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  • Fluid intake  (1)
  • Key words: Hermansky-Pudlak syndrome—CD63—Granulophysin.  (1)
  • microtubules  (1)
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    The Gene for Lysosomal Protein CD63 Is Normal in Patients with Hermansky-Pudlak Syndrome (1998)
    Springer
    Lung 176 (1998), S. 249-256 
    Details
    ISSN: 1432-1750
    Keywords: Key words: Hermansky-Pudlak syndrome—CD63—Granulophysin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Hermansky-Pudlak syndrome (HPS) is one of the few genetic disorders associated with severe pulmonary fibrosis. Fifty percent of affected patients die as a result of respiratory insufficiency. Fibrosis is thought to be caused by the accumulation of ceroid, an insoluble fluorescent lipoprotein, both extracellularly and in the lysosomes of alveolar macrophages. In addition to pulmonary fibrosis, HPS is characterized by oculocutaneous albinism and a reduction in the number of platelet dense bodies. CD63 is a protein that was described originally in platelet lysosomes. It localizes to the membranes of melanosomes and platelet dense bodies. CD63 is decreased dramatically in the lysosomes and dense bodies of patients with HPS. We theorized that CD63, a membrane protein common to lysosomes, melanosomes, and platelet dense bodies, may play a role in HPS. We sought to characterize the gene coding for this protein in HPS lymphoid cell lines. The coding region for CD63 was sequenced in control and HPS cell lines. Messenger RNA from HPS and normal cell lines was examined by Northern analysis. Genomic DNA from the same cell lines was examined by Southern analysis and polymerase chain reaction (PCR). CD63 protein in lymphoid cell lines and peripheral blood monocytes was compared by Western analysis. We found no mutations in the coding region of CD63 in an HPS cell line. We also found no diminution in the quantity of CD63 RNA by Northern analysis and no gross defects in the structural gene by PCR and Southern analysis, suggesting that the CD63 structural gene, promoter, and untranslated regions were normal. Western analysis showed that the 43-kDa protein was present in control and HPS lymphoid cell lines and peripheral blood monocytes in equivalent amounts. Although CD63 is an attractive candidate for the primary defect of HPS, the disease is probably not caused by a mutation in the CD63 gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00007607
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Selective reduction of anaphase B in quinacrine-treated PtK1 cells (1989)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 14 (1989), S. 220-229 
    Details
    ISSN: 0886-1544
    Keywords: microtubules ; mitosis ; kinetochore ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Quinacrine, an acridine derivative which competitively binds to ATP binding sites, has previously been shown to cause the reorganization of metaphase spindle microtubules (MTs) due to changes in interactions of non-kinetochore microtubules (nkMTs) of opposite polarity (Armstrong and Snyder: Cell Motil. Cytoskeleton 7:10-19, 1987). In the study presented here, mitotic PtK1 cells were treated in early anaphase with concentrations of quinacrine ranging from 2 to 12 μM to determine energy requirements for chromosome motion. The rate and extent of chromosome-to-pole movements (anaphase A) were not affected by these quinacrine treatments. The extent of anaphase B (kinetochore-kinetochore separation) was reduced with increasing concentrations of quinacrine. Five micromolar quinacrine reduced the extent of kinetochore-kinetochore separation by 20%, and addition of 12 μM quinacrine reduced the kinetochore-kinetochore separation by 40%. To determine the role of nkMTs in anaphase spindle elongationquinacrine-treated metaphase cells were treated with hyperosmotic sucrose concentrations, and spindle elongation was measured (Snyder et al.: Eur J. Cell Biol. 39:373-379, 1985). Metaphase cells treated with 2-10 μM concentrations of quinacrine for 2-5 min reduced spindle lengths by 10-50% prior to 0.5 M sucrose treatment for 5 min. This treatment showed a significant reduction in the ability of sucrose to induce spindle elongation in cells pretreated with quinacrine. As spindle length and birefringence was reduced by quinacrine treatment, sucrose-induced elongation was concomitantly diminished. These data suggest that quinacrine-sensitive linkages are necessary for anaphase B motions. Reduction in these linkages and/or MT length in the nkMT continuum may reduce the ability of the nkMTs to hold compression at metaphase. This form of energy is thought to drive a significant proportion of normal anaphase B in PtK1 cells and sucrose-induced metaphase spindle elongation.
    Additional Material: 11 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970140208
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of hydration state on plasma testosterone, cortisol and catecholamine concentrations before and during mild exercise at elevated temperature (1994)
    Springer
    European journal of applied physiology 69 (1994), S. 294-300 
    Details
    ISSN: 1439-6327
    Keywords: Dehydration ; Fluid intake ; Testosterone ; Cortisol ; Catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This investigation examined the influence of pre-exercise hydration status, and water intake during low intensity exercise (5.6 km · h−1 at 5% gradient) in the heat (33° C), on plasma testosterone (TEST), cortisol (CORT), adrenaline (A), and noradrenaline (NA) concentrations at baseline (BL), pre-exercise (PRE), and immediately (IP), 24 h (24 P), and 48 h postexercise (48 P). Ten active men participated in four experimental treatments. These treatments differed in preexercise hydration status [euhydrated or hypohydrated (HY, −3.8 (SD 0.7)% body mass)] and water intake during exercise (water ad libitum or no water intake during exercise, NW). There were no significant changes in TEST, CORT, or A concentrations with time (BL, PRE, IP, 24 P, and 48 P), or among treatments. However, significant increases from BL and PRE plasma NA concentrations were observed at IP during all four treatment conditions. In addition, HY + NW resulted in significantly higher plasma NA concentrations at IP compared to all other treatments. These results suggest that moderate levels of hypohydration during prolonged, low intensity exercise in the heat do not influence plasma TEST, CORT, or A concentrations. However, plasma NA appears to respond in a sensitive manner to these hydration and exercise stresses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00392033
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    Paper (German National Licenses)
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