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  • 1
    Electronic Resource
    Electronic Resource
    Abnormality of Long-Chain Fatty Acids in Erythrocyte Membrane Sphingomyelin from Patients with Adrenoleukodystrophy (1981)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 36 (1981), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have devised an analytical method for the determination of fatty acid composition of erythrocyte membrane sphingomyelin by chemical ionization mass spectrometry combined with capillary column gas-liquid chromatography. Fatty acid composition of erythrocyte membrane sphingomyelin from 8 patients with adrenoleukodystrophy (ALD) and 16 healthy controls were examined by this method. The ratio of hexacosanoic acid (C26.0) to docosanoic acid (C22:0) in erythrocyte membrane sphingomyelin from ALD patients was 2.6-fold higher than that of the controls. This result suggests that biochemical diagnosis of ALD is possible by the analysis of fatty acid composition of erythrocyte membrane sphingomyelin. Furthermore, it demonstrates that biochemical abnormality in ALD is the generalized abnormal metabolism of very long-chain saturated fatty acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1981.tb01698.x
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  • 2
    Electronic Resource
    Electronic Resource
    Decreased Phosphorylation Levels of TrkB Neurotrophin Receptor in the Spinal Cords from Patients with Amyotrophic Lateral Sclerosis (2000)
    Springer
    Neurochemical research 25 (2000), S. 239-245 
    Details
    ISSN: 1573-6903
    Keywords: TrkB ; tyrosine kinase ; brain-derived neurotrophic factor (BDNF) ; phosphotyrosine ; amyotrophic lateral sclerosis (ALS)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Amyotrophic lateral sclerosis (ALS) is characterized by the selective degeneration of specific populations of cranial and spinal motor neurons. In this study, we examined the expression of the high affinity functional receptor for BDNF, TrkB, and assessed the functional state of TrkB by examining the level of phosphorylation on tyrosine residues in ALS spinal cords. The data showed that TrkB-immunoprecipitates prepared from cell-free lysates of ALS spinal cords by use of an anti-TrkB antibody contained much more TrkB protein than from controls. These TrkB proteins expressed in ALS spinal cords, however, are much less phosphorylated on tyrosine residues than those of controls. Moreover, RT-PCR analysis of TrkB mRNA in ALS spinal cords demonstrated that the expression of Trk B mRNA is also upregulated in ALS spinal cords compared with those of controls. These data strongly suggest that there exists an abnormality in TrkB-mediated intracellular signaling in ALS spinal cords and shed a light on the possibility of the therapeutic intervention by normalizing this intracellular signaling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007575504321
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Bile Reflux due to Disturbed Gastric Movement Is a Cause of Spontaneous Gastric Ulcer in W/Wv Mice (1999)
    Springer
    Digestive diseases and sciences 44 (1999), S. 1177-1183 
    Details
    ISSN: 1573-2568
    Keywords: GASTRIC ULCER ; PROTON PUMP INHIBITOR ; MUCOSAL PROTECTIVE DRUGS ; BILE REFLUX
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract c-Kit is a receptor tyrosine kinase, and it isencoded by the mouse W locus. Mutant W/Wvmice develop spontaneous gastric antral ulcers. The aimof the present study was to investigate the pathogenesis of these gastric ulcers and to examine theeffects of two antiulcer drugs; a proton pump inhibitor(2{[4-(3-methoxypropoxy)-3-methylpyridine-2-yl]methyl-sulfinyl}-1H-benzimidazole sodium salt, rabeprazole) and a mucosal protective drug(geranylgeranylacetone, GGA), on the gastric ulcers. Theinhibition of the gastric acid secretion by rabeprazole(30 mg/kg body weight, subcutaneous injection once a dayfor six weeks) significantly increased the gastriculcer formation compared to the controls. In contrast,the GGA treatment (100 mg/kg body weight, oraladministration for six weeks) significantly inhibited the ulcer formation. Bile reflux was seen inthese mutant mice, and they showed no cyclic intensecontractions in the gastric antrum. These resultssuggest that bile reflux due to the disturbance ofgastric antral movement is a cause of the spontaneousgastric ulcers in W/Wv mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026684425642
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  • 4
    Electronic Resource
    Electronic Resource
    Unglycosylated Trk protein does not co-localize nor associate with ganglioside GM1 in stable clone of PC12 cells overexpressing Trk (PCtrk cells) (2000)
    Springer
    Glycoconjugate journal 17 (2000), S. 233-237 
    Details
    ISSN: 1573-4986
    Keywords: Trk ; ganglioside GM1 ; signal transduction ; glycolipids enriched microdomain (GEM) ; glycosylation ; tunicamycin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Our previous studies have shown that acidic glycosphingolipid, ganglioside GM1 (GM1), is an endogenous regulator of high affinity nerve growth factor receptor, Trk, which is an essential factor for the normal development and differentiation of neuronal cells by forming a complex with Trk. GM1 is also known to be a major constituent of caveola or glycosphingolipid-enriched microdomain (GEM) of the plasma membrane. In order to study the effect of the glycosylation of Trk on the formation of GM1-Trk complex and subcellular distribution of this protein, we generated PC12 cells stably overexpressing Trk (PCtrk). Pretreatment of this stable clones with tunicamycin, a potent inhibitor of N-glycosylation, caused the appearance of unglycosylated Trk core protein. These unglycosylated Trk can hardly respond to its ligand, NGF. Sucrose density gradient analysis revealed that unglycosylated Trk core protein was recovered in high density fractions, whereas most of GM1 is present in low density fractions corresponding to caveola or GEM fractions. Moreover, these unglycosylated Trk proteins lose their ability to form a complex with GM1, although GM1 is present in the same high density fractions. These data strongly suggest that spatial segregation of GM1 from the Trk protein by the inhibition of the glycosylation of Trk might be an important molecular mechanism for the unresponsiveness to NGF. Moreover, the binding site of GM1 in the Trk protein might act as an important determinant for the normal trafficking of the Trk protein within the cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026597408790
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    Paper (German National Licenses)
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