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91.
92.
Inhibition of in vivo tumorigenicity and invasiveness of a human glioblastoma cell line transfected with antisense uPAR vectors 总被引:1,自引:0,他引:1
Yoshinori Go Shravan K. Chintala Sanjeeva Mohanam Ziya Gokaslan Boyapati Venkaiah Rolf Bjerkvig Kazunari Oka Garth L. Nicolson Raymond Sawaya Jasti S. Rao 《Clinical & experimental metastasis》1997,15(4):440-446
Our previous studies showed that glioblastomas express increased urokinase-type plasminogen activator receptors (uPARs) in comparison to low-grade gliomas (Yamamoto et al., Cancer Res., 54, 5016-5020, 1994). To explore whether downregulation of uPAR inhibits tumor formation and invasiveness, a human glioblastoma cell line was transfected with a cDNA construct corresponding to 300 bp of the human uPAR's 5¢ end in an antisense orientation, resulting in a reduced number of uPA receptors. Co-culture studies with tumor spheroids and fetal rat brain aggregates showed that antisense SNB19-AS1 cells expressing reduced uPAR failed to invade fetal rat brain aggregates. Intracerebral injection of SNB19-AS1 stable transfectants failed to form tumors and were negative for uPAR expression in nude mice. Thus uPAR appears in this model to be essential for tumorigenicity and invasion of glioblastomas in vivo. 相似文献
93.
Koh Nakazawa Nobuo Itoh Hui-Jun Duan Yuichi Komiyama Hidekazu Shigematsu 《Pathology international》1992,42(9):662-666
A 73-year-old Japanese man with a history of partial gastrectomy due to gastric cancer 4 years previously was admitted because of intermittent fever. The patient developed abdominal pain, erythema, and myalgia in addition to the fever during the final clinical course, and died of acute heart failure. Autopsy disclosed atrophy of the left lobe of the liver and acute myocardial infarction. Neither metastasis nor recurrence of the cancer was observed. Small and medium-sized arteries of the visceral organs showed various stages of necrotizing vasculitis with narrowing of the lumina. The vasculitis was most prominent in the left lobe of the liver and in the heart. Narrowing of the portal vein due to portal tract inflammation in addition to vasculitis of the hepatic arteries may have induced ischemia and infarction, which had resulted in atrophy of the left hepatic lobe. Acta Pathol Jpn 42: 662–666, 1992. 相似文献
94.
Yoshihiko Takahashi Yuichi Takiguchi Takayuki Kuriyama Tadaaki Miyamoto 《Clinical & experimental metastasis》1998,16(2):149-157
A clone of NIH3T3 transformant (H3) can yield subcutaneous tumors and experimental pulmonary metastasis in nude mice. Compared
to H3 in culture, the cells after in vivo tumor growth (H3-N) acquired enhanced tumorigenicity and metastatic ability. Also, indirect immunofluorescence revealed that
cellular fibronectin (c-FN) of H3-N was decreased remarkably. We have studied the interactions between H3 and extracellular
matrices to elucidate these phenomena. In the present study, we observed the effect of NIH3T3, H3, and H3-N cultured in type
I collagen gel. Morphologically in the collagen gel, NIH3T3 assumed an extensive elongated fiber-like shape, H3 assumed a
moderately elongated shape, and H3-N assumed a round or spindle shape with short pseudopodia. Compared to conventional cultures
on dishes, cell proliferation of all three types was suppressed in collagen gel, but the degree of the suppression was least
in H3-N. As a result, H3-N grew fastest in collagen gel. The variants which acquired growth advantage in the subcutaneum of
mice also kept it in collagen gel. H3 cells were cultured in type I collagen gel for 4 weeks, a period comparable to that
of tumor formation in nude mice. The cells after this long-term culture (H3-C) acquired enhanced tumorigenicity and metastatic
ability nearly equal to that of H3-N. FACS analysis revealed that the c-FN of H3-C had decreased to a value comparable to
that of H3-N. This means that type I collagen gel as well as subcutaneous tissues could select variants of H3 with less c-FN
through proliferation. Moreover, it is suspected that lattices of type I collagen regulate cell proliferation of fibroblast
via c-FN.
This revised version was published online in August 2006 with corrections to the Cover Date. 相似文献
95.
Adjuvant Activity of 6-Amino-6-Deoxy-Muramyldipeptides and Their Acylamino Derivatives on the Induction of Delayed Hypersensitivity to Azobenzenearsonate-N-Acetyl-l-Tyrosine in Guinea Pigs 下载免费PDF全文
Ichiro Azuma Hiroyuki Okumura Ikuo Saiki Yoshiro Tanio Makoto Kiso Akira Hasegawa Yuichi Yamamura 《Infection and immunity》1981,32(3):1305-1308
The 6-amino-6-deoxy-N-acetylmuramyldipeptides and their 6-acylamino derivatives were shown to be active as adjuvants on the induction of delayed-type hypersensitivity to azobenzenearsonate-N-acetyl-l-tyrosine in guinea pigs. However, 6-acylamino-6-deoxy-N-(acyl)muramyldipeptides were inactive as adjuvants. 相似文献
96.
Thioredoxin (TRX) is an endogenous redox (reduction/oxidation) regulator that has cytoprotective effects against various types of oxidative stresses. Exposure to excessive levels of white light induces retinal photoreceptor damage. To test the cytoprotective effect of overexpressed TRX against retinal photooxidative damage, both TRX transgenic (trx-tg) mice and C57BL/6 (wild type) mice were exposed to intense white fluorescent light. The amounts of oxidized and tyrosine-phosphorylated proteins decreased in the neural retinas of the trx-tg mice compared to the wild type mice after light exposure. The electroretinographic amplitudes were higher and the formation of oxidized DNA was lower in trx-tg mice compared to wild type mice after light exposure. These results suggest that overexpression of TRX suppresses retinal photooxidative damage. TRX intensification may be a useful therapeutic strategy to prevent retinal photic injury. 相似文献
97.
Liver cell membrane antibody detected by protein A and isolated rabbit liver plasma membrane in sera of patients with chronic liver diseases 总被引:1,自引:1,他引:1 下载免费PDF全文
G Toda Y Ikeda N Hashimoto M Yamazaki M Torii H Oka 《Clinical and experimental immunology》1983,54(3):661-670
Using the plasma membrane fraction isolated from rabbit liver (RLPM), we detected non-species specific IgG antibody against liver cell surface membrane in the sera from the patients with chronic liver diseases. The sea were treated with dithiothreitol and iodoacetamide, and absorbed with sufficient amount of actin isolated from rabbit striated muscles. The antibody was detected by incubation of RLPM with the treated and absorbed sera and subsequent determination of IgG bound to RLPM by 125I-staphylococcal protein A. It was found mainly in the patients with autoimmune hepatitis (12 of 28) and liver cirrhosis (eight of 24). It occurred more frequently in HBsAg negative liver cirrhosis than in HBsAg positive forms (six of 13 vs two of 11). The frequency of the antibody was low in chronic hepatitis except autoimmune hepatitis, and primary biliary cirrhosis. Thus the antibody against RLPM was an immunological marker of autoimmune hepatitis and HBsAg negative liver cirrhosis. The occurrence did not correlate with those of anti-smooth muscle antibody, anti-nuclear antibody and anti-mitochondrial antibody. In two cases of autoimmune hepatitis, the antibody against RLPM decreased with clinical improvement induced by corticosteroids. 相似文献
98.
Takusa Y Fukao T Kimura M Uchiyama A Abo W Tsuboi Y Hirose S Fujioka H Kondo N Yamaguchi S 《Molecular genetics and metabolism》2002,75(3):227-234
Very-long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is clinically classified into severe, intermediate, and myopathic forms. We identified mutations in three unrelated Japanese patients with VLCAD deficiency: two with the myopathic form and one with the intermediate form, all compound heterozygotes of K264E/M437V, A416T/1798delA, and P89S/IVS16-3delAA, respectively. We characterized four missense mutations, K264E, M437V, A416T, and P89S, by transisent expression analysis, using SV40-transformed fibroblasts derived from a VLCAD-null patient, as recipient cells. In transient expression of the wild-type VLCAD cDNA, VLCAD activity at 30 degrees C was higher than at 37 degrees C. Moreover, this temperature-sensitive character is more evident in all the mutant proteins tested than in wild type. Based on characterization of the five missense mutations identified in four Japanese patients, including data on one patient with the myopathic form previously reported, patients with the nonsevere forms (intermediate or myopathic forms) have missense mutations with residual activities in at least one allele. Expression analysis at 30 degrees C may be more useful for evaluating these missense mutations, compared with that at 37 degrees C. 相似文献
99.
To help understand the molecular mechanisms of Pasteurella multocida toxin (PMT) action, we searched for a cellular protein interacting with PMT. The ligand overlay assay revealed a 60-kDa cellular protein that binds to a region from the 840th to 985th amino acids of the toxin. This protein was identified as vimentin by peptide mass fingerprinting. The N-terminal head domain of vimentin was further found to be responsible for the binding to the toxin. 相似文献
100.
Yuji Narita Hideaki Kagami Hiroshi Matsunuma Yosuke Murase Minoru Ueda Yuichi Ueda 《Journal of artificial organs》2008,11(2):91-99
Previous attempts to create small-caliber vascular prostheses have been limited. The aim of this study was to generate tissue-engineered small-diameter vascular grafts using decellularized ureters (DUs). Canine ureters were decellularized using one of four different chemical agents [Triton-X 100 (Tx), deoxycholate (DCA), trypsin, or sodium dodecyl sulfate (SDS)] and the histology, residual DNA contents, and immunogenicity of the resulting DUs were compared. The mechanical properties of the DUs were evaluated in terms of water permeability, burst strength, tensile strength, and compliance. Cultured canine endothelial cells (ECs) and myofibroblasts were seeded onto DUs and evaluated histologically. Canine carotid arteries were replaced with the EC-seeded DUs (n = 4). As controls, nonseeded DUs (n = 5) and PTFE prostheses (n = 4) were also used to replace carotid arteries. The degree of decellularization and the maintenance of the matrix were best in the Tx-treated DUs. Tx-treated and DCA-treated DUs had lower remnant DNA contents and immunogenicity than the others. The burst strength of the DUs was more than 500 mmHg and the maximum tensile strength of the DUs was not different to that of native ureters. DU compliance was similar to that of native carotid artery. The cell seeding test resulted in monolayered ECs and multilayered alpha-smooth muscle actin-positive cells on the DUs. The animal implantation model showed that the EC-seeded DUs were patent for at least 6 months after the operation, whereas the nonseeded DUs and PTFE grafts become occluded within a week. These results suggest that tissue-engineered DUs may be a potential alternative conduit for bypass surgery. 相似文献