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)

Paroxysmal nocturnal hemoglobinuria, first described in the late 19th century, is an acquired disorder characterized by hemoglobinemia and hemoglobinuria. The major clinical manifestation of PNH is chronic intravascular hemolysis of various severity. Patients-mostly young adults - may also present with episodes of abdominal or back pain. Common cause of death is thrombosis especially of the hepatic veins. Granulocytopenia and thrombocytopenia may be the initial manifestation of PNH, indicating that the disorder is a primary bone-marrow disease, affecting not only the erythrocytes but also other peripheral blood cells and the haematopoietic stem cell. The course of the disease is variable. Partial complete recovery was described, but also fatal thrombosis. The major phenotypic expression of PNH is an increased susceptibility of the erythrocytes to the lytic action of complement in vitro. The enhanced complement susceptibility is most probably due to membrane defects: two membrane proteins regulating the complement cascade in PNH cells were missing, the decay-accelerating factor, DAF, inhibiting the activation of the lytic complement complex and the C8 binding protein, C8bp, which interferes with the lytic process. Aside from the lack of the complement regulators also other membrane defects have been described (e.g. of acetylcholinesterase or alkaline phosphatase). The proteins as well as DAF and C8bp are linked to the cell membrane via a phosphatidylinositol (PI) anchor, leading to the speculation that the disease results from a deficiency in the post-translational PI anchoring mechanism. The diagnosis of PNH is based on the Hamtest, but will be extended to the quantitation of the above described membrane proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Paroxysmal nocturnal hemoglobinuria]. 218 38

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire x Landrace x Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of treatment of growing swine with aflatoxin and T-2 toxin. 224 Jul 92

Microwave-stimulated enzyme incubations for acetylcholinesterase, 5'-nucleotidase, alkaline phosphatase, lactate dehydrogenase, malate dehydrogenase, succinic dehydrogenase and isocitric dehydrogenase were studied, and compared with incubations in a waterbath. Temperature settings of 37 degrees C and 50 degrees C were used, and the incubation times were varied from 30 seconds to 30 minutes. The desired temperature of the incubation solution was reached in the microwave oven within 1 minute, whilst in the waterbath it took 10 to 25 minutes. The microscopic results for alkaline phosphatase and succinic dehydrogenase at a temperature setting of 50 degrees C were superior in the microwave method for incubation times less than 15 minutes. It is postulated that the increased reaction product of alkaline phosphatase and succinic dehydrogenase is due to a temperature effect, which has to be large enough to be of practical value. For the other enzymes studied, microwave-stimulated incubations were no better than the conventional incubations at corresponding temperatures. For 5'-nucleotidase there were aspecific lead deposits in the microwave method. All enzymes performed at the elevated, unphysiological temperature of 50 degrees C proved to have advantages, except for 5'-nucleotidase, whilst for malate dehydrogenase there was an aspecific reduction of the colour developer at this temperature.
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PMID:Microwave-stimulated brain enzyme incubations are possible at the unphysiological condition of 50 degrees C. 224 28

In 34 patients (16 women and 18 men) with acute leukaemias (8 with acute lymphoblastic leukaemia and 26 with acute myeloblastic leukaemia), as yet untreated, the serum levels were determined of conjugated cholic acid, bilirubin, aspartate aminotransferase (AspAT), alanine aminotransferase (AlAT), alkaline phosphatase (AP), lactate dehydrogenase (LDH) and cholinesterase (Chol). Serum conjugated cholic acid level was determined by radioimmunoassay. The mean values of AP and Chol activity were within the range of normal values in this laboratory, the values of AspAT and AlAT were slightly above this range, and LDH value exceeded twice this normal range. The mean bilirubin concentration was within normal range. The greatest changes were noted in conjugated cholic acid values, the mean value exceeded five times the upper normal range (1.0 mumol/l). In 30 patients (88%) the conjugated cholic acid level in the serum was above 1.0 mumol/l, in the remaining 4 cases it was above the mean value for the control group. No correlation was found between conjugated cholic acid and any of the determined parameters. These results point out that the serum level of conjugated cholic acid may be a valuable parameter for assessment of hepatocellular function in acute leukaemias.
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PMID:[Serum cholic acid levels in patients with acute leukemia]. 225 Dec 7

During an ultra-long-distance race (1000 km in 20 days) the influence of running was examined on the enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), gamma-glutamyl-transferase (GGT), and glutamate dehydrogenase (GLDH) with regard to their release from the liver cells or their induction. Furthermore the liver synthetic capacity was assayed by measuring the enzyme activity of cholinesterase and the concentration of serum albumin during the race. Of the 110 participants, 55 finished the race and only the results of these runners were used in our study. AP increased continuously from day 0 (mean = 102 U/L) to day 19 (mean = 120 U/L). A fivefold increase of AST and a twentyfold increase of CK up to day 3 was followed by a significant decrease towards the end of the race. ALT rose as well up to day 6 from a mean value of 8 U/L to 24 U/L but remained at this level. Surprising was the individual increase of the enzymes GLDH (up to twentyfold) and GGT (up to sixfold) in more than half of the finishers on various days indicating liver cell injuries. The activity of CHE and the concentration of serum albumin decreased during the race, both were significantly correlated.
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PMID:Ultra-long-distance running and the liver. 228 82

Dichlorvos was applied as spray at 1 and 2% concentrations daily for a period of 28 and 21 consecutive days, respectively to buffalo calves. Animals sprayed with 1% dichlorvos displayed mild to moderate clinical signs of toxicosis during the 4th week of exposure. The higher concentration (2%) produced clinical signs of poisoning after 12-16 applications, and was lethal to one of three animals. Daily spraying of dichlorvos at both concentrations inactivated erythrocyte cholinesterase (ChE) (15-21%), plasma ChE (17-20%) and serum carboxylesterase (5-10%) within 3 days. The extent of inhibition of esterases was increased with repeated treatment and maximal inhibition of erythrocyte ChE (80-89%), plasma ChE (81-91%) and serum carboxylesterase (33-54%) with 1 and 2% concentrations was observed on the 28th and 21st day after start of application, respectively. In surviving animals, blood esterases remained inactivated to the extent of 14-65% on the 14th day after the termination of treatment. Dichlorvos at both concentrations significantly (P less than 0.01) elevated the serum levels of aspartate aminotransferase, alanine aminotransferase, acid phosphatase and alkaline phosphatase. The activities of these enzymes in surviving animals recovered to control values within 14 days after the final application of dichlorvos.
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PMID:Effects of repeated topical application of dichlorvos on blood enzymes and its toxicity in buffalo calves (Bubalus bubalis). 236 59

The effect of ultraviolet (uv) light on embryonic development was examined in the ascidian Styela clava. uv irradiation (3.0 x 10(-3) J mm-2) of the entire surface of fertilized eggs during ooplasmic segregation prevented gastrulation, sensory cell induction, and embryonic axis formation. The uv-irradiated embryos completed ooplasmic segregation and cleaved normally, but vegetal blastomeres did not invaginate at the beginning of gastrulation, sensory cells in the larval brain did not develop tyrosinase or melanin pigment, and the larval tail did not develop. Endoderm, epidermis, and muscle cells differentiated in the uv-irradiated embryos, however, as evidenced by expression of endodermal alkaline phosphatase (AP), an epidermal-specific antigen, and alpha-actin, myosin heavy chain, and acetylcholinesterase (AChE) in muscle cells. Higher doses of uv light (6.0-9.0 x 10(-3) J mm-2) suppressed expression of the epidermal antigen and muscle cell markers, whereas the development of endodermal AP was insensitive. Irradiation at various times between fertilization and the 16-cell stage revealed that gastrulation, sensory cell differentiation, and axis formation are sensitive to uv light only during ooplasmic segregation. Irradiation of restricted regions of the zygote during ooplasmic segregation showed that the uv-sensitive components are localized in the vegetal hemisphere. The absorption characteristics of the uv-sensitive components suggest that they are nucleic acids. The results show that uv-sensitive components that specify gastrulation, sensory cell induction, and embryonic axis formation are localized in the vegetal hemisphere of Styela eggs.
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PMID:Ultraviolet irradiation during ooplasmic segregation prevents gastrulation, sensory cell induction, and axis formation in the ascidian embryo. 237 59

The time change of laboratory variables in cirrhosis was studied by analysis of data from 488 patients with cirrhosis included in a controlled clinical trial of long-term prednisone vs. placebo. In the placebo group, a marked regression towards normal was seen within 3 months of entry into the trial (increase in serum albumin, acetylcholinesterase, cholesterol, hemoglobin and decrease in erythrocyte sedimentation rate). The subsequent course did not show a clear pattern, except for a slight increase in serum bilirubin and decrease in albumin. When studied in relation to the time of death in patients dying from a "hepatic" cause, marked increase in bilirubin and decrease in prothrombin index, albumin and cholesterol were seen in the year prior to death with little change before that time. In the prednisone group, a more marked decrease in bilirubin, SGOT, alkaline phosphatase, gamma-globulin, sulfobromophthalein retention, erythrocyte sedimentation rate and increase in leukocytes, prothrombin index and cholesterol were seen during the first 3 months. In relation to time of death from a "hepatic" cause, similar changes were seen as in the placebo group except that alkaline phosphatase increased and cholesterol did not decrease. A beneficial effect of prednisone on survival, as expressed by a previously developed therapeutic index, was associated with decrease in SGOT, alkaline phosphatase and gamma-globulin within the first 3 months. An increase in SGOT during prednisone seemed to be associated with harmful effects of therapy.
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PMID:Changes of laboratory variables with time in cirrhosis: prognostic and therapeutic significance. 241 49

Decay-accelerating factor (DAF) is an integral membrane protein that inhibits amplification of the complement cascade on the cell surface. We and other investigators have shown that DAF is part of a newly characterized family of proteins that are anchored to the cell membrane by phosphatidylinositol (PI). The group includes the variant surface glycoprotein (VSG) of African trypanosomes, the p63 protein of Leishmania, acetylcholinesterase (AChE), alkaline phosphatase, Thy-1, 5'-nucleotidase, and RT6.2--an alloantigen from rat T cells. The structure of the membrane anchor has been best characterized for VSG, but chemical studies of the membrane anchors of AChE and Thy-1 suggest that similar glycolipid moieties anchor these proteins to the cell surface. In the VSG, the membrane anchor consists of an ethanolamine linked covalently to an oligosaccharide and glucosamine; the entire complex is anchored to the cell membrane by PI. Immunologically, this glycolipid defines an epitope, the cross-reacting determinant (CRD), that is only revealed after removal of the diacyl glycerol anchor by a phospholipase C. By Western blotting, we show here that DAF-S (DAF released from the membrane by PI-specific phospholipase C [PIPLC]) also contains CRD. Using a newly developed immunoradiometric assay (IRMA) in which the solid-phase capturing antibody is a monoclonal antibody to DAF and the second antibody is anti-CRD, we have been able to quantitate DAF-S. By IRMA, we show that the reaction between anti-CRD and DAF-S is specific, since the binding is competitively inhibited only by the soluble form of the VSG. These observations further support the concept that the glycolipid anchors of this new family of proteins have similar structures. DAF is also found as a soluble protein in various tissue fluids as well as in Hela cell supernatants. No evidence for the presence of the CRD epitope was found on these proteins, suggesting that these forms of DAF are not released from the surface of cells by endogenous phospholipases.
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PMID:Decay-accelerating factor (DAF) shares a common carbohydrate determinant with the variant surface glycoprotein (VSG) of the African Trypanosoma brucei. 243 27

In patients with paroxysmal nocturnal hemoglobinuria (PNH) the RBCs, neutrophils (PMNs), monocytes, and platelets derived from the abnormal clone are deficient in the complement-regulatory protein decay-accelerating factor (DAF). RBC acetylcholinesterase (AChE) and leukocyte alkaline phosphatase (LAP) activities are also characteristically low. DAF, AChE, and LAP are known to be anchored within cell membranes to glycophospholipid-containing phosphatidylinositol (PI). Because PNH progenitors contain DAF that appears to be lost with maturation, it has been proposed that this disorder results from abnormal tethering of these and possibly other proteins to membrane PI. We were puzzled, therefore, that our two PNH patients consistently had normal LAP levels. Consequently, we studied their isolated PMNs to compare DAF and LAP activities in individual cells. PMNs were separated by flow cytometry into DAF-positive and -negative populations by using rabbit anti-DAF antiserum and fluorescein-conjugated goat antirabbit IgG. In both patients the majority of PMNs were DAF deficient, and these cells contained very little alkaline phosphatase activity. In contrast, the smaller, DAF-positive cell populations were phosphatase replete. This is the first demonstration that abnormalities in DAF and LAP activity occur in the same PNH PMN population and strengthens the hypothesis that defective anchoring of proteins to membrane glycophospholipid underlies the pathophysiology of this disorder.
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PMID:The population of paroxysmal nocturnal hemoglobinuria neutrophils deficient in decay-accelerating factor is also deficient in alkaline phosphatase. 245 46


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