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V Kumar PM Carabateas JA Dority WG Earley JP Mallamo C Subramanyam LD Aimone B Ault DL DeHaven Hudkins MS Miller 《Canadian Metallurgical Quarterly》1995,38(10):1826-1830
Replacement of the pyridinium ring of 6,11-ethanobenzo[b]quinolizinium cations with thiazolium (4a and 4b) and N-methylimidazolium (4c and 4d) resulted in equipotent compounds in the [3H]TCP binding assay. The corresponding N-methyl-1,2,4-triazolium analogs were less potent in this assay. The thiazolium derivative 4b, with a Ki = 2.9 nM, is being evaluated as a possible neuroprotective N-methyl-D-aspartic acid (NMDA) antagonist. 相似文献
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J Lorenz K Wilhelm M Kessler C Peschel U Schwulera R Lissner WG Struff E Huland C Huber WE Aulitzky 《Canadian Metallurgical Quarterly》1996,2(7):1115-1122
Safety, local and systemic immunomodulation, and tumor response to treatment with aerosolized natural interleukin 2 (nIL-2) applied five times a day were studied in a Phase I trial in 16 patients with pulmonary malignancies refractory to conventional therapy. The toxicity of inhaled nIL-2 was different from that observed after systemic administration. Reversible airway irritation causing a nonproductive cough represented the dose-limiting toxicity. Mild to moderate reduction of the vital capacity and forced expiratory volume (FEV1) with minor effects on relative FEV1, peak expiratory flow, airway resistance, and PaO2 was experienced by individual patients. In 14 patients suffering from pulmonary metastases due to renal cell cancer, one durable complete response, one partial response, and one mixed response were observed. Inhalation of nIL-2 aerosol resulted in a dose-dependent expansion of pulmonary immunocompetent cells in bronchoalveolar lavage fluid. Posttreatment bronchoalveolar lavage showed an activated lymphocyte phenotype with increased HLA-DR expression. The only systemic biological effect detectable in peripheral blood was a marked increase of soluble interleukin 2 receptor serum levels. We conclude that treatment with aerosolized nIL-2 is an effective means for site-specific immunomodulation and deserves further investigation for the treatment of malignant and inflammatory lung disease. 相似文献
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Time-dependent thrombolytic resistance is a critical problem in thrombolytic therapy for acute myocardial infarction. Platelets have been regarded as the main source of plasminogen activator inhibitor-1 (PAI-1) found in occlusive platelet-rich clots. However, endothelial cells are also known to influence the fibrinolytic capacity of blood vessels, but their ability to actively mediate time-dependent thrombolytic resistance has not been fully established. We will show that, in vitro, tumor necrosis factor-alpha-stimulated endothelial cells secrete large amounts of PAI-1 over a period of hours, which then binds to fibrin and protects the clot from tissue plasminogen activator-induced fibrinolysis. In vivo, endothelial cells covering atherosclerotic plaques are influenced by cytokines synthesized by plaque cells. Therefore, we propose that continuous activation of endothelial cells in atherosclerotic blood vessels, followed by elevated PAI-1 secretion and storage of active PAI-1 in the fibrin matrix, leads to clot stabilization. This scenario makes endothelial cells a major factor in time-dependent thrombolytic resistance. 相似文献
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WG Dickerson 《Canadian Metallurgical Quarterly》1996,15(6):60, 62, 66-60, 62, 69
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MK Danks MR Warmoth E Friche B Granzen BY Bugg WG Harker LA Zwelling BW Futscher DP Suttle WT Beck 《Canadian Metallurgical Quarterly》1993,53(6):1373-1379
Five cell lines selected for resistance to the cytotoxicity of inhibitors of DNA topoisomerase II have point mutations in the gene that codes for the M(r) 170,000 form of this enzyme. In each case, the mutation results in an amino acid change in or near an ATP binding sequence of the M(r) 170,000 isozyme of topoisomerase II. We used single-strand conformational polymorphism analysis to screen for similar mutations in other drug-resistant cell lines or in leukemic cells from patients previously treated with etoposide or teniposide. We also analyzed the region of the gene that codes for amino acids adjacent to the tyrosine at position 804 of topoisomerase II which binds covalently to DNA. CEM/VM-1, CEM/VM-1-5, and HL-60/AMSA human leukemic cell lines were used as controls; 3 of 3 known mutations were detected by migration differences of polymerase chain reaction products from the RNA extracted from these three lines. A previously unknown mutation was found in the tyrosine 804 region of the M(r) 170,000 topoisomerase II expressed by CEM/VM-1 and CEM/VM-1-5 cells. Sequence analysis showed that substitution of a T for a C at nucleotide 2404 resulted in an amino acid change of a serine for a proline at amino acid 802. No mutations in any of the ATP binding sequences or in the tyrosine 804 region were detected in polymerase chain reaction products from RNA extracted from human leukemia HL-60/MX2 or CEM/MX1 cells (both cell lines selected for resistance to mitoxantrone) or in human myeloma 8226/Dox1V cells (selected for resistance by simultaneous exposure to doxorubicin and verapamil). No mutations were detected in polymerase chain reaction products from RNA extracted from blasts of 15 patients with relapsed acute lymphocytic leukemia, previously treated with etoposide or teniposide. We conclude that: (a) single-strand conformational polymorphism analysis is useful for screening for mutations in topoisomerase II; (b) resistance to the cytotoxicity of inhibitors of DNA topoisomerase II is not always associated with mutations in ATP binding sequences or the active site tyrosine region of M(r) 170,000 topoisomerase II; and (c) mutations similar to those detected in drug resistant cells selected in culture have not been identified in blast cells from patients with relapsed acute lymphocytic leukemia, previously treated with etoposide or teniposide. 相似文献
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F Deák á Horváth á Kiss Z Seres A Galonsky CK Gelbke H Hama L Heilbronn D Krofcheck WG Lynch DW Sackett HR Schelin MB Tsang J Kasagi T Murakami 《Canadian Metallurgical Quarterly》1995,52(1):219-227
An extruding wire knife was used to give adult male CFHB rats a minimally traumatic unilateral mechanical lesion of the medial forebrain bundle. In addition, some rats received bilateral intrastriatal injections of one of three fluorescent retrograde tracers either eight days before or eight days after the lesion. Injections made after the lesion revealed that about half of the animals had complete lesions of the nigrostriatal tract, while the other half were incompletely lesioned, the mean proportion of non-axotomized neurons being 23%. Over the 10 weeks following the lesions, the number of tyrosine hydroxylase-immunoreactive cells in the lesioned substantia nigra fell linearly, reaching a mean of 29% of that of the control substantia nigra. In the animals which were completely lesioned, neuronal survival at 10 weeks varied between 6 and 12%. That the disappearance of tyrosine hydroxylase-immunoreactive neurons was due to cell death rather than the loss of tyrosine hydroxylase itself was confirmed by labelling the cells with Fluoro Gold before axotomy; the tracer was seen in survival neurons, microglia and in a few involuted neurons which continued to be tyrosine hydroxylase-immunoreactive. This percentage of neurons surviving axotomy corresponds to the proportion of substantia nigra neurons which project to the contralateral striatum, and these neurons were in the region of the substantia nigra from which the contralateral projection originated. It is concluded that following mechanical transection of the nigrostriatal tract, all truly axotomized substantia nigra neurons die over a period of about 10 weeks. 相似文献