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Biomedical subjects

J Johnson

Publications and source records attributed to J Johnson.

At least 541 records · Page 30Linked to original sources
PubMed1986

Activation of chicken liver fructose- 1,6-bisphosphatase by oxidized glutathione.

Treatment of chicken liver fructose- 1,6-bisphosphatase with oxidized glutathione (GSSG) leads to an increase in activity. This activation is markedly enhanced if treatment is performed in the presence of AMP or Mn2+. The effects of AMP and Mn2+ appear to be synergistic. The maximal activation is over 13-fold and is accompanied by the disappearance of 4 sulfhydryl groups per molecule of enzyme. Both fructose 1,6-bisphosphate and fructose 2,6-bisphosphate can largely prevent this activation. Activation can be reversed by dithiothreitol or cysteine. It appears that GSSG activates this enzyme by thiol/disulfide exchanges with the enzyme's specific sulfhydryl groups.

Adenosine Monophosphate↗
PubMed1986

Dose- and time-dependent binding and kinetics of pindolol in patients with congestive heart failure.

Dose- and time-dependent pharmacokinetics and plasma protein binding of pindolol were studied in patients with idiopathic cardiomyopathy who had mild to moderate congestive heart failure. The binding and plasma concentrations of pindolol at various times following the oral administration of single 5- and 10-mg doses and multiple 10-mg doses were determined. The binding of pindolol to plasma protein was time-dependent, increasing from 26% on the first day to 31% during the third day of treatment (P less than .05); this was probably due to increased alpha-1-acid glycoprotein concentration. Analysis of the plasma concentration-time data indicated dose-independent pharmacokinetics. Pindolol pharmacokinetics were time-dependent in one patient. Absorption and elimination half-lives ranged between 0.05 to 0.6 and 1.6 to 7.2 hours, respectively.

Adult↗
PubMed1986

The influence of pindolol and hydrochlorothiazide on blood pressure, and plasma renin and plasma lipid levels.

After three weeks' administration of placebo, three groups of eight patients with moderate hypertension were randomly assigned to single daily dose, double-blind treatment with either pindolol 15 mg, hydrochlorothiazide 50 mg, or a combination of both for eight weeks. All determinations were made 24 hours after ingestion of a dose. Reductions in supine, sitting, and standing systolic and diastolic blood pressure were greater in patients receiving hydrochlorothiazide than in those administered pindolol; however, the greatest reductions were registered in individuals receiving combination therapy. Mean basal plasma renin activity rose significantly from 0.45 +/- 0.44 to 1.42 +/- 1.31 ng/mL/hr and from 0.67 +/- 0.46 to 1.27 +/- 0.83 ng/mL/hr in patients receiving hydrochlorothiazide and combination therapy, respectively, but there was no change in those administered pindolol. Hydrochlorothiazide and combination therapy increased mean total cholesterol levels from 247 +/- 25 to 263 +/- 37 mg/dL and 198 +/- 36 to 211 +/- 33 mg/dL, respectively, at eight weeks, and both increased mean triglyceride concentrations at two weeks. Pindolol did not show any tendency to alter lipid levels. Pindolol should be given twice daily. At 15 mg daily, it has little or no effect on basal plasma renin activity or plasma lipid levels.

Adult↗
PubMed1986

Neurochemical and behavioral consequences of mild, uncontrollable shock: effects of PCPA.

The present experiments examined the role of the serotonergic system in the behavioral deficit produced by uncontrollable shock. In Experiment 1: Establishment of model, the behavioral potential of the Sprague-Dawley rat was defined. When exposed to mild uncontrollable stress such as a 0.8 mA electric footshock, a significant percentage of rats developed a shock escape deficit which was evident when subsequently placed in a shock escape paradigm. Serotonin depletion was produced by chronic treatment with p-chlorophenylalanine. Biogenic amine levels and 5-HT levels were monitored in various brain areas using HPLC. Following chronic treatment with PCPA, the shock escape capability of the Sprague-Dawley rat was assessed. The severe depletion of 5-HT in various brain regions was highly correlated with a dramatic improvement in the shock escape scores. Thus, the detrimental effects of exposure to a mild course of inescapable shock can be prevented by chronic treatment with PCPA. These experiments implicate the serotonergic system as a possible mediator of the "learned helplessness" phenomenon.

Animals↗
PubMed1986

Stability of sublines in the R3327-H rat prostatic tumor.

Over several years of in vivo maintenance passage the R3327-H rat prostatic tumor has given rise to nine unique sublines in our laboratory. Some have emerged under selective treatment pressure while others apparently represent spontaneous or random modulation. Each new subline embodied an altered histology, growth rate, metastatic pattern or treatment sensitivity in comparison to its parent subline. However, each has been subsequently passaged enough times to provide evidence of considerable phenotypic stability, a notable point in view of the R3327 tumor's well known potential for modulation.

Animals↗
PubMed1986

The effects of thiazide diuretics upon plasma lipoproteins.

In a double-blind, placebo-controlled, crossover study in 16 hypertensives, 4 weeks of 50 mg hydrochlorothiazide twice daily, caused significant elevations in total plasma cholesterol, high density lipoprotein (HDL)-cholesterol, low density lipoprotein (LDL)-cholesterol, very low density lipoprotein (VLDL)-cholesterol and triglycerides. Significant elevations in fasting plasma glucose and in plasma insulin were observed, but no correlation between individual lipid elevations and either glucose or insulin elevations was apparent. The metabolic effects developed within 2 weeks, and dissipated within 4 weeks. Changes induced within 4 weeks of treatment with hydrochlorothiazide were unaltered at 6 months. Hydrochlorothiazide induces elevation of all lipoprotein cholesterol fractions and VLDL-triglyceride. However, as the important ratio between LDL- and HDL-cholesterol is unchanged, coronary risk may be unchanged.

Adult↗
PubMed1986

A comparison of the effects of end-to-side portacaval shunting and side-to-side mesocaval shunting on hepatic haemodynamics in the dog.

Functional liver blood flow and hepatic artery flow were measured before and after either end-to-side portacaval or side-to-side mesocaval shunting in dogs. Functional liver blood fell by approximately 50% following both portacaval and mesocaval shunting. The hepatic artery response was variable after both portacaval and mesocaval shunts. It is concluded that side-to-side mesocaval shunts do not preserve hepatic blood flow or produce a greater compensatory increase in hepatic artery flow than conventional portacaval shunts.

Animals↗
PubMed1986

"Transeducation".

Explore the source record for details and available documents.

Allied Health Personnel↗
PubMed1986

Physiological and electrophysiological consequences of etoposide-induced blood-brain barrier disruption.

The present study investigates the effects of etoposide-induced blood-brain barrier (BBB) disruption on systemic blood pressure (SBP), intracranial pressure (ICP), and electroencephalographic (EEG) activity. A total of 29 rats were divided into two groups. In Group 1, 8 control animals received intracarotid normal saline; in Group 2, 21 animals received intracarotid etoposide. SBP, ICP, and EEG were monitored continuously under general anesthesia and controlled ventilation after tracheostomy. Intravenous Evans blue dye was used for determination of BBB disruption. Although none of the Group 1 animals showed BBB disruption, 57% of the animals in Group 2 showed marked BBB disruption (3+). A slight but statistically significant increase in ICP was noted in the Group 2 animals with 3+ BBB disruption, although lesser degrees of barrier disruption (1+ or 2+) resulted in no significant alteration in ICP. The amplitude and frequency of the EEG decreased significantly ipsilateral to the side of intracarotid infusion in all animals with 3+ barrier disruption with a tendency to return toward normal within 2 hours. The degree of transient EEG change observed correlates well with the degree of barrier disruption, potentially allowing clinical determination of BBB disruption by this method.

Animals↗
PubMed1986

Biochemical and epitope analysis of the 17-1A membrane antigen.

The antigen recognized by the monoclonal anti-colon carcinoma antibody 17-1A was found to be a 37 kD glycoprotein in three human colon carcinoma cell lines. The 17-1A antigen (17-1A Ag) contains asparagine-linked carbohydrates as determined by inhibition of glycosylation with tunicamycin. After reduction of 17-1A precipitates with 2-mercaptoethanol two bands of 33 and 40 kD were obtained from the cell lines DLD-1 and HT-29, but only one band from cell line WiDr. Four new MAbs generated against fresh colon carcinoma tissue were shown to be directed against the 17-1A Ag by immunoprecipitation and Western blotting. Two of these MAbs appear to define a novel epitope on the 17-1A Ag as judged from cross-blocking experiments and idiotype expression. Immunohistochemical analysis revealed that the 17-1A Ag is distinctly expressed on a variety of normal and malignant epithelial tissues.

Antigen-Antibody Complex↗
PubMed1986

Etoposide induced blood-brain barrier disruption in rats: duration of opening and histological sequelae.

The intracarotid infusion of the antineoplastic compound etoposide enhances blood-brain barrier (BBB) permeability. In a rat model system, the functional reversibility and anatomic sequelae of etoposide induced BBB disruption were investigated. Etoposide, in a dose range from 3.0 to 22.5 mg/kg, was infused into the left internal carotid artery of Sprague-Dawley rats. BBB disruption was evaluated by the appearance in the infused hemisphere of systemically administered Evans blue dye and quantitatively by the ratio of counts of the technetium labeled chelate of diethylenetriaminepentaacetic acid in the infused to the noninfused hemisphere. Functional reversibility of altered BBB permeability was investigated at three dose levels of etoposide (3.0, 15.0, and 22.5 mg/kg) by the administration of Evans blue dye at the time of etoposide infusion and the administration of the technetium labeled chelate of diethylenetriamine-pentaacetic acid at varying time intervals after etoposide infusion. Fourteen groups of 12 rats each were studied to define the time course of altered BBB permeability at these three doses. The anatomic sequelae of etoposide induced BBB disruption were investigated at varying time intervals (up to 3 weeks) after intracarotid etoposide infusion. Nineteen rats were examined after sacrifice by intracardiac fixation perfusion with 10% formalin. Each brain was sectioned coronally and examined under light microscopy after hematoxylin and eosin staining. Evidence of BBB disruption was seen at all dose levels of etoposide. The degree of BBB disruption increased with increasing doses of etoposide. The duration of altered BBB permeability increased from less than 1 day at 3.0 mg/kg to between 3 and 4 days at 22.5 mg/kg. Histological studies revealed no evidence of parenchymal damage, although at 4 days postdisruption, a mild perivascular lymphocytic infiltration was noted in the infused hemisphere. Etoposide infusion and subsequent BBB disruption were well tolerated by all test animals. In a rat model system the intracarotid infusion of etoposide is capable of producing prolonged reversible BBB disruption.

Animals↗