Showing papers by "Howard Hughes Medical Institute published in 1977"

Abnormalities of leukotaxis in atopic dermatitis.

Abstract: Leukocyte chemotaxis studies were performed in 14 patients with atopic dermatitis. Monocyte chemotactic responsiveness (MCR), polymorphonuclear leukocyte (PMN) chemotactic responsiveness (PCR), and patient serum inhibition of normal monocyte chemotaxis were evaluated. The most common defect noted was depressed MCR. This was found in 8 of the 14 patients and was associated with a chemotactic inhibitor in the serum of 5 of 6 of the 8 with depressed MCR whose sera were so tested. Depressed PCR was found in 3 of 10 patients studied. Ten of the 14 patients had depressed chemotaxis of at least one cell type. Depressed chemotaxis was not related to the presence of infection, to the serum IgE level, or to the severity of the eczema, and it could not be produced in vitro by incubating normal cells with histamine or IgE myeloma. These studies demonstrate a high frequency of leukocyte chemotactic abnormalities in patients with severe atopic dermatitis. Elucidation of the clinical significance of the leukotactic abnormalities observed and determination of whether they are basic or secondary to the disease process must await further study.

Positions of sea urchin (Strongylocentrotus purpuratus) histone genes relative to restriction endonuclease sites on the chimeric plasmids pSp2 and pSp17

Abstract: The positions of the several sea urchin histone genes on the eukaryotic fragments of the chimeric plasmids pSp2 and pSp17 have been mapped relative to the Eco RI and Hind III restriction endonuclease sites on the plasmids. Two principal mapping methods using the electron microscope have been used: (a) the R-loop procedure and a new modification thereof to map the genes on duplex DNA; (b) the gene 32-ethidium bromide technique to visualize RNA-DNA hybrids on single strands of DNA. It is known that there are two histone genes, H3 and H2A, on pSp17. There are two Eco RI sites at the two junctions of the procaryotic segment with the eucaryotic segment on the plasmid. We show, by an electron microscope method, that for H2A, with a length of 0.52 kilobases (kb), one end of the gene is situated 0.02 to 0.03 kb from one RI site, and that there is a Hind III site within this gene at about 0.13 kb from the end phe other RI site of this plasmid. The H4 gene lies between H2B and H1. The ms the incubation temperature is raised up to a temperature just below that at which strand dissociation of the duplex DNA occurs.

Characterization of B cell subpopulations by velocity sedimentation, surface ia antigens and immune function.

Abstract: An in vitro splenic focus assay for B cell cloning was used to analyze the responses of primary and secondary B cells obtained after fractionation on (1 × g) velocity sedimentation gradients. When nonimmune adult bone marrow cells are fractionated, the small cell (slowly sedimenting) fraction contains the majority of primary B cells specific for the 2,4-dinitrophenyl determinant (DNP). When nonimmune adult spleen cells are fractionated, all of the cell fractions contain B cells specific for DNP or for fluorescein (FL), and the large and medium cell fractions contain approximately 50 % of the activity. There is a differential expression of IgM vs. IgG1 anti-hapten monoclonal antibody, in that the majority of primary splenic B cells which give rise to clones producing only IgM antibody are found predominantly in the large and medium cell fractions. All of the cell fractions contain B cells which can generate clones producing both IgM and IgG1, or only IgG1 antibody. Ia-“negative” B cells which give rise to clones producing only IgM antibody are found in the large and medium cell fractions, whereas all the cell fractions contain la-positive B cells. When secondary spleen cells are fractionated, all of the cell fractions contain secondary B cell activity. The large and medium cell fractions contain half of the DNP-specific secondary B cells, whereas the medium and small cell fractions contain more secondary B cells specific for FL or hemocyanin. The large and medium cell fractions of secondary spleen cells are not enriched for B cells giving rise to clones producing only IgM antibody.

Reexamination of the Second Messenger Hypothesis of Glucagon and Catecholamine Action in Liver

Abstract: Glucagon causes a rapid activation of cAMP-dependent protein kinase in rat liver parenchymal cells which correlates well with the accumulation of cAMP. Full activation of phosphorylase or inactivation of glycogen synthase is achieved with half-maximal activation of protein kinase. Epinephrine stimulates glycogen breakdown and gluconeogenesis in these cells mainly by mechanisms involving α-adrenergic receptors and not β-receptors. Activation of α-receptors results in rapid activation of phosphorylase and inactivation of glycogen synthase without accumulation of cAMP or activation of cAMP-dependent protein kinase. Activation of β-receptors causes a transient rise in cAMP and a short-lived activation of protein kinase with correspondingly little stimulation of glycogenolysis and gluconeogenesis.