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Biomedical subjects

L F Barker

Publications and source records attributed to L F Barker.

At least 73 records · Page 4Linked to original sources
PubMed1976

Double-blind evaluation of 5-mum final filtration to reduce postinfusion phlebitis.

A double-blind study was conducted to determine the effectiveness of 5-mum final filtration in preventing phlebitis secondary to intravenous fluid administration. An experimental administration set which contained distal portion of the tubing was used for patients randomly assigned to receive filtered intravenous solutions. An identical administration set minus the filter was used in the control group to allow double-blind evaluation of the injection site. Data were collected on 49 patients whose average age was eight years and one month. Most patients had a primary diagnosis of acute lymphocytic or myelocytic leukemia or solid tumor. The patients' injection sites were evaluated daily for clinical findings of phlebitis (erythema, induration, heat, erythematous-streak and discomfort). The incidence of phlebitis was significantly lower (p less than 0.01) in patients receiving filtered intravenous solutions. For the patients in this study, filtration of intravenous fluids with a 5-mum mesh filter appeared to be a feasible and effective means of reducing postinfusion complications.

Drug Contamination↗
PubMed1975

Hepatitis B antigen and antibody in active chronic hepatitis and other liver diseases in Australia. A multicenter collaborative study.

In a multicenter cooperative study, sera from 85 patients with active chronic hepatitis (ACH) were examined for the presence of hepatitis B (Australia) antigen (HBAg) by radioimmunoassay (RIA) and antibody to HBAg (anti-HBAg) by RIA and passive hemagglutination (PHA), the most sensitive currently available techniques. In addition, sera from 83 patients with other liver diseases 98 other hospital patients, and 67 healthy controls were tested. HBAg was detected in 3 of the 85 patients (four percent) with ACH. In a further 3 patients (four percent) anti-HBAg was detected. Thus, 6 patients with ACH (seven percent) had evidence of present or prior infection with the hepatitis B virus (HBV). HBAg was also detected in 7 of the patients with other liver diseases, 2 of the other hospital patients, and none of the healthy controls. Anti-HBAg was detected in 17 of the non-ACH subjects. These results indicate that neither persistent nor prior self-limited infection with HBV is a major factor in the pathogenesis of ACH in Australia.

Acute Disease↗
PubMed1975

Evaluation of hepatitis B antigen testing in federally licensed blood banks in the United States.

Between August 1972 and January 1974, the Burear of Biologics distributed four panels of 20 coded serum samples to all federally licensed blood banks for hepatitis B antigen testing. Initially, all but six blood banks reported results by counterelectrophoresis (CEP) only, but by January 1974, 152 of 247 banks reported results by radioimmunoassay (RIA). On the four panels distributed, correct results were reported for 63 to 83% of all potentially detectable samples by CEP and for 98 to 100% of all samples potentially detectable by RIA. Perfect scores were obtained by only 5 to 25% of blood banks using CEP but by 77 to 100% using RIA. Nonreproducible results on duplicate reactive samples, included to evaluate internal consistency, ranged from 0.5 to 25% by CEP and from zero to 5% by RIA. These results demonstrate greater reliability in addition to greater sensitivity of "third generation" RIA testing in comparison with "second generation" CEP testing.

Blood Banks↗
PubMed1975

Effects of cyclophosphamide on hepatitis B virus infection and challenge in chimpanzees.

The role of antibodies to the surface antigen of hepatitis B virus (HBsAg) and to the hepatitis B core antigen (HBcAg) and of cell-mediated immunity in hepatitis B virus infections and in resistance to challenge was studied in six chimpanzees. Two chimpanzees were studied during primary hepatitis B virus infection while being treated with cyclophosphamide (5-15 mg/kg im three times per week). Cyclophosphamide treatment may have predisposed these chimpanzees to chronic hepatitis B virus infections. Four other chimpanzees convalescent from primary hepatitis B virus infection (subtype ayw) were challanged with hepatitis Bvirus; two were callenged with heterologous virus (subtype adw) without immunosuppression, and two were challenged with homologous virus (subtype syw)while being treated with cyclophosphamide. Chimpanzees with residual humoral immunity, demonstrable by serum antibodies against the group determinant a and subdeterminant y of HBsAg, resisted challenge with either heterologous or homologous hepatitis B virus despite cyclophosphamide immunosuppression in the latter case. Antibodies to the hepatitis B virus core did not appear necessary for protection against hepatitis B virus infection in these chimps.

Animals↗
PubMed1975

Hepatitis B virus infection in chimpanzees: titration of subtypes.

Thirty-four chimpanzees were inoculated with sera containing the adw, ayw, adr, or ayr subtype of hepatitis B surface antigen (HBs Ag). Twenty-nine of the animals became infected with hepatitis B virus, and in every instance the subtype of HBs Ag in the infected animal was the same as the subtype in the inoculum. Infectivity titers were established for the adw and ayw inocula. The patterns of serologic events varied in the infected animals but included most of the typical patterns of serologic change seen in human cases of type B hepatitis. Mild disease, manifested by elevated concentrations of serum enzymes and changes detected by liver biopsy, occurred in 23 of the 29 infected animals.

Animals↗
PubMed1975

Experimental infection of chimpanzees with hepatitis A virus.

The susceptibility of chimpanzees to viral hepatitis type A was examined with immine electron microscopy. Of four seronegative infant chimpanzees, two were inoculated with a hepatitis A acute-phase stool filtrate rich in 27 nm virus-like hepatitis A antigen (HA Ag) particles, and two were inoculated with an HA Ag-negative preinfection stool filtrate. One of each pair of chimpanzees was inoculated intravenously, the other orally. One month later both chimpanzees that had received the HA Ag-positive filtrate developed biochemical, histologic, and clinical evidence of acute viral hepatitis. HA Ag particle (27 nm) were detected in their stools by immune electron microscopy; particle shedding followed a pattern similar to that in human volunteers. Immune electron microscopy also showed that antibody HA Ag had developed in the convalescent-phase sera of the infected chimpanzees. Control animals remained free of illness at this time but did develop hepatitis three to five weeks after exposure to the two infected chimpanzee-. The infectious inoculum was titrated in two additional seronegative chimpanzees. It was concluded that hepatitis a can be successfully transmitted to seronegative chimpanzees. Moreover, these studies provide further evidence that the 27-nm virus-like HA Ag particle is the etiologic agent of viral hepatitis type A.

Animals↗
PubMed1975

Hepatitis B surface antigen (HBS Ag) subtypes and indices of clinical disease.

Serial serum samples of prospectively studied patients exposed to plasma containing both adw and ayw subtypes of hepatitis B surface antigen (HBS Ag) were studied for the relationship of HBS Ag subtype to several indices of clinical type B hepatitis. Seventy-four patients circulated HBS Ag that could be subtyped; 50 subtype adw, 22 ayw, and 2 adyw. Although the average incubation period among adw cases was shorter than among ayw cases (P less than 0.05), no additional significant differences were detected between these two groups of patients when analyzed for severity and chronicity of disease. The chronic HBS Ag carrier state developed in 16% (8 of 50) adw cases and in 9% (2 of 22) ayw cases, but this difference was not statistically significant. Judging from these data, it was concluded that the severity and outcome of type B hepatitis are probably independent of HBS Ag subtypes d and y.

Carrier State↗
PubMed1975

Food and Drug Administration regulations and licensure.

The regulatory requirements of the Food and Drug Administration for products that are defined as drugs and/or biologics are extensively documented in the applicable sections of the Code of Federal Regulations. They include broad requirements for good manufacturing practices and a number of general requirements for matters such as sterility, stability, pyrogens, and labeling. In addition, for biological products, specific standards are published for comment in the Federal Register and then as final rules prior to the acceptance of license applications for new products. The major criteria for such products are safety and effectiveness when the products are used prudently as directed in accompanying circulars. It is generally sound practice to obtain extensive toxicologic and pharmacologic knowledge of potential new products prior to embarking on clinical trials. These trials must be described in investigational new drug applications (INDs), if the products will be entered into interstate commerce. Clinical trials should be planned and conducted using sound scientific and ethical principles in order to obtain objective evidence of clinical effectiveness without unduly jeopardizing the participants in such studies.

Biological Products↗
PubMed1975

Hepatitis B core antigen and antibody.

Two distinct antigen-antibody systems are associated with the hepatitis B virus: the hepatitis B surface antigen (HBsAg, Australia antigen) and antibody (anti-HBs) and the recently characterized hepatitis B core antigen (HBcAg) and antibody (anti-HBc, anti-core). HBsAg is found in the serum of patients acutely or chronically infected with the hepatitis B virus (HBV) and is represented on electron microscopy of such serum as 20 nm spherical and tubular structures and as the surface component of the 42 nm Dane particle. The core antigen of the HBV is associated with a 27 nm viral nucleocapsid particle present in the nuclei of infected hepatocytes and with the inner, core component of the Dane particle. These two HBV antigens have been shown to be antigenically distinct by immune electron microscopy. Immunization studies have demonstrated that both antigens are capable of eliciting distinct, humoral and cell-mediated immune responses in guinea pigs. Analysis of immune responses to HBcAg during the course of type B hepatitis provides a clearer understanding of this disease and anti-HBc may serve as a sensitive marker for the presence of the chronic HBsAg carrier state.

Animals↗
PubMed1975

The interaction of rheumatoid factor with hepatitis B surface antigen-antibody complexes.

A solid phase radioimmunoassay was developed in which the hepatitis B surface antigen was adsorbed to the surface of plastic beads. When the antigen-coated beads were incubated with human IgG antibody against hepatitis B surface antigen, immune complexes were formed on the solid phase surface. IgM rheumatoid factor was found to bind to the hepatitis B surface antigen-antibody complexes but not to the antigen or the IgG antibody alone. Since both hepatitis B surface antigen-antibody complexes and rheumatoid factor are commonly present in type B viral hepatitis, it is suggested that rheumatoid factor may play a role in the pathogenesis of this viral disease in man.

Antibodies, Viral↗
PubMed1974

Hepatitis B core antigen: immunology and electron microscopy.

TWO DISTINCT VIRAL ANTIGENS ARE ASSOCIATED WITH THE HEPATITIS B VIRUS: the hepatitis B surface antigen (HB(s)Ag, Australia antigen) and the hepatitis B core antigen (HB(c)Ag). HB(s)Ag, purified from the serum of asymptomatic human HB(s)Ag carriers, and HB(c)Ag, purified from the liver of a chimpanzee acutely infected with hepatitis B virus, were examined by serological and immune electron microscopic methods. Antisera raised against HB(s)Ag reacted with the outer, surface component of the Dane particle and with the 20-nm spherical and tubular particles present in HB(s)Ag-positive serum, but not with the internal component of the Dane particle or with purified HB(c)Ag particles. Antisera raised against purified HB(c)Ag particles reacted with the internal component of the Dane particle and with HB(c)Ag, but not with the surface of the Dane particle or with the 20-nm spherical and tubular particles associated with HB(s)Ag. Purified HB(c)Ag particles, 27 nm in diameter, demonstrated distinct subunits. The infectious form of hepatitis B virus appears to be represented by the 42-nm Dane particle composed of a 27-nm nucleocapsid core component (HB(c)Ag) surrounded by an antigenically and morphologically distinct lipoprotein surface component (HB(s)Ag).

Animals↗