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  • 1
    ISSN: 1432-1440
    Keywords: Lipoproteidlipase ; Lipoproteide ; Hyperlipoproteinämie Typ V ; Lipoprotein lipase ; Lipoproteins ; Type V Hyperlipoproteinemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The effects of the main lipoprotein density classes on the human adipose tissue lipoprotein lipase activity were studied. A dose-dependent stimulation of lipoprotein lipase activity was obtained for HDL and, to a lesser extent, for VLDL on a constant weight basis. LDL exerted virtually no effect. At higher concentrations, HDL as well as VLDL inhibited the stimulated lipolytic activity. In type V hyperlipoproteinemia, the stimulating effect of VLDL and of HDL was significantly lower, whereas the inhibiting action of HDL was markedly increased.
    Notes: Zusammenfassung Die Effekte der einzelnen Lipoproteidfraktionen des Plasmas auf die Aktivität der Lipoproteidlipase des menschlichen Fettgewebes wurden untersucht. HDL (high density lipoproteins) und, in geringerem Ausmaß, VLDL (very low density lipoproteins) bewirkten eine dosisabhängige Stimulierung der Aktivität der Lipoproteidlipase. LDL (low density lipoproteins) übten praktisch keinen Effekt aus. In höheren Konzentrationen hemmten sowohl HDL als auch VLDL die stimulierte lipolytische Aktivität. Bei Patienten mit Hyperlipoproteinämie Typ V war der stimulierende Effekt der VLDL und HDL viel geringer, die Hemmwirkung der HDL jedoch deutlich stärker ausgeprägt.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Liver cirrhosis ; Lipoproteins ; LCAT ; Hepatic lipase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 12 patients with unequivocal post-alcoholic end-stage liver cirrhosis were compared with 12 healthy controls with regard to the plasma concentrations of lipids, lipoproteins (by rate zonal ultra-centrifugation) and apolipoproteins of high-density-lipoproteins (HDL) (by disc electrophoresis), as well as to the activities of lecithin-cholesterol acyltransferase (LCAT) in plasma and of hepatic lipase (HL) in post-heparin plasma. The cirrhotic group showed the following differences (all significant at thep〈0.01 level) from the control group: Total cholesterol, HDL-cholesterol, very-low-density-lipoproteins (VLDL), HDL, and HL were decreased. Intermediate-density-lipoproteins (IDL) were not detectable in the cirrhotic group. Low-density-lipoproteins (LDL) did not differ significantly from controls. However, LDL from cirrhotic patients contained more triglycerides but less esterified and free cholesterol (allp〈0.01). The percentage apolipoprotein composition of HDL did not differ significantly between controls and cirrhotics. Surprisingly, LCAT acivity in plasma as well as the ratios between esterified and free cholesterol in plasma, LDL, and HDL were nearly identical in both groups. It seems likely that LCAT activity decreases only in the states of acute or subacute liver injury or of biliary obstruction. Severe chronic liver damage as in our cases of end-stage liver cirrhosis without any signs of acute liver injury exhibits apparently no defect in cholesterol esterification.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Hepatic lipase ; Lipoproteins ; Hyperlipemia ; Intermediate-density lipoproteins (IDL)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The main lipoprotein density classes, namely very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3 were investigated with respect to their influence on hepatic lipase (HTGL) activity in vitro. Lipoproteins from pooled normal plasma (NP) and from pooled hyperlipemic plasma (HP) were prepared by means of sequential ultracentrifugation. Hepatic lipase was determined radioenzymatically after preincubation with protamine sulfate. It could be demonstrated that IDL from HP were able to stimulate HTGL activity by approximately 100% above the baseline value. HDL3 from both NP and HP revealed an inhibiting effect on HTGL activity. VLDL, LDL, and HDL2 exhibited no significant effect on HTGL activity. It is speculated that HTGL could possibly represent a second pathophysiological pathway for the catabolism of IDL in hyperlipemia but this presumption is supported by only a few investigations in vivo.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1912
    Keywords: Tachykinins ; Calcitonin gene related peptide ; Neutrophils ; Monocytes ; Chemotaxis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Polymorphonuclear leukocytes (PMNL) are a component of the inflammatory response to neurogenic mediators. Using the micropore filter approach, the authors studied the chemoattracting properties of tachykinins, including substance P (SP), neurokinin A (NKA) and neurokinin B (NKB), and that of calcitonin gene-related peptide (CGRP) for human PMNL in vitro and now show that SP in near nanomolar concentrations stimulates locomotion of human PMNL. Locomotion of PMNL is induced by SP, aminoterminal SP (1–9) and the SP receptor antagonist [d-pro2, d-trp7,9]-SP (DPDT) but not by carboxyterminal SP (3–11), NKA, NKB, or CGRP suggesting that the aminoterminal amino acids arginine and proline, are essential residues of SP in activation of PMNL locomotion. In contrast, the migratory effect of SP on monocytes resides in the carboxyterminal SP amino acid sequence, which is in agreement with carboxyterminal, SP receptor-mediated chemotaxis of human monocytes previously shown by others. From the known structure-activity relationships for SP receptors it is concluded that induction of PMNL migration by SP does not involve neurokinin-1 (NK-1), NK-2 or NK-3 receptors. “Checkerboard” analysis reveals that PMNL locomotion by SP is not dependent on concentration gradients and thus represents chemokinesis, which is enhancement of speed and/or frequency of locomotion. One cannot exclude that this action of SP on PMNL is mediated by the aminoterminal sequence via yet unknown SP “receptors”. Since structure-activity relationships appear to be similar to the mast cell degranulating actions of tachykinins, which also critically depend on the aminoterminal sequence, it may correspondingly be regarded as non-receptorial mechanism, due to membrane interaction of the basic groups in the N-terminal region of the peptide.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1912
    Keywords: Somatostatin ; Octreotide ; Neutrophils ; Raspiratory burst ; Chemotaxis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Growth hormone, prolactin and somatostatin are polypeptide hormones of the neuroendocrine and peripheral nervous systems. In vitro, these have opposing effects on cells of the immune system. We compared the effects of these peptides on activation of neutrophils using a recombinant preparation of human growth hormone, human prolactin and octreotide, a long acting analog of somatostatin. In the absence of growth hormone, octreotide did not affect either neutrophil locomotion or respiratory burst. Octreotide, however, significantly antagonized growth hormone-induced activation of neutrophils for enhanced respiratory burst as well as growth hormone-induced inhibition of stimulated migration. As the effect of growth hormone on neutrophils is mediated by the prolactin receptor, its inhibition by octreotide was also tested using prolactin as priming agent. Data indicate comparable effects of octreotide on priming of neutrophils by prolactin. The effect of octreotide was dose-dependent and appeared to be selective, as activation of neutrophil respiration burst by γ-interferon, and inhibition of stimulated migration by tumor necrosis factor-α were unaffected by octreotide. The present study suggests that octreotide may act on neutrophils directly by antagonizing growth hormone or prolactin at the cellular level.
    Type of Medium: Electronic Resource
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