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D Harker

Publications and source records attributed to D Harker.

11 recordsLinked to original sources
PubMed2005

Deep Impact: observations from a worldwide Earth-based campaign.

On 4 July 2005, many observatories around the world and in space observed the collision of Deep Impact with comet 9P/Tempel 1 or its aftermath. This was an unprecedented coordinated observational campaign. These data show that (i) there was new material after impact that was compositionally different from that seen before impact; (ii) the ratio of dust mass to gas mass in the ejecta was much larger than before impact; (iii) the new activity did not last more than a few days, and by 9 July the comet's behavior was indistinguishable from its pre-impact behavior; and (iv) there were interesting transient phenomena that may be correlated with cratering physics.

Cosmic Dust↗
PubMed1991

Two-dimensionally infinite polyhedra with vertices related by symmetry operations.

It is shown that an infinitely extended polyhedron of one sheet composed of plane polygons of finite size, and in which all the vertices are related to one another by symmetry operations, can always be constructed by folding a stiff, unstretchable sheet (such as a piece of paper). It is also shown that only 11 such polyhedra have faces that are regular polygons; these polygons are equilateral triangles and squares. The 4 of these 11 polyhedra that are not known to have been published previously are presented here.

Journal Article↗
PubMed1987

Characterization of the enzymatic defect in late-onset muscle phosphofructokinase deficiency. New subtype of glycogen storage disease type VII.

Human phosphofructokinase (PFK) exists in tetrameric isozymic forms, at least in vitro. Muscle and liver contain homotetramers M4 and L4, respectively, whereas red cells contain five isozymes composed of M (muscle) and L (liver) type subunits, i.e., M4, M3L, M2L2, and ML3, and L4. Homozygous deficiency of muscle PFK results in the classic glycogen storage disease type VII characterized by exertional myopathy and hemolytic syndrome beginning in early childhood. The genetic lesion results in a total and partial loss of muscle and red cell PFK, respectively. Characteristically, the residual red cell PFK from the patients consists of isolated L4 isozyme; the M-containing hybrid isozymes are completely absent. In this study, we investigated an 80-yr-old man who presented with a 10-yr history of progressive weakness of the lower limbs as the only symptom. The residual red cell PFK showed the presence of a few M-containing isozymes in addition to the predominant L4 species, indicating that the genetic lesion is a "leaky" mutation of the gene coding for the M subunit. The presence of a small amount of enzyme activity in the muscle may account for the atypical myopathy in this patient.

Aged↗
PubMed1986

Regional assignment of human liver-type 6-phosphofructokinase to chromosome 21q22.3 by using somatic cell hybrids and a monoclonal anti-L antibody.

The three structural loci encoding human phosphofructokinase, a key regulatory enzyme of glycolysis, are located on separate chromosomes. The gene coding for the liver-type subunit PFKL has previously been assigned to chromosome 21. We have used a subunit- and human-specific monoclonal antibody to liver PFK to detect the expression of human PFKL in hamster X human hybrid cell lines. A cell line carrying an 8;21 translocation which contains all of chromosome 21 except the band 21q22.3 was negative for the expression of PFKL whereas cell lines carrying the reciprocal 8;21 translocation were positive. In addition, a cell line with a ring chromosome 21 containing a breakpoint which excluded the distal part of the q22.3 band was negative for expression of PFKL. These results indicate that human PFKL is located on chromosome 21q22.3.

Animals↗
PubMed1978

Colored lattices.

Combinations of translations and color permutations are derived that leave a periodic array of colored points-a colored lattice-apparently unchanged. It is found that there are three types of colored lattices: (1) those in which all rows and nets have more than one color, (2) those in which there are rows with only one color, and (3) those in which there are both rows and nets with only one color. The color permutation groups of colored lattices are all Abelian. The direct product of three independent cyclic subgroups is required by type 1, but only two are required by type 2; in type 3 the color permutation group consists of the n powers of a cyclic permutation of all n colors present-i.e., the group consists of a single cycle.

Journal Article↗
PubMed1978

Effect of rotational symmetry on colored lattices.

A colored lattice L(c) has a geometrical lattice L. A subgroup lattice L' of L and each of its cosets consist of like-colored points, each coset having a different color. The index of L' in L is given by Delta, the determinant of the matrix (t(jk)) that converts L into L'. This is the order of the factor group {L/L'}, and is also the number n of colors present. The crystal systems-i.e., the combinations of rotational symmetry axes-of L(c), L, and L' are all the same, but L and L' may have different centerings; this results in 39 combinations of centerings, called here the 39 symmetry types of colored lattices. These types are tabulated here, together with the special forms taken by (t(jk)) and the formulas for Delta. In only 7 of the 39 types can the number of colors be arbitrary; in most types certain numbers of colors are impossible.

Journal Article↗
PubMed1972

Myelin membrane structure as revealed by x-ray diffraction.

The present work consists of a new interpretation of the data presented in the article entitled "X-Ray Diffraction of Myelin Membrane. II" by C. K. Akers and D. F. Parsons (1970, Biophys. J.10:116). It will be shown that the projection of the electron density onto the normal to the myelin multilayer derived by these authors is no more consistent with their data than another electron density function, or, perhaps, its negative. (A density function and its negative are related as follows: one of them is a certain density distribution, the other is the same function subtracted from a constant uniform density. Two density functions so related produce identical diffracted intensities.) The Fourier series for the projection of the electron density onto the normal to the myelin multilayer has coefficients +/-[hI(h)](1/2) where I(h) are the intensities of the five orders of reflection; data from which these can be estimated are presented by Akers and Parsons. The sequence of signs found here is + - - + + for the positive density (or - + + - - for the negative one). Quantitative agreement exists between the five X-ray diffraction data of Akers and Parsons and the same intensities calculated from the new model of the myelin structure described here. In this model the myelin double layer, 171 A thick, consists of a central lipid layer 72.4 A thick covered on both surfaces by protein layers 6.9 A thick; these protein layers are covered, in turn, by other lipid layers 42.4 A thick. Minor modifications of this model will no doubt be required to produce agreement between the observed and calculated intensities of the higher order reflections.

Animals↗
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