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)

This study was undertaken to examine the influence of hospitalization on the nutritional status of cancer patients. We examined 126 patients consecutively admitted to the Istituto Nazionale Tumori of Milan. At admission, all patients underwent standard evaluations, including actual weight, percentage weight loss, arm circumference, triceps skinfold, serum proteins, serum albumin, total iron binding capacity, cholinesterase and peripheral lymphocytes. Finally, from all patients a 24-h dietary recall was obtained, in order to calculate calorie and protein intake. All the patients underwent another evaluation after 1 week of hospitalization; after 2 weeks only 37 of them were evaluated again, since some were operated, some were treated with radio-chemotherapy, some were discharged or had died. Results showed that after one week of hospitalization some variables were significantly altered, such as arm circumference in male patients, serum proteins, cholinesterase, total iron binding capacity, peripheral lymphocytes, calorie and protein intake. A significant weight loss was seen after 2 weeks. The reduced calorie and protein assumption was correlated with depletion of some of the nutritional variables (body weight, arm circumference in males, total iron binding capacity, serum albumin, cholinesterase, lymphocytes). Our data show that hospitalization plays an important role in deterioration of nutritional status in our patient population, and this problem is generally overlooked by the clinicians primarily involved in the care of cancer patients.
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PMID:Impact of hospitalization on the nutritional status of cancer patients. 366 Apr 76

A study was undertaken to identify the nutritional parameters associated with a high risk of postoperative sepsis. The nutritional status of 162 cancer patients subjected to clean or clean-contaminated elective surgery was preoperatively evaluated according to the following parameters: percentage weight loss, arm circumference, triceps skinfold, arm muscle circumference, creatinine-height index, total serum protein, serum albumin, total iron-binding capacity, cholinesterase, peripheral lymphocytes, complement C3-C4 components, and skin tests. Patients were followed postoperatively according to a precise protocol to classify them as infected or noninfected. Postoperative sepsis was present in 40 patients who had significantly different mean values for four nutritional parameters from those of 114 patients with no complications, ie, total serum protein, 6.60 vs 6.99 g/dl, p = 0.008; serum albumin, 3.39 vs 3.66 g/dl, p = 0.001; total iron-binding capacity 301.32 vs 337.17 mmg/dl, p = 0.006; and cholinesterase, 2389.77 vs 2770.10 mU/ml, p = 0.005. Moreover, the relative risk and the attributable risk for these variables were evaluated and the significance was tested by the chi 2 test. By using multiple logistic analysis it appeared that only total serum protein and total iron-binding capacity gave an independent contribution to the risk of postoperative sepsis, while serum albumin disappeared and cholinesterase became non significant when the contribution of the first two variables was accounted for. It was also possible to identify, in a small number of patients, combinations of two variables that were associated with a very high risk of postoperative sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:"Nutritional" markers as prognostic indicators of postoperative sepsis in cancer patients. 392 22

In recent years nutritional status gained greater attention as a surgical risk factor. This study analyzes the frequency of malnutrition in surgical patients with solid and operable tumors, the relation to the type of tumor and stage of the disease. In addition, the clinical value of the measurements carried out is discussed. The analysis was performed in 100 cancer patients (34 gastric cancer, 56 colorectal cancer, and 10 breast cancer). The nutritional assessment included individual dietary habits, ideal weight/height, triceps skinfold, arm muscle circumference, creatinine-height index, serum protein, albumin, prealbumin, cholinesterase, transferrin, total peripheral lymphocytes, and skin tests. The results were compared with international standards or normal plasma concentrations respectively. Most patients suffered from an alternation of the nutritional parameters indicating malnutrition, mostly Kwashiorkor-Marasmus Mix. Patients with gastrointestinal cancer, especially gastric cancer showed more often a decline of the nutritional status than patients with breast cancer. Malnutrition became more severe with advanced disease. The parameters examined revealed varying significance with respect to the assessment of the nutritional status. Some measurements showed little clinical importance; the reasons are discussed.
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PMID:[Significance of the nutritional status of surgical patients]. 393 Sep 1

Mononuclear cell (MNC) leukemia was identified in 26-month-old F344 rats by splenomegaly, reduced red blood cell counts, and elevated white blood cell counts. Atypical MNC were predominant in spleen and blood with acentric nuclei and red cytoplasmic granules. Pentose shunt, glycolytic, and Krebs cycle enzyme activities were elevated 2- to 11-fold in the enriched MNC fraction (Ficoll-Paque density gradients, 1.077 g/ml) isolated from spleen. A leukemic MNC line was derived from one of the spontaneously leukemic donors and then maintained in vivo by s.c. transfer of 2 X 10(7) spleen cells into 7-8-week-old syngeneic recipients. In these serial transplantation experiments leukemia that was clinically and morphologically indistinguishable from spontaneous leukemia in 104-week-old rats was induced in 22-24-week-old rats. Enhanced enzyme activity in MNC was not essential to maintain the phenotypic expression of Fischer rat leukemia. The pattern of biochemical response in spleen MNC from transplanted cases was the opposite of that previously noted in spontaneously leukemic rats, with 50-70% decreases in the specific activities of pentose shunt enzymes and malate dehydrogenase. Reversal of the expression of these enzymes in MNC may be related to a difference in the growth rate of the tumors or to selective proliferation of the transplanted leukemic cells. In addition acetylcholinesterase activity decreased 35-85% in MNC of spleen and blood. Transplantable MNC from F344 rats provide abundant tumorigenic material with a novel biochemical expression that may be useful in the study of chemotherapeutic intervention.
Cancer Res 1985 Sep
PMID:Comparison of the morphology and enzyme activity of mononuclear cells from Fischer 344 rats with either spontaneous or transplanted leukemia. 402 16

Serum levels of various hydrolytic enzymes in prostatic cancer patients with or without bone metastasis were compared with those in patients with prostatic hypertrophy and in the control subjects. The enzymes tested included 11 aminopeptidases, 2 endopeptidases, dipeptidyl carboxypeptidase, esterase, acetyl cholinesterase, and RNase. Although most of the enzymatic levels tended to be decreased in the cancer patients without bone metastasis, they tended to be increased in those with metastasis as well as in the patients with prostatic hypertrophy. Thus, bone metastasis is an important factor affecting the serum levels of hydrolytic enzymes in cancer patients. Of the enzymes tested, RNase was unique in that its serum levels were significantly increased regardless of the existence of bone metastasis. This enzyme may become a marker of malignancy.
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PMID:Different tendencies of changes in hydrolytic enzyme activities in sera from prostatic cancer patients with or without bone metastasis. 608 28

The regulation of cyclic adenosine 3':5'-monophosphate (cAMP)-binding protein in N-18 neuroblastoma cells in tissue culture was studied by the covalent incorporation of 8-azido-cyclic adenosine 3':5'-[32P]monophosphate, together with the techniques of sodium dodecyl sulfate:polyacrylamide gel electrophoresis and autoradiography. Greater than 95% of the total cAMP binding activity of N-18 neuroblastoma cells was identified as being regulatory subunits of the type I (RI) and type II (RII) species, with RI being the predominant form of the two (RI:RII = 3:1). The specific activity of RI but not of RII increased 3-fold when cells were grown in medium containing 1% rather than 10% fetal calf serum. Under the same conditions, the specific activity of acetylcholinesterase increased 3- to 5-fold. The increase in RI was inversely related to the serum concentration in the medium and was specific for cells at the stationary phase of growth. An increase in intracellular cAMP, concomitant with the increase in RI, was also observed. Morphological examination of stationary-phase neuroblastoma cells maintained in medium containing 1% fetal calf serum suggested the presence of a high proportion of highly-differentiated cells. It is proposed that the regulatory control of RI cAMP-binding protein by serum may involve modulation of intracellular cAMP and that the expression RI may be used as a biochemical index of differentiation in mouse neuroblastoma cells.
Cancer Res 1980 Nov
PMID:Regulation of cyclic adenosine 3':5'-monophosphate-binding protein in N-18 mouse neuroblastoma cells. 625 72

We have demonstrated that incubation of rat liver microsomes with N-hydroxy-2-acetylaminofluorene (N-OH-AAF) leads to formation of a 2-nitrosofluorene-membrane lipid adduct. This adduct exists as a nitroxyl free radical, termed N-O-LAF, in its oxidized state. When microsomes were incubated with the sulfhydryl binding agent, rho-hydroxymercuribenzoate, a larger amount of N-OL-LAF formed. We interpret this as a slowdown in the rate of endogenous chemical reduction of carcinogen-membrane lipid adduct. In this paper we present evidence that N-OH-AAF is deacetylated by a microsomal enzyme to form N-hydroxy-2-aminofluorene and this is then oxidized to 2-nitrosofluorene which adds covalently to membrane lipid double bonds to form N-O-LAF. Various antioxidants, peroxidase inhibitors, and P450 substrates and inhibitors were ineffective in altering the amount of N-O-LAF formed from N-OH-AAF; but two esterase inhibitors, dietyl-rho-nitrophenylphosphate and alpha-toluene-sulfonyl fluoride, prevented N-O-LAF formation. Of the following purified enzymes tested: porcine liver carboxyl esterase, pepsin, chymotrypsin, cathepsin D, ficin, papain, leucine aminopeptidase, Naja naja phospholipase, acetylcholinesterase (type I), trypsin (type I and V) and epoxide hydrase; only carboxyl esterase was effective in deacetylating N-OH-AAF.
Cancer Biochem Biophys 1980
PMID:The deacetylation of N-hydroxy-2-acetylaminofluorene by rat liver microsomes and carboxyl esterase. 626 Mar 32

The expression of a adenosine cyclic 3':5'-monophosphate (cAMP)-binding protein, regulatory subunit of the type I cAMP-dependent protein kinase (Rl), and its functional significance in the differentiation of N-18 mouse neuroblastoma cells were examined. 8-Azidoadenosine cyclic 3':5'-[32P]monophosphate, a photoaffinity-labeling analog of cAMP, and high-resolution sodium dodecyl sulfate-polyacrylamide gel electrophoresis were used to identify and quantitate cAMP-binding proteins in cell extracts. The induction of differentiation of N-18 mouse neuroblastoma cells, initiated either by adding dibutyryl adenosine cyclic 3':5'-monophosphate to the growth medium or by culturing cells in medium supplemented with 1% fetal calf serum, led to a 3-fold increase in the amount of 8-azidoadenosine cyclic 3':5'-[32P]monophosphate incorporated into Rl, when assayed in vitro. This increased incorporation was attributable to an increase in the amount of Rl rather than to an increase in the affinity of Rl for 8-azidoadenosine cyclic 4':5'-[32P]monophosphate. The subunit molecular weight, isoelectric point, and immunoreactivity of Rl were found to be identical to that of the regulatory subunit of the type I cAMP-dependent protein kinase purified from bovine skeletal muscle. The increase in Rl was not accompanied by an increase in the cAMP-dependent protein kinase activity. DEAE-cellulose column chromatography confirmed the induction of Rl as a free cAMP-binding protein in the differentiated neuroblastoma cells. The possibility of a growth-dependent regulation of Rl was also examined. Addition of 2% dimethyl sulfoxide to cultures of N-18 mouse neuroblastoma cells inhibited cell growth without increasing the specific activity of Rl. Dimethyl sulfoxide had no effect on neurite outgrowth or acetylcholinesterase activity, two parameters characteristic of differentiated cells. The fact that the induction of Rl coincided with differentiation of the neuroblastoma cells suggests that the expression of Rl may be used as a biochemical index of differentiation in these cells. The presence of a free cAMP-binding protein, not associated with cAMP-dependent protein kinase in neuroblastoma cells, raises important considerations concerning the action of cAMP in the regulation of growth and differentiation.
Cancer Res 1981 Nov
PMID:Induction of the regulatory subunit of type I adenosine cyclic 3':5'-monophosphate-dependent protein kinase in differentiated N-18 mouse neuroblastoma cells. 627 81

(R, S)-alpha-Fluoromethylornithine (alpha-FMO), a catalytic irreversible inhibitor of ornithine decarboxylase (L-ornithine carboxy-lyase, EC 4.1.1.17), induced the differentiation of N2a mouse neuroblastoma cells. The effect of alpha-FMO was concentration dependent; approximately 50% of the cell population exhibited neurite outgrowth in the presence of 1 mM alpha-FMO, while higher concentrations caused severe growth inhibition and cell death. The effect of 1 mM alpha-FMO on neuroblastoma differentiation was potentiated greatly by 0.1 to 0.2 mM N6,O2'-dibutyryl adenosine cyclic 3':5'-monophosphate (Bt2cAMP) causing more than 90% of the cell population to differentiate morphologically with thick and long processes; 0.1 to 0.2 mM Bt2cAMP, by itself, had no effect on cell growth and did not induce neurite outgrowth. The effect of alpha-FMO, either by itself or in combination with 0.1 to 0.2 mM Bt2cAMP, on the morphological differentiation of mouse neuroblastoma cells was reversed by the addition of exogenous putrescine or spermidine. The morphological differentiation of mouse neuroblastoma cells induced by 1 mM alpha-FMO plus 0.2 mM Bt2cAMP was accompanied by increases of the regulatory subunit of the type I cAMP-binding protein and acetylcholinesterase activity. These results indicate that the modulation of cellular polyamine contents may be important in neuroblastoma cell differentiation.
Cancer Res 1983 Jun
PMID:Effects of inhibitors of ornithine decarboxylase on the differentiation of mouse neuroblastoma cells. 630 69

Changes in the acetylcholinesterase activity, thermal and osmotic stability of erythrocyte membranes of the cancer patients are found as compared with this activity of erythrocyte membranes of donors. No differences were detected in the rate of phosphate anion transfer through the erythrocyte membranes in the examined persons. The data obtained show that the development of malignant tumours is followed by the changes in the structural and functional state of surface components of erythrocyte membranes.
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PMID:[Various structural-functional characteristics of erythrocyte membranes in malignant growths]. 649 57


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