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

Edema

 
 
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Disease relevance of Edema

  • In these mice, VEGF induced, through IL-13-dependent and -independent pathways, an asthma-like phenotype with inflammation, parenchymal and vascular remodeling, edema, mucus metaplasia, myocyte hyperplasia and airway hyper-responsiveness [1].
  • Pathological increases in vascular leakage lead to edema and swelling, causing serious problems in brain tumors, in diabetic retinopathy, after strokes, during sepsis and also in inflammatory conditions such as rheumatoid arthritis and asthma [2].
  • Mice lacking PI3Kgamma did not form edema after intradermal injection of adenosine and when challenged by passive systemic anaphylaxis [3].
  • Transdermal nicotine therapy at doses of 44 mg produced a significantly greater frequency of nausea (28%), vomiting (10%), and erythema with edema at the patch site (30%) than did a 22-mg dose (10%, 2%, and 13%, respectively; P < .01 for each adverse effect) [4].
  • These results indicate that PGE2 plays a major role in tissue edema, hyperalgesia, and IL-6 production at sites of inflammation, and they suggest that selective pharmacologic modulation of PGE2 synthesis or activity may provide a useful means of mitigating the symptoms of inflammatory disease [5].
 

Psychiatry related information on Edema

 

High impact information on Edema

  • Compared to histamine, which causes constriction of airways and edema formation, the leukotrienes are three to four orders of magnitude more potent and the effects have longer duration [11].
  • RESULTS: Adverse effects of STI571 were minimal; the most common were nausea, myalgias, edema, and diarrhea [12].
  • As compared with placebo, prophylactic infusions of C1 inhibitor resulted in significantly lower daily symptom scores for the severity of edema of the extremities (P<0.01), larynx (P<0.05), abdomen (P<0.05), and genitourinary tract (P<0.05) [13].
  • Mutations at the alpha-globin locus are the most common class of mutations in humans, with deletion of all four adult alpha-globin genes resulting in the perinatal lethal condition haemoglobin Barts hydrops fetalis [14].
  • Glucose phosphate isomerase deficiency as a cause of hydrops fetalis [15].
 

Chemical compound and disease context of Edema

  • Captopril in idiopathic edema [16].
  • EF, a calmodulin- and Ca2+-dependent adenylate cyclase, is responsible for the edema seen in the disease [17].
  • Trypsin and tryptase directly signal to neurons to stimulate release of these neuropeptides, which mediate inflammatory edema induced by agonists of proteinase-activated receptor 2 [18].
  • A possible explanation for this is that other dipsogenic sites are involved which are beyond the interventricular foramen and that SFO lesions produce an obstruction by edema or debris at the foramen which blocks access of cerebrospinal fluid-borne angiotensin to those sites [19].
  • Liver necrosis and perhaps the induction of lung edema and neoplasia as well as other effects of thiono-sulfur-containing compounds are more likely the result of the covalent binding of the electrophilic S-oxides or S-dioxides or carbene derivatives of these S-oxides and S-dioxides to tissue macromolecules [20].
  • Bivariable and multivariable logistic regression models were used to identify comorbid illnesses, demographic characteristics, other medications, and PD features associated with increased risk of pedal edema among individuals taking pramipexole [21].
  • Cotreatment with spantide attenuated peritracheal edema in captopril-treated DPPIV-deficient rats (P = .005 vs captopril-treated DPPIV-deficient rats and P = .57 vs saline-treated DPPIV-deficient rats) [22].
 

Biological context of Edema

 

Anatomical context of Edema

  • Complete Freund's adjuvant-induced mast cell degranulation as well as edema and neutrophil infiltration, which occurred weakly in mast cell-deficient WBB6F(1)-W/W(v) mice, did not occur in NMU-deficient mice [28].
  • Treatment of rats with the mast cell degranulator 48/80 to deplete these cells of their stores of histamine and serotonin abolished completely the ability of TRAP to produce edema [29].
  • Hydrostatic lung edema in response to acute increases in pulmonary artery pressure was not affected by AQP5 deletion [30].
  • In mice, intracolonic administration of PAR1 agonists led to an inflammatory reaction characterized by edema and granulocyte infiltration [31].
  • Kinin generation may contribute to the asthmatic response directly through edema formation and smooth muscle contraction and by augmenting release and/or production of preformed (histamine) and secondary mediators such as leukotrienes and platelet-activating factor [32].
 

Gene context of Edema

  • IL-2 induced massive lymphocytic infiltration in the liver and lung and moderate infiltration in the kidney in association with organ edema and dysfunction [33].
  • Therapeutic administration of a selective COX-2 inhibitor, SC-58125, rapidly reversed paw edema and reduced the level of PGE2 in paw tissue to baseline [34].
  • AQP1 facilitates hydrostatically driven lung edema but is not required for active near-isosmolar absorption of alveolar fluid [35].
  • The molecular nature of a severe multisystemic disorder with a recurrent nonimmune hydrops fetalis was identified as deficiency of GDP-Man:GlcNAc(2)-PP-dolichol mannosyltransferase, the human orthologue of the yeast ALG1 gene (MIM 605907) [36].
  • Chronic transgenic delivery of PlGF-2 to murine epidermis resulted in a significantly increased inflammatory response, associated with more pronounced vascular enlargement, edema, and inflammatory cell infiltration than seen in wild-type mice [37].
  • The most increased, neuronal pentraxin 2 (NPTX2, 7-fold change), was predictive of survival in tumors with the highest levels of edema, in contrast to VEGF (hazard ratio, 2.73; 95% CI, 1.49-5.02; P=0.049) [38].
 

Analytical, diagnostic and therapeutic context of Edema

 

References

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