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排序方式: 共有422条查询结果,搜索用时 15 毫秒
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Zusammenfassung Luftnot gehört zu den häufigsten und besonders belastenden Symptomen bei Patienten mit einer inkurablen Tumorerkrankung. Grundsätzlich sind direkt tumorbedingte, tumor- und therapieassoziierte sowie tumorunabhängige Ursachen zu unterscheiden. Die spezifische Behandlung umfasst zunächst den Ausschluss iatrogener Ursachen, Punktion bei Ergüssen, Heparinbehandlung bei Pulmonalarterienembolien, Einlage von Stents, Steroidtherapie und ggf. bronchodilatorische Therapie. Zur symptomatischen Behandlung werden Opioide, Sauerstoff, Anxiolytika und inhalative Maßnahmen eingesetzt. 相似文献
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The presence of immunosuppressive ''p15E-like'' factors in the serum and urine of patients suffering from malign and benign breast tumours. 总被引:1,自引:2,他引:1
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H Stger M Wilders-Truschnig H Samonigg M Schmid T Bauernhofer A Tiran M Tas H A Drexhage 《Clinical and experimental immunology》1993,93(3):437-441
Autoantibodies in sera from patients with systemic lupus erythematosus (SLE) and onchocerciasis recognize calreticulin (CaR), a calcium-binding protein, as antigen. In this study we present the immunological properties of two synthetic peptides prepared to correspond to the 1-24 and 7-24 amino acid sequence of CaR. In contrast to information previously reported for the recombinant protein, the CaR-peptide analogues appeared immunoreactive to anti-Ro/SSA autoimmune sera. Human sera from patients with SLE, Sjögren's syndrome (SS), rheumatoid arthritis (RA), as well as mixed connective tissue disease (MCTD), demonstrated a positive autoimmune response (binding of antibodies), to the CaR-peptide analogues. These findings suggest that anti-calreticulin autoantibodies are not restricted to any disease specificity. 相似文献
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Matthias Wicklmayr Günther Dietze Bernulf Günther Richard Schifmann Ingolf Böttger Reinhard Geiger Hans Fritz Hellmut Mehnert 《Inflammation research》1980,10(4):339-343
The influence of synthetic bradykinin (BK) on disturbed protein and carbohydrate metabolism was studied in chemical and manifest maturity-onset diabetics, in surgical patients and in alloxan diabetic rats. BK,mixed with insulin and injected subcutaneously twice daily in alloxan diabetic rats lowered the morning blood glucose concentration in a dose-dependent way, whereas in a control group treated with insulin only no decrease was seen. Accelerated local blood flow or enhanced vascular permeability as a cause of increased glucose uptake could be ruled out by control experiments using papaverine and eledoisin. Better metabolic control in the BK/insulin-treated group was also indicated by lower arterial levels of free fatty acids and of -hydroxybutyrate, normalized hepatic glycogen content and better growth of body weight. In healthy man an intravenous infusion of BK (80 g/h) did not influence normal fasting blood glucose concentrations, whereas elevated glucose levels in maturity-onset diabetics were continuously reduced within 100 min by 12.2±1.4%. A comparable diabetic group receiving saline alone showed no spontaneous drop of blood glucose concentration. An improvement of pathological carbohydrate metabolism by infusion of BK i.v. could also be demonstrated using the intravenous glucose tolerance test in chemical and manifest maturity-onset diabetics and in surgical patients: in all groupsk values of the glucose tolerance test were significantly increased by BK. This effect was neither due to stimulated insulin release nor to changed glucose pool or to increased renal glucose loss, which was even reduced by BK. Interestingly, normalk values in healthy volunteers were not further improved by BK. A stimulated protein breakdown, which occurs after surgery due to peripheral insulin resistance, can also be restricted by intravenous infusion of BK: in surgical patients urinary nitrogen excretion was reduced by 50% during infusion of BK and was accelerated again after cessation of the infusion. These results indicate that BK can improve the efficacy of exogenous insulin in insulin-deficient animals and depressed insulin sensitivity in maturity-onset diabetics and surgical patients. 相似文献
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Bendicht U. Pauli Hellmut G. Augustin-Voss Marwan E. El-Sabban Robert C. Johnson Daniel A. Hammer 《Cancer metastasis reviews》1990,9(3):175-189
Summary The initial, site-specific colonization of secondary organs by blood-borne cancer cells appears to be mediated by endothelial cell adhesion molecules. These molecules are part of the organ-specific microvascular phenotype and are regulated through complex interactions of the endothelium with the extracellular matrix (e.g., distinct matrix macromolecules and growth factors). They are inducedin vitro by growing unspecific (large vessel) endothelial cells on extracts of organ-specific biomatrices. In many respects, these molecules are similar to the various classes of chemically different adhesion molecules that regulate lymphocyte traffic, but are believed to be distinct from the inducible adhesion molecules that govern leukocyte adhesion during acute episodes of inflammation. Biochemical and biophysical data indicate that preference of tumor cell adhesion to organ-specific microvascular endothelium may not require qualitative differences of such homing receptors between endothelia, but may be explained on the basis of quantitative receptor differences as well as differences of receptor avidity. Following adhesion, the metastatic cascade proceeds by the establishment of metabolic conduits between the endothelium and adherent tumor cells. This heterotypic coupling represents an early step in the extravasation of cancer cells from the microvasculature, initiating endothelial cell retraction from its basement membrane and recanalization around the arrested tumor cell. These events, together with local growth promoting effects exerted by the metastasized organ, are believed to provide the basis for Paget's seed and soil hypothesis of metastasis. 相似文献
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Emilia A. Korhonen Aino Murtomki Sawan Kumar Jha Andrey Anisimov Anne Pink Yan Zhang Simon Stritt Inam Liaqat Lukas Stanczuk Laura Alderfer Zhiliang Sun Emmi Kapiainen Abhishek Singh Ibrahim Sultan Anni Lantta Veli-Matti Leppnen Lauri Eklund Yulong He Hellmut G. Augustin Kari Vaahtomeri Pipsa Saharinen Taija Mkinen Kari Alitalo 《The Journal of clinical investigation》2022,132(15)
Vascular endothelial growth factor C (VEGF-C) induces lymphangiogenesis via VEGF receptor 3 (VEGFR3), which is encoded by the most frequently mutated gene in human primary lymphedema. Angiopoietins (Angs) and their Tie receptors regulate lymphatic vessel development, and mutations of the ANGPT2 gene were recently found in human primary lymphedema. However, the mechanistic basis of Ang2 activity in lymphangiogenesis is not fully understood. Here, we used gene deletion, blocking Abs, transgene induction, and gene transfer to study how Ang2, its Tie2 receptor, and Tie1 regulate lymphatic vessels. We discovered that VEGF-C–induced Ang2 secretion from lymphatic endothelial cells (LECs) was involved in full Akt activation downstream of phosphoinositide 3 kinase (PI3K). Neonatal deletion of genes encoding the Tie receptors or Ang2 in LECs, or administration of an Ang2-blocking Ab decreased VEGFR3 presentation on LECs and inhibited lymphangiogenesis. A similar effect was observed in LECs upon deletion of the PI3K catalytic p110α subunit or with small-molecule inhibition of a constitutively active PI3K located downstream of Ang2. Deletion of Tie receptors or blockade of Ang2 decreased VEGF-C–induced lymphangiogenesis also in adult mice. Our results reveal an important crosstalk between the VEGF-C and Ang signaling pathways and suggest new avenues for therapeutic manipulation of lymphangiogenesis by targeting Ang2/Tie/PI3K signaling. 相似文献
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Hellmut Marx 《Journal of molecular medicine (Berlin, Germany)》1940,19(39):1007-1009
Ohne Zusammenfassung 相似文献
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