Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new subclass of mouse IgG for which we propose the name IgG3 has been shown to have a mol wt of 150,000 consistent with an L(2)H(2) structure, and is present in normal mouse serum at a concentration of 0.1-0.2 mg/ml. Its molecular weight, low carbohydrate content, glycopeptide analysis, and C-terminal analysis are all typical of the IgG class. The intact protein had a strong tendency to form noncovalent aggregates with itself which were dissociable in acid. Upon papain digestion an Fab fragment of 47,000 mole wt was generated along with an Fc fragment which was insoluble at neutral pH. As for its biology, the protein did not fix complement, was not cytophilic for gammaG2 receptor sites on macrophages, and did not show passive cutaneous anaphylaxis. It was very efficiently transported across the placenta so that its concentration in the newborn was twice that in the serum of the mother, compared to the concentration of IgG1 and IgG2 proteins which were only present at one-third the concentration of that found in the serum of the mother. The Fc fragment of this protein reacted with and was solubilized by the staphylococcal A protein which also precipitated the intact immunoglobulin. In addition, the myeloma protein which was the prototype for this gammaG subclass exhibited binding activity for levan which was localized to the Fab fragment.
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PMID:A new mouse immunoglobulin: IgG3. 513 63

Arachidonic acid is metabolized to prostaglandins and thromboxane via the cyclooxygenase pathway and to leukotrienes B4, C4, D4, and E4 via the lipooxygenase pathway. A possible role played by leukotrienes in cardiogenic shock resulting from anaphylaxis prompted us to investigate the action of these compounds on coronary vessels and myocardial contractility. In this study leukotriene B4 (LTB4) and C4 (LTC4) were injected directly into the left circumflex (LCx) coronary artery of nine anesthetized Suffolk sheep. LTB4 had no effect on coronary artery blood flow or myocardial contractility, but 3 X 10(-9) mole induced profound transient circulating neutropenia, reflecting the potent chemotactic and chemokinetic properties of this compound. Injecting as little as 1.6 X 10(-11) mole of LTC4 caused a 14.5 +/- 4.3% (mean +/- SE) reduction of LCx coronary artery flow while 1.6 X 10(-10) mole caused a 26.5 +/- 3.7% decrease of LCx coronary artery flow and an 18.1 +/- 3.2% decrease in systolic shortening of the myocardial region supplied by the LCx coronary artery. Since the decrease in systolic shortening was far greater than that expected on the basis of the reduction in coronary artery flow, we postulate that LTC4 has a direct negative inotropic effect. FPL 55712, a receptor antagonist of leukotrienes C4, D4, and E4, blocked the vasoconstriction induced by LTC4 but only partially blocked the negative inotropic effects of LTC4. LTC4 is a potent vasoconstrictor and negative inotropic agent and may play an important role in anaphylactic shock.
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PMID:Effects of leukotrienes B4 and C4 on coronary circulation and myocardial contractility. 630 44

Although mediator release from mast cells and basophils plays a central role in the pathogenesis of human allergic disease, biochemical studies have been restricted to rat peritoneal mast cells and basophilic leukemia cells because they could be easily purified. We have used two new techniques of cell separation to purify human lung mast cells to 98% homogeneity. Lung cell suspensions were obtained by dispersion of chopped lung tissue with proteolytic enzymes. Mast cells were then purified from the suspensions by countercurrent centrifugal elutriation and affinity chromatography. The purified mast cells released both histamine and slow-reacting substance of anaphylaxis (SRS-A) (leukotriene C and D) during stimulation with goat anti-human IgE antibody. Moreover, these preparations were able to generate significant quantities of SRS-A (32 +/- 7 x 10(-17) LTD mole-equivalents/mast cell) at all stages of purification, indicating that a secondary cell is not necessary for the antigen-induced release of SRS.
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PMID:Generation of leukotrienes by purified human lung mast cells. 711 13

Pepsin-digested rabbit antibody (5S) provoked reverse passive cutaneous anaphylaxis in the guinea pig, but was somewhat less effective, mole for mole, than the native antibody. Fixation of guinea pig complement by the pepsin-digested antibody could not be demonstrated either in vitro or in vivo. Splitting of the 5S fragment into two monovalent fragments (3.5S) markedly reduced the capacity to provoke reverse passive cutaneous anaphylaxis.
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PMID:Passive cutaneous anaphylaxis with antibody fragments. 1394 Jul 85