Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a prospective study we compared the usefulness of various laboratory tests (albumin, alpha-1-proteinase inhibitor (A1PI), cholinesterase (CHE), C-reactive protein, erythrocyte sedimentation rate, hematocrit) and activity indices (CDAI, VHAI) in relation to the disease activity by endoscopic criteria. Except for hematocrit highly significant differences (p less than 0.0005) of the mean values of all test results were found for patients without or with slight mucosal lesions compared with patients with severe inflammation of the mucosa. Further analysis of the data indicates the highest test efficiency (84%), sensitivity (80%), and specificity (88.6%) for CHE. CHE showed good correlations to all other tests; the highest correlation was found between CHE and VHAI (r = -0.78). We suggest that a suppression of CHE synthesis mediated by endotoxins and cytokines rather than an increased intestinal loss explains the decreased CHE in severe Crohn's disease. It is concluded from the data that CHE is a useful test to assess the inflammatory activity of Crohn's disease.
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PMID:Evaluation of different laboratory tests and activity indices reflecting the inflammatory activity of Crohn's disease. 141 Dec 85

We have used a panel of well-characterized monoclonal antibodies (MoAbs) to examine the blood cells of a patient with a novel form of congenital dyserythropoietic anemia (CDA) characterized by intra-erythroblastic and intra-erythrocytic membranous inclusions. Twelve antibodies defining three nonoverlapping epitope groups on the extracellular domain of CD44 all failed to react with the red blood cells (RBCs) of the patient. A rabbit antibody to the cytoplasmic domain of CD44 from normal RBCs failed to react with the patient's RBC ghosts. In contrast, the patient's lymphocytes, granulocytes, and monocytes showed apparently normal CD44 expression. Bone marrow preparations stained with CD44 antibodies and visualized with 125I antimouse Ig (F(ab')2) followed by autoradiography showed positive staining of lymphocytes and myeloid cells but not of most orthotolidine-positive erythroblasts. The patient's RBCs also gave weaker than normal reactions with MoAbs of anti-LWab specificity while MoAbs to glycophorins A, B, and C, Rh polypeptides, CD47, CD55, CD58, CD59, acetylcholinesterase, and Lutheran and Kell glycoproteins all gave normal reactions. Agglutination tests with human blood grouping sera demonstrated that the RBCs of the patient have the unique phenotype In(a-b-), Co(a-b-) and that they also lack the high incidence RBC antigen AnWj. The phenotype In(a-b-) would be expected because these antigens are known to be expressed on CD44. There is also some evidence associating the AnWj antigen with CD44. However, the CO blood group locus is on chromosome 7p whereas that for CD44 is on chromosome 11p. Quantitative binding assays using 125I-labeled Fab fragments of CD44 antibodies did not show any evidence for reduced levels of CD44 on RBCs from the parents of the patient or from her unaffected sister. The parents and sister had the common Colton blood group phenotype [Co(a+b-)]. Neither deficiency of CD44 nor absence of Colton antigens are general features of CDA because erythrocytes from patients with CDA I, CDA II, CDA III, and two other unclassified CDAs had normal expression of CD44 and normal Colton blood group phenotypes. Further analysis of the defect(s) present in the patient's erythroid cells may provide useful information regarding membrane assembly and the regulation of differentiation in normal erythroid cells.
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PMID:A novel form of congenital dyserythropoietic anemia associated with deficiency of erythroid CD44 and a unique blood group phenotype [In(a-b-), Co(a-b-)]. 750 39

Acute phase proteins and markers of proteosynthetic activity reflect the clinical activity in Crohn's disease (CD). The impact of anti-tumor necrosis factor antibody (anti-TNF) therapy on serum levels of acute phase proteins and proteosynthetic markers was studied. Fourteen patients with active CD were treated with 5 mg per kg of anti-TNF in intravenous infusion. Clinical activity (assessed by Crohn's disease activity index - CDAI), alpha-1-acid glycoprotein, haptoglobin, cholinesterase and prealbumin were assessed before and in months 1 and 5 after treatment. A sustained decrease in CDAI was observed. This was accompanied by a significant decrease in alpha-1-acid glycoprotein and haptoglobin in month 1 (p=0.005 and p=0.01, respectively) while in month 5 the levels of both acute phase proteins rose significantly (p=0.003 for alpha-1-acid glycoprotein and p=0.02 for haptoglobin). Cholinesterase and prealbumin significantly increased in month 1 after the treatment (p=0.02 and p=0.0006, respectively), the increase was sustained in cholinesterase while prealbumin levels diminished in month 5. We conclude that the clinical improvement after anti-TNF therapy for CD is accompanied by changes of acute phase proteins and proteosynthetic markers. The assessment of these laboratory markers may be useful in the management of CD patients treated with anti-TNF.
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PMID:Changes in acute phase proteins after anti-tumor necrosis factor antibody (infliximab) treatment in patients with Crohn's disease. 1262 12