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MeSH Review

Passive Cutaneous Anaphylaxis

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Disease relevance of Passive Cutaneous Anaphylaxis

  • In this study, spontaneous procoagulant activity (PCA) was measured in circulating mononuclear cells to determine whether elevated PCA correlated with the presence of proliferative glomerulonephritis in patients with systemic lupus erythematosus (SLE) [1].
  • The PCA response was antigen specific: peripheral blood mononuclear cells (PBM) from donors sensitive to PPD or tularemia showed an increase in PCA only in response to the sensitizing antigen [2].
  • The binding properties and the regional densities of histamine H(1) receptors were studied in brain of rats with portacaval anastomosis (PCA) and in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy (HE) [3].
  • This project was undertaken to study the survival properties of various prostate cells, including normal (NHP), BPH (benign prostate hyperplasia), primary carcinoma (PCA), and metastatic prostate cancer cells (LNCaP, PC3, and Du145), in the absence of trophic factors [4].
  • IgE injected i.p. 24 hr before the sensitization with IgE anti-ovalbumin (OVA) completely inhibited both IgE- and IgG2a-induced passive cutaneous anaphylactic (PCA) reactions at a dose (2.5 mg/100 g body weight) that resulted in peak serum concentrations of 150 micrograms IgE IR162/ml [5].

Psychiatry related information on Passive Cutaneous Anaphylaxis


High impact information on Passive Cutaneous Anaphylaxis

  • Subsequently, the plasma is removed, medium added, and procoagulant activity (PCA) and secretion of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) measured after 18-h incubation [11].
  • The levels of PCA, TNF-alpha, and IL-6 obtained with plasma from shock patients were not different from those induced by plasma from 10 meningococcal patients without shock or with plasma from healthy persons [11].
  • The inflammatory reactions investigated were a passive cutaneous anaphylaxis (PCA) reaction and responses elicited by intradermal soluble inflammatory mediators (platelet-activating factor, leukotriene B4, C5a des Arg), arachidonic acid, and zymosan particles [12].
  • The magnitude of the monocyte PCA response increased in response to an increase in the allogeneic stimulator/T clone responder ratio, and third-party allogeneic cells were unable to elicit the PCA-inducing lymphokine signals from T inducer clones [13].
  • In eight patients with SLE but with no apparent active renal disease, PCA was not elevated above normal basal levels [1].

Chemical compound and disease context of Passive Cutaneous Anaphylaxis


Biological context of Passive Cutaneous Anaphylaxis

  • The kinetics of the endothelial PCA responses to TNF and IL-1 were similar, demonstrating a rapid rise to peak activity at approximately equal to 4 hr, and a decline toward basal levels by 24 hr [19].
  • These multiple effects on cholesterol homeostasis and pool sizes strongly suggest that PCA can reverse the progressive accumulation of cholesterol in body tissues of FH patients [20].
  • Cell differentiation in a myeloid direction induced by retinoic acid or DMSO led to a diminished PCA, while not affecting the fibrinolytic activity [21].
  • Dietary administration of PCA also caused significant decreases in the labeling index of bromodeoxyuridine and the number and area of silver-stained nucleolar organizer regions per cell nucleus, known as cell proliferation indices, of the tongue squamous epithelium (P < 0.05) [22].
  • A serially transplantable, primary human PCA, designated CWR22, exhibits a clonal cytogenetic aberration, causes high elevations of prostate specific antigen in the peripheral blood of nude mice, and is unusually responsive to androgen deprivation as compared with other xenografts [23].

Anatomical context of Passive Cutaneous Anaphylaxis

  • The median levels of PCA, TNF-alpha, and IL-6 were 5, 0, and 4%, respectively, of the monocyte activities induced by normal plasma boosted with purified N. meningitidis (Nm)-LPS (2,500 pg/ml; net LPS-boosted capacity, 100%) [11].
  • Induction of PCA by rTNF was concentration dependent (maximum, 500 units/ml), time dependent, reversible, and blocked by cycloheximide and actinomycin D, and it occurred without detectable endothelial cell damage [19].
  • In the present study, we investigated the effect of cyclosporine A (CsA) on the lipopolysaccharide (LPS)-induced procoagulant activity (PCA) in human monocytes/macrophages [24].
  • Irradiation of nonadherent lymphocytes before mixing them with FMLP and adherent cells abolishes their ability to amplify PCA [25].
  • Data indicate that both CD8+ and CD4+ Th1, but not Th2, T cells can help TF production and PCA [26].

Associations of Passive Cutaneous Anaphylaxis with chemical compounds

  • The PCA was tissue factorlike in that Factors VII and X were required for expression of the activity, whereas Factor VIII was not [2].
  • In all four dogs who escaped from DOCA, the PCA was widely patent and the mean pressure gradient was only 1.6 cm H2O [27].
  • In addition, PCA caused a net efflux of accumulated tissue cholesterol as demonstrated by reductions in the rapidly exchangeable and total exchangeable masses of body cholesterol [20].
  • We conclude that YFP PCA can detect weak and transient protein interactions in the secretory pathway and hence is a powerful approach to study luminal processes involved in protein secretion [28].
  • METHODS AND RESULTS: In endothelium-denuded IMA and PCA and less so in IMV, FR139317 and BQ-123 (in PCA only) shifted the concentration-contraction curves to ET-1 parallel to the right [29].

Gene context of Passive Cutaneous Anaphylaxis

  • YFP PCA analysis revealed the oligomerization of ERGIC-53 and its interaction with MCFD2, as well as its lectin-mediated interaction with cathepsin Z [28].
  • PCA induced by IFN-gamma, IL-1 beta, and TNF-alpha depended largely on tissue factor expression, as evidenced by experiments with factor X-deficient plasma and antitissue factor antibodies [30].
  • Interferon-gamma (IFN-gamma), interleukin-1 beta (IL-1 beta), and tumor necrosis factor-alpha (TNF-alpha) were strong macrophage PCA inducers [30].
  • PCA prevented activation of caspase-8 and caspase-3 upon treatment with FasL [16].
  • Together, these results suggest that anticancer effects of GSE in PCA be mediated via impairment of EGFR-ERK1/2-Elk1-AP1-mediated mitogenic signaling and activation of JNK causing growth inhibition and apoptosis, respectively [31].

Analytical, diagnostic and therapeutic context of Passive Cutaneous Anaphylaxis

  • The results revealed a dose-dependent decrease in PCA muscle tone caused by pontine microinjections of carbachol [32].
  • We also tested PCA and ICA using PLS in a simulated event-related fMRI data to show their similar detection [33].
  • The development of parasites, the expression of resistance after sensitization, and the intensity of delayed type hypersensitivity (DTH), Ag-mediated blast transformation (AMBT), IgG2a, passive cutaneous anaphylaxis, and IgE-mediated antibody-dependent cell-mediated cytotoxicity responses against S. mansoni or control Ag were ascertained [34].
  • In situ hybridization analysis showed that the PCA reaction sites treated with antisense TGF-beta1 oligonucleotides exhibited no detectable levels of TGF-beta1 and L-histidine decarboxylase mRNA after anti-DNP IgE stimulation, whereas the PCA reaction sites treated with sense TGF-beta1 oligonucleotides possessed significant amounts of their mRNA [35].
  • BACKGROUND.--The purpose of this study is a prospective assessment of morphine sulfate administration by intermittent intravenous (IV) injections (Int-IV) vs patient-controlled analgesia (PCA) in patients in the emergency department (ED) with sickle cell crisis pain [36].


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  11. Net inflammatory capacity of human septic shock plasma evaluated by a monocyte-based target cell assay: identification of interleukin-10 as a major functional deactivator of human monocytes. Brandtzaeg, P., Osnes, L., Ovstebø, R., Joø, G.B., Westvik, A.B., Kierulf, P. J. Exp. Med. (1996) [Pubmed]
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  14. The participation of macrophages, glomerular procoagulant activity, and factor VIII in glomerular fibrin deposition. Studies on anti-GBM antibody-induced glomerulonephritis in rabbits. Tipping, P.G., Holdsworth, S.R. Am. J. Pathol. (1986) [Pubmed]
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  21. Combined procoagulant activity and proteolytic activity of acute promyelocytic leukemic cells: reversal of the bleeding disorder by cell differentiation. Wijermans, P.W., Rebel, V.I., Ossenkoppele, G.J., Huijgens, P.C., Langenhuijsen, M.M. Blood (1989) [Pubmed]
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