Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We thought that nutritional parameters in laboratory data might be able to express quality of life (QOL). Therefore, in 70 patients with malignant chest diseases (NSCLC, 42 patients; SCLC, 15; lung metastasis, 7; others, 6), the correlation between nutritional parameters of total protein (Tp), serum albumin (Alb), and serum (cholinesterase (ChE] and Karnofsky Performance Status scale (KPS) was investigated. Then, in 24 patients with them (NSCLC, 12; SCLC, 6; lung metastasis, 4; others 2), Alb and ChE were compared to the EORTC Core Quality of Life Questionnaire and Lung Cancer-Specific Questionnaire Module (QS). Results were as follows: 1) KPS and nutritional parameters correlated (Tp. r = 0.55, p less than 0.001; Alb, r = 0.60, p less than 0.001, ChE, r = 0.60; p less than 0.001). 2) The cores for Functional Status (FS) and Disease and Treatment-related symptoms (Sym) in QS and parameters of Alb and ChE correlate (FS v.s. Alb, p less than 0.01; Sym v.s. Alb, p less than 0.01; FS v.s. ChE, p less than 0.05; and Sym v.s. ChE, p less than 0.05). Moreover, the scores of Psychological Distress in QS and Alb showed a correlation (p less than 0.05). It is considered that nutrition and part of QOL (KPS and FS + Sym in QS, that is to say, "objective" functional activity and "subjective" functional activity and symptoms) correlate, and that nutritional parameters are useful to evaluate QOL.
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PMID:[Quality of life (QOL) and nutrition]. 202 88

The preoperative serum-protein-status of 91 patients was investigated with a laboratory-screening in order to find out the patients with a malnutrition and consequently with a high risk of postoperative complications. The diagnosis was the basis for the classification in groups. There were no significant differences between values of our patients and normal values of a control group in protein, albumin, prealbumin, transferrin, cholinesterase, alpha-1-antitrypsin and haemopexin. Nutrition parameters are of limited value of preoperative risk-screening in operable lung cancer patients.
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PMID:[Preoperative status of serum proteins in lung surgery patients]. 748 67

The hematopoietic stimulating activity of a human lung cancer cell line, MC-1, was investigated. The protein fraction (MC-1 protein) was prepared from the serum-free culture supernatant of MC-1 cells using hydroxyapatite and concanavalin A-agarose columns. In serum-containing cultures, MC-1 protein stimulated colony formation by megakaryocyte colony-forming units (CFU), erythroid burst-forming units and granulocyte/macrophage (GM) CFU. The stimulating effect was strongest for megakaryocyte CFU. The factor having megakaryocyte colony-stimulating activity was shown to be a protein whose molecular weight was determined to be 23,000 daltons by gel filtration. By various analyses, this protein was shown to be molecularly different from the heretofore-identified cytokines that may affect megakaryocytopoiesis, i.e., interleukin-1 (IL-1), IL-2, IL-3, IL-6, IL-7, IL-11, granulocyte colony-stimulating factor (CSF), macrophage CSF, GM-CSF, leukemia inhibitory factor, stem cell factor and tumor necrosis factor. Under serum-free conditions, MC-1 protein augmented murine megakaryocyte colony formation in the presence of murine IL-3 and increased the acetylcholinesterase activity of purified murine megakaryocytes. It was also shown that MC-1 protein stimulated human megakaryocyte colony formation. It was concluded that MC-1 cells produce a megakaryocyte potentiator which is molecularly different from any heretofore-identified cytokines.
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PMID:A novel megakaryocyte potentiator produced by MC-1 human lung cancer cell line. 829 93

Bronchopulmonary infection affects the prognosis of lung cancer patients. Thus, we investigated the relationship between the prognosis of bronchopulmonary infectious diseases and their causative bacteria isolated by transtracheal aspiration (TTA) in lung cancer patients. In the present study, we determined which factor is more predisposing for the outcome of bronchopulmonary infections, the type of causative bacteria or the host nutritional status. A total of 107 lung cancer patients, which consisted of 105 males and 5 females (mean age 67.3 +/- 8.0), were included in this study. The study was conducted from 1981 to 1994. They were classified into the survival group and the deceased group. Causative agents of infection were compared between these 2 groups. S. pneumoniae, alpha-Streptococcus sp., M. catarrhalis, and Neisseria sp. were predominant in organisms isolated from TTA-specimens of lung cancer patients with bronchopulmonary infections, regardless of prognosis. Nutritional status, as determined by serum levels of cholinesterase, albumin, and cholesterol, was poor in the deceased group than in the survival group. These results indicate that the outcome of bronchopulmonary infections in lung cancer patients are affected mainly by the nutritional status of the host.
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PMID:[Analysis of prognosis of bronchopulmonary infectious disease with lung cancer]. 913 26

Peroxisome proliferator-activated receptor gamma (PPAR-gamma) is a member of the nuclear receptor superfamily of ligand-dependent transcription factors that has been shown to play a major role in adipocyte and monocyte/macrophage differentiation. Recent work has also suggested a role for PPARgamma in cell cycle control and/or differentiation of other cell types including breast and lung cancer cells. Using reverse transcription-PCR, we now show for the first time that human neuroblastoma (nb) cells express PPARbeta and -gamma, but not -alpha. Using the LA-N-5 nb cell line, we have determined that the natural PPARgamma ligand 15-deoxy-delta prostaglandin J2, as well as the synthetic PPARgamma agonist GW1929, can stimulate the differentiation of nb cells, as evidenced by the inhibition of cell proliferation, neurite outgrowth, increased acetylcholinesterase activity, and the reduction of N-myc expression. We have also demonstrated that PPARgamma is expressed in primary nb and, furthermore, that the expression of this receptor correlates with the maturational stage of the nb cells. Taken together, these studies have implicated a role for PPARgamma in peripheral nerve cell biology and suggest that the PPARgamma signaling pathway is involved in the regulation of nb cell growth and differentiation.
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PMID:Novel expression and function of peroxisome proliferator-activated receptor gamma (PPARgamma) in human neuroblastoma cells. 1120 25

A 55-year-old woman with congenital myotonia (Becker type), diagnosed by muscle biopsy and gene examination, underwent a right lower lobectomy assisted with thoracoscopy for lung cancer. After epidural tube replacement at T 9-10, general anesthesia was introduced with propofol 2.5 mg x kg(-1) and fentanyl 2.5 mcg x kg(-1). Vecuronium was administered prudently for muscle relaxation assessed with T 1 response (%) and train-of-four (TOF) ratio (%). T 1 response decreased to 50% 3 min and disappeared 4 min after vecuronium administration. Then she was intubated with a double lumen endobronchial tube. T 1 increased 25% within 27 min and 75% in 40 min. Surgery was uneventful and completed in 180 min. At the end of the operation, there was neither fading of twitch responses nor tetanic responses, and TOF ratio returned to 100%. An acetylcholinesterase inhibitor was not given. She was extubated when normal spontaneous breathing, clear consciousness and adequate pharyngeal reflex were present 25 min after discontinuing propofol. There were no perioperative adverse events including hyperthermia and myoglobinuria related to malignant hyperthermia. In conclusion, we managed the anesthesia for a patient with congenital myotonia (Becker type) with thoracic epidural anesthesia and total intravenous anesthesia. Non-depolarizing muscle relaxant could be used safely at the same dose as that used in non-myotonic patients, and did not cause malignant hyperthermia.
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PMID:[Anesthetic managements of a patient with congenital myotonia (Becker type)]. 1558 85

The possible functional role of voltage-gated Na(+) channel (VGSC) expression in controlling endocytic membrane activity in human small-cell lung cancer (SCLC) cell lines (H69, H209, H510) was studied using uptake of horseradish peroxidase (HRP). The normal human airway epithelial (16HBE14o) cell line was used in a comparative approach. Uptake of HRP was vesicular, strongly temperature-sensitive and suppressed by cytoskeletal poisons (cytochalasin D and colchicine), consistent with endocytosis. Compared with the normal cells, HRP uptake into SCLC cells was kinetically more efficient, resulting in more than four-fold higher uptake under optimized conditions. Importantly, HRP uptake into SCLC cells was inhibited significantly by the specific VGSC blocker tetrodotoxin, as well as lidocaine and phenytoin. These effects were dose-dependent. None of these drugs had any effect on the uptake into the 16HBE14o cells. Uptake of HRP into SCLC cells was reduced by approximately 66% in Na(+)-free medium and was partially ( approximately 30%) dependent on extracellular Ca(2+). The possibility that the endocytic activity in the H510 SCLC cells involved an endogenous cholinergic system was investigated by testing the effects of carbachol (a cholinergic receptor agonist) and eserine (an inhibitor of acetylcholinesterase). Both drugs inhibited HRP uptake, thereby suggesting that basal cholinergic activity occurred. It is concluded that VGSC upregulation could enhance metastatic cell behavior in SCLC by enhancing endocytic membrane activity.
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PMID:Small-cell lung cancer (human): potentiation of endocytic membrane activity by voltage-gated Na(+) channel expression in vitro. 1615 2

The probable involvement of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in cancer and the relevance of cholinergic responses for lung cancer growth prompted us to study whether cholinesterase activity of human lung is altered by malignancy. Surgical pieces of non-small lung carcinomas (NSLC) and their adjacent non-cancerous tissues (ANCT) were analysed for AChE and BChE activities. AChE activity in adenocarcinoma (AC) was 7.80 +/- 5.59 nmol of substrate hydrolysed per min and per mg of protein (mU/mg), the same as in their ANCT (8.83 +/- 4.72 mU/mg; P = 0.823); in large cell carcinoma (LCC), 7.52 +/- 3.32 mU/mg, approximately 50% less than in their ANCT (15.39 +/- 5.66 mU/mg; P = 0.043); and in squamous cell carcinoma (SCC), 1.39 +/- 0.58 mU/mg, 80% less than in ANCT (6.08 +/- 2.88 mU/mg; P = 0.003). BChE activity was 5.85 +/- 3.20 mU/mg in AC and 9.56 +/- 3.38 mU/mg in ANCT (P = 0.022); 2.94 +/- 2.01 mU/mg in LCC and 6.50 +/- 6.63 mU/mg in ANCT (P = 0.068); and 4.49 +/- 2.30 mU/mg in SCC and ANCT 6.56 +/- 4.09 mU/mg (P = 0.026). Abundant AChE dimers and fewer monomers were identified in lung and, although their distribution was unaffected by cancer, the binding with concanavalin A revealed changes in AChE glycosylation between SCC and their ANCT. The fall in BChE activity affected all molecules, with a strong decrease of the amphiphilic tetramers. Western blotting revealed protein bands with the expected mass of the principal AChE subunits, and the deeper intensity of the protein signal in SCC than in healthy lung, in lanes loaded with the same units of AChE activity, supported an augment in the amount of AChE protein/unit of AChE activity in SCC. The increased availability of acetylcholine in neoplastic lung, resulting from the fall of cholinesterase activity, may enhance cholinergic signalling and contribute to tumour progression.
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PMID:Cholinesterase activity of human lung tumours varies according to their histological classification. 1627 77

Previous studies have shown that the cholinergic system plays a pivotal rule in small cell lung cancer (SCLC) cell growth through an autocrine loop that activates the nicotinic cholinergic receptor, which together with the activation of this receptor by nicotine links SCLC evolution with tobacco use. Non-small cell lung cancer (NSCLC) is the most common form of lung cancer and is also linked to tobacco use. Here we describe the presence of molecules of the cholinergic system in NSCLC samples and cell lines and investigate the implications of the cholinergic system in cell growth regulation. Cholino-acetyltransferase (ChAT), vesicular acetylcholine transporter (VAChT) and acetylcholinesterase (AChE) were observed in NSCLC tumor biopsies and in NSCLC cell lines. Polymeric alkylpyridinium salts (poly-APS) are AChE inhibitors isolated from the crude extract of the marine sponge, Reniera sarai. These metabolites were characterized as a mixture of two polymers of 3-octylpyridinium, including 29 and 99 monomeric units. Exposure of normal lung fibroblast and NSCLC cell lines to poly-APS revealed a selective cytotoxicity for cancer cells as compared to the normal fibroblast cell lines. FACS analysis indicated poly-APS induced apoptosis in NSCLC cells but not in normal lymphocytes. Non-toxic doses of poly-APS also potently reduced NSCLC cell-cell adhesion in suspension cultures. The limited toxicity of poly-APS on normal cells was confirmed by injection in the caudal vein of mice. No overt effects on health parameters, such as weight gain and physical behavior, were observed, and histological analysis of major organs did not reveal differences between the treated animals as compared to controls. These data demonstrate that NSCLC cells express cholinergic molecules that may be involved in cell growth regulation and that the cholinesterase inhibitor, poly-APS, shows selective toxicity toward NSCLC cells while having no apparent toxicity towards normal cells and tissue in vitro and in vivo.
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PMID:Marine sponge-derived polymeric alkylpyridinium salts as a novel tumor chemotherapeutic targeting the cholinergic system in lung tumors. 1708 75

In non-neuronal contexts, ACh (acetylcholine) is thought to be involved in the regulation of vital cell functions, such as proliferation, differentiation, apoptosis and cell-cell interaction. In airways, most cells express the non-neuronal cholinergic system, each containing a specific set of components required for synthesis, signal transduction and ACh hydrolysis. The aim of the present study was determine the expression of cholinergic system components in bronchial aspirates from control subjects and patients with lung cancer. We conducted an analysis of cholinergic components in the stored soluble and cellular fraction of bronchial aspirates from non-cancerous patients and patients diagnosed with lung cancer. The results show that the fluid secreted by human lung cells contains enough AChE (acetylcholinesterase) activity to control ACh levels. Thus these findings demonstrate that: (i) AChE activity is significantly lower in aspirates from squamous cell carcinomas; (ii) the molecular distribution of AChE in both bronchial cells and fluids consisted of amphiphilic monomers and dimers; and (iii) choline acetyltransferase, nicotinic receptors and cholinesterases are expressed in cultured human lung cells, as demonstrated by RT-PCR (reverse transcriptase-PCR). It appears that the non-neuronal cholinergic system is involved in lung physiology and lung cancer. The physiological consequences of the presence of non-neuronal ACh will depend on the particular cholinergic signalling network in each cell type. Clarifying the pathophysiological actions of ACh remains an essential task and warrants further investigation.
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PMID:Cancer-associated differences in acetylcholinesterase activity in bronchial aspirates from patients with lung cancer. 1821 Dec 61


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