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S Oja

Publications and source records attributed to S Oja.

6 recordsLinked to original sources
PubMed1997

The inhibitory role of nitric oxide in the control of porcine and human sphincter of Oddi activity.

BACKGROUND: The possible role of nitric oxide in the regulation of the sphincter of Oddi is not known in species with a resistor-like sphincter of Oddi such as humans and pigs. METHODS: Sphincter of Oddi perfusion manometry and simultaneous electromyography (EMG) were recorded transduodenally in eight anaesthetised pigs. Acetylcholine (4 micrograms/kg) was given intra-arterially, with or without sodium nitroprusside (10-100 micrograms/kg), an exogenous nitric oxide donor. For in vitro studies the sphincter was removed from the eight pigs and from six patients undergoing pancreaticoduodenectomy, cut into rings, and the amplitude of contraction was measured in an ex vivo bath. Each ring was stimulated with acetylcholine (100 microM) and KCl (125 mM). The stimulation was repeated after incubation with L-NAME (a stereospecific competitive inhibitor of nitric oxide synthase), with L-NAME plus L-arginine (a substrate for nitric oxide synthase), and with sodium nitroprusside. The sphincter rings were then submersed in liquid nitrogen and stored. Immunohistochemical analysis was used to localise nitric oxide synthase in the pig and human sphincter specimens. RESULTS: In vivo EMG revealed 2-3 phasic bursts per minute with the basal pressure variation 6-40 mm Hg. Acetylcholine induced a large electrical burst and the pressure increased by (mean (SE)) 20 (10) mm Hg (p < 0.01) for 17 (4) seconds. After sodium nitroprusside (10 micrograms/kg) acetylcholine did not induce pressure changes and electrical activity was almost abolished. In vitro, L-NAME increased the KCl induced sphincter contraction in both pig and human specimens (p < 0.01). In human, but not in pig, specimens L-NAME increased the amplitude of acetylcholine induced contraction (p < 0.01). L-Arginine partly reversed the effect of L-NAME in both pig and human specimens. Sodium nitroprusside decreased the acetylcholine and KCl induced contractions in both pig and human specimens. Immunohistochemical studies localised nitric oxide synthase to rich plexi of nerve fibres in the mucosa and the muscle in both pig and human sphincter of Oddi. CONCLUSIONS: The sphincter of Oddi in both pigs and humans has endogenous nitric oxide synthase activity and immunoreactivity. Inhibition of endogenous nitric oxide production enhances contractility while exogenous nitric oxide decreases sphincter contractility and electrical activity.

Acetylcholine↗
PubMed1994

Normal vector magnetocardiogram. I. Correlation with the normal vector ECG.

The vector magnetocardiogram (VMCG) has been measured with the corrected unipositional VMCG lead system and analyzed statistically in 290 normal subjects. The morphologic study of the QRS waveforms showed that in the right-to-left (X) component, the triphasic qRs waveform appeared in 55% of the subjects. The superoinferior (Y) component was characterized by a prominent S wave in 96% of the subjects, and the anteroposterior (Z) component was also characterized by a prominent S wave in 95% . The VMGs were compared with the vector electrocardiograms (VECG) recorded in a subgroup of 200 subjects, in whom both the VMCG and VECG were available for computer analysis. The normal variability of the spatial vector magnitude measurements was significantly greater in the VMCG than in the VECG. Some similarities were observed in the waveforms of the time-averaged QRS complexes between the VMCG and VECG. Multiple linear regression analysis between the VMCG and VECG showed that maximally 27, 45, and 41% of the variation in the instantaneous QRS X, Y, and Z amplitudes of the VMCG, respectively, could be explained by the instantaneous X, Y, and Z amplitudes of the VECG.

Adolescent↗
PubMed1994

Normal vector magnetocardiogram. II. Effect of constitutional variables.

The effects of age, sex, height, weight, and dimensions of the thorax on the vector magnetocardiogram (VMCG) were studied in 290 normal subjects. The effect of sex on 141 VMCG parameters was tested with the Mann-Whitney U test, and the effects of age and body dimensions on the male and female subjects were tested with the Kruskal-Wallis H test. Similar analyses were applied for a comparison of the vector electrocardiogram (VECG) in a subgroup of 200 normal subjects. Sex had the most pronounced effect on the VMCG, a total of 58% of the instantaneous time-normalized QRS and T amplitude parameters were significantly (P < .01) different in men and women (47% for the VECG). In women, the absolute VMCG amplitudes were, on average, about 60% of those in men. In the VECG, the corresponding portion was about 85%. In men and women, 50 and 26% of the time-normalized amplitude parameters, respectively, were significantly (P < .01) affected by age; the main effect was a decrease in most VMCG amplitudes with increasing age. In the VECG, the corresponding effect was not as statistically significant. The effect of constitutional variables of the body on the VMCG and VECG was, in most cases, not statistically significant. Multiple correlation analysis showed that the five noncardiac factors together explained, at most, 16 and 28% of the variability in the instantaneous, time-normalized QRS amplitudes for men and women, respectively. In the VECG, these figures were 13 and 18%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Promotion and inhibition of activation-induced apoptosis in T-cell hybridomas by oncogenes and related signals.

The Two Signal: Death/Survival Model suggests that cellular proliferation and physiological cell death should be intimately associated such that, in the absence of external influences, a normal cell departing from rest will have an equal probability of undergoing either process. The c-Myc protooncogene product has been implicated in cell cycle progression and in the control of gene expression, and more recently c-Myc has also been seen to promote apoptotic cell death. As predicted from the model, c-Myc-induced apoptosis is inhibited by growth factors or other anti-apoptotic signals including those provided by some oncogenes. Here, we discuss experiments that test the Two Signal: Death/Survival Model in the phenomenon of activation-induced apoptosis in T-cell hybridomas. Ligation of the antigen receptor on these cells leads to activation, resulting in cytokine production and apoptosis. Inhibition of c-Myc expression by addition of antisense oligodeoxynucleotides or transforming growth factor beta inhibits this form of apoptosis. Because c-Myc is known to bind to several cellular proteins, including Max, we further examined the effects of expression of a dominant negative Max on activation-induced apoptosis. We found that this Max mutant, which interferes with the function of the Myc/Max heterodimer, inhibits the induction of apoptosis by antigen receptor ligation. Thus, both Myc and Max play roles in activation-induced apoptosis, presumably via control of gene expression. Further, as predicted, signals generated from growth factor receptors or the v-Abl oncogene interfere with activation-induced apoptosis. In contrast, the anti-apoptotic effects of Bcl-2 are not active in this form of apoptosis. Finally, a role for Fas/Fas-ligand interactions in activation-induced apoptosis is considered.

Animals↗