Biomedical subjects
J Miller
Publications and source records attributed to J Miller.
Calcium-mediated changes in related malignant and nonmalignant mouse epidermal cell lines.
Two epidermal cell lines of common origin, one tumorigenic and the other not, have been grown in media of different Ca2+ concentrations (low: 0.07 mM; normal: 1.4 mM; high: 10 mM). At normal Ca2+ levels, both cell lines had similar growth rates. The growth rates were reduced at both higher and lower Ca2+ concentrations, with greater inhibition of the tumorigenic than the nontumorigenic cells. At a given level of Ca2+, the 2 cell lines could not be distinguished in their polyacrylamide gel patterns by protein staining, by [125I]concanavalin A reactivity, and by lactoperoxidase iodination. Changes in surface membrane proteins with Ca2+ concentrations were observed by lactoperoxidase iodination, whereas the other techniques, which measure total cell proteins or glycoproteins, showed no substantial variation.
Factors affecting the autologous mixed lymphocyte reaction in kidney transplantation.
In long-term well adapted kidney transplant recipients we have found a close correlation between the T helper (TH):T suppressor/cytotoxic (TS/C) subset ratios and the presence of T cells that respond in the autologous mixed lymphocyte reaction (AMLR). In 21 recipients with T cell E rosette levels ranging between 53 and 86% and TH:TS/C ratios between 0.15 to 2.10, ratios of greater than 0.8 correlated with AMLR responses (13/13), and ratios of less than 0.8 with AMLR nonreactivity (7/7). By contrast, the allogeneic MLR showed no apparent correlation with the TH:TS/C ratios or with the AMLR pre- or postoperatively. It was found that the AMLR in 22 of 23 normal individuals was markedly inhibited by autologous T cells obtained from peripheral blood lymphocytes, exposed to 3,000 rad (Tx) and added as a third component to the cultures. In contrast, 13 of 13 kidney transplant recipients failed to exhibit this Tx AMLR inhibitory cell population. The "naturally occurring" T inhibitory cells, fractionated by an affinity column chromatography procedure into x-irradiated TH and TS/C subsets, inhibited the AMLR to the same extent as unseparated Tx cells. In cell interchange studies performed in four of five HLA identical donor-recipient pairs the Tx cells of the (normal) donor inhibited the recipient AMLR (immunosuppressed), but recipient Tx cells failed to inhibit the donor AMLR. Finally T cells, primed in AMLR and allogeneic MLR for 10 d were tested for AMLR or allogeneic MLR inhibitory activity. Allogeneic MLR primed x-irradiated cells, inhibited both the AMLR and allogeneic MLR while AMLR x-irradiated primed cells inhibited neither reaction. The Tx AMLR inhibitor found in normal peripheral blood, appears to be a cell that is highly sensitive to the effects of biologic or pharmacologic immunosuppressive agents.
Reciprocal gastropancreatic modulations for the release of somatostatin-like immunoreactivity, glucagon, and insulin in the rat.
In order to assess the interrelationships between stomach and pancreas regarding the secretions of somatostatin-like immunoreactivity (SLI), glucagon (IRG), and insulin (IRI), concentrations of the three hormones were assayed in portal plasma and portal blood flow was measured in enterectomized rats before and after the selective removal of stomach or pancreas. Portal plasma SLI, IRG, and IRI concentrations were significantly increased by i.v. arginine in control rats (pancreas + stomach present). After gastrectomy, SLI, IRG, and IRI concentrations were, respectively, 52 +/- 13% (N = 15; P less than 0.005), 234 +/- 40% (P less than 0.001), and 119 +/- 15% (NS) of the pregastrectomy values. A decreased SLI secretion, an increased IRG release, and an unmodified basal IRI release were estimated by portal flow measurement. The A- and B-cell responses to arginine in the gastrectomized rats were significantly higher than in the control rats, while the D-cell response was no longer detectable. After pancreatectomy, by contrast, SLI concentrations were 360 +/- 75% of the prepancreatectomy values (N = 12; P less than 0.001). This reflected an actual increment of SLI release, taking into account the concomitant measurement of portal blood flow. The concentrations of IRG declined by 51 +/- 5% (P less than 0.001) and IRI was no longer measurable. A- and B-cell responses to arginine also were no longer detectable. These results suggest that in these experimental conditions (1) the stomach restrained pancreatic A- and B-cell responses to arginine, perhaps through the SLI released from the stomach and (2) the pancreas restrained gastric SLI secretion, perhaps through insulin.
Mouse monoclonal antibody (WI-MN-1) against malignant melanoma.
A mouse monoclonal antibody, WI-MN-1, was raised against G-361 melanoma cell line. Reactivity of this antibody was characterized by indirect immunofluorescence against 22 cell lines and normal and neoplastic human tissues. Positive reactions were seen against three melanoma cell lines (G-361, HT-144, and MeWo). It also reacted against an epidermoid carcinoma cell line (Hep-2) and amnion cells (WISH). The antibody failed to react against cell lines derived from granulocytic leukemias, lymphocytic leukemias, Burkitt's lymphoma, carcinoma of the lung, carcinoma of the cervix, carcinoma of the colon, carcinoma of the breast, astrocytoma, and a human monocytoid cell line. Mouse melanoma and mouse fibroblast cell lines were also nonreactive. Similarly, there was no reaction against human peripheral blood, bone marrow, spleen, lymph node, thymus, breast, lung, stomach, heart, brain, kidney, liver, skin, or testis. The antibody was also tested by indirect immunofluorescence against 17 samples of metastatic malignant melanoma which were removed from 13 patients. WI-MN-1 gave positive reaction against 16 of these specimens, and it reacted with the cryostat section in the immunoperoxidase test, delineating neoplastic melanoma from the normal brain tissue. The antibody precipitated Mr 105,000 and 38,000 antigens from biosynthetically labeled G-361 cells. It was suggested that WI-MN-1 was a useful addition to the panel of monoclonal antibodies against melanoma-associated antigens.
Inhibitory effect of a fava bean component on the in vitro development of Plasmodium falciparum in normal and glucose-6-phosphate dehydrogenase deficient erythrocytes.
We examined the hypothesis that G-6-PD deficiency associated with fava bean ingestion confers resistance to malaria by studying the in vitro interactions between malaria parasites (Plasmodium falciparum), human erythrocytes with varying degrees of G-6-PD deficiency, and isouramil (IU), a fava bean extract that is known to cause oxidant stress and hemolysis of G-6-PD-deficient erythrocytes. Untreated G-6-PD-deficient and normal erythrocytes supported the in vitro growth of P. falciparum equally well. However, after pretreatment with IU, G-6-PD-deficient erythrocytes did not support parasite growth in vitro, whereas growth remained high in normal erythrocytes. Parasite growth was proportional to the G-6-PD activity of the IU-treated erythrocytes. In contrast, when parasitized erythrocytes were exposed to IU, parasites even in normal erythrocytes were destroyed. Ring forms were much less sensitive than late trophozoites and schizonts. The results suggest that there are two modes by which IU affects the development of P. falciparum and demonstrate in vitro that G-6-PD deficiency confers resistance against malaria under conditions of fava-bean-associated oxidant stress.
The inhibitory effect of human immune sera upon the in vitro development of Plasmodium falciparum.
Sera from patients who had recovered from malaria were examined for their capacity to inhibit the growth of Plasmodium falciparum in vitro. The sera were dialysed to eliminate any residual drugs taken by the donor. IgG purified from inhibitory sera was found to be as effective as the original sera. The inhibitory activity of some of the immune serum was pronounced after the second day in culture. This may suggest that the mechanism of action of antibodies affects the merozoites which appear for a short period in the two day cycle of the parasite. There was no correlation between antibody titre measured by IFA and the inhibitory capacity of the sera: some samples with high IFA titres did not inhibit the growth while some with low IFA titres inhibited the parasite. Autoantibodies directed against the erythrocytes, which were found in some sera, had no antimalarial inhibitory role and the absorption of them did not alter the inhibitory effect. There were more inhibitory sera among Nigerian than amount Thai and Ethiopian sera. The experiments were performed with a Nigerian strain and therefore the results may be explained by differences between the various falciparum strains of malaria.
A Gower Street scandal. The Samuel Gee lecture 1982.
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Intracochlear implants: potential histopathology.
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Nursing image. Influencing the image with newspaper features.
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Replanning of an intensive therapy unit.
Considerable effort is needed when replanning an intensive therapy unit to avoid repeating mistakes in design, such as lack of windows and an impractical working area. Early consultation with the nursing and medical staff primarily responsible for such a unit is essential. The considerable technological innovations in intensive care will require flexibility in the future if they are to be incorporated into existing facilities.
Malpractice premiums rise in Britain.
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Acute refractory congestive cardiac failure following allogeneic bone marrow transplantation.
A young woman aged 18 years underwent allogeneic bone marrow transplantation for severe acute aplastic anaemia. In the 3 weeks following this procedure the platelet count remained between 10 and 30 X 10 q/l, and from the 21st day after the transplant there was relentless progression of congestive cardiac failure resulting in the patient's death 4 days after its onset. Autopsy showed widespread subendocardial haemorrhage and extensive bleeding between the myocardial fibres resulting in refractory cardiac failure. These findings are compatible with drug-induced cardiotoxicity.
Curriculum unfair to dental students?
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Structural alterations in J regions of mouse immunoglobulin lambda genes are associated with differential gene expression.
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Concurrent sickle-cell anemia and alpha-thalassemia: effect on severity of anemia.
We studied 47 patients with sickle-cell anemia to determine the effect of alpha-thalassemia on the severity of their hemolytic anemia. We diagnosed alpha-thalassemia objectively by using alpha-globin-gene mapping to detect alpha-globin-gene deletions, studying 25 subjects with the normal four alpha-globin-genes, 18 with three, and four with two. The mean hemoglobin, hematocrit, and absolute reticulocyte levels (+/- S.D.) were 7.9 +/- 0.9 g per deciliter (4.9 +/- 0.6 mmol per liter), 22.9 +/- 2.9 per cent, and 501,000 +/- 126,000 per cubic millimeter, respectively, in the non-thalassemic group; 9.8 +/- 1.6 g per deciliter (6.1 +/- 1.0 mmol per liter), 29.0 +/- 5.0 per cent, and 361,000 +/- 51,000 per cubic millimeter in the group with three alpha-globin genes; and 9.2 +/- 1.0 g per deciliter (5.7 +/- 0.6 mmol per liter), 27.5 +/- 3.0 per cent, and 100,000 +/- 15,000 per cubic millimeter in the group with two alpha-globin genes. Deletion of alpha-globin genes was also accompanied by a decreased mean corpuscular hemoglobin concentration (MCHC) in post-reticulocyte erythrocytes and by increased hemoglobin F levels. The decreased intraerythrocytic hemoglobin S concentration and elevated hemoglobin F levels associated with alpha-thalassemia appear to diminish the degree of hemolytic anemia found in sickle-cell disease.
Preparation of creatine kinase-MM isoenzymes from canine and human tissues.
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