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Biomedical subjects

G Simon

Publications and source records attributed to G Simon.

At least 181 records · Page 10Linked to original sources
PubMed1989

Transcriptional activation of homologous and heterologous genes by the hepatitis B virus X gene product in cells permissive for viral replication.

The potential of the hepadnavirus X gene product to activate gene expression in trans was tested through a series of cotransfections of X expression vectors with a variety of potential targets for transactivation. The X gene products from human hepatitis B virus (HBV), woodchuck hepatitis virus, and ground squirrel hepatitis virus are all equally active in augmenting the expression of a wide array of target promoters in both permissive and nonpermissive cells. Using the HBV genome itself as the source of X protein, we demonstrate that transactivation of HBV and heterologous genes occurs when X protein is expressed in its native state during productive infection of permissive cells. Run-on transcription analysis indicates that this transactivation occurs at the level of primary transcription.

Genes, Viral↗
PubMed1988

Tritium labeling of a powerful methylphosphonate inhibitor of cholinesterase: synthesis and biological applications.

7-(Methylethoxy phosphinyloxy)-1-methyl-quinolinium iodide (MEPQ), a powerful anti-cholinesterase methylphosphonate ester, was labeled with tritium (9 Ci/mmol) at the methylphosphonyl moiety (TCH2P(O)(OR)X) by an iodine-tritium replacement reaction. Kinetic measurements of the rate of inhibition of acetylcholinesterase (AChE) by [3H]MEPQ and its rate of hydrolysis in alkaline solution confirmed the identity of [3H]MEPQ with authentic MEPQ, which was prepared by the same reaction sequences. Gel-filtration experiments verified the radiospecificity of [3H]MEPQ. In vitro radiolabeling of both AChE and butyrylcholinesterase along with the whole-body autoradiography of [3H]MEPQ-treated mice suggests that [3H]MEPQ is a convenient marker for studying biological systems containing these esterases.

Acetylcholinesterase↗
PubMed1988

Pathophysiology of increased urinary N-acetyl-beta-D-glucosaminidase activity in human hypertension: effect of cilazapril therapy.

To investigate the pathophysiology of elevated urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in human hypertension, total and fractional urinary NAG activities were correlated with Li clearance, a measure of proximal renal tubular Na reabsorption, in 15 white hypertensive subjects, aged 56 years, and in 13 normotensive control subjects. In 11 hypertensive subjects, the measurements were repeated after 2 months of antihypertensive therapy with the converting enzyme inhibitor cilazapril (2.5 or 5.0 mg daily). Urinary NAG activity was increased in hypertensives and correlated directly with Li clearance in both hypertensive and normotensive subjects. Li clearance and urinary NAG activity were reduced by antihypertensive therapy. The findings indicate an inverse correlation between urinary NAG activity and proximal renal tubular Na reabsorption, suggesting that NAG is reabsorbed in the proximal renal tubules with Na and other proteins. High Li clearance and urinary NAG activity in hypertension are in part functional and, therefore, reversible disturbances of renal function.

Acetylglucosaminidase↗
PubMed1988

Relationship between dog saphenous vein reactivity and Na content.

The physiological significance of the wide range of spontaneous variation in the total Na content of the dog saphenous vein (SV) was investigated. The SV of pentobarbital-anesthetized male mongrel dogs was perfused in vitro with the dogs' own venous blood, and its reactivity to acetylcholine (ACh) and norepinephrine (NE) was measured. The contralateral SV was removed for measurements of total and intracellular (Li exchange at 4 degrees C) Na and K content, DNA content, and muscle width. Reactivity to ACh correlated directly with total and extracellular SV Na content, and reactivity to NE correlated directly with total and intracellular K content. Reactivity to NE was unrelated to ACh reactivity, plasma NE concentration, or venous wall DNA content or muscle width. ACh-mediated venoconstriction was approximately 10 times more sensitive to inhibition by amiloride, an inhibitor of Na-entry pathways, than NE-mediated venoconstriction. The finding that extracellular Na content is a marker of reactivity to ACh is compatible with experimental evidence that the mode of action of ACh may be the stimulation of Na influx. The positive correlation between the K content and reactivity of veins to NE suggests that there is a link between intracellular K content and the release of Ca from the sarcoplasmic reticulum in response to NE.

Acetylcholine↗
PubMed1987

Antihypertensive and hormonal responses to beta-blockade with intrinsic sympathomimetic activity: pindolol versus epanolol.

After a 2-week placebo period, 30 men, aged 60 years (mean), with mild or moderate hypertension were randomly assigned to one of three treatment groups: pindolol, 10 mg b.i.d.; epanolol, 200 mg b.i.d.; and epanolol, 400 mg q.d. At the end of the placebo period and of 4 weeks of active treatment, heart rate, blood pressure, plasma renin activity (PRA), and nonepinephrine (NE) concentration of subgroups of subjects, were measured during isoproterenol infusion (30 ng/kg.min-1 for 15 min) and submaximal ergometric exercise (89 W, mean). Sitting heart rates were reduced with 200 mg b.i.d. epanolol (p less than 0.01) but unchanged with pindolol and 400 mg q.d. epanolol. Reductions of systolic and diastolic blood pressures occurred in all treatment groups but were most pronounced with pindolol. Isoproterenol-induced cardioacceleration and rise in PRA and plasma NE concentration were abolished by pindolol but only attenuated by epanolol. Pindolol also abolished the isoproterenol-induced reduction in diastolic blood pressure; epanolol had no effect on it. The hemodynamic and hormonal responses to exercise were attenuated by pindolol and epanolol in proportion to their beta-blocking activities. In the doses used, epanolol had moderate beta 1-selective blocking action. The intrinsic sympathomimetic activity of epanolol is dose dependent.

Adrenergic beta-Antagonists↗