Genetic variation detected among flavivirus genomes is consistent with the established serological relatedness between JEV and other members of flaviviruses. The secondary structure of the JEV genome is deduced and discussed concerning its involvement in genome replication. 相似文献