Visualization and function studies of the cerebrospinal fluid space with 99mTc sulfide colloid.
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Biomedical subjects
Publications and source records attributed to R Ramirez.
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We investigated the effect of gamma interferon and phorbol ester (TPA), on the expression of HLA class II molecules of myeloid leukaemic cell lines K562, U937, KG-1, HL-60 and ML-2. Gamma interferon induced the expression of HLA-DR but not HLA-DQ on HL-60 and ML-2, increased the expression of HLA-DR and DQ on U937 and induced the expression of HLA-DQ on KG-1. TPA treatment did not affect the expression of HLA class II antigens on U937 and KG-1 and induced the expression of HLA-DR and HLA-DQ on HL-60 and ML-2. TPA treatment did not affect the HLA phenotype of K562 but gamma interferon did induce HLA class I molecules. Thus, gamma interferon cannot only increase the expression of HLA products already expressed on the cells but can also induce the de novo synthesis of these molecules on myeloid leukaemic cell lines.
Although natural killer (NK) activity is not restricted by the major histocompatibility complex (MHC), it has been suggested that the level of expression of MHC antigens by target cells may influence their lysis by NK cells. We have studied the NK susceptibility of 20 cell lines obtained from primitive and metastatic human tumours and the K562 cell line treated with gamma-interferon, phorbol ester TPA and tumour factor NK-RIF. When the levels of MHC class I antigen expression on the human tumour cell lines and their NK susceptibility were compared, no relationship between these two parameters was observed. Furthermore the treatment of K562 with either gamma-interferon, TPA or NK-RIF decreased its NK susceptibility independently of MHC class I expression. These results indicate that the MHC class I antigen is not the only factor directly involved in NK susceptibility and suggest that other membrane structures modulated by gamma-interferon, TPA or NK-RIF may also influence NK susceptibility.
Treatment of rabbit aortic endothelial cells or human umbilical vein cells for as little as 1 day with 25 micrograms/ml of beta-migrating very low density lipoprotein (beta-VLDL), but not low density lipoprotein (LDL), caused an increased binding of human peripheral blood monocytes to the endothelium. This increase was maximal by 24 hours but was not significant at 4 hours of pre-incubation with beta-VLDL. Neutrophil binding was not significantly stimulated by beta-VLDL treatment of endothelial cells, while endotoxin (LPS) treatment of endothelial cells stimulated both neutrophil and monocyte binding. Antibody to leukocyte function-associated-antigen-1 and to Mo2 inhibited binding to both beta-VLDL-stimulated and LPS-stimulated cells by 25%. The fact that both rabbit and human cells were stimulated by beta-VLDL to bind human monocytes suggests that some mechanisms regulating binding are conserved between species. These studies suggest that beta-VLDL acts like a chronic inflammatory mediator to cause a sustained increase in binding of monocytes to the endothelium.
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The time-course of changes in the blood plasma cortisol level during activation of the positive reinforcement system was studied in experiments on adult chinchilla male rabbits. The self-stimulation status of the brain lateral hypothalamus was utilized as a model for positive reinforcement. The basal cortisol level in intact rabbits, determined by means of radioimmunoassay, was equal to 5.31 +/- 0.87 micrograms% over a period of 10 to 2 hours p.m. The blood collection procedure, using the method of the ear marginal vein dissection, increases the cortisol concentration 30 minutes after blood collection by 19.4%, i.e. augments its level up to 6.37 +/- 0.90 micrograms%. A significant rise (P less than 0.01) of hormone release into the blood (two-fold) is seen 5 to 15 minutes following the self-stimulation test. Cortisol level remains heightened 1 hour after the self-stimulation experiment. The intensity of the corticotropic activity was not dependent on the hypothalamus, stimulated by force or by animals themselves. On the basis of the data obtained it is concluded that the hormonal response is directly dependent both on hypothalamic electric stimulation and on the motivative mechanism activation. The very positive reinforcement, timing to the post-stimulating period and being of full value only during the adaptive behavioral act, is not stress-inducing.
We present the humoral immunological findings in 18 patients with ulcerative colitis and two with Crohn's disease. All of them had the disease for 3 months to five years. Fifteen were hispanics and five from European origin. There were ten males and ten females, and an average age of 38 years. All patients had active disease from clinical and endoscopy points of view. Thirteen patients had abnormal values in one of the immunoglobulins and normal in seven patients. IgA was increased in eleven, normal in seven and decreased in two. IgG increased in two, decreased in one and normal in seventeen cases. IgM was found to be increased in five and normal in the rest. IgA secretory determination in saliva, was performed twelve patients and was positive in all of them. Antinuclear antibodies were negative in eight. Anti-smooth muscle were positive in three of fifteen. Anti-mitochondrial were present in one and negative in thirteen. Values of C3 and C4 were lower than normal in 3 and 2 cases respectively from 4 cases studied. CH50 was decreased in 2 of 11 cases studied. In the patients, no correlation was found between low complement values, the positivity of auto antibodies and the clinical parameters previously mentioned. We conclude that there is quantitative alterations of the humoral response and it is necessary the immunological study in persons with inflammatory bowel disease others studies are needed to establish the real value of these findings.