[Alteration of onset of pancuronium and vecuronium by priming principle].
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Biomedical subjects
Publications and source records attributed to M Kinjo.
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A clinicopathologic autopsy study of the vascular changes in the kidneys of 100 patients with systemic lupus erythematosus was undertaken. Necrotizing arteritis was found in seven patients, mucinous intimal thickening in nine, onion-skin intimal thickening in two, and renal vein thrombosis in two. Active necrotizing arteritis was present most frequently in the arterioles and interlobular arteries, with healing necrotizing arteritis predominating in the arcuate and interlobar arteries. These events were closely related to the activity of glomerular lesions, and immunologic vascular injury seemed to be the causative factor. Rapidly progressive renal failure and severe hypertension had characterized the clinical courses of the patients. Mucinous intimal thickening, present in the arterioles and interlobular arteries, had been accompanied by accelerated hypertension. Although dialysis or accelerated hypertension may have been causes, other factors, including glucocorticoid therapy, must be considered. In one patient with class II lupus nephritis, renal vein thrombosis was considered the cause of the nephrotic syndrome. These vasculopathies, often detected in patients with lupus at autopsy, seem to alter the clinical course.
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Interaction based on possible chemical affinity of an amino acid for tRNA was examined as a model for the aminoacylation of primitive tRNA without aid of an enzyme system. Two types of reaction were carried out and compared. One was the acyl linkage of amino acid to the 5'-terminal phosphate of a tRNA activated as an imidazolide. The other was the incorporation of an amino acid activated as an imidazolide into 2'(3')-hydroxyl groups of intact tRNA. Both types of reaction indicated that none of the amino acids tested had any selectivity for the tRNAs examined. However, the rates of reaction with a given tRNA were different among amino acids. In the second type of reaction, amino acids were found mainly at loop-out regions of tRNA, but not at either its 5'- or 3'-terminal sites.
The keratin pattern of newborn mouse epidermis was investigated during terminal differentiation. In highly pure fractions of basal and suprabasal cells, obtained by Percoll density gradient centrifugation, we identified two sets of mRNA-encoded proteins: a basal set of 58.5, 52, and 47 kd subunits and a suprabasal set of 67 and 60 kd subunits. The large subunits of each set were alkaline to neutral, while the small subunits were acidic. Polyclonal antibodies against the suprabasal, acidic 60 kd protein and the basal, alkaline 58.5 kd protein selectively recognized their antigens in immunoblots of NEPHGE -resolved keratins and decorated the corresponding epidermal compartments in frozen sections. The antibody to the suprabasal 60 kd protein also recognized distinct cells in the basal cell layer. Quantification of this cell population revealed a 10% cell fraction, morphologically indistinguishable from the total cell population, that, in addition to expressing basal keratin proteins, was already synthesizing suprabasal keratin subunits.
Two rat ascites hepatoma lines, AH130, originating from a azodye-induced liver carcinoma, and AH130F(N), spontaneously derived from the AH130 line during serial i.p. transplantation were analyzed for their intermediate filament protein expression by one and two-dimensional gel electrophoresis, in vitro translation of their mRNAs and immunolocalization using antisera against distinct subunits and compared with intermediate filament expression of normal hepatocytes. Normal rat hepatocytes synthesize mainly two keratin subunits at 55 and 47 kDa. The AH130 hepatoma line maintains the expression of these proteins, however, in addition also synthesizes a 40-kDa keratin subunit and large amounts of vimentin. In contrast, the AH130F(N) hepatoma line has lost the ability to express keratin subunits; its intermediate-sized filament compound is apparently built up only by vimentin. Even by means of the sensitive immunoblotting technique using antisera against the normal hepatocyte keratin subunits, no keratin synthesis can be demonstrated in this line. The marked differences in the metastatic capacity of the two hepatoma lines make them promising tools to investigate a possible involvement of intermediate-sized filament expression in the process of tumor spreading.
The intermediate-filament proteins in Sarcoma 180 ascites cells and solid tumors generated by s.c. injection of ascites cells in NMRI or nude mice were analyzed by one- and two-dimensional gel electrophoresis and identified by immunological methods. The ascites form of Sarcoma 180 coexpresses keratin and vimentin, whereas the solid tumor ceases to synthesize keratins but continues to express vimentin. These reversible changes in the expression of intermediate-filament proteins may be due to a change in the differentiation program induced by environmental conditions like growth with or without cell contact.
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Thromboplastic and fibrinolytic activities of 8 lines of cultured human gastric cancer cells were estimated both in cell lysate and serum-free supernatant fraction. Furthermore, cell lysates with differing levels of thromboplastic activity were injected intravenously into congenitally athymic nude mice and the role of this activity in thrombus formation was examined. Thromboplastic and fibrinolytic activities of the cell lysate and the serum free-supernatant fraction varied from one line to another. There was no apparent correlation between these activities and the degree of histological differentiation of the original tumor. The thromboplastic activity was factor VII-dependent and factor IX-independent, indicating that it was attributable to tissue thromboplastin, although some factor VII-independent thromboplastic activity was also included in the cell lysate of two lines. Intravenous injection of the cell lysate with high thromboplastic activity produced more thrombi in the lung than that with low thromboplastic activity. This suggests that thromboplastic activity of cancer cells might play a significant role in the development of the hypercoagulable state in patients with gastric cancer.
In 1977 Porsolt proposed a new behavioral test, using mice, for screening antidepressants. He stated that antidepressants selectively reduce the immobility of mice in a forced swimming situation. The test is useful, but lacks objectivity in its evaluation of immobility and does not successfully screen 'false positive' drugs. A new 'behavioral despair' test was thus designed involving a small water wheel set in a water tank. Mice placed on this apparatus turned the wheel vigorously but, when they abandoned attempts to escape from the water the wheel stopped turning. The number of rotations of the water wheel were counted. All antidepressants tested increased the number of rotations. However, tranquillizers, anticholinergics and antihistaminics were not effective. We suggest that this water wheel test is more appropriate as screening test for antidepressants than Porsolt's test with regard to both objectivity and specificity.
Protein and non-protein amino acids were synthesized following hydrolysis of products obtained by high frequency discharge techniques applied to model atmospheres consisting of N2 as a nitrogen source together with CH4 and/or CO2 as a carbon source. Highest yields were obtained in the absence of CO2 and from mixtures rich in CH4. Amino acids would indeed be expected on the frozen surface of Titan with its CH4-N2 atmosphere.
Catalytic action of histone on peptide formation from phenylalanyl adenylate was studied. A peptide bond formation from phenylalanyl adenylate releases two protons. The proton release was increased in the presence of histone at a higher concentration. The catalytic action seems to be due to basic circumstance induced by histone, since (1) basic condition enhanced the proton release; (2) basic amino acid did not enhance the proton release.
Lewis lung carcinoma cells were implanted in the foot-pads of mice and the effects of the plasminogen-plasmin inhibitor tranexamic acid (t-AMCHA) and of the plasminogen activator urokinase on metastasis were examined by electron microscopy. The intravascular tumour cells were not associated with thrombus formation in either control or urokinase-treated mice. Polymerized fibrin deposition around tumour cells and thrombi composed of fibrin and platelets was observed only in the mice given t-AMCHA. This suggests that the inhibition of fibrinolysis by tACC caused fibrin deposition and thrombus formation around intravascular tumour cells, which prevented release of the cells from primary foci to form secondary tumours. On the other hand, fibrinolysis induced by urokinase prevented thrombus formation, and accelerated cell release from primary foci.
Formation of hematogenous metastasis in the congenitally athymic nude mice (nu/nu) and their heterozygous ones (nu/+) was compared 2 weeks after an intravenous injection of xenogeneic tumor cells of rat ascites hepatoma cells (AH 130) with high thromboplastic activity. AH 130 cells formed large numbers of metastatic foci in the lungs of nu/nu recipients, while they developed into only temporary growth of metastatic foci with subsequent regression in nu/+ mice. Cellular reaction to arrested tumor cells in the pulmonary vessels was composed of large mononuclear cells, and was extensive and prominent in nu+/mice in comparison with nu/nu mice 3 days after the injection of the tumor cells. The results suggest that mononuclear cells reaction is closely related to suppression of growth of micrometastasis. This is considered as a model that highly immunogenic tumor cells attenuated and could be rejected in relation to immunological mechanisms.
The effect of acute and chronic stress on escape behavior, brain norepinephrine (NE) concentration and beta-receptor binding was examined, and the mechanism of adaptation to chronic stress was discussed in terms of both behavioral and neurochemical standpoint. The rats were divided into an acute stress group (AS), chronic stress group (CS) and control group (C). The rats of AS experienced a single stress session. The rats of CS received 5 separate sessions. The rats of each group were examined by escape test, or killed for the purpose of measurement of beta-receptor binding and NE concentration 30 min after the final shock. The latency of escape test of AS was significantly greater than that of C. On the other hand, the latency of CS, and cortex beta-receptor binding of CS was significantly lower than that of C. However, beta-receptor binding of hypothalamus of AS and CS was not different from that of C. These results indicate that adaptation to chronic stress occurs with respect to escape behavior, and its neurochemical background relates with the acceleration of NE turnover and down regulation of beta-receptor sensitivity of cerebral cortex.
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