200,511 research outputs found
Ueber die akademische Bibliothek zu Wittenberg / von M. Fr. Heinr. Ludw. Leopold
No full textVorlageform des Erscheinungsvermerks: Gedruckt mit Meltzerischen Schriften, 180
Ein Zusatz zu dem Artikel «Inhibition» von S. I. Meltzer
No full textEIN ZUSATZ ZU DEM ARTIKEL «INHIBITION» VON S. I. MELTZER
Le Physiologiste Russe (-)
Le Physiologiste Russe (2) (a0005)
Ein Zusatz zu dem Artikel «Inhibition» von S. I. Meltzer (2) (p0246
Macrophage activation for tumor cytotoxicity: tumoricidal activity by macrophages from C3H/HeJ mice requires at least two activation stimuli
No full textMacrophages from C3H/HeN mice treated in vivo with Mycobacterium bovis, strain BCG or in vitro with supernatants from antigen-stimulated leukocyte cultures (lymphokines) were cytotoxic to tumor cells in vitro. Macrophage tumoricidal activity, however, did not develop after identical in vivo or in vitro treatment of cells from endotoxin (LPS)-unresponsive C3H/HeJ mice. Increasing time of macrophage incubation in lymphokines, concentration of lymphokines or number of lymphokine-treated macrophages added to tumor cells did not evoke tumoricidal activity. Similarly, varying time of macrophage collection after BCG infection, number of BCG organisms in the infectious inoculum or numbers of macrophages from BCG-infected mice added to tumor cells also did not evoke cytotoxic activity. The tumorical defect of macrophages from C3H/HeJ mice appeared highly selective: C3H/HeN responses to BCG infection in c3H/HeN and C3H/HeJ mice were indistinguishable: moreover, no difference was detected between these strains in production of macrophage activation factors. Thus, despite normal inflammatory reactions, normal production of lymphokines and extensive experimental manipulation of single activation stimuli, macrophages from C3H/HeJ mice did not express tumoricidal activity in vitro. Nevertheless, macrophages from C3H/HeJ mice could develop tumoricidal activity under appropriate conditions. Macrophages from in vivo immune reactions (BCG infection, Con A injection), but not from irritant-induced peritoneal exudates, developed full cytotoxic activity after exposure to certain in vitro stimuli. These stimuli include microgram/ml concentrations of LPS and certain factors in lymphokine supernatants or supernatants from a T-cell lymphoma line. The effect of LPS but not that of lymphokines or lymphoma culture supernatants was abrogated by polymyxin B. These data suggest that the ultimate expression of macrophage cytotoxicity may depend upon certain signals from the milieu of immune reactions. These expression signals, derived from bacterial organisms or from soluble mediators of immune responses, provide the necessary and final stimulus for macrophage activation. The tumoricidal defect of macrophages from C3H/HeJ mice reflects a genetic inability of these cells to respond to environmental expression signals
Origins of the Great Inflation
No full textThe Great Inflation from 1965 to 1984 is the climactic monetary event of the last part of the 20th century. This paper analyzes why it started and why it continued for many years. Like others, it attributes the start of inflation to analytic errors, particularly the widespread acceptance of the simple Keynesian model with its implication that monetary and fiscal policy should be coordinated. In practice, that meant that the Federal Reserve financed a large part of the fiscal deficit. This paper gives a large role to political decisionmaking. Continuation of inflation depended on political choices, analytic errors, and the entrenched belief that inflation would continue.Inflation (Finance) ; Economic history ; Monetary policy
Macrophage activation for tumor cytotoxicity: Development of macrophage cytotoxic activity requires completion of a sequence of short-lived intermediary reactions
No full textMacrophages from endotoxin (LPS)-unresponsive C3H/HeJ mice fail to develop tumoricidal activity after any of several in vivo or in vitro treatments that induce cytotoxicity with cells from LPS-responsive C3H/HeN mice. Under certain conditions, however, these macrophages could become tumoricidal: macrophages from in vivo immune reactions such as those induced by BCG infection, but not cells from irritant-induced peritoneal exudates, developed full cytotoxic capability after further exposure in vitro to microgram per milliliter concentrations of LPS or to supernatants from antigen-stimulated leukocyte cultures (lymphokines). Capacity of macrophages from BCG-infected C3H/HeJ mice to become tumoricidal after LPS exposure was gradually lost with time in culture and was absent by 24 hr. Requirements for at least two activation stimuli for cytotoxic activity with C3H/HeJ macrophages could also be fulfilled entirely in vitro: cells cultured in lymphokines plus LPS were fully tumoricidal; macrophages cultured in either agent alone were not cytotoxic. Similar interactions between lymphokines and LPS could be demonstrated with macrophages from LPS-responsive C3H/HeN mice. Tumoricidal activity by C3H/HeN macrophages cultured in lymphokines plus nanogram per milliliter concentrations of LPS was considerably greater than that by cells cultured in either agent alone. LPS and lymphokines were synergistic in their action on macrophage cytotoxicity. The synergistic effect of LPS on cytotoxicity by lymphokine activated macrophages was evident after a 15-min pulse and was not dependent upon fluid-phase LPS. Synergistic action, however, was dependent upon 1.) treatment sequence: LPS was active only if given simultaneously with or after lymphokine treatment; LPS exposure before lymphokine treatment was ineffective, and 2.) treatment interval: capacity of lymphokine-treated macrophages to express cytotoxic activity after LPS exposure decayed with time in culture and was lost by 24 hr. Thus, macrophage activation for tumor cytotoxicity in both C3H/HeJ and C3H/HeN mice was the final result of a cascade of short-lived intermediary reactions in a defined sequence. Tumoricidal activity of fully activated cells and responsiveness of each noncytotoxic precursor cell to activation stimuli were all short lived macrophage reactions. Present evidence suggests that none of these reactions was reversible. Completion of each state of macrophage activation was completely dependent upon the simultaneous presence of localized activation signals and macrophage precursors able to respond
Macrophage activation for tumor cytotoxicity: increased lymphokine responsiveness of peritoneal macrophages during acute inflammation
No full textPeritoneal inflammation induced by sterile irritants led to accumulation of macrophages that were more responsive to lymphokines than macrophages from resident cell populations of untreated mice. Lymphokine responsiveness was quantitated by measurement of macrophage-mediated tumor cytotoxicity induced by supernatants from antigen-stimulated immune spleen cell cultures. Tumor cytotoxicity by lymphokine-activated inflammatory macrophages was about 10-fold greater than that by equal numbers of lymphokine-treated resident cells. Analysis of the time course of activation and of lymphokine dose-response demonstrated that the increased responsiveness of inflammatory cells was a consequence of quantitative changes. Lymphokine-responsive cells in both resident and inflammatory populations were identical; the numbers of response cells increased with inflammation. Changes in numbers of lymphokine-responsive cells during acute inflammation were coincident with similar changes in numbers of peroxidase-positive macrophages. This finding suggested that the increased lymphokine responsiveness of inflammatory cells was dependent upon influx of young peroxidase-positive mononuclear phagocytes rather than stimulation of resident macrophages. This concept was further strengthened by the finding that whole body x-irradiation diminished the numbers of both peroxidase-positive and of lymphokine-responsive macrophages in inflammatory and resident cell populations. These data suggest that the lymphokine-responsive precursor or the activated tumoricidal macrophage during both steady-state and acute inflammatory conditions was the newly formed blood-derived mononuclear phagocyte. The 10-fold increase in numbers of lymphokine responsive macrophages in peritoneal exudate over resident cell populations reflected a similar increase in macrophage turnover induced by inflammation
Macrophage activation for tumor cytotoxicity: regulatory mechanisms for induction and control of cytotoxic activity.
No full textImperfect Information and the Meltzer-Richard Hypothesis
No full textStandard models of voting on redistribution generate a clear-cut prediction: redistribution increases in income skewness. (the Meltzer-Richard hypothesis) Empirical evidence on this issue is mixed. Changes in income skewness are often accompanied by developments in redistribution into the opposite direction. This paper argues that it is important to distinguish between sources of changes in income skewness, polarization and upward mobility which both have the same impact on income skewness. In a model with imperfect information, these developments affect redistribution in different ways. While polarization generates a positive relation between income skewness and redistribution, upward mobility can have the opposite effect
Macrophage activation for tumor cytotoxicity: mechanisms of macrophage activation by lymphokines.
No full text[No abstract available
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