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Biomedical subjects

M Brown

Publications and source records attributed to M Brown.

At least 721 records · Page 40Linked to original sources
PubMed1982

Discrete subgenomic DNA fragments in incomplete particles of adenovirus type 2.

Discrete subgenomic DNA fragments were found in three out of thirty-two preparations of adenovirus type 2 incomplete particles grown in human Hep-2 cells and examined over the course of 1 year. One preparation contained three fragments corresponding to 5, 14 and 19% of the genome, another contained a 37% fragment and the third a 40% fragment. Each fragment hybridized exclusively to the left end of the genome. Digestion of the nick-translated 37% fragment with HindIII confirmed that it contained the left 37.3% of the genome. Synthesis of these fragments was not dependent on high input multiplicity of infection. Comparable fragments were not found in unpackaged DNA from the corresponding infected cells. This is consistent with the hypothesis that such fragments are generated during virus assembly or, alternatively, may reflect the very small proportion of these fragments relative to the pool of unpackaged DNA within the cells. The possibility that they are generated by errors in DNA replication is discussed.

Adenoviruses, Human↗
PubMed1982

Serological and biochemical analysis of the PlA1 alloantigen of human platelets.

A solid phase platelet antibody assay has been developed which rapidly and sensitively detects PlA1 antibodies. The three-step assay is performed by: (1) adhering platelets to the wheels of a microtitre plate, (2) incubating the platelets with test serum, and (3) adding radiolabelled Staphylococcal protein A which binds to the Fc domain of IgG antibodies. Immune reactions are detected by overnight autoradiography. Characterization of the PlA1 antigen was performed by using PlA1 antisera in immune precipitation assays. A 90 000 dalton molecular weight species was precipitated from PlA1 positive human and dog platelets.

Adult↗
PubMed1982

Adenoassociated virus has a unique chromatin structure.

The organization of intranuclear adenoassociated virus DNA (AAV) was examined following micrococcal nuclease digestion of nuclei prepared from cells coinfected with AAV type 2 (AAV-2) and adenovirus type 2 (Ad2). Blot-hybridization analysis of the DNA with AAV-2, Ad2, and cellular DNA probes revealed that AAV-2 chromatin has a unique structure, which upon nuclease digestion gives rise to a smear of oligomeric DNA fragments from 600-2200 base pairs in length with only a very faint band about 160 base pairs and no discrete multimers. This structure was similar to, but distinguishable from, Ad2 chromatin and completely unrelated to eukaryotic chromatin.

Adenoviruses, Human↗
PubMed1982

Specific high affinity binding sites for somatostatin-28 on pancreatic beta-cells: differences with brain somatostatin receptors.

Saturable and high affinity binding sites have been obtained for an iodinated somatostatin-28 (SS-28) analog, [Leu8,D-Trp22,125I-Tyr25] SS-28, in a membrane preparation from hamster insulinoma, mainly composed of pancreatic beta-cells. Specific binding is maximal after 1 hour incubation at 22C and represents 65% of the total binding. KD for [Leu8,D-Trp22,Tyr25] SS-28 is 0.25 nM with the number of sites corresponding to 68 fmol/mg protein. The KD for SS-28 (1nM) is more than 5 times lower than that for SS-14. SS-28 analogs, such as [D-Trp22] SS-28 and analogs which selectively inhibit insulin release in vivo (Des-Asn5[D-Trp8,D-Ser13] SS-14 and Des-Asn19[D-Trp22,D-Ser27] SS-28), are the most potent compounds in this assay. C-terminal replacement of L-cysteine by D-cysteine reduces the apparent affinity of SS analogs. Unrelated peptides and the inactive analog Des-Trp8-SS-14 have no affinity for insulinoma binding sites. There are differences between the insulinoma SS binding sites and those monitored under similar conditions from rat cerebral cortex. In cerebral cortex, SS-14 and SS-28 have similar affinity for the binding sites, and the insulin selective analogs are less potent than SS-14. It is concluded that pancreatic beta-cells, as well as brain, possess high affinity binding sites for SS, but that they differ in some of their pharmacological properties.

Adenoma, Islet Cell↗
PubMed1982

Immunologic memory to phosphorylcholine III. IgM includes a fine specificity population distinct from TEPC 15.

Group I and group II variable regions expressed in the PC-KLH memory response may originate from distinct germ-line genes or group II may arise by somatic mutation of group I (TEPC 15) germ-line genes. A current version of the somatic mutation hypothesis proposes that somatic mutation is activated by the class switch from IgM to IgG or IgA. If group II results from somatic mutation during class switching, group II IgM antibodies would not exist. This prediction was tested in the present experiments. Group I and group II antibodies were separated from whole serum by affinity chromatography on PC-Sepharose. An ELISA was used to characterize the fine specificity and idiotype of the isolated antibody populations. Group I antibodies were inhibited by both PC and NPPC haptens and were T15 idiotype-positive. Group II antibodies were inhibited appreciably only by NPPC and were negative for the T15 idiotype. The purified group II antibodies contained a significant IgM component, and high levels of group II IgM were detected during the early secondary response to PC-KLH. These observations are inconsistent with the hypothesis that group II originates by somatic mutation activated by the class switch. These results strongly suggest that one or more of the germ-line genes (V, D, or J) of groups I and II are different. Alternatively, if group II antibodies arise from group I by somatic mutation, this mutation must occur before class switching.

Animals↗
PubMed1982

Immunologic memory to phosphorylcholine. II. PC-KLH induces two antibody populations that dominate different isotypes.

We examined the fine specificity of the memory response to phosphorylcholine (PC) using an enzyme-linked immunosorbent assay (ELISA) that measures the relative abilities of PC analogs to inhibit the binding of antibody to antigen. Along with the usual haptens (phosphorylcholine, L-alpha-glycerophosphorylcholine, and choline) these studies included as an inhibitor p-nitrophenyl phosphorylcholine, a compound that is homologous to the structure of the PC antigen in a protein conjugate. Evaluation of the fine specificity profiles revealed two populations of antibody elicited by PC-KLH, which were unequally dominant among the various immunoglobulin classes and IgG subclasses. Group I antibodies exhibited a similar or slightly greater avidity for PC than for NPPC and constituted the majority of IgM, IgA, and IgG3 antibodies. Group II antibodies, which were expressed primarily by IgG1, IgG2a, and IgG2b antibodies, possessed significant avidity only for NPPC. Possible mechanisms that would link IgM, IgA, and IgG3 to similar variable regions while excluding IgG1, IgG2a, and IgG2b from the same grouping are discussed.

Animals↗
PubMed1982

Bone marrow infarction in sickle cell anemia: correlation with hematologic profiles.

Bone marrow infarction was investigated by 99mTc-sulfur colloid imaging in 42 patients with sickle cell anemia (SS) over a period of 2 yr. Marrow defects were demonstrated in 28 patients (66.6%), and in 15 (aged 19--52 yr), they were matched by roentgenographic evidence of medullary bone infarction. Repeated images showed no change in the size or site of these defects. Among 13 patients (aged 6--32 yr), all in crisis when initially examined, marrow defects were not associated with roentgenographic changes, and in many cases, repeated images showed resolution or decrease in size of the defects in 3--6 mo, even if the limb had been swollen and the marrow defect large. Among 14 patients (aged 18--36 yr), all asymptomatic at the time of study, no defects were found. Comparison of hematologic variables revealed a higher mean hemoglobin and hematocrit level among those with marrow infarcts (p less than 0.0001). High levels of HbF, or the presence of alpha-thalassemia, did not protect against marrow infarction. Pulmonary fat embolism was not observed. 99mTc-sulfur colloid marrow imaging was considered to provide more useful information in the initial management of bone pain and swelling in sickle cell crisis than either roentgenographs or conventional 99mTc-methyldiphosphate bone images.

Adolescent↗