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Biomedical subjects

D Stevenson

Publications and source records attributed to D Stevenson.

At least 127 records · Page 7Linked to original sources
PubMed1974

Antiviral activity of 3-methyleneoxindole.

3-Methyleneoxindole (MO), an oxidation product of the plant auxin indole-3-acetic acid, can selectively inhibit the replication of herpes-, mengo-, polioviruses, and Sindbis virus. The antiviral action of MO, a sulfhydryl binding compound, is neutralized by 2-mercaptoethanol if the latter is added soon after exposure of infected cells to MO. If addition of 2-mercaptoethanol is delayed, the antiviral action of MO appears to be irreversible. Data are presented which indicate that the antiviral action of MO is not mediated by interferon.

Animals↗
PubMed1972

Ethics report.

Explore the source record for details and available documents.

Ethics, Dental↗
PubMed1966

Effect of interferon on polymerization of single-stranded and double-stranded mengovirus ribonucleic acid.

Gordon, Irving (University of Southern California, Los Angeles), Sara S. Chenault, Douglas Stevenson, and Jean D. Acton. Effect of interferon on polymerization of single-stranded and double-stranded mengovirus ribonucleic acid. J. Bacteriol. 91:1230-1238. 1966.-The effect of interferon on actinomycin-resistant mengovirus ribonucleic acid (RNA) replication in L cells was investigated to determine whether defective or partially polymerized RNA products were made and whether synthesis of any specific class of virus RNA was prevented. RNA labeled with uridine-C(14) was extracted in hot and cold phenol and analyzed by zonal sucrose density centrifugation. Both single- and double-stranded infectious RNA peaks were identified. Interferon treatment caused almost complete depression of uridine-C(14) incorporation throughout linear sucrose gradients except in the 4S region, and no infectivity was detectable in any fraction. These inhibitory effects are attributable to the action of interferon, because they were reversed when cultures were treated with actinomycin D simultaneously with interferon. The results, with those of other investigators, indicate that the step at which interferon interrupts virus multiplication is between the events immediately after uncoating and the formation of template "minus" strands; under the conditions of our experiments, no partially polymerized virus RNA products were made.

Carbon Isotopes↗
PubMedDate not supplied

Detection of anti-HBc IgM following prednisone treatment in patients with chronic active hepatitis B virus infection.

The effect of a short course of prednisone therapy on serum IgM type antibody to the hepatitis B core antigen (anti-HBc IgM) was studied in 14 male patients with chronic active type B hepatitis. Eleven patients (78.5%) became positive for serum anti-HBc IgM either during or shortly after prednisone withdrawal. Detection of anti-HBc IgM correlated with an increase in hepatitis B virus specific DNA-polymerase activity and was followed by a rise in serum transaminase levels. Six patients with histologic evidence of cirrhosis developed anti-HBc IgM which lasted six or more months after prednisone therapy and had a rapid onset of hepatic decompensation manifested by encephalopathy with ascites and/or variceal bleeding. In 17 untreated chronic active type B hepatitis patients who served as controls, anti-HBc IgM was detected at low levels in only a single serum sample from each of two patients during the same observation period.

DNA-Directed DNA Polymerase↗
PubMedDate not supplied

Impaired antibody synthesis in patients with chronic hepatitis B infection.

In vitro synthesis of the anti-HBc, anti-HBs and polyclonal IgG and IgM classes of antibodies were determined from supernatants of peripheral blood mono-nuclear cells cultured in the presence of pokeweed mitogen. Thirty-seven patients with chronic hepatitis B and 10 healthy control subjects whose sera were positive for anti-HBs formed the study group. Twenty-four of 37 patients showed histologic evidence of chronic active hepatitis B while the remaining 13 patients had chronic persistent hepatitis B. Lymphocytes from chronic persistent hepatitis B, chronic active hepatitis B and healthy controls secreted similar levels of IgM. However, IgG synthesis was markedly impaired (p less than 0.002) in the chronic persistent hepatitis B group as compared with healthy controls or chronic active hepatitis B patients. In vitro anti-HBc production and serum anti-HBc titers correlated directly with hepatocellular inflammation and inversely with serum hepatitis B virus DNA. Anti-HBc synthesis was significantly higher in chronic active hepatitis B patients who exhibited a more pronounced hepatocellular damage when compared to chronic persistent hepatitis B patients who had little or no liver cell injury.

Adult↗
PubMedDate not supplied

A pilot study on the effects of prednisone withdrawal on serum hepatitis B virus DNA and HBeAg in chronic active hepatitis B.

We investigated the efficacy of a short course of prednisone therapy in 20 patients with histologic evidence of chronic active hepatitis B. Sixteen of 20 prednisone-treated patients who were initially serum hepatitis B virus DNA-positive had a transient elevation of their serum ALT activity on withdrawal of prednisone. Subsequently, 14 of these 16 patients (87.5%) became persistently negative for serum hepatitis B virus DNA, and 10 also lost their HBeAg. In addition, there was a significant fall in serum ALT levels and HBsAg titers up to 12 months of follow-up in the prednisone-treated group. Five of 20 (25%) prednisone-treated patients experienced a transient episode of hepatic decompensation coinciding with the peak of enzyme elevation. To contrast, only 3 of 15 (20%) initially hepatitis B virus DNA-positive matched untreated patients followed during the same time period became negative for serum hepatitis B virus DNA, and no significant changes in serum ALT values or HBsAg titers were noted over the 12-month study period. Thus, patients with chronic active hepatitis B appear to be responsive to immunologic manipulation with prednisone as indicated by a pronounced rebound immune response and clearance of hepatitis B virus DNA with improvement in liver disease activity.

Adult↗