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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Exudates and Transudates

 
 
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Disease relevance of Exudates and Transudates

  • Delayed-type hypersensitivity (DTH) responses specific for the phosphorylcholine (PC) hapten were induced in BALB/c mice by immunization with syngeneic peritoneal exudate cells (PEC) coupled with diazotized phenyl-phosphoryl-choline [1].
  • Pretreatment of murine peritoneal exudate macrophages with 1-5 U/ml rIFN-gamma or rIL-2, or higher concentrations of IFN-alpha or IFN-beta greatly stimulated ADCC to Rl lymphoma targets [2].
  • The recently described inhibition of DNA synthesis (IDS) assay, which measures antitumor effector (E) cell function by the quantitation of decreases in tritiated thymidine incorporation of target tumor cells, was used to analyze the nonspecific effector activity of peritoneal exudate cells (PEC) from mice infected intraperitoneally with BCG [3].
  • 2) The 9 patients with lower ascitic fluid than plasma CEA levels (medians: 29 and 140 ng/ml, respectively) had transudates and negative cytology examinations but did have demonstrable liver metastases [4].
  • Exudates of dicotyledonous plants contain specific phenolic signal molecules, such as acetosyringone, which serve as potent inducers for the expression of the virulence (vir) regulon of the phytopathogen Agrobacterium tumefaciens [5].
 

Psychiatry related information on Exudates and Transudates

  • However, a spot of haptoglobin alpha-1 chains (13.5 kDa; approximate pI 4.6) was found to be present in the majority of 2-D CSF maps from the dementia cases, suggesting a high-molecular-weight transudate type of alteration in the blood-brain barrier with considerable frequency in AD [6].
 

High impact information on Exudates and Transudates

 

Chemical compound and disease context of Exudates and Transudates

  • In a second group of hearts, the normoxic control levels of adenosine in the transudates (42 +/- 7 pmol/ml) and coronary effluents (62 +/- 17 pmol/ml) were increased with hypoxia by 174 and 1,178%, respectively [12].
  • Constant-flow perfused rat hearts were used to study: 1) the effect of hypoxia on isoproterenol (ISO)-induced increase in interstitial adenosine, as estimated with epicardial surface transudates, and 2) the role of endogenous adenosine in hypoxic depression of ISO-induced contractile responses [13].
  • Deacylation of lipopolysaccharide in whole Escherichia coli during destruction by cellular and extracellular components of a rabbit peritoneal inflammatory exudate [14].
  • Mac-2, a 30-35-kDa galactose-binding protein, is synthesized at similar levels in murine peritoneal exudate macrophages whether recruited in response to an intraperitoneal pathogen Mycobacterium microti, to sterile inflammatory stimuli such as thioglycollate broth, or to concanavalin A [15].
  • Thioglycolate-elicited peritoneal exudate macrophages from C3H/HeJ mice were rendered cytolytic for P815 mastocytoma cells in a two-signal tumoricidal assay that used recombinant interferon-gamma (rIFN-gamma; 1 to 10 U/ml) as a "priming" signal and butanol-extracted lipopolysaccharide (But-LPS; 0.1 to 5 micrograms/ml) as a "trigger" signal [16].
 

Biological context of Exudates and Transudates

  • This paper explores the nature of the cross-reactions at the T-cell level among the branched-chain copolymers (T,G)-A--L, (phi,G)-A--L, (H,G)-A--L, and G-A--L, as well as a related linear terpolymer, GAT, in a variety of mouse strains using the peritoneal exudate T-lymphocyte-enriched cells (PETLES) proliferation assay [17].
  • The time course of the induction of inducible nitric oxide synthase (iNOS) protein in the pouch tissue was found to coincide with the production of NO2-. Dexamethasone inhibited both iNOS protein expression and NO2- synthesis in the fluid exudate (IC50 = 0.16 mg/kg) [18].
  • Both drugs reduced PGE2 concentrations in inflammatory exudates by 50-70%, but aspirin was considerably more potent than salicylate in inhibiting thromboxane B2 production in clotting blood [19].
  • Gel retardation and methylation interference assays showed that stimulation of TNF-alpha gene transcription in peritoneal exudate macrophages was accompanied by induction of DNA-binding proteins that recognized with different affinities four elements related to the kappa B consensus motif and a Y-box motif [20].
  • Extracellular 14-kDa phospholipases A2 (PLA2) in inflammatory exudates can contribute to bacterial phospholipid (PL) degradation during phagocytosis of Escherichia coli by polymorphonuclear leukocytes (PMN) and are highly active toward E. coli treated with the bactericidal/permeability-increasing protein (BPI) purified from PMN [21].
 

Anatomical context of Exudates and Transudates

 

Associations of Exudates and Transudates with chemical compounds

  • Human peripheral blood PMNs exposed to PGE2 (as in exudates) switched eicosanoid biosynthesis from predominantly LTB4 and 5-lipoxygenase (5-LO)-initiated pathways to LXA4, a 15-LO product that "stopped" PMN infiltration [27].
  • Indomethacin treatment did not prevent the formation of a peritoneal inflammatory exudate or peritoneal oil granulomatous tissue, although it had a mild inhibitory effect on the intensity of the cellular inflammation, particularly after extensive treatment of greater than 100 d [28].
  • For example, mouse resident peritoneal exudate cells (PEC) lysed TNP CRBC and bacillus Calmette-Guérin-activated PEC lysed both TNP CRBC and TNP tumor targets [29].
  • Likewise, peritoneal exudate leukocytes of beige mice (the murine counterpart of CHS) contained correspondingly reduced levels of their major neutral protease, a serine enzyme of mol wt 27,000 [30].
  • Here, we report that lipidomic analysis of exudates obtained in the resolution phase from mice treated with ASA and docosahexaenoic acid (DHA) (C22:6) produce a novel family of bioactive 17R-hydroxy-containing di- and tri-hydroxy-docosanoids termed resolvins [23].
 

Gene context of Exudates and Transudates

  • Also, in BLTR transgenic mice, 5-LO expression and product formation were selectively increased in exudates, demonstrating that receptor overexpression amplifies proinflammatory circuits [31].
  • Despite absence of CCR5, intracerebral infection invariably resulted in lethal T cell-mediated meningitis, and quantitative and qualitative analysis of the inflammatory exudate cells did not reveal any significant differences between gene-targeted mice and wild-type controls [32].
  • In bone marrow (BM) neutrophils isolated from rac2(-/-) mice generated by gene targeting, we previously reported that PMA-induced superoxide production was reduced by about 4-fold, which was partially corrected in TNF-alpha-primed BM neutrophils and in peritoneal exudate neutrophils [33].
  • Thioglycollate, proteose-peptone, or IL-1 elicited peritoneal exudate cells were found to bind 125I-IL-1 alpha in a specific and saturable manner [34].
  • Histologically, at day 7 after AIA induction, exudate and infiltrate in the knee joint was similar in Fc gamma RI-/- and Fc gamma RIII-/- and significantly higher (230% and 340%) in Fc gamma RII-/- mice if compared to controls [35].
 

Analytical, diagnostic and therapeutic context of Exudates and Transudates

References

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