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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 772 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford BSL : Blackwell Science Ltd
    Clinical & experimental allergy 30 (2000), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: It has previously been demonstrated that the level of nerve growth factor (NGF) is increased in serum from humans with allergic diseases and asthma.〈section xml:id="abs1-2"〉〈title type="main"〉AimA question raised by these observations is whether NGF could be released from degranulating mast cells during an allergic reaction. The aim of this study was to investigate if NGF is released from mast cells after activation through cross-linkage of the high-affinity IgE receptor.〈section xml:id="abs1-3"〉〈title type="main"〉MethodsMouse and human in vitro cultured mast cells were activated by IgE and specific antigen, stem cell factor or lipopolysaccharide. Release of NGF was measured by ELISA and mRNA expression was detected by RT PCR.〈section xml:id="abs1-4"〉〈title type="main"〉ResultsWe found that mast cells not only express NGF transcripts, but also release NGF polypeptide in response to IgE and specific antigen. Activation of mouse mast cells for 30 min induced significant release of NGF (32.9 ± 1.3 pg/2 × 106 cells) compared to spontaneous release (13.9 ± 2.7 pg/2 × 106 cells) (P 〈 0.01). Similarly, activation of human cultured mast cells also resulted in a significant increase of NGF release (733 ± 310 pg/3 × 105 cells) compared to spontaneous release (9.2 ± 4.0 pg/3 × 105 cells). Two other mast cell secretogogues studied, stem cell factor and lipopolysaccharide, were not able to induce release of NGF.〈section xml:id="abs1-5"〉〈title type="main"〉ConclusionThis study provides evidence that NGF could be specifically released by stimuli causing an allergic reaction, and mast cells can thereby be the source of NGF in IgE-mediated allergic diseases. Our findings add further support for a close correlation between NGF and mast cells that could be of importance for the allergic inflammation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 33 (2003), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Mast cells are a potent source of mediators that regulate the inflammatory response in allergy and asthma. Mast cells can be activated through different receptors, for example, via cross-linkage of the high-affinity IgE receptor (FcɛRI) and by adenosine acting on specific receptors. We have recently described mast cell survival of an IgE receptor activation by up-regulation of the anti-apoptotic gene A1.Objective To compare mast cell survival and expression of A1 after activation through the FcɛRI and by an adenosine agonist.Methods Bone marrow-derived, cultured mouse mast cells (BMCMC) were activated either with IgE+antigen or with the adenosine receptor agonist 5′-N-ethylcarboxamido adenosine (NECA). Release of β-hexosaminidase, cell viability, phosphorylation of Akt and IkB-α, and expression of pro-survival and pro-apoptotic genes were measured after activation.Results Activation of BMCMC with NECA caused the release of β-hexosaminidase, although to a lesser extent than after FcɛRI activation (33% and 98%, respectively). Activation by both NECA and FcɛRI stimulated phosphorylation of Akt (Ser473 and Thr308) and IkB-α (Ser32), both of which are implicated in the regulation of cell survival. However, only cells that were activated through FcɛRI, but not by NECA, expressed A1 and exhibited an increased survival rate compared to the control.Conclusion These results show that adenosine receptor activation of BMCMC does not induce the same survival programme in mast cells as does activation through FcɛRI. These findings may be important for understanding the role that mast cells play in asthma provoked by different stimuli.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Nuclear Inst. and Methods in Physics Research, B 92 (1994), S. 213-216 
    ISSN: 0168-583X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Solid State Communications 45 (1983), S. 281-283 
    ISSN: 0038-1098
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 1108 (1992), S. 210-214 
    ISSN: 0005-2736
    Keywords: Aluminum ; Barnacle fiber ; Citrate ; Sodium ion efflux
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-2242
    Keywords: Molecular markers ; Sorghum bicolor ; Phenetics ; Genetic diversity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The genetic diversity of sorghum, as compared to corn, is less well characterized at the genetic and molecular levels despite its worldwide economic importance. The objectives of this study were to: (1) investigate genetic diversity for restriction fragment length polymorphism (RFLPs) and random amplified polymorphic DNAs (RAPDs) in elite sorghum lines, (2) compare similarities based on molecular markers with pedigree relationships, and (3) examine the potential of RFLPs and RAPDs for assigning sorghum lines to the A/B (sterile) and R (restorer) groups. Using four restriction enzymes, polymorphism was detected with 61% of the RFLP probes used, compared to 77% of the random primers. One hundred and sixteen (64%) probe-enzyme combinations yielded multiple-band profiles compared to 98% of the random primers. RFLP profiles generated 290 polymorphic bands compared to 177 polymorphic RAPDs. Pair-wise comparisons of polymorphic RFLPs and RAPDs were used to calculate Nei and Jaccard coefficients. These were employed to generate phenograms using UPGMA and neighborjoining clustering methods. Analysis of RFLP data with Jaccard's coefficient and neighbor-joining clustering produced the phenogram with the closest topology to the known pedigree.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-2242
    Keywords: Key words Restriction fragment length polymorphism ; Zea mays L. ; Quantitative resistance ; Oligogenic ; Gene mapping
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Breeding maize for gray leaf spot (GLS) resistance has been hindered by the quantitative nature of the inheritance of GLS resistance and by the limitations of selection under less than optimumal disease pressure. In order to identify the quantitative trait loci (QTLs) controlling GLS resistance, a cross was made between B73 (susceptible) and Va14 (resistant) to generate a large F2 population. Six GLS disease assessments were made throughout the disease season for over 1000 F2 plants in 1989, and for 600 F2-derived F3 lines replicated in two blocks in 1990. RFLP analysis for 78 marker loci representing all ten maize chromosomes was conducted in 239 F2 individuals including those with the extreme GLS disease phenotypes. The GLS disease scores of the three field evaluations, each averaged over six ratings, were separately used for the interval mapping in order to determine the consistency of the QTL effects. The heavy GLS disease pressure, meticulous disease ratings, and large population size of this study afforded us the sensitivity for detecting QTL effects. QTLs located on three chromosomes (1, 4, and 8) had large effects on GLS resistance, each explaining 35.0–56.0%, 8.8–14.3%, and 7.7–11.0% of the variance, respectively. These three QTL effects were remarkably consistent across three disease evaluations over 2 years and two generations. Smaller QTL effects were also found on chromosomes 2 and 5, but the chromosome-5 effect might be a false positive because it was not repeatable even in the same location. The chromosome-1 QTLs had the largest effect or highest R2 reported for any quantitative trait to-date. Except for the chromosome-4 gene, which was from the susceptible parent B73, the resistance alleles at all QTL were derived from Va14. The resistance QTLs on chromosomes 1 and 2 appear to have additive effects, but those on chromosomes 4 and 8 are dominant and recessive, respectively. Significant interaction between the QTLs on chromosomes 1 and 4 was detected in all three evaluations. Cumulatively, the four QTLs identified in this study explained 44, 60, and 68% of the variance in F2, and in F3 replications 1 and 2, respectively.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Sensors and Actuators B: Chemical 11 (1993), S. 129-131 
    ISSN: 0925-4005
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Electrical Engineering, Measurement and Control Technology
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 0003-2670
    Keywords: Chromium ; Ores ; Rare earth elements ; Thorium
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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