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Biomedical subjects

E Long

Publications and source records attributed to E Long.

At least 37 records · Page 2Linked to original sources
PubMed1983

Evaluation of the Phadebact CSF test for detection of the four most common causes of bacterial meningitis.

A five-center collaborative study was undertaken to determine the suitability of the Phadebact CSF test kit and the Phadebact group B Streptococcus reagent for routine use by clinical laboratories to detect antigens of common organisms causing bacterial meningitis. The kits employ staphylococcal protein A coagglutination to detect the antigens of Haemophilus influenzae types a, b, c, d, e, and f, Neisseria meningitidis groups A, B, C, Y, and W135, Streptococcus pneumoniae (83 serotypes), and group B Streptococcus. A total of 2,817 individual tests were performed on 577 cerebrospinal fluid specimens. The percent positive specimens detected by coagglutination was as follows: overall, 84%; H. influenzae, 97%; group B Streptococcus, 75%; S. pneumoniae, 71%; and N. meningitidis, 58%. Eighty-five of the specimens were also tested by counterimmunoelectrophoresis. Coagglutination was more sensitive than counterimmunoelectrophoresis because it detected 74% of the positive specimens, whereas counterimmunoelectrophoresis detected only 65%. No false-positive results were obtained with coagglutination. The Phadebact CSF test kit is recommended for routine use in screening cerebrospinal fluid samples for antigens of the common organisms causing bacterial meningitis along with the Gram stain and culture for delayed confirmation of the rapid results.

Agglutination Tests↗
PubMed1982

A molecular map of the immune response region from the major histocompatibility complex of the mouse.

A stretch of 200 kilobases (kb) of DNA from the I region of the mouse major histocompatibility complex has been cloned and characterized. It contains the genes for the biochemically defined class II proteins E alpha, E beta and A beta. DNA blot analyses suggest that the I region may contain only 6-8 class II genes. Correlation of our molecular map with the genetic map of the I region confines two of the five I subregions, I-J and I-B, to less than 3.4 kb of DNA at the 3' end of the E beta gene where a hotspot for recombination has been observed. Indeed, the I-A and I-E subregions may be contiguous. If so, the I-B and I-J subregions are not encoded in the I region between the I-A and I-E subregions.

Animals↗
PubMed1982

The presence of Schistosoma mansoni in Montserrat Leeward Islands.

Following the discovery in two villages in Montserrat of five individuals who were passing Schistosoma mansoni ova in their stools, a house to house survey was undertaken in November 1978 to determine the prevalence of the infection. From 158 persons residing in the two villages 137 faecal samples were received. Of these 14% were positive for S. mansoni ova. The enzyme linked immunosorbent assay (ELISA) was performed on finger-prick blood samples collected on chromatography paper. In the ELISA 16% of the 132 persons tested were positive. In comparison with the stool examination, the ELISA showed a 53% sensitivity and a 92% specificity. It was recommended that the individuals passing schistosome eggs should be treated.

Adolescent↗
PubMed1980

Factors affecting the acquisition of resistance against Schistosoma mansoni in the mouse. The effect of varying the route and the number of primary infections, and the correlation between the size of the primary infection and the degree of resistance that is acquired.

Mice given primary infections of Schistosoma mansoni by percutaneous or subcutaneous routes were found to acquire a higher degree of resistance against homologous challenge after 7--8 weeks than mice infected intraperitoneally. Mice infected by the intraperitoneal route tended to have smaller worm burdens than those infected with the same number of cercariae by the other two routes and this may, in part, have contributed to the relative lack of efficacy of intraperitoneal infections in inducing resistance to re-infection. The same degree of resistance was acquired after primary percutaneous infection irrespective of whether it was administered in 3 equivalent weekly doses, or the same total number of cercariae was administered as a single infection. The same degree of resistance was also observed when a percutaneous challenge was administered on the same or a different skin site to that which received the percutaneous primary infection. The degree of resistance to re-infection acquired after a percutaneous primary infection correlated well with the size of the primary worm burden and the number of eggs in the intestine and liver, but did not correlate with the number of eggs in the lungs.

Animals↗
PubMed1978

Factors affecting the acquisition of resistance against Schistosoma mansoni in the mouse. I. Demonstration of resistance to reinfection using a model system that involves perfusion of mice within three weeks of challenge.

The degree of resistance acquired by Schistosoma mansoni-infected mice against homologous challenge has been determined by perfusion of the animals within three weeks of the challenge, at which time the challenge-derived organisms were morphologically distinguishable from the primary infection which induced the resistance. The method has been compared with assays based on determination of the number of organisms migrating through the lung, and with perfusions at a later time when the challenge has matured. The results obtained with the three week perfusion method, showing that resistance was acquired by eight weeks after a primary infection, were confirmed by the longer survival of, and reduced egg excretion rates and tissue egg burdens in the experimental animals relative to respective challenge control animals. However, some discrepancy in challenge-derived worm numbers was found between animals perfused three weeks after challenge and those autopsied at later times. The possible reasons for this difference are discussed. The degree of resistance that was acquired was to some extent dependent on the size of the challenge infection.

Animals↗
PubMed1978

Factors affecting the acquisition of resistance against Schistosoma mansoni in the mouse. 2. The time at which resistance to reinfection develops.

Mice developed a partial resistance against homologous challenge with Schistosoma mansoni as early as two weeks after primary infections of 35 to 75 cercariae, and the degree of protection increased to an apparent maximum by 6 weeks. Animals given a primary infection of only 25 cercariae required a longer period to acquire maximum resistance.

Animals↗
PubMed1976

DNA-dependent RNA polymerase C from Xenopus laevis ovaries. Ability to transcribe intact double-stranded DNA.

DNA-dependent RNA polymerase C, partially purified from Xenopus laevis ovaries, has been resolved by DEAE-Sephadex chromatography in two forms, eluting at 0.2 M and 0.3 M ammonium sulfate, respectively. Both are sensitive to high concentrations of alpha-amanitin (200 mug/ml). Their ionic strength dependence and divalent cation requirements are indistinguishable. Quantitatively, RNA polymerase C represents the major form of RNA polymerase activity solubilized from the ovaries. Both RNA polymerases C are able to transcribe efficiently either high-molecular-weight Xenopus DNA or intact adenovirus DNA, as compared to nicked DNA. In contrast, RNA polymerase A has little activity on an intact DNA template. The salt dependence of the RNA polymerases C activity is different on the two kinds of template. Nicked DNA is efficiently transcribed up to a salt concentration of 100 mM ammonium sulfate. On intact DNA, optimal transcription is obtained at 40 mM ammonium sulfate and is inhibited by higher salt concentrations.

Amanitins↗
PubMedDate not supplied

Functional interaction between human T-cell protein CD4 and the major histocompatibility complex HLA-DR antigen.

Mature T cells segregate phenotypically into one of two classes: those that express the surface glycoprotein CD4, and those that express the glycoprotein CD8. The CD4 molecule is expressed primarily on helper T cells whereas CD8 is found on cytotoxic and suppressor cells. A more stringent association exists, however, between these T-cell subsets and the major histocompatibility complex (MHC) gene products recognized by their T-cell receptors (TCRs). CD8+ lymphocytes interact with targets expressing class I MHC gene products, whereas CD4+ cells interact with class II MHC-bearing targets. To explain this association, it has been proposed that these 'accessory' molecules bind to monomorphic regions of the MHC proteins on the target cell, CD4 to class II and CD8 to class I products. This binding could hold the T cell and its target together, thus improving the probability of the formation of the trimolecular antigen: MHC: TCR complex. Because the TCR on CD4+ cells binds antigen in association with class II MHC, it has been difficult to design experiments to detect the association of CD4 with a class II molecule. To address this issue, we devised a xenogeneic system in which human CD4 complementary DNA was transfected into the murine CD4-, CD8- T-cell hybridoma 3DT-52.5.8, the TCR of which recognizes the murine class I molecule H-2Dd. The murine H-2Dd-bearing target cell line, P815, was cotransfected with human class II HLA-DR alpha, beta and invariant chain cDNAs. Co-culture of the parental T-cell and P815 lines, or of one parental and one transfected line resulted in a low baseline response. In contrast, a substantial increase in response was observed when CD4+ 3DT-52.5.8 cells were co-cultured with HLA-DR+ P815 cells. This result strongly indicates that CD4:HLA-DR binding occurs in this system and that this interaction augments T-cell activation.

Animals↗