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Biomedical subjects

J Cunningham

Publications and source records attributed to J Cunningham.

At least 217 records · Page 12Linked to original sources
PubMed1983

Serum-induced enhancement of peripheral blood mononuclear cell mediated cytotoxicity towards human target cells in systemic lupus erythematosus.

Sera from 6 out of 18 patients with systemic lupus erythematosus (SLE) were found to be capable of producing marked increases of cytotoxicity in several established human target cell lines when co-cultured with normal human peripheral blood mononuclear cells (PBM). Fractionation studies indicated that the cytotoxicity-inducing activity resided in IgG containing fractions and that the effector cells were Fc-receptor positive. By contrast, sera from 27 normal controls produced little or no cytotoxicity when similarly co-cultured with the same target cell lines and normal PBM. Any slight reactivity that occasionally occurred against a single cell line was, on serum fractionation, either labile or associated with albumen containing fractions. These findings raise the possibility that antibody-dependent cellular cytotoxicity could provide an additional pathogenetic mechanism in patients with SLE.

Adult↗
PubMed1982

Hypernatremia induced by maximal exercise.

A short burst of intensive exercise (100-m swim lasting one minute and resulting in a 12-fold rise in the level of blood lactate) resulted in frank hypernatremia (serum sodium level, greater than 150 mEq/L) in 30% to 40% of well-trained athletes. In contrast, less intensive exercise (800-m swim lasting ten minutes and resulting in a sevenfold rise in the level of blood lactate) failed to cause a rise in serum sodium level despite comparable elevations in hematocrit reading and serum protein levels. Hypernatremia induced by intensive exercise cannot be explained by losses in body fluid or solute ingestion, but is probably a consequence of a shift of hypotonic fluid from the extracellular to the intracellular compartment. Thus, the mechanism of exercise-induced hypernatremia may be unique, as compared with other clinically recognized forms of hypernatremia.

Adolescent↗
PubMed1982

Chronic acidosis with metabolic bone disease. Effect of alkali on bone morphology and vitamin D metabolism.

Chronic metabolic acidosis and osteomalacia developed in two patients following urinary diversion. Good clinical, biochemical, and histologic responses were seen following treatment with alkali alone (vitamin D was not given), despite the presence of markedly impaired glomerular filtration in one of the patients. Plasma 25-hydroxyvitamin D and 1 alpha, 25-dihydroxyvitamin D concentrations were normal before and during treatment in one of the patients and in the other were low before and normal during treatment. The results show that successful treatment of the osteomalacia of chronic acidosis is not necessarily accompanied by changes in the plasma levels of vitamin D metabolites and that even when marked glomerular dysfunction coexists with acidosis and osteomalacia, treatment with alkali may be more appropriate than the administration of vitamin D analogues.

Acidosis↗
PubMed1982

Cyclic GMP concentration in ovarian tissue after administration of gonadotrophin to prepubertal rats.

The weights, protein concentrations, and concentrations of cyclic AMP and cyclic GMP in the ovaries of prepubertal rats have been measured after induction of follicular growth by administration of pregnant mare serum gonadotrophin (PMSG). Three phases of ovarian growth, the follicular growth phase, the preovulatory phase and the luteal phase were investigated. Ovulation was induced by administration of human chorionic gonadotrophin (hCG). During the follicular phase, ovarian weight, protein content and the content of both cyclic AMP and cyclic GMP increased 2-3 days after administration of PMSG. Administration of hCG 65h after PMSG caused a rapid rise in the concentration of cyclic AMP but the concentration of cyclic GMP tended to fall. During the luteal phase the concentrations of both cyclic nucleotides decreased.

Animals↗
PubMed1982

Long-term complications of MOPP chemotherapy in patients with Hodgkin's disease.

Two hundred and sixty-three patients in long-term remission from Hodgkin's disease were evaluated for complications of chemotherapy. All patients were interviewed by telephone conversation and reported complications were documented by chart review. Treatment consisted of mantle and para-aortic irradiation in 127 patients, total nodal irradiation (TNI) in 32, TNI and MOPP in 34, and mechlorethamine, vincristine, prednisone, and procarbazine (MOPP) chemotherapy alone or with lesser irradiation in 70. In this study, greater than 90% of the men who received MOPP remain infertile. In contrast, a substantial portion of female patients treated with MOPP chemotherapy have retained normal menses (58%) and only a small proportion have had persistent amenorrhea (9%). Five of eight female patients desiring families after MOPP chemotherapy have had normal children. The risk of developing a major infection requiring hospitalization was greatest in those patients who had received TNI and MOPP chemotherapy. The risk of developing a herpes zoster infection was greatest during or within the first year following therapy and was greatest in those patients receiving combined radiation therapy and chemotherapy. Nearly 100% of patients continue to lead normal lives following treatment for Hodgkin's disease. Only a small percent of patients (1.5%) have been totally disabled following treatment.

Adolescent↗
PubMed1982

Influence of mediastinal adenopathy on site and frequency of relapse in patients with Hodgkin's disease.

Between April 1969 and July 1979, 267 patients with surgically staged IA-IIB Hodgkin's disease and 31 with clinically staged IIE or IV Hodgkin's disease were treated; disease was limited to the area above the diaphragm. Three separate groups of patients with mediastinal adenopathy were identified. Patients with disease limited to the mediastinum had a favorable prognosis, and treatment with mantle followed by para-aortic irradiation has resulted in 85% relapse-free survival and 100% overall survival at 8 years. Surgically staged patients with large diameter mediastinal adenopathy (greater than 0.33 of the thoracic diameter) have a high relapse rate with radiation therapy alone. The use of combined modality therapy has reduced the risk of relapse in these patients, but the survival remains higher whether MOPP is used initially or at relapse. Clinically staged IIE patients or stage IV patients with extensive extranodal disease limited to the thoracic cavity were treated with chemotherapy and involved- or extended-field irradiation. These patients had a 5-year survival of 66% with large mediastinal adenopathy and 90% with lesser mediastinal disease.

Hodgkin Disease↗
PubMed1981

Impaired response of plasma renin activity to tilting after renal transplantation.

1. Changes in plasma renin activity, plasma noradrenaline, pulse rate and blood pressure after tilting were measured in normal subjects and in patients with renal transplants. 2. There was a marked difference between the renin responses in the two groups, the increases in plasma renin activity in the control subjects being much greater than those in the transplanted patients. 3. Activation of the sympathetic nervous system after tilting, as indicated by changes in pulse rate, blood pressure and plasma noradrenaline, was similar in the two groups. 4. We conclude that the ability of the transplanted kidney to increase plasma renin activity after tilting is impaired, probably as a result of sympathetic denervation of the kidney during transplantation. The results suggest a dominant role of the sympathetic nervous system in the mediation of renin release after tilting.

Adult↗
PubMed1981

Specific inhibition of anti-self reactivity following exposure of neonatal rats to lymphocytes with anti-neural activity.

Not only did newborn rats prove to be resistant to the adoptive transfer of responses against central nervous system tissues following the injection of lymphocytes from rats sensitized against syngeneic spinal cord, but such recipients were also subsequently resistant as adults to the active induction of an immune response following challenge with syngeneic cord. This resistance to active immunization against syngeneic spinal cord as adults was associated with the absence of lymphocytes with anti-neural activity and with the appearance of cells able to suppress such activity, after challenge. Interference by the lymphocytes of resistant rats with anti-neural responses was restricted to those responses directed against syngeneic neural cells.

Animals↗
PubMed1981

Migration of lymphocytes sensitized against syngeneic and allogeneic spinal cord after infusion into susceptible and resistant syngeneic and semi-allogeneic hosts.

Lymphocytes from rats that had been sensitized against spinal cord were infused into unsensitized hosts, and the ability of cells subsequently recovered from the thoracic duct lymph of these recipients to mount anti-neural responses was tested. Lymph from normal recipients frequently contained reactive lymphocytes during the 4 days following infusion of sensitized cells, whereas cells that had been recovered from transfused rats, resistant to encephalomyelitis as a result of neonatal treatment, were almost invariably benefit of activity. If lymphocytes reactive against allogeneic neural cells were passaged through F1 hybrids of the lymphocyte and sensitizing allogeneic tissue strains, loss or retention of their ability to attack allogeneic neural cells was determined by the method of sensitization of the original lymphocyte donor.

Animals↗
PubMed1981

On the mechanism by which veratridine causes a calcium-independent release of gamma-aminobutyric acid from brain slices.

1 The mechanisms by which veratridine increases the release of gamma-aminobutyric acid (GABA) from brain slices have been studied.2 Exposure of superfused cerebro-cortical, nigral or cerebellar slices to veratridine (5 muM) or KCl (50 mM) caused large increases in the efflux of [(3)H]-GABA.3 Reduction of the external Ca concentration [Ca](o) to zero had strikingly different effects on the veratridine and K-evoked release of [(3)H]-GABA. The K-evoked release from all three areas was greatly reduced in Ca-free medium, but the veratridine-evoked release from cerebeller slices was not affected, and the release of [(3)H]-GABA from cortical and nigral slices was increased three fold. The potentiation of the veratridine evoked release of GABA which occurred in Ca-free medium was not due to the reduction in divalent ions, because it still occurred in medium in which the Ca was replaced by an equivalent amount of Mg.4 The veratridine-evoked release of [(14)C]-glycine from slices of spinal cord was also significantly increased in Ca-free medium. In contrast, the release of cortical [(3)H]-noradrenaline and [(14)C]-acetylcholine caused by the alkaloid was greatly diminished in Ca-free medium.5 The veratridine but not the K-evoked release of [(3)H]-GABA was abolished when the external Na concentration [Na](o) was reduced to zero and by tetrodotoxin (TTX) (0.2 muM). Cl-free medium did not affect the veratridine-evoked release of [(3)H]-GABA or its potentiation by Ca-free medium.6 Exposure of the tissue to depolarizing concentrations of external K ([K](o) = 120 mM) did not abolish the veratridine evoked release of [(3)H]-GABA or its potentiation by Ca-free medium.7 Pre-incubation of cortical slices with L-2,4, diaminobutyric acid (DABA), or substitution of Na in the superfusion medium with Li, did not affect the veratridine-evoked release of [(3)H]-GABA, indicating that the alkaloid does not stimulate GABA efflux by a carrier-mediated transport process.8 Exposure of the tissue to ruthenium red (10 muM) increased the veratridine evoked release of [(3)H]-GABA in both normal and in Ca-free medium but almost abolished the K-evoked release.9 It is suggested that veratridine causes GABA release by increasing the permeability of the nerve terminals to Na. In normal medium, the resulting influx of Ca(2+) ions through voltage-dependent Ca(2+) channels may be involved in triggering the release of GABA. However, a major part of the GABA efflux appears to be triggered by the release of Ca(2+) ions from intraterminal mitochondria, which results from the increase in[Na](i). Since Ca(2+) ions antagonize the action of veratridine, the potentiation of the drug-evoked release of GABA that occurs in Ca-free medium, might be due to the absence of the antagonistic Ca(2+) ions. The resulting greater increase in Na entry and [Ca](i) caused by Ca release from intracellular stores, must presumably more than balance the contribution normally made by any influx of extracellular Ca(2+).

Acetylcholine↗
PubMed1981

Serum antibody and opsonic responses after immunization with pneumococcal vaccine in kidney transplant recipients and controls.

We immunized 31 renal transplant patients and 6 control subjects with a pneumococcal vaccine containing 14 capsular polysaccharides. Antibody levels to Streptococcus pneumoniae types 3 and 6A were measured by a radioimmunoassay, and opsonic activity to S. pneumoniae types 3 and 6B was determined by using a luminol-enhanced chemiluminescence phagocytic assay on serum samples obtained before and 1 month after immunization. There was a 10.2-fold and a 2.9-fold increase in antibody to S. pneumoniae type 3 (P less than 0.005) and type 6A (P less than 0.01), respectively, but only a 1.3-fold (P greater than 0.05) and 1.1-fold (P greater than 0.05) increase in opsonic activity. For S. pneumoniae type 3, changes in opsonic activity correlated well with antibody concentration (P less than 0.05). However, for S. pneumoniae type 6, these two tests correlated poorly (P greater than 0.05). This poor correlation suggests that concentrations of antibody to type 6A polysaccharide which are achieved after immunization may not be opsonically active in vitro against S. pneumoniae type 6B.

Antibodies, Bacterial↗
PubMed1981

Reactivity of neuro-antigen-sensitized lymphocytes against syngeneic, allogeneic and tolerated allogeneic neural tissue.

Lymphocytes reactive against cultured cerebellar cells were collected from rats that had been sensitized against a variety of preparations. While cells with in vitro reactivity were invariably present in lymph from rats which were to develop encephalomyelitis, the reverse did not apply. Challenge with either neural or non-neural allogeneic tissue sensitized effectively against allogeneic neural tissue. Challenge of homograft-tolerant rats with either syngeneic or tolerated allogeneic spinal cord sensitized against neural tissues of tolerated strain.

Animals↗
PubMed1981

The role of suppressor T cells in the expression of autoimmune haemolytic anaemia in NZB mice.

The course of haemolytic anaemia in NZB mice has been altered by injection of spleen cells from diseased mice into younger ones before the onset of clinical disease. Recipients greater than 6 weeks of age developed early-onset autoimmune disease, recipients less than 6 weeks of age developed early-onset autoimmune disease, recipients less than 6 weeks of age recovered from early induced disease and showed a delay in the onset of spontaneous disease as compared with untreated NZB mice. This delay was due to the induction in the young mice of splenic suppressor cells. These cells were non-adherent to nylon wool and suppressed autoantibody formation on transfer to old Coombs-positive recipients. Suppressor cells active against autoantibody formation on transfer to old Coombs-positive recipients. Suppressor cells active against autoantibody-producing cells may be present in young untreated NZB mice, but not in sufficient numbers to suppress autoantibody production on adoptive transfer to Coombs-positive; however, when Ig-negative cells from the spleens of very young NZB mice were transferred together with Ig-positive cells from Coombs-positive donor mice to irradiated NZB recipients, the autoantibody production of the transferred B cells was suppressed in some cases. Suppressor cell activity could also be induced by co-culture of spleen cells from old Coombs-positive and young Coombs-negative NZB mice in vitro.

Anemia, Hemolytic, Autoimmune↗