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Biomedical subjects

J Gordon

Publications and source records attributed to J Gordon.

At least 505 records · Page 28Linked to original sources
PubMed1976

On long-term survivals in non-Hodgkin's lymphoma with 'gentle' treatment.

Eighty-seven cases of non-Hodgkin's lymphomas from the Southern California Permanente Medical Group have been reviewed. The patients were treated between 1953 and 1960, all in an era of 'minimal' radiotherapeutic and chemotherapeutic treatment. The favourable prognostic factors for long-term survival using gentle treatment are, firstly, nodular pattern, presenting in clinically localised Stages I and II and, secondly, diffuse well-differentiated lymphocytic lymphoma (DLWD) presenting either in a localised or generalised fashion. In this series moderate dose irradiation (2500 rad) to involved areas with or without modest chemotherapy has resulted in the survival of 26 out of 32 DLWD patients for more than five years and in most cases for over ten years.

Adult↗
PubMed1976

Binding of thiostrepton to ribosomes from thiostrepton-sensitive and -resistant Bacillus subtilis strains.

Binding of [(35)S]thiostrepton to ribosomes from thiostrepton-sensitive and -resistant strains of Bacillus subtilis was studied. Ribosomes from thiostrepton-resistant strains bound relatively little thiostrepton compared with ribosomes from thiostrepton-sensitive B. subtilis. In addition, ribosomes from revertant strains that were obtained as thiostrepton-sensitive revertants from thiostrepton-resistant strains bound [(35)S]thiostrepton similarly to ribosomes from the sensitive parental strain.

Anti-Bacterial Agents↗
PubMed1975

Identification of a ribosomal protein necessary for thiostrepton binding to Escherichia coli ribosomes.

A ribosomal protein necessary for thiostrepton binding to Escherichia coli ribosomes has been identified using the following criteria: 1. A loss in the thiostrepton binding ability of the ribosome was correlated with the selective removal of ribosomal protein L11. This was achieved by a comparison of the thiostrepton binding ability of 50 S ribosomal subunits treated with 1 M NH4C1 and 50% ethanol at 37 degrees which still contained protein L11, and subunits treated successively at 0 degrees and 37 degrees in the same medium, from which protein L11 had been removed. 2. The thiostrepton binding ability of a ribosomal core containing only seven proteins, produced by treatment of 50 S subunits with 4 M LiC1, was fully restored by the rebinding of protein L11, obtained by Sephadex G-100 fractionation of the 1 M LiC1 split protein fraction from 50 S subunits. In addition, treatment of the 1 M LiC1 split protein fraction with an IgG specific for protein L11, uniquely inhibited the restoration of activity. 3. Thiostrepton binding to the 4 M LiC1 core, reconstituted with the 1 M LiC1 split protein fraction, was blocked by treatment with a monovalent antibody fragment (Fab) prepared against protein L11, but not by treatment with antibodies specific for the proteins of the 4 M LiC1 core. We conclude, therefore, that protein L11 is required for the ribosomal binding of thiostrepton.

Anti-Bacterial Agents↗
PubMed1975

Host resistance in sepsis and trauma.

Host resistance to infection was measured by the in vivo response to 5 delayed hypersensitivity antigens and to sensitivity and challenge by dinitrochlorobenzene (DNCB) in 55 seriously ill or injured patients and in 50 preoperative patients. A close correlation between infections, septicemia, death related to infection and anergy was found in the postoperative and post injury patients and was predictive of these complications in the patients studied preoperatively. Decreased body cell mass was noted in both the anergic and non-anergic patients which was consistent with protein-calorie malnutrition but the two groups were not significantly different. A serum factor which inhibited cellular immunity in vitro was found in 4 patients. This factor disappeared in the two patients who recovered. The study suggests the therapeutic value of the in vivo measurement of delayed hypersensitivity in seriously ill and especially preoperative patients in whom specific or non-specific stimulation of cell mediated immunity might alter the risk of infection.

Adolescent↗
PubMed1975

Amelioration of hypoglycemia in a patient with malignant insulinoma during the development of the ectopic ACTH syndrome.

A patient with functioning islet cell carcinoma is described who had amelioration of her hypoglycemia during the development of ectopic ACTH syndrome. Moon facies and hyperkalemic metabolic acidosis were also present in this patient, features uncommonly seen in the actopic ACTH syndrome. At autopsy, she was found to have active tuberculosis. Prophylactic antituberculous therapy should be given to high-risk patients with the ectopic ACTH syndrome. High doses of ACTH may be palliative in refractory hypoglycemic states.

Adenoma, Islet Cell↗
PubMed1975

The immune response of mice treated with anti-mu antibodies: the effect on antibody-forming cells, their precursors and helper cells assayed in vitro.

Previous studies have shown that mice treated from birth with heterologous anti-mu antiserum are severely immunosuppressed with respect to numbers of splenic plaque-forming cells (PFC) to sheep red blood cells (SRBC) in all immunoglobulin classes. In this study we have investigated, using in vitro techniques, the cellular site of the deficit created by anti-mu. The primary PFC response of spleen cells originating from anti-mu-treated mice was completely suppressed in vitro. The response was restored by the addition to the cultures of B cells but not T cells. T cells were derived from normal spleens which had been depleted of B lymphocytes and adherent cells by filtration through cotton wool columns, or by educated thymus cells obtained from the spleens of lethally irradiated mice injected with syngeneic thymocytes and SRBC. Restoration of the PFC response of spleen cells from anti-mu-treated mice by normal B cells suggested that a cellular deficiency rather than an activity process by inhibitory cells was the cause of the imunosuppression. Also, co-culturing spleen cells from normal and suppressed mice did not reveal the presence of inhibitory cells. Spleen cells from x-irradiated mice, injected with bone marrow from anti-mu-suppressed mice, gave rise to PFC cells when cultured with SRBC and normal T cells, suggesting that stem cells giving rise to B cell were not affected by anti-mu treatment. Similarly, educated thymus cells derived from suppressed mice could provide helper function when reconstituted in vitro with normal B cells. Exposure of normal bone marrow and spleen cells to anti-mu serum prior to passage through syngeneic x-irradiated recipients demonstrated that spleen cells were much more sensitive than were bone marrow cells to suppression by anti-mu antibodies. It is concluded that the target of anti-mu antibody is a mu-chain bearing B cell precursor to the IgM-, IgG-, and IgA-producing cell.

Animals↗