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Biomedical subjects

J Cunningham

Publications and source records attributed to J Cunningham.

At least 235 records · Page 13Linked to original sources
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↗
PubMed1980

Recognition of histocompatibility determinants controls reactivity of auto-sensitized lymphocytes against neural tissues.

Thoracic duct lymphocytes from rats sensitized against syngeneic spinal cord rapidly produce damage in cultures of syngeneic cerebellar cells but coexist indefintely with allogeneic cultures. Lymphocytes from donors that have been sensitized against allogeneic spinal cord attack cultures of syngeneic and specific allogeneic cerebellum but not cells from rats of a third, unrelated strain.

Animals↗
PubMed1980

Oxidative metabolism of 4-aminobutyrate by rat brain mitochondria: inhibition by branched-chain fatty acid.

The oxidation of 4-aminobutyric acid (GABA) by nonsynaptosomal mitochondria isolated from rat forebrain and the inhibition of this metabolism by the branched-chain fatty acids 2-methyl-2-ethyl caproate (MEC) and 2.2-dimethyl valerate (DMV) were studied. The rate of GABA oxidation, as measured by O2 uptake, was determined in medium containing either 5 or 100 mM-[K+]. The apparent Km for GABA was 1.16 +/- 0.19 mM and the Vmax in state 3 was 23.8 +/- 5.5 ng-atoms O2 x min-1 x mg protein-1 in 5 m M-[K+]. In a medium with 100 mM-[K+] the apparent Km was 1.11 +/- 0.17 mM and Vmax was 47.4 +/- 5.7 ng-atoms O2 x min-1 x mg protein-1. The Ki for MEC was determined to be 0.58 +/- 0.24 or 0.32 +/- 0.08 mM, in 5 or 100 mM-[K+], respectively. For DMV, the Ki was 0.28 +/- 0.05 or 0.34 +/- 0.06 mM, in 5 or 100 mM-[K+] medium, respectively. The O2 uptake of the mitochondria in the presence of GABA was coupled to the formation of glutamate and aspartate; the ratio of oxygen uptake to the rate of amino acid formation was close to the theoretical value of 3. Neither the [K+] nor any of the above inhibitors had any effect on this ratio. The metabolism of exogenous succinic semialdehyde (SSA) by these same mitochondria was also examined. The Vmax for utilization of oxygen in the presence of SSA was much greater than that found with exogenously added GABA, indicating that the capacity for GABA oxidation by these mitochondria is not limited by SSA dehydrogenase. In addition, the branched-chain fatty acids did not inhibit the metabolism of exogenously added SSA. Thus, the inhibitors examined apparently act by competitively inhibiting the GABA transaminase system of the mitochondria.

Animals↗
PubMed1980

The "bull's-eye" falciform ligament: a sonographic finding of portal hypertension.

The umbilical vein may dilate as a collateral in portal venous hypertension and become visible within the echodense fat of the falciform ligament. The resulting "bull's-eye" appearance was visible in 5/47 (11%) of patients with cirrhosis secondary to alcohol abuse. It was not visualized in any patients with cholelithiasis who had no evidence of cirrhosis. When demonstrated by ultrasound, this finding should suggest portal venous hypertension.

Adult↗
PubMed1979

Psychopathology in self-identified female-to-male transsexuals, homosexuals, and heterosexuals.

The comparative self-esteem and psychological well-being of female-to-male transsexuals, homosexuals, and heterosexuals (patient and nonpatient) were studied. Results indicated that individual candidates for sex-change surgery varied appreciably in self-concept and adjustment, and as a group were indistinguishable from psychiatric controls. Nonpatient homosexuals and heterosexuals demonstrated the most positive self-esteem and level of adjustment.

Adolescent↗
PubMed1979

Gutta-percha points of apicoectomy. To push or to pull?

A gutta-percha root-filling point placed during apicoectomy may be condensed by the application of pressure to its coronal end or tension to its apical end. Scanning electron microscopy clearly demonstrates the effect that these techniques have on the adaptation of the root filling to the canal. The pressure method would appear to produce the more satisfactory result.

Apicoectomy↗
PubMed1979

Warfarin skin necrosis. The role of factor VII.

Necrosis of cutaneous and subcutaneous tissue is a rare complication of therapy of with oral anticoagulants, and is related to the use of loading-dose regimes. Three cases are reported, and demonstrate that the principal histopathological feature is thrombosis within the subcutaneous vasculature. The effect of large doses of anticoagulant on the levels of the vitamin K dependent clotting factors provides a satisfactory model for the temporal sequence of events in this syndrome. The occurrence of intravascular thrombosis with low or absent levels of Factor VII indicates that the intrinsic clotting system is of primary importance in venous thrombosis. This complication of anticoagulant therapy is not seen if loading-dose regimes are avoided.

Aged↗
PubMed1979

A deterministic model for measles.

A deterministic model of recurrent epidemics is constructed using a non linear relationship between infection rate and number of contacts. Epidemic waves which are not damped are predicted and a relationship between community size and the period of recurrence is established. A possible explanation of measles outbreaks is suggested.

Adolescent↗