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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 604 (1990), 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
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: TLX antigens have been found on most peripheral blood cells, trophoblasts, seminal vesicle cells and sperms. These antigens seem to be associated with the membrane co-factor protein (MCP) and the CD46 antigen. Alloantibodies to TLX antigens with FctRII-blocking features were obtained by transfusion of leucocytes or platelets. Preliminary population studies revealed that alloantibodies to TLX/CD46/MCP recognize four overlapping specificities. The terminology TLX-B was introduced with specificities TLX-BI, B2, B3, B4 and frequencies obtained in the population were: 38%, 46%, 42% and 26%, respectively. Family studies showed an independent segregation of the TLX and HLA alleles.At the cellular protein on trophoblast, the alloantibody detected a glycoprotein of 66-67 kDa molecular mass, which may correspond to the a chain of the TLX/CD46/MCP isotypes. A direct association of the alloantibody with FctRII could be excluded thus its FctR blocking feature is probably based on an indirect functional effect.After transfusion and in pregnancy the induction of TLX alloantibody production depended on the mismatching in the TLX/CD46/MCP phenotypes. Probable associations were revealed in the case of recurrent habitual abortion between the lack of FCTR blocking antibody production and the matched TLX specificities of the couples. After transfusion, TLX alloantibody production with FCTR and MLR blocking function was induced only when the recipient was lacking the TLX specificities expressed on the donor cells. Suppression of MLR was found only when TLX specificity in sera corresponded to the TLX specificity of the effector cell. The immunopathological importance of these findings in transplantation and reproductive medicine has yet to be clarified.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The present study investigated the pharmacological properties of excitatory P2X receptors and P2X2 and P2X5 receptor subunit expression in rat-cultured thoracolumbar sympathetic neurons. In patch-clamp recordings, ATP (3–1000 µm; applied for 1 s) induced inward currents in a concentration-dependent manner. Pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonate (PPADS; 30 µm) counteracted the ATP response. In contrast to ATP, α,β-meATP (30 µm; for 1 s) was virtually ineffective. Prolonged application of ATP (100 µm; 10 s) induced receptor desensitization in a significant proportion of sympathetic neurons in a manner typical for P2X2−2 splice variant-mediated responses. Using single-cell RT-PCR, P2X2, P2X2−2 and P2X5 mRNA expression was detectable in individual tyrosine hydroxylase-positive neurons; coexpression of both P2X2 isoforms was not observed. Laser scanning microscopy revealed both P2X2 and P2X5 immunoreactivity in virtually every TH-positive neuron. P2X2 immunoreactivity was largely distributed over the cell body, whereas P2X5 immunoreactivity was most distinctly located close to the nucleus. In summary, the present study demonstrates the expression of P2X2, P2X2−2 and P2X5 receptor subunits in rat thoracolumbar neurons. The functional data in conjunction with a preferential membranous localization of P2X2/P2X2−2 compared with P2X5 suggest that the excitatory P2X responses are mediated by P2X2 and P2X2−2 receptors. Apparently there exist two types of P2X2 receptor-bearing sympathetic neurons: one major population expressing the unspliced isoform and another minor population expressing the P2X2−2 splice variant.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Excitatory ATP responses in rat cultured thoracolumbar sympathetic neurones are mediated by somatic P2X2 receptors. The present study investigated a possible role of axonal P2X2 as well as P2X7 receptors on the same preparation. Confocal laser scanning microscopy demonstrated P2X2 and P2X7 immunoreactivity along the axons as well as P2X7 immunoreactivity surrounding the cell nuclei. P2X7 mRNA expression was detected in individual neurones using a single-cell RT–PCR approach. Adenosine triphosphate (ATP) caused a significant increase in axonal Ca2+ concentration which was dependent on external Ca2+ but insensitive to depletion of the cellular Ca2+ pools by cyclopiazonic acid. Pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonate (PPADS; 30 µm) virtually abolished the ATP response, whereas brilliant blue G (0.1 µm), a selective P2X7 receptor antagonist, had no effect. Dibenzoyl-ATP (BzATP; 100 µm) induced a much smaller increase in axonal [Ca2+] concentration than ATP at equimolar concentrations. The response to BzATP was distinctly reduced by PPADS but not by brilliant blue G. The overall pharmacological profile of the axonal P2X receptors resembled closely that of the somatic P2X2 receptors. In conclusion, the present data suggest the occurrence of axonal excitatory P2X2 receptors in thoracolumbar sympathetic neurones. However, the functional significance of axonal and (peri)-nuclear P2X7 receptors has still to be proven.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The nonspecific P2 receptor antagonist pyridoxalphosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS), the nonspecific P1 receptor antagonist 8-(p-sulphophenyl)-theophylline (8-SPT) and the combination of both were applied by retrograde microdialysis into the nucleus accumbens (NAc) before and during feeding of 18-h food-deprived rats. In addition to the registration of behavioural parameters, such as the amount and duration of food intake, the feeding-induced changes in dopamine (DA) concentration and the concomitant changes of neuronal activity in the NAc and the ventral tegmental area (VTA) were simultaneously determined. The perfusion with PPADS (20 µm) diminished the amount of food intake and the duration of feeding. Furthermore, the P2 receptor antagonist blocked the feeding-induced DA release and prevented the feeding-elicited changes of the electroencephalography (EEG) power distribution which was characterised by an increase in the power of the 8.0–13.0-Hz frequency band in the NAc and the VTA. The effects of PPADS could be completely prevented by the concomitantly perfused adenosine receptor antagonist 8-SPT (100 µm). When given alone, 8-SPT increased the amount of food ingested, the duration of feeding and the EEG power of the higher frequency range, particularly between 19.0 and 30.0 Hz, in both the NAc and the VTA. The feeding-elicited DA release was supplemented to the enhanced DA level caused by the perfusion with 8-SPT in an additive manner. The P2 and P1 receptor antagonists interact antagonistically in the modulation of feeding behaviour and the feeding-induced changes of EEG activity suggesting that both endogenous extracellular ATP and adenosine are involved in the regulation of the feeding-associated mesolimbic neuronal activity in a functionally antagonistic manner.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cord blood (CB) as a new source for bone marrow transplantation represents advantageous features concerning stem cell and leucocyte compartments and function. We attempted to get more information about the phenotypes and function of CB cells by investigating their cell surface markers and also the production of IL-2, IFN-γ and IL-6 by mitogen and alloantigen stimulation. The CB cells were characterized by a low proportion of CD3+ T cells, CD4+ T subpopulation, activated T cells and CD3+ CD16/CD56+ cytotoxic cells, suggesting reduced graft versus host potential. The significant increase of CD19/CD3 double positive cells and decrease of CD19/HLA-DR double positive mature B cells reflect that immature B cells exist in CB. In the functional studies, a 27- and 5-fold reduction was observed in the production of IFN-γ by CB cells stimulated with PHA and allogeneic cells, respectively. The production of IL-2 in PHA-stimulated CB cells also showed a 50% determination. Decrease in the production of these cytokines by CB cells is supported by the decline of the proportion of CD3+ T cells. However, an increase was observed in the production of IL-6 by CB cells stimulated with allogeneic cells as compared with the controls. These results suggest a difference in the functional activity of the T helper cell subsets between the CB and peripheral blood and/or differences in the functional maturity of T helper cell subsets and B cells in these compartments.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1438-2199
    Keywords: Rat striatum ; Medium spiny neuron ; Adenosine AZA receptor ; NMDA receptor channel ; Whole-cell patch clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Whole-cell patch clamp experiments were carried out in rat striatal brain slices. In a subset of striatal neurons (70–80%), NMDA-induced inward currents were inhibited by the adenosine AZA receptor selective agonist CGS 21680. The non-selective adenosine receptor antagonist 8-(p-sulphophenyl)-theophylline and the AZA receptor selective antagonist 8-(3chlorostyryl) caffeine abolished the inhibitory action of CGS 21680. Intracellular GDP-β-S, which is known to prevent G protein-mediated reactions, also eliminated the effect of CGS 21680. Extracellular dibutyryl cAMP, a membrane permeable analogue of cAMP, and intracellular Sp-cAMPS, an activator of cAMP-dependent protein kinases (PKA), both abolished the CGS 21680-induced inhibition. By contrast, Rp-cAMPS and PKI 14–24 amide, two inhibitors of PKA had no effect. Intracellular U-73122 (a phospholipase C inhibitor) and heparin (an inositoltriphosphate antagonist) prevented the effect of CGS 21680. Finally, a more efficient buffering of intracellular Ca2+ by a substitution of EGTA (11 mM) by BAPTA (5.5 mM) acted like U-73122 or heparin. Hence, AZA receptors appear to negatively modulate NMDA receptor channel conductance via the phospholipase C/inositoltriphosphate/Ca2+ pathway rather than the adenylate cyclase/PKA pathway.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Adenosin ; AIDS-Demenz ; Alzheimer Demenz ; EAE ; K+-Kanäle ; spannungsabhängige ; Mikroglia ; Multiple Sklerose ; Proliferation ; Purinozeptoren ; Regeneration Zytotoxizität ; Key words Adenosine ; AIDS-dementia ; Alzheimer’s dementia ; EAE ; K+-channels ; voltage-dependent ; Microglia ; Multiple sclerosis ; Proliferation ; Purinoceptors ; Regeneration ; Cytotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Microglia are the resident macrophages of the brain. They are the central cellular element to initiate defense mechanisms against destructive environmental influences and to facilitate regenerative processes. No other cell type of the brain is endowed with a comparably comprehensive, immunocompetent machinery like microglia. It encompasses cell proliferation, migration and differentiation into full-blown macrophages able to present antigen and to phagocytose cell debris. Relatively little is known about these stages of microglia activation on the cellular and molecular level, although microglia have been described as a separate cell type of the brain as early as in the 30ies of this century by P. del Rio Hortega. This review summarizes the data that have accumulated until now in this respect and tries to embed them into a clinical framework. Special focus has been given to the role of this cell type in the development and progression of Multiple Sclerosis, HIV-associated dementia and Alzheimer’s disease.
    Notes: Zusammenfassung Mikrogliazellen sind residente Makrophagen des Gehirns. In dieser Funktion sind sie das zentrale zelluläre Element für die Einleitung von Abwehrmechanismen gegen schädigende Umwelteinflüsse und für regenerative Prozesse. Kein anderer Zelltyp des Gehirns verfügt über das umfassende, immunokompetente Repertoire, wie es die Mikrogliazellen besitzen. Es erstreckt sich von der Proliferation über die Migration bis zur Differenzierung in ausgereifte Makrophagen, die Antigen präsentieren und Zelltrümmer phagozytieren. Auf zellulärer und molekularer Ebene ist über diese Stadien der Mikrogliaaktivierung noch recht wenig bekannt, obwohl sie schon in den 30er Jahren von P. del Rio Hortega als eigenständiger Zelltyp des Gehirns beschrieben wurden. Diese Übersicht faßt Daten, die bisher auf diesen Ebenen vorliegen, zusammen und diskutiert sie im Kontext ihrer klinischen Relevanz. Insbesondere konzentrieren sich die Ausführungen auf die Bedeutung dieses Zelltyps bei Entstehung und Progression der multiplen Sklerose, der HIV-assoziierten Demenz und der Alzheimer Erkrankung.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 344 (1990), S. 62-63 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 52-58 
    ISSN: 1432-1912
    Keywords: Substance P ; Tachykinins ; Capsaicin ; Neurotransmission ; Rabbit ear artery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rabbit isolated ear arteries were perfused at a constant flow and stimulated with field pulses (5 Hz, 5 impulses). Different tachykinins and capsaicin depressed stimulation-induced vasoconstriction, substance P (SP) being the most potent inhibitor. The rank order of potency of the tachykinins was, SP ∼ physalaemin ∼ eledoisin〉SP-methylester; that of SP and its C-terminal fragments, SP∼SP-(2–11)∼SP-(4–11)〉SP-(6–11). SP-(1–9) was inactive. The SP antagonist (Arg5,d-Trp7,9,Nle11)SP-(5–11) 10 μmol/l shifted the concentration-response curve of SP to the right (pA2=5.43), whereas it did not reduce the action of capsaicin. Another SP antagonist (d-Pro4,d-Trp7,9,10)SP-(4–11) 10 μmol/l failed to affect the SP depression. Neither antagonist changed vasoconstriction by itself. Pretreatment of the arteries with a mixture of yohimbine, propranol, atropine, diphenhydramine, burimamide, methysergide and indomethacin, all 1 μmol/l, did not influence the effect of SP or capsaicin. Only the inhibition by SP, but not that by capsaicin was abolished after mechanical destruction of the endothelium. SP, physalaemin and eledoisin, all 3 μmol/l, reduced vasoconstriction by noradrenaline or histamine; capsaicin 30 μmol/l depressed noradrenaline-induced vasoconstriction. In arteries preincubated with3H-noradrenaline, electrical stimulation (1 Hz, 120 pulses) triggered an increase in the outflow of tritium and evoked vasoconstriction. SP 1 μmol/l did not change either basal or stimulation-evoked tritium outflow, whereas it reduced vasoconstriction. In conclusion, SP depresses nerve stimulation-induced vasoconstriction solely by changing smooth muscle contractility; the receptor activated seems to belong to the SP-P type. Under the conditions of these experiments there is no indication for a similar effect of endogenous SP.
    Type of Medium: Electronic Resource
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