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Biomedical subjects

L F Barker

Publications and source records attributed to L F Barker.

At least 37 records · Page 2Linked to original sources
PubMed1980

Hepatitis-associated markers in the American Red Cross volunteer blood donor population. I. Trends in HBsAg detection, 1975--1978.

From January 1975 to December 1978, 19,140,169 units of blood were collected by the American Red Cross at 57 regional locations. Each unit was tested for hepatitis B surface antigen (HBsAg) by a single commercial radioimmunoassay test system. A total of 15,954 donations were reported reactive, representing a rate of HBsAg reactivity of 0.83/1,000 units tested. The rate during 1975 was 0.94/1,000 units tested, decreasing to 0.71/1,000 units tested in 1978 (p < 0.005). The prevalence of HBsAg among first-time donors was 2.08/1,000 during 1977 and 1978, 2.7 times higher than that calculated for repeat donors (0.77/1,000 donors). Substantial geographic variation in the prevalence and rate of detection of HBsAg was observed.

Blood Donors↗
PubMed1980

Hepatitis-associated markers in the American Red Cross volunteer blood donor population. ii. Distribution of level of HBsAg reactivity by radioimmunoassay and occurrence of nonspecific reactivity.

During the year 1978 this laboratory evaluated the specificity of all samples found reactive for hepatitis B surface antigen (HBsAg) by 44 of 57 regions of the American Red Cross Blood Services. Radioimmunoassay detected a total of 1.921 HBsAg-reactive sampled among more than three million donor units tested. A vast majority (96%) of the samples had high level of HBsAg (greater than or equal to 20 ng/ml). Only about 50% of the samples with low level of HBsAg (less than 20 ng/ml) were reactive in reversed passive hemagglutination. There were 13 samples that were repeatable for HBsAg but were considered nonspecific as they were nonneutralizable in radioimmunoassay, 2 donors who showed nonspecific reactivity were further tested and it was found that the reactivity in radioimmunoassay persisted for more than 9 months, and this reactivity was also detectable by a second commercial kit for HBsAg. Antibodies to core and surface antigen were not found in any of the nine samples that were tested. The explanation of this nonspecific reactivity is unclear, but the data suggest that the nonspecific factor(s) may be an inherent property of the sample rather than a deficiency of the test reagents.

Antibody Specificity↗
PubMed1980

Hepatitis-associated with markers in the American Red Cross volunteer blood donor population. III. Influence of donor selection practice upon HBsAg prevalence.

The American Red Cross collects blood from a number of defined subsets of the donor population and teh proportion of blood collected from each subset varies widely from center to center. A large part of the variation in prevalence of HBsAg may be related to variations in the proportion of blood collected from plants and factories, military units and schools or colleges. We have derived a regression equation, significant at the p less than 0.001 level, which links HBsAg prevalence with these collection parameters. Using this equation, we were able to predict the prevelance of HBsAg among first-time donors in 6 of the 9 geographic divisions of the United States with an accuracy exceeding 10%. The predictions for the remaining division were within 35% of the actual value. Correlation studies were supported by measurements of true donor prevalence in three blood centers.

Blood Donors↗
PubMed1979

Serologic response in human hepatitis A: detection of antibody by radioimmunoassay and immune adherence hemagglutination.

An indirect solid-phase radioimmunoassay (RIA) for detection of antibody to the hepatitis A antigen (anti-HAV) was developed using polystyrene pearls as the solid phase and hepatitis A antigen (HAAg) extracted from marmoset livers. This RIA was compared to an immune adherence hemagglutination assay (IAHA) which employed HAAg derived from the stools of chimpanzees collected during acute hepatitis A. Anti-HAV was detected in the sera of 15 humans with naturally acquired hepatitis A infection. Sensitivity and specificity were greater using the RIA, permitting the detection of anti-HAV as early as the time of onset of jaundice. Either seroconversion or a significant increase in the titer of anti-HAV was demonstrated following hepatitis A exposure in paired sera from six patients by both techniques. No significant difference in anti-HAV responses was noted between patients with icteric compared to anicteric hepatitis A or between children and adults with hepatitis A.

Adolescent↗
PubMed1979

Simultaneous acute infections with hepatitis A and hepatitis B viruses in a chimpanzee.

The unexpected occurrence of a hepatitis B virus (HBV) infection in a chimpanzee experimentally inoculated with hepatitis A virus (HAV) provided an opportunity to examine the course of simultaneous acute infections with both agents. A chimpanzee inoculated intravenously with HAV developed elevated levels of aminotransferases in serum, detectable excretion of hepatitis A antigen in feces, and a marked antibody response to HAV. During the acute phase of this experimentally induced infection with HAV, the chimpanzee simultaneously developed an HBV infection. The latter was characterized by jaundice, a second increase in levels of aminotransferases in serum, and the appearance in serum of hepatitis B surface antigen (HBsAg), hepatitis B e antigen, antibody to hepatitis B core antigen, and, later, antibody to HBsAg. During the acute phase of both HAV and HBV infections, marked histopathologic inflammatory changes were observed in serial liver biopsy specimens. In this chimpanzee, the concurrent acute infection with both HAV and HBV occurred in association with marked liver damage.

Acute Disease↗
PubMed1978

Transmission of hepatitis B virus infection by transfusion of frozen-deglycerolized red blood cells.

Chimpanzees were used to determine the ability of prior freezing of red blood cells to prevent the transmission of Type B post-transfusion hepatitis. Four units of human whole blood were each inoculated with 10(6) infectious doses of hepatitis B virus. Although all units became HBsAg negative after freezing and deglycerolization, hepatitis B virus infection developed in all four chimpanzees when these units were transfused. Two of these chimpanzees had only serologic evidence of infection, including the development of HBsAg and antibody to both the hepatitis B surface and core antigens; in these animals, the incubation periods were prolonged (24 to 25 weeks). In contrast, the other two animals also had elevated serum glutamic pyruvic transaminase (peaks of 190 and 461 IU per liter) and had a more rapid onset. There was no hepatitis B virus infection in two nontransfused controls. Our results do not support the use of frozen red blood cells for the prevention of post-transfusion hepatitis.

Alanine Transaminase↗
PubMed1978

Transmission of non-A, non-B hepatitis from man to chimpanzee.

Non-A, non-B hepatitis was transmitted to four colony-born chimpanzees by intravenous inoculation of human sera. Two chimpanzees were inoculated with serum from a patient with a clinical and serological diagnosis of chronic non-A, non-B hepatitis whose blood appeared to transmit this disease to a nurse following accidental needle-stick, and the other two chimpanzees were inoculated with serum from either of two former blood-donors whose HBsAg-negative blood appeared to transmit clinically recognisable hepatitis, and who were found to have raised serum-aminotransferase levels 1 1/2 and 5 years later. Serum-aminotransferase levels rose in all four chimpanzees, beginning 2--4 weeks after inoculation: peak alanine-aminotransferase values were 210 to 328 I.U./l. Evidence of hepatitis was present in liver biopsy specimens from all four chimpanzees, beginning 8--10 weeks after inoculation. None showed serological evidence of infection with hepatitis A virus, hepatitis B virus, cytomegalovirus, or Epstein-Barr virus.

Alanine Transaminase↗
PubMed1978

Childhood acute lymphocytic leukemia: study VIII.

This controlled study of children with ALL was designed to test the efficacy and toxicity of one-, two-, three- and four-drug therapy during remission and whether more aggressive therapy in the first eight weeks prolongs remission in patients with features associated with a particularly poor prognosis. After inducing remission with prednisone, vincristine and asparaginase, patients received cranial irradiation and IT methotrexate and were randomized to receive: 1--methotrexate alone; 2--methotrexate plus mercaptopurine; 3--same as in group 2 plus cyclophosphamide; and 4--same as in group 3 plus arabinosyl cytosine. Patients with CNS leukemia at diagnosis received IT methotrexate weekly during the induction period and a higher dose of CNS irradiation. Patients with anterior mediastinal enlargement at diagnosis received radiotherapy to the mass during the induction period. Patients who failed to attain bone marrow remission after four weeks of therapy were given daunorubicin and prednisone for 2--4 additional weeks. Of the 282 patients entering this study between January 1972 and November 1975, 268 (95%) attained complete remission and 228 (85%) were randomized to receive continuation chemotherapy with 1, 2, 3 or 4 drugs. In Group 1 (methotrexate alone), 14 of 20 patients relapsed and 9 developed leukoencephalopathy without antecedent CNS leukemia apparently due to higher doses of intravenous methotrexate; in Groups 2, 3 and 4 the results were equivalent, but without leukoencephalopathy in initial CR. The addition of cyclophosphamide and arabinosyl cytosine increased toxicity and complications without demonstrably increasing the leukemocidal effect. In the 40 patients given additional early therapy, the modalties employed in this study did not prolong remission.

Adolescent↗
PubMed1978

Effect of ethanol during hepatitis B virus infection in chimpanzees.

To determine whether the use of ethyl alcohol (ethanol, C2H5OH) may increase the liver damage caused by hepatitis B virus infection, ethanol was infused into four chimpanzees on one or two occasions during the course of natural or experimentally induced hepatitis B virus infections. A fifth chimpanzee, without active hepatitis B virus infection, served as a control. Moderate elevations of serum aspartate or alanine aminotransferases occurred in four of the five chimpanzees, including the control chimpanzee, in direct association with ethanol infusion; pre-existing enzyme elevations persisted in a fifth chimpanzee. No alteration occurred in the titers of hepatitis B surface antigen or of antibody to hepatitis B core antigen in three of the four infected chimpanzees. There was no significant alteration in the course of hepatitis B virus infection by ethanol infusion in these chimpanzees.

Acute Disease↗