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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 47 (1969), S. 891-892 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1424
    Keywords: Microglia ; Granulocyte/macrophage colony-stimulating factor ; Whole-cell recording ; Outward K+ currents ; Frequency-independent K+ current ; Peptide toxins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Voltage-gated whole-cell currents were recorded from cultured microglial cells which had been developed in the presence of the macrophage/microglial growth factor granulocyte/macrophage colony-stimulating factor. Outward K+ currents (I K) were most prominent in these cells. I Kcould be activated at potentials more positive than −40 mV. Half-maximal activation of I Kwas achieved at −13.8 mV and half-maximal inactivation of I Kwas determined at −33.8 mV. The recovery of I Kfrom inactivation was described by a time constant of 7.9 sec. For a tenfold change in extracellular K+ concentration the reversal potential of I Kshifted by 54 mV. Extracellularly applied 10 mm tetraethylammonium chloride reduced I K by about 50%, while 5 mm 4-aminopyridine almost completely abolished I K. Several divalent cations (Ba2+, Cd2+, Co2+, Zn2+) reduced current amplitudes and shifted the activation curve of I Kto more positive values. Charybdotoxin (IC50 = 1.14 nm) and noxiustoxin (IC50=0.89 nm) blocked I Kin a concentration-dependent manner, whereas dendrotoxin and mast cell degranulating peptide had no effect on the current amplitudes. The outward K+ currents showed a frequency dependence when depolarizing pulses were applied at a frequency of 1 Hz. A frequency-independent outward current (I K′) characterized by the same activation behavior as I Kwas detected. I K′was blocked completely by 10 nm charybdotoxin or by 10 nm noxiustoxin. In contrast to its effect on I K, 10 mm tetraethylammonium chloride did not reduce I K′.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0378-1119
    Keywords: Recombinant DNA ; genomic library ; monoclonal antibody
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 7 (1978), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 3H-serotonin-release from labelled gp-platelets is established as a sensitive method for testing a new biological activity of gp-C3a anaphylatoxin in an autologous situation. Time-, dose- and temperature-dependent release reactions as well as specific inhibition by carboxypeptidase Band anti-C3a antibodies show that C3a is a potent and specific inducer of platelet activation. Inactive C3a does not induce 3H-serotonin-release but specifically inhibits the action of C3a on platelets.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 8 (1978), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 3H-serotonin release from guinea-pig platelets was demonstrated to be the consequence of C3a binding to these cells. A Scatchard analysis of dose-response data of the 125I-C3a binding pattern to guinea-pig platelets pointed to the existence of binding sites with high and low affinity for the C3a molecule (HA and LA receptors). HA receptors are specific for C3a with intact C-terminal arginine. whereas C3adesarg only interacts with LA receptors. The release of serotonin may be induced by a combined reaction of C3a with HA receptors and LA receptors on the platelet membrane.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0584
    Keywords: Adult respiratory distress syndrome ; Acute leukemia ; Neutropenia ; Granulocyte colony ; stimulating factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Adult respiratory distress syndrome (ARDS) in patients suffering from acute leukemia usually occurs during chemotherapy-induced neutropenia. In addition, intensified chemotherapy with high-dose cytosine arabinoside and mediastinal irradiation may contribute to the development of ARDS. This complication is usually refractory to conservative treatement with antibiotics, steroids, and mechanical ventilation. In this report, we describe a 25-year-old patient with acute lymphoblastic leukemia who developed ARDS during the phase of chemotherapy-induced neutropenia. Subcutaneous administration of granulocyte colony-stimulating factor (G-CSF) at doses of 300–600 μg/day led to a prompt increase of peripheral granulocyte counts. With resolution of neutropenia, respiratory function gradually improved, and mechanical ventilatory support was stopped after 2 weeks. From this observation we surmise that the application of G-CSF may be an effective therapeutic approach for preventing the fatal outcome of ARDS in leukemia patients with bone marrow aplasia.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 6 (1983), S. 283-326 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary and Conclusion During the last decade considerable progress has been made to characterize intimate functional links between macrophages, a major cellular component of immunoinflammatory responses, and the complement system representing the major humoral mediator of inflammation. Macrophages of various species and tissue sites have been shown to synthesize and release most of the complement components providing these cells with their own \ldpericellular\rd complement system. Circumstantial evidence for the assembly of both classical and alternative pathway convertases has been adduced. An intricate network of feedback loops involving endogenous and extrinsic factors operates to adjust complement production to acute requirements, for example augmenting production in the face of accelerated turnover at sites of inflammation, and returning it to baseline levels once the inflammatory stimulus has subsided, in order to maintain a fine-tuned balance. The molecular mechanisms underlying regulation of complement synthesis by macrophages are beginning to be elucidated by use of gene technology. On the other hand, complement activation products exert a number of effects on macrophages via specific surface receptors causing internalization of offending agents, microbes, and immune complexes, promotion of intracellular killing, controlling migration behavior, inducing release of potent biologic substances such as lysosomal enzymes, arachidonic acid metabolites, and interleukin 1. In these interactions, two important humoral mediator systems of inflammation, the complement system and the arachidonic acid cascade, are functionally linked at the level of the macrophage. Stimulation of the release of immunomodulating compounds from macrophages invoke a role for complement in immune regulation. This multifacetted interplay is of particular importance considering the mobility of macrophages that allows them to gain almost unrestricted access to sites of ongoing immunoinflammatory responses. The time seems to have come to abandon the petrified thinking in socalled systems as, for instance, humoral versus cellular, specific versus unspecific, and to proceed to interlocking functions guided by physiology proper.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical microbiology & infectious diseases 19 (2000), S. 385-387 
    ISSN: 1435-4373
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The purpose of the study was to analyze the distribution of the macrolide-resistance genes in 134 erythromycin-resistant Staphylococcus aureus blood-culture isolates collected at 15 German university hospitals. The most prevalent resistance gene was ermC (68/134; 50.7%), followed by ermA (52/134; 38.8%), ereB (10/134; 7.5%), and mrsA/msrB (4/134; 6%). The least common genes were ermB (3/134; 2.2%) and ereA (1/134; 0.7%). Overall, resistance to erythromycin was predominantly due to the presence of two erm genes, although with different distributions, depending on the methicillin-resistance pattern.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1434-9949
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0584
    Keywords: Acute Leukemia ; Streptococcus mitis ; Septicemia ; Neutropenia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Eight neutropenic patients with acute lymphocytic or nonlymphocytic leukemia had septicemia due to different strains ofStreptococcus mitis (St. mitis), a microorganism not commonly recognized as a special pathogen in leukemic patients. Four of the patients had been treated with high-dose cytosine arabinoside as part of the cytostatic regimen, six had a central venous line and four patients had oral lesions prior to the infection. Selective gut decontamination consisted of co-trimoxazole/colistin in five patients and quinolones in three patients. The first three patients died, either due to interstitial pneumonia with the adult respiratory distress syndrome (ARDS), or due to infection-triggered disseminated intravascular coagulation despite prompt empiric antibiotic therapy including vancomycin. The other patients improved after empiric supplementation of penicillin G (30 Mega/day) to the antibiotic regimen. Beginning ARDS in two of these patients dramatically responded to high-dose steriods. We conclude thatSt. mitis is a major pathogen in neutropenic leukemic patients. Infection appears to occur independently of acute leukemic cell type, regimen of selective gut decontamination, venous access, visible oral lesions or treatment with highdose cytosine arabinoside. The clinical course of our patients raises questions about the value of commonly recommended empiric antibiotic regimens, which were clearly ineffective to control infections withSt. mitis in this patient group. Our data indicate that immediate antibiotic therapy with penicillin G is indicated and may be life-saving for suspectedSt. mitis infections in neutropenic leukemic patients.
    Type of Medium: Electronic Resource
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