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F Gaskin

Publications and source records attributed to F Gaskin.

50 records · Page 3Linked to original sources
PubMed1975

The formation of filamentous structures from iodinated neurotubules.

The porcine neurotubule and its basic subunit were found to be modified in vitro by iodination of amino acids (principally tyrosine) using lactoperoxidase. Iodide ion, H2O2, or lactoperoxidase singly or in any pairwise combination had virtually no effect on neurotubules. However, when all three reagents were present, permitting covalent iodination, it was found that at 0.1 iodotyrosines per tubulin dimer the microtubules unravel to form structures which morphologically resemble strands of protofilaments twisted or wound around each other. These abnormal tubules are stable at room temperature and 4 degrees C. Both monomers of tubulin are labeled to approximately the same extent. Iodinated tubulin (0.1 iodotyrosines/dimer) is unable to assemble in vitro under normal assembly conditions. Heavily iodinated microtubules (8 iodines per tubulin dimer) are similar in morphology to the slightly iodinated structures.

Animals↗
PubMed1973

Microtubule assembly in the absence of added nucleotides.

Microtubule assembly is enhanced by the addition of 1 M sucrose or 4 M glycerol to the reassembly mixture. Tubulin can be purified from guinea pig brain readily and in good yield by two cycles of assembly in glycerol-containing solutions. The tubules assembled in glycerol and sucrose are more stable than tubules formed in the absence of these compounds. Assembly occurs in glycerol or sucrose in the absence of ATP or GTP, but is greatly accelarated by their presence.

Adenosine Triphosphate↗
PubMed1972

An interstrain difference in cholesterol synthesis in vitro in mice, dependent upon a difference in endogenous NADPH-generating capacity.

Earlier experiments have shown that significantly more endogenously generated NADPH is available for reduction of corticosterone in liver homogenates from C57BL/10 male mice than in those from the DBA/2 strain. To test the effect of this interstrain difference upon a representative NADPH-requiring biosynthetic pathway in vitro, the biosynthesis of cholesterol from mevalonic acid was studied in homogenates of livers from the two strains of mice, with and without addition of an NADPH-generating system. The incorporation of mevalonic acid into cholesterol in homogenates from the C57BL/10 strain is little affected by omission of the NADPH-generating system, but in the DBA/2 strain, addition of an NADPH-generating system is necessary to elevate the level of cholesterol synthesis to that of the C57BL/10 strain. Without this addition, the DBA/2 homogenate mainly produces lanosterol and other precursors of cholesterol which require NADPH for their further metabolism.

Animals↗
PubMedDate not supplied

The effects of 13-cis retinoic acid and interferon-alpha in chronic myelogenous leukemia cells in vivo in patients.

The effects of the administration of a 3-day course of 13-cis retinoic acid in combination with interferon a [RA/IFN] on the leukemia cells was measured in vivo in 43 patients with chronic myelogenous leukemia. The administration of RA/IFN was associated with a significant fall in the white blood cell count of patients with chronic-phase disease and with a fall in the percentage S-phase cells in CML patients regardless of the stage of their leukemia. In two thirds of the patients studied the administration of RA/IFN was also associated with an increase in marrow apoptosis. The cytokine combination also suppressed bcl-2 and myc expression in a minority of patients and such expression appears to be associated with response to a treatment regimen which includes RA/IFN. These studies are the first to directly assess the effects of the combination of RA/IFN on chronic myelogenous leukemia cells in vivo in patients. These effects, if seen in other malignant diseases, could account for the therapeutic benefit which has been associated with the administration of this combination of biological agents to patients with malignant disease.

Adult↗
PubMedDate not supplied

Lupus glomerulonephritis revisited 2004: autoimmunity and end-organ damage.

Histopathology of the kidney and clinical presentation are critical factors in the diagnosis of immune-mediated glomerulonephritis (GN). The histological manifestations of glomerular injury are shared by multiple underlying mechanisms. Work from our laboratory and from other investigators shows that antinuclear, antihistone or anti-dsDNA antibodies are neither required nor sufficient for development of lupus GN. In addition, antibody to dsDNA can be generated by mechanisms other than loss of tolerance to chromatin. Genetic analyses demonstrate that although there is some interaction between autoantibody production and renal disease, the phenotypes are regulated by distinct genetic intervals. Furthermore, renal failure is not an essential outcome of the immune-complex deposition and proliferative lupus GN. These data are also supported by published studies from systemic lupus erythematosus (SLE) patients. The immune regulation of lupus GN is distinct from other organ-specific diseases and not influenced by CD25(+) or NK1.1(+) regulatory T cells. Thus, fatal GN may depend upon a kidney-reactive T-cell response that, in turn, may be regulated by gender and intrinsic end-organ factors. The data discussed in this review call for a re-evaluation of the current paradigms for pathogenesis of SLE. An interactive model separating autoimmunity from end-organ susceptibility for the pathogenesis of SLE is proposed.

Animals↗