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D Popp

Publications and source records attributed to D Popp.

23 records · Page 2Linked to original sources
PubMed1988

Cause of changes in the thin filament-associated reflexions on activation of frog muscle--myosin binding or conformational change of actin.

Although the intensity increase of the 5.9 nm layer-line (5.9 L.L.) on activation can potentially be informative, systematic investigation is left to be done. The present study is aimed to assign the cause of the intensity increase. Using the synchrotron radiation, X-ray diffraction patterns were recorded from live sartorius or semitendinosus muscle of the frog (mostly at a temperature of 3-4 degrees C) either on the "Imaging Plates", a newly developed X-ray image recording system, or with the fast linear detector. The Imaging Plates enabled us to measure the disorientation of the thin filaments in the contracting muscle, so that the intensity profiles of the layer-lines were corrected for the disorientation. After the correction, a slight inward shift of the intensity peak of 5.9 L.L. was measured which is associated with the intensity increase on activation at 4 degrees C. At higher temperatures, 5.9 L.L. increases less. The extent of the intensity increase is linearly related to the sarcomere overlap, whereas the outer part of the 2nd actin layer-line (2nd L.L.) is as high as 60% at 10% overlap. The rise of the intensity of 5.9 L.L. is as fast as that of 2nd L.L., but much faster than the changes of the equatorial reflexions and the tension rise. Although these results do not let us assign the cause, some properties are elucidated of the structural change which causes the intensity increase.

Actins↗
PubMed1985

A mutation in the beta-globin gene detected in the progeny of a female mouse treated with ethylnitrosourea.

A mouse with a variant hemoglobin was discovered during electrophoretic screening of (C57BL/6J X DBA/2J)F1 progeny of females treated with ethylnitrosourea. The variant trait was transmitted as a simple Mendelian alternate at the Hbb locus in all crosses except those involving the original carrier of the mutation. The proband mouse which received the mutation directly from the mutagen-treated parent was a germinal mosaic for the mutant and normal Hbbs alleles. The mutant allele was designated Hbbs2. The mutant haplotype specifies both an electrophoretically fast hemoglobin band and a hemoglobin band in the normal beta single hemoglobin position. Thus, the mutation has altered one of the tandemly duplicated genes at the Hbbs locus. A comparison of the relative concentrations of the two hemoglobins in Hbbs2 mice demonstrates preferential expression of the mutant gene, possibly analogous to the enhanced expression of Hbbdmaj in the Hbbd haplotype. Analysis of the amino acid sequence of the variant beta-globin revealed that the valine at position 60 was changed to glutamic acid. The simplest mutation mechanism for such an alteration is an A X T----T X A transversion.

Animals↗
PubMed1983

Studies on lung surfactant replacement in respiratory distress syndrome. Rapid film formation from binary mixed liposomes.

Binary mixed liposomes were prepared from dipalmitoylphosphatidylcholine (DPPC) and a minor compound, e.g., egg phosphatidylglycerol (PG) at a ratio of 9:1. Using different preparative techniques, large unilamellar vesicles (LUV), small unilamellar vesicles (SUV) or multilamellar vesicles (MLV) were obtained and were studied with an electron microscope for morphology, with a Wilhelmy balance for spreading and surface tension lowering potential, and in the surfactant-depleted isolated rat lung for their ability to restore expiratory lung capacity. Only the simultaneous investigation of phospholipids by negative staining and thin sectioning allows unequivocal classification of liposomes. The surface-active structures prepared with the technique of Bangham et al. (Bangham, A.D., Hill, M.W. and Miller, N.G.A. (1974) in Methods in Membrane Biology (Korn, E., ed.), Vol. 1, pp. 1-68, Plenum Press, New York) at room temperature are LUV. LUV containing DPPC:PG at a ratio of 9:1 rapidly spread to a film with high surface tension lowering potential. Within 5 min after injection into the subphase they rise to the surface and form a film at the air/liquid interface able to lower the surface tension to less than 1 mN/m at compression. SUV of the same chemical composition, however, are immediately surface-active only when spread directly onto the surface. MLV exhibit poor surface activity. LUV or pure DPPC, applied onto the surface, are weakly surface active within 5 min. DPPC vesicles injected into the subphase at 37 degrees C do not adsorb to any film with surface tension lowering potential in this time. The minor compounds PE, PI, PS, PA, lysoPC enable DPPC to form surface-active films after application on saline at 37 degrees C. Removal of surfactant decreases the expiratory lung capacity of the isolated rat lung from 49.7 to 12.4% at 4 cmH2O. After substitution with natural surfactant, the expiratory lung capacity is twice that of the washed lung (25.9%), but the original distensibility of the native lung is not restituted. The effect of LUV containing DPPC:PG at a ratio of 9:1 is also remarkable (21.2%).

Animals↗
PubMed1980

Hyperkalemia and hyperglycemic increments in plasma potassium in diabetes mellitus.

The frequency of persistent or intermittent hyperkalemia in patients with diabetes is unknown. In 405 predominantly insulin-treated patients, major hyperkalemia was not common (< 5.0 mEq/L in 2.5%). In ten insulin-treated patients sampled hourly from 8 AM through 8 PM, major intermittent hyperkalemia was not detected (< 4.8 mEq/L in all samples). However, mean plasma potassium values paralleled mean glucose values; these variables were significantly correlated in seven of ten patients. In contrast, there were no relationships between plasma potassium and plasma free insulin, glucagon, epinephrine, or norepinephrine values. We conclude that (1) hyperkalemia--fasting or intermittent--does not occur commonly in patients with diabetes, and (2) hyperglycemia, but not insulin or epinephrine lack or glucagon excess, appears to be a direct determinant of plasma potassium but is not a sufficiently potent determinant to commonly produce clinically important hyperkalemia in insulin-treated diabetic patients.

Adolescent↗