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  • 1
    Keywords: brain ; PEPTIDE ; RECEPTOR ; CELLS ; EXPRESSION ; BLOOD ; CELL ; IN-VIVO ; INHIBITION ; MODEL ; NEW-YORK ; ACCUMULATION ; MICE ; BLOOD-FLOW ; blood flow ; FLOW ; ALZHEIMERS-DISEASE ; cytokines ; TARGET ; TRANSPORT ; MOUSE ; TRANSGENIC MICE ; STRESS ; transgenic ; PRODUCT ; RAGE ; CEREBRAL-BLOOD-FLOW ; CEREBROSPINAL-FLUID ; CLEARANCE ; DEMENTIA ; INTERACTS ; MOUSE MODEL ; PARENCHYMA ; PRECURSOR PROTEIN ; SQUIRREL-MONKEY ; TRANSGENIC MODEL ; VASCULATURE ; WALL
    Abstract: Amyloid-beta peptide (Abeta) interacts with the vasculature to influence Abeta levels in the brain and cerebral blood flow, providing a means of amplifying the Abeta-induced cellular stress underlying neuronal dysfunction and dementia. Systemic Abeta infusion and studies in genetically manipulated mice show that Abeta interaction with receptor for advanced glycation end products (RAGE)-bearing cells in the vessel wall results in transport of Abeta across the blood-brain barrier (BBB) and expression of proinflammatory cytokines and endothelin-1 (ET-1), the latter mediating Abeta-induced vasoconstriction. Inhibition of RAGE-ligand interaction suppresses accumulation of Abeta in brain parenchyma in a mouse transgenic model. These findings suggest that vascular RAGE is a target for inhibiting pathogenic consequences of Abeta-vascular interactions, including development of cerebral amyloidosis
    Type of Publication: Journal article published
    PubMed ID: 12808450
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  • 2
    Keywords: APOPTOSIS ; CELLS ; SURVIVAL ; Germany ; PATHWAY ; DEATH ; DISEASE ; GENE ; PROTEIN ; METABOLISM ; MICE ; ALZHEIMERS-DISEASE ; ACID ; CELL-SURVIVAL ; MOUSE ; CELL-DEATH ; MUTATION ; MUTATIONS ; XENOPUS ; DIET ; AMYLOID-BETA-PEPTIDE ; neurodegeneration ; 2-METHYL-3-HYDROXYBUTYRYL-COA DEHYDROGENASE-DEFICIENCY ; ERAB ; HSD10 ; organic aciduria
    Abstract: Deficiency of the mitochondrial enzyme 2-methyl-3-hydroxybutyryl-CoA dehydrogenase involved in isoleucine metabolism causes an organic aciduria with atypical neurodegenerative course. The disease-causing gene is HSD17B10 and encodes 17 beta-hydroxysteroid dehydrogenase type 10 (HSD10), a protein also implicated in the pathogenesis of Alzheimer's disease. Here we show that clinical symptoms in patients are not correlated with residual enzymatic activity of mutated HSD10. Loss-of-function and rescue experiments in Xenopus embryos and cells derived from conditional Hsd17b10(-/-) mice demonstrate that a property of HSD10 independent of its enzymatic activity is essential for structural and functional integrity of mitochondria. impairment of this function in neural cells causes apoptotic cell death whilst the enzymatic activity of HSD10 is not required for cell survival. This finding indicates that the symptoms in patients with mutations in the HSD17B10 gene are unrelated to accumulation of toxic metabolites in the isoleucine pathway and, rather, related to defects in general mitochondrial function. Therefore alternative therapeutic approaches to an isoleucine-restricted diet are required
    Type of Publication: Journal article published
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  • 3
    ISSN: 0190-7409
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine , Education , Psychology
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0800
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0983
    Keywords: Key words Toeprinting ; Maize ; Mitochondria ; Transcription
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The maize mitochondrial atpA promoter has been well-characterized using in vitro transcription. The functional elements of this promoter comprise a central domain extending from –7 to +5 relative to the transcription start site, and an upstream domain of 1–3 bp that is purine-rich and centered around positions –11 to –12. As a first step in characterizing the transcriptional machinery, exonuclease-III mapping (toeprinting) was used to map the borders of DNA-protein interactions using either a 107-bp wild-type template or transcriptionally-inactive templates containing linker-scanning mutations. These experiments revealed that, with a wild-type promoter, protein factors occupy as much as 36 bp, from positions –20 to +16 relative to the transcription initiation site. Protein-binding patterns were altered when the linker-scanning mutants were used, suggesting that either the number or conformation of DNA-binding proteins could account for their inability to promote transcription initiation.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-5233
    Keywords: Key words Nonenzymatically glycated albumin ; Endothelium ; Aorta
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Diabetic mice (6 weeks duration) were studied to assess the interaction of advanced glycation endproduct-modifed albumin (AGE-Alb) with micro- and macrovascular endothelium, and to evaluate the alterations induced in the ultrastructure of the lung, kidney, and aorta. [125I]-AGE-Alb and AGE-Alb-Au were perfused in situ in the vasculature; the total uptake was quantitated by spectrometry, and the endothelial pathways of AGE-Alb-Au and the morphological alterations of the vascular beds were examined by electron microscopy. The results showed that [125I]-AGE-Alb (0.567 µM) was taken up specifically and saturably by all organs studied, and particularly by the lung. AGE-Alb-Au endocytosis and transcytosis occurred in the pulmonary and aortic endothelia, and were enhanced in diabetic animals. Also in diabetic animals, AGE-Alb-Au was detected throughout the kidney glomerular basement membrane (GBM) and within open filtration slits of podocytes, suggesting altered barrier function. The structural modifications progressed, and at the end of the experimental period, in the lung ∼28% of the capillaries and ∼25% of the alveoli became compressed or even collapsed, due to the hyperplasia of extracellular matrix and interstitial connective tissue. The presence of adherent intravascular macrophages suggests the development of an inflammatory immune process. The structural modifications observed in kidney glomeruli included thickening (∼30%) of the GBM and the disappearance of diaphragms between the cellular processes of podocytes. The aortic endothelium displayed luminal foldings, increased number (2.8-fold) of Weibel-Palade bodies, and proliferation of basal lamina. Together, the results show that in diabetes there is enhanced vascular uptake of AGE-Alb and significant pathomorphological changes of micro- and macrovessels.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1433-2965
    Keywords: Thorotrast ; Thorium ; Dual-energy X-ray absorptiometry ; DXA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 69-year-old woman presented with a 20-year history of back pain and a 10 cm height loss. She had received an injection of the contrast agent, Thorotrast, at age 23. There was no history of fluoride exposure. Multiple vertebral compression fractures were seen on radiographs. Dual-energy X-ray absorptiometry (DXA) scans revealed high normal bone mineral content on the spine and, on whole body scan, visualization of the liver and spleen regions. Given the attenuation coefficient of thorium and the thorium concentrations reported for liver, spleen and vertebral bodies, it is likely that thorium was visualized in the liver and spleen and that it caused spurious elevation in her DXA bone mineral content values.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-5233
    Keywords: Endothelium ; Endocardium ; Streptozotocin-induced diabetes ; Hyperlipidemia ; Atrium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The structural alterations of endocardial endothelial cells of the heart right atrium and left ventricle were investigated in Golden Syrian hamsters subjected to streptozotocin-induced diabetes and to a combination of diabetes and diet-induced hyperlipidemia. Animals were examined at time intervals ranging from 2 weeks to 6 months. Anionic sites of the endothelial plasmalemma were visualized by in situ perfusion of cationized ferritin. The results indicated that: (a) both atrial and ventricular endocardial endothelium are affected in streptozotocin-induced diabetes: endothelium converts from continuous into a fenestrated type, (b) although the anionic charge of the plasmalemma decreased in advanced diabetes, the newly formed fenestrae highly bound cationized ferritin, (c) combined diabetes and hyperlipidemia induced more severe alterations of endocardial endothelium: new permeable endothelial structures were formed (transendothelial channels, open intercellular junctions, fused plasmalemmal vesicles), and the cells became particularly enriched in cytoskeleton (intermediate filaments and microtubules), (d) the thick subendocardial layer of connective tissue contained, in the combined experimental model, macrophage-derived foam cells indicative for the occurrence of alterations of atherosclerotic type.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-5233
    Keywords: Key words  Endothelium ; Endocardium ; Streptozotocin-induced diabetes ; Hyperlipidemia ; Atrium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract   The structural alterations of endocardial endothelial cells of the heart right atrium and left ventricle were investigated in Golden Syrian hamsters subjected to streptozotocin-induced diabetes and to a combination of diabetes and diet-induced hyperlipidemia. Animals were examined at time intervals ranging from 2 weeks to 6 months. Anionic sites of the endothelial plasmalemma were visualized by in situ perfusion of cationized ferritin. The results indicated that: (a) both atrial and ventricular endocardial endothelium are affected in streptozotocin-induced diabetes: endothelium converts from continuous into a fenestrated type, (b) although the anionic charge of the plasmalemma decreased in advanced diabetes, the newly formed fenestrae highly bound cationized ferritin, (c) combined diabetes and hyperlipidemia induced more severe alterations of endocardial endothelium: new permeable endothelial structures were formed (transendothelial channels, open intercellular junctions, fused plasmalemmal vesicles), and the cells became particularly enriched in cytoskeleton (intermediate filaments and microtubules), (d) the thick subendocardial layer of connective tissue contained, in the combined experimental model, macrophage-derived foam cells indicative for the occurrence of alterations of atherosclerotic type.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0584
    Keywords: Endothelial Cells ; Thromboxane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Bovine aortic endothelial cells in culture were incubated with endotoxin. The amount of thromboxane A2 synthesized was then determined by a specific radioimmunoassay for thromboxane B2. After a lag of several hours the cells changed their shape and parallel to the change in cell shape release of thromboxane B2 occurred. At 24h the amount of thromboxane B2 generated in response to endotoxin was 200-fold above baseline. Thromboxane B2 generation could be blocked by aspirin and the specific thromboxane synthetase inhibitor UK 37248. The endotoxin effect was dependent on protein and RNA synthesis as evidenced by the inhibitory action of cycloheximide (1.5μM) and actinomycin D (2μm).
    Type of Medium: Electronic Resource
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