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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 123 (1991), S. 0 
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Physiology 68 (2006), S. 67-95 
    ISSN: 0066-4278
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine , Biology
    Notes: Because of the anatomy, function, and nonregenerative nature of the myocardium, inflammation in this tissue is not well tolerated. Nevertheless, various diseases of the heart are characterized by inflammatory responses involving the effector mechanisms of innate and adaptive (lymphocyte-dependent) immunity. The innate immune response to ischemia-reperfusion injury is, by far, the most common cause of myocardial inflammation. Innate responses may have beneficial influences that preserve myocardial function in the short term but may be maladaptive in chronic states. Adaptive responses in the myocardium occur with infection or loss of tolerance, and lead to myocarditis. Given the narrow margin for benefit of cardiac inflammation, special regulatory mechanisms likely raise the threshold, compared to other tissues, for the induction and persistence of adaptive immune responses. These mechanisms include strong central and peripheral T cell tolerance to heart antigens and induction of anti-inflammatory feedback mechanisms involving cytokines such as interferon-??.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 111 (1982), S. 213-217 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The phenothiazine, trifluoperazine, and the mitogenic lectins, phytohemagglutinin (PHA) and Concanavalin A (Con A), were tested for their effects on human lymphocyte plasma membrane Ca-activated Mg-ATPase and ATP-dependent calcium uptake. Trifluoperazine completely inhibited Ca-uptake when present from the start of the assay at concentrations of 100 m̈M or more. When added during measurement of calcium uptake, trifluoperazine reduced the rate of vesicular calcium accumulation but was unlike the calcium ionophore, A23187, which caused a rapid release of accumulated calcium from the vesicles. Trifluoperazine also inhibited membrane vesicle Ca-ATPase activity, but this inhibition was nonspecific since the Mg-ATPase and Na, K-ATPase activities were inhibited to similar extents at the same concentration of the phenothiazine. In contrast, concentrations of PHA and Con A, which are mitogenic for lymphocytes, did not cause any change in Ca-uptake when added to suspensions of membrane vesicles. Con A had no effect and PHA had a weak inhibitory effect on Ca-ATPase activity.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Supramolecular Structure 14 (1980), S. 65-75 
    ISSN: 0091-7419
    Keywords: lymphocyte ; calcium ; phytohemagglutinin ; A23187 ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Calcium has been suggested as an internal second messenger when lymphocytes are stimulated by mitogens to enter the cell cycle. We have assessed the effect of 2 lymphocyte stimulants, the plant lectin phytohemagglutinin (PHA) and the calcium ionophore A23187, on human lymphocyte nucleic acid synthesis, total cell calcium content, and 4 5Ca labeling. We have used an ultrasensitive method for the measurement of total cell calcium in the same samples used for radiolabeling. Mitogenic concentrations of A23187 (∼ .25 μ mole/liter) caused an increase in both total cell calcium and 4 5Ca labeling. These increases were almost completely blocked by inhibitors of mitochondrial respiration, suggesting that the calcium increment after ionophore treatment was located in the mitochondria. In contrast, total cell calcium was not altered at optimal mitogenic PHA concentrations (0.1 μg/ml and above). However, at the minimum PHA concentrations that caused stimulation (0.025 to 0.1 μg/ml), the dose response of 4 5Ca uptake was very similar to that of DNA sysnthesis. Importantly, we could not stimulate DNA synthesis with PHA without increasing lymphocyte 4 5Ca labeling. Thus, an increase in total cell calcium is not essential for mitogenesis; however, an increase in 4 5Ca exchange is closely associated with the mitogenic effects of A23187 and PHA.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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