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  • 1990-1994  (2)
  • 1955-1959
  • 1992  (2)
  • Life and Medical Sciences  (2)
  • supercritical fluid chromatography
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  • 1990-1994  (2)
  • 1955-1959
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  • 1
    Electronic Resource
    Electronic Resource
    A multiplanar anatomic study of the cervical proximal nerve roots and spinal nerves (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Clinical Anatomy 5 (1992), S. 433-440 
    Details
    ISSN: 0897-3806
    Keywords: anatomy ; spine ; sheath ; Life and Medical Sciences ; Miscellaneous Medical
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: An anatomic study focused on the proximal cervical spinal nerves has not been reported. Therefore, we dissected the cervical spinal nerves of three cadavers and examined stained sections in parasagittal and axial planes through the proximal cervical spinal nerves and root sheaths. These studies documented distinct segments of the spinal nerve which had not been completely described in the previous anatomic studies. The sheath originates from the dural sac as a common sleeve, divides into two sleeves, one containing the ventral root and one the dorsal root, and then distal to the dorsal root ganglion fuses again into one sleeve. A space, the interradicular cleft, separates the dorsal and ventral portions of the sleeve. The proximal segment of the spinal nerve proper distal to the dorsal root ganglion is composed of multiple small fascicles surrounded by a dense epineurium. The presence of an interradicular cleft in the cervical nerve root sheath and of fascicles in the cervical spinal nerve has significance for imaging of the cervical spinal nerves and for the pathogenesis of symptoms in cases of partial compression. © 1992 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ca.980050603
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Dihydropyridine calcium antagonist modulates cholesterol metabolism and eicosanoid biosynthesis in vascular cells (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 48 (1992), S. 393-400 
    Details
    ISSN: 0730-2312
    Keywords: calcium channel blocker ; atherosclerosis ; LDL ; LDL-receptor ; vascular smooth muscle ; PGI2 ; cyclic AMP ; cyclooxygenase ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Recent clinical studies have shown that calcium channel blockers can retard and possibly reduce the angiographic progression of coronary artery disease. Calcium channel blockers also inhibit dietary-induced atherosclerosis in animal models of this disease. In this study, we delineate potential cellular and molecular mechanisms by which nicardipine, a dihydropyridine calcium antagonist, may alter lipoprotein and cholesterol trafficking, affect the regulatory signal transduction pathways involved in accelerating cholesteryl ester (CE) catabolism in vascular smooth muscle cells, and modulate cell-cell interactions of vascular and inflammatory cells. We demonstrate in arterial smooth muscle cells that nicardipine increases (1) LDL binding, uptake, and degradation, (2) RNA transcript levels for the LDL receptor, (3) CE catabolic activity, (4) PGI2 release, and (5) RNA transcript levels for cyclooxygenase. Furthermore, nicardipine blocked cytokine-induced monocyte adhesion to endothelial cells and smooth muscle cells. Taken together, these findings support the hypothesis that nicardipine may function as an anti-atherosclerotic agent by promoting CE catabolism and cholesterol clearance and by reducing monocyte adhesion to the activated endothelium.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240480408
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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