Quantitative structure-activity relationships of antineoplastic drugs: nitrosoureas and triazenoimidazoles.
Explore the source record for details and available documents.
Amides↗
Biomedical subjects
R Engle
Publications and source records attributed to R Engle.
Psychoendocrinology of ego disintegration.
Explore the source record for details and available documents.
17-Hydroxycorticosteroids↗
Hepatitis B virus DNA in the sera of HBsAg carriers: a marker of active hepatitis B virus replication in the liver.
Sera and liver biopsies from 30 Italian patients, carriers of HBsAg for at least 3 years, were examined for markers of hepatitis B virus (HBV) infection by serological assays and immunofluorescence. Biopsies were analyzed for HBcAg, HBsAg, and delta antigen by immunofluorescence; sera were assayed for HBsAg/anti-HBs, HBcAg/anti-HBc, HBeAg/anti-HBe, delta/anti-delta, HBV-specific DNA polymerase activity and the presence of HBV DNA. HBcAg, HBeAg, and DNA polymerase tests were positive in the sera of 71, 86, and 57%, respectively, of carriers with intrahepatic HBcAg. HBV DNA was detected in 100% of patients expressing HBcAg in the liver with a strong correlation between the concentration of serum DNA and the intensity of HBcAg immunofluorescence in the liver. HBV DNA was detected in the sera of 63% of carriers with intrahepatic delta where the other markers of HBV replication (HBeAg, DNA polymerase) were undetectable. The assay for serum HBV DNA appears to be an excellent noninvasive method for detecting active replication of HBV in HBsAg carriers.
Carrier State↗
Viral hepatitis in Colombia: a study of the "hepatitis of the Sierra Nevada de Santa Marta".
The prevalences of hepatitis B virus (HBV), hepatitis delta virus and hepatitis A virus infections were studied in two regions of Colombia. In Bogota, 10 of 53 patients with acute hepatitis were HBsAg positive and three of these were hepatitis D antigen positive. Hepatitis A virus was the major cause of acute hepatitis in this group. In 366 healthy controls from Bogota, 1.6% were HBsAg positive and 7.1% had at least one marker of HBV infection. In northern Colombia, individuals from three villages with outbreaks of the fulminant "hepatitis of the Sierra Nevada de Santa Marta" were tested. The prevalences of HBsAg (1.8 to 23%) and HBV infection (35 to 93%) were generally high and varied from village to village; 60% of the HBsAg carriers in one village were positive for antibody to hepatitis D antigen, and two individuals in the outbreak area had circulating hepatitis D antigen. The findings suggest that HBV and the associated hepatitis delta virus are etiologic factors in the "hepatitis of the Sierra Nevada de Santa Marta."
Adolescent↗
Serial passage of hepatitis delta virus in chronic hepatitis B virus carrier chimpanzees.
Five consecutive passages of hepatitis delta virus in hepatitis B virus carrier chimpanzees were performed in order to further characterize the infectious and pathogenic nature of this naturally occurring defective virus. Three animals received identical inocula at fourth passage in order to assess individual animal variation as a factor in the course of infection and disease. Acute hepatitis delta virus infection occurred in all hepatitis B virus carrier chimpanzees as demonstrated by coincident intrahepatic hepatitis delta antigen, serum hepatitis delta antigen and serum hepatitis delta virus RNA followed by seroconversion to antibody to hepatitis delta antigen. In all animals, acute hepatitis was temporally associated with hepatitis delta virus infection and was self-limited. The incubation period to hepatitis shortened with passage, whereas biochemical and histologic evidence of liver diseases increased. The marked increase in liver disease with passage was not associated with increasing markers of hepatitis delta virus replication or expression, thus indicating that adaptation to the chimpanzee by serial passage resulted in increased hepatitis delta virus virulence. The duration of hepatitis due to hepatitis delta virus infection in three chimpanzees which received the same inoculum varied from 1 to 8 months. The observations of passage adaptation and individual host variation in this experimental model of hepatitis delta virus disease parallel known pathogenic variations in human hepatitis delta virus infection.
Animals↗
Serological markers of hepatitis B virus and hepatitis D virus infections in Greek adults with primary hepatocellular carcinoma.
Primary hepatocellular carcinoma (PHC) has been linked etiologically to chronic hepatitis B virus (HBV) infection by epidemiologic and molecular lines of evidence. Serologic evidence of HBV and hepatitis delta virus (HDV) infection was assessed in sera from 47 Greek patients with PHC. Radioimmunoassays for the detection of serological markers of HBV and HDV infections and molecular hybridization techniques for the detection of HBV DNA sequences were used. Serological evidence of HBV infection was found in 93.6% of PHC patients. Of the 47 patients, 20 (42.6%) were positive for HBsAg, 43 (91.5%) were positive for anti-HBc and 21 (44.7%) were positive for anti-HBs. Anti-HBe was detected in a high percentage (90%) of HBsAg positive PHC patients. Anti-HBc IgM was also detected in 90% of HBsAg positive PHC patients; in contrast, HBV DNA was detected only in 5% of them. None of the 47 patients had serological evidence of HDV infection. These data show that HBV appears to be the principal etiological agent of PHC in Greece.
Adult↗
An outbreak of fulminant hepatitis delta in the Waorani, an indigenous people of the Amazon basin of Ecuador.
An outbreak of delta hepatitis occurred during 1998 among the Waorani of the Amazon basin of Ecuador. Among 58 people identified with jaundice, 79% lived in four of 22 Waorani communities. Serum hepatitis B surface antigen (HBsAg) was found in the sera of 54% of the jaundiced persons, and 14% of asymptomatic persons. Ninety-five percent of 105 asymptomatic Waorani had hepatitis B core (HBc) IgG antibody, versus 98% of 51 with jaundice. These data confirm that hepatitis B virus (HBV) infection is highly endemic among the Waorani. Sixteen of 23 (70%) HBsAg carriers identified at the onset of the epidemic had serologic markers for hepatitis D virus (HDV) infection. All 16 were jaundiced, where as only two of seven (29%) with negative HDV serology were jaundiced (P = .0006). The delta cases clustered in families, 69% were children and most involved superinfection of people chronically infected with HBV. The data suggest that HDV spread rapidly by a horizontal mode of transmission other than by the sexual route.
Adolescent↗