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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Zeitschrift für Rheumatologie 57 (1998), S. 399-408 
    ISSN: 0340-1855
    Keywords: Schlüsselwörter Schwangerschaftsinduzierte Algodystrophie ; Kalziummetabolismus ; Kalzitonintherapie ; Key words Pregnancy-associated osteoporosis ; calcium metabolism ; calcitonin treatment ; algodystrophy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Pregnancy-induced algodystrophy is per se a rare, possibly too rarely diagnosed disease, since patients with algodystrophy may be misdiagnosed as having unspecific backache, musculoskeletal problems, and ligament pain associated with pregnancy. However, when clinical signs of beginning algodystrophia are present, immediate investigations and therapy are necessary for relief of pain and in order to prevent complications. The aim of this paper is to summarize our current knowledge on this disease. Furthermore, the clinical course and diagnostic evaluation are described in two cases with pregnancy-induced algodystrophy. The authors question the common distinction between pregnancy-induced and post-pregnancy algodystrophy, which result in a disturbed bone and calcium metabolism, but discuss both entities similary.
    Notes: Zusammenfassung Die schwangerschaftsinduzierte Algodystrophie ist eine seltene Erkrankung, die zudem kaum diagnostiziert wird, da die Beschwerden häufig als statische oder ligamentäre, durch die Schwangerschaft bedingte Probleme verkannt werden. Eine rechtzeitige Diagnosestellung ist jedoch ebenso wie die Einleitung einer adäquaten Therapie notwendig, um Komplikationen zu verhindern sowie Schmerzen zu bekämpfen. In dieser Arbeit wird über den aktuellen Kenntnisstand zu dieser Erkrankung berichtet. Darüber hinaus werden anhand von zwei Erkrankungsfällen der klinische Verlauf und die phasenspezifische Diagnostik und Therapie dargestellt. Im Ergebnis unserer klinischen Beobachtungen stellen wir die bisher übliche Trennung von schwangerschaftsinduzierter Algodystrophie und postpartaler Osteoporose in Frage und diskutieren die Vermutung, daß es sich hierbei um zwei Krankheitsbilder handelt, die sich über die Störung des Knochen- und Kalziummetabolismus gegenseitig beeinflussen.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Bioscience reports 12 (1992), S. 109-114 
    ISSN: 1573-4935
    Keywords: energy metabolism ; oxygen consumption ; thymocytes ; ConA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The influence of ConA on the energy metabolism of quiescent rat thymocytes was investigated by measuring the effects of inhibitors of protein synthesis, proteolysis, RNA/DNA synthesis, Na+K+-ATPase, Ca2+-ATPase and mitochondrial ATP synthesis on respiration. Only about 50% of the coupled oxygen consumption of quiescent thymocytes could be assigned to specific processes using two different media. Under these conditions the oxygen is mainly used to drive mitochondrial proton leak and to provide ATP for protein synthesis and cation transport, whereas oxygen consumption to provide ATP for RNA/DNA synthesis and ATP-dependent proteolysis was not measurable. The mitogen ConA produced a persistent increase in oxygen consumption by about 30% within seconds. After stimulation more than 80% of respiration could be assigned to specific processes. The major oxygen consuming processes of ConA-stimulated thymocytes are mitochondrial proton leak, protein synthesis and Na+K+-ATPase with about 20% each of total oxygen consumption, while Ca2+-ATPase and RNA/DNA synthesis contribute about 10% each. Quiescent thymocytes resemble resting hepatocytes in that most of the oxygen consumption remains unexplained. In contrast, the pattern of energy metabolism in stimulated thymocytes is similar to that described for Ehrlich Ascites tumour cells and splenocytes, which may also be in an activated state. Most of the oxygen consumption is accounted for, so the unexplained process(es) in unstimulated cells shut(s) off on stimulation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Bioscience reports 12 (1992), S. 381-386 
    ISSN: 1573-4935
    Keywords: energy metabolism ; oxygen consumption ; thymocytes ; ConA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The influence of ConA on the energy metabolism of quiescent rat thymocytes was investigated by measuring the effects of inhibitors of protein synthesis, proteolysis, RNA/DNA synthesis, Na+K+-ATPase, Ca2+-ATPase and mitochondrial ATP synthesis on respiration. Only about 50% of the coupled oxygen consumption of quiescent thymocytes could be assigned to specific processes using two different media. Under these conditions the oxygen is mainly used to drive mitochondrial proton leak and to provide ATP for protein synthesis and cation transport, whereas oxygen consumption to provide ATP for RNA/DNA synthesis and ATP-dependent proteolysis was not measurable. The mitogen ConA produced a persistent increase in oxygen consumption by about 30% within seconds. After stimulation more than 80% of respiration could be assigned to specific processes. The major oxygen consuming processes of ConA-stimulated thymocytes are mitochondrial proton leak, protein synthesis and Na+K+-ATPase with about 20% each of total oxygen consumption, while Ca2+-ATPase and RNA/DNA synthesis contribute about 10% each. Quiescent thymocytes resemble resting hepatocytes in that most of the oxygen consumption remains unexplained. In constrast, the pattern of energy metabolism in stimulated thymocytes is similar to that described for Ehrlich Ascites tumour cells and splenocytes, which may also be in an activated state. Most of the oxygen consumption is accounted for, so the unexplained process(es) in unstimulated cells shut(s) off on stimulation.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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