SEARCH · PubMed Health

Results for “ADE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 667 records · Page 37Linked to original sources

PubMed1992

Post-marketing surveillance of probucol (Sinlestal) in Japan.

We surveyed the efficacy and safety of probucol (Sinlestal) in 6,002 patients with hyperlipidemia during the past six years between Oct., 1984 and Sep., 1990. Probucol was usually administered for more than 8 weeks at a dose of 500 mg per day and effects on serum lipids and adverse drug events (ADEs) were investigated. Total cholesterol (TC), triglycerides (TG) and HDL cholesterol (HDL) significantly decreased by 16-20%, 6-9% and 15-20% respectively. Further, LDL cholesterol (LDL) decreased by 15-19%. ADEs were reported in 2.7% (161/6,002 subjects), but severity was mild or moderate. In addition to survey in 6,002 patients, the effect on regression of xanthomas and safety in long-term administration of over one year was investigated in 44 and 142 patients, respectively. Regression of xanthoma was observed in 63.6% (28/44 subjects). Probucol was well tolerated in long-term administration. These PMS results showed probucol to possess good therapeutic efficacy and safety.

Adult↗

PubMed2005

FDG PET and CT in locally advanced adenocarcinomas of the distal oesophagus. Clinical relevance of a discordant PET finding.

AIM: The incidence of adenocarcinomas of the distal oesophagus (ADE) has dramatically increased in Western countries. The clinical importance of a FDG PET finding discordant with CT was determined in patients with locally advanced ADE. In addition, tumour standardized uptake values (SUV) were correlated with patient survival. PATIENTS, METHODS: 40 consecutive patients were analyzed retrospectively. All patients underwent an attenuation corrected FDG PET scan (neck, chest, abdomen) and contrast enhanced helical CT of the chest and abdomen. PET and CT scans were reviewed independently and concomitantly with respect to metastases in predefined lymph node sites and organs. Any discordance between PET and CT was assessed for clinical relevance. Clinical relevance was defined as a change in the overall therapeutic concept (curative vs. palliative). Follow-up imaging and histological evaluation served as the gold standard. Mean tumour SUVs were determined by 1.5 cm regions of interest placed over the tumour's maximum. RESULTS: When read independently from the CT scan FDG PET indicated a clinically relevant change in tumour stage in 9/40 patients (23%) and a non-relevant change in 11/40 patients (28%). PET was correct in 5/9 patients (56%) with clinically relevant discordances. In 4/9 patients PET was incorrect (3 false positive due to suspicion of M1-lymph nodes or lung metastases, 1 false negative in disseminated liver metastases). With concomitant reading, PET indicated a clinically relevant change in tumour stage in 6/40 patients (15%) and a non-relevant change in 5/40 patients (13%). PET was correct in 5/6 patients (83%) with clinically relevant discordances. The patient with disseminated liver disease remained the single false negative. Overall, the benefit from PET was based on its higher diagnostic accuracy at organ sites. Tumour SUV did not correlate with patient survival. CONCLUSION: About half of discordances between FDG PET and CT are clinically relevant. Concomitant reading of PET and CT is advisable as it reduces the overall rate of discordances and enhances the accuracy of PET in clinical relevant discordances (from 56% to 83%).

Adenocarcinoma↗

PubMed2005

Effect of bar-code technology on the incidence of medication dispensing errors and potential adverse drug events in a hospital pharmacy.

We performed a direct observation prepost study to evaluate the impact of barcode technology on medication dispensing errors and potential adverse drug events in the pharmacy of a tertiary-academic medical center. We found that barcode technology significantly reduced the rate of target dispensing errors leaving the pharmacy by 85%, from 0.37% to 0.06%. The rate of potential adverse drug events (ADEs) due to dispensing errors was also significantly reduced by 63%, from 0.19%to 0.069%. In a 735-bed hospital where 6 million doses of medications are dispensed per year, this technology is expected to prevent about 13,000 dispensing errors and 6,000 potential ADEs per year.

Clinical Pharmacy Information Systems↗

PubMed2006

Recent study lauds automated surveillance.

ADEs detected at a rate 3.6 times that of voluntary reporting at a university hospital and 12.3 times that at a community hospital. Goal of system is not just to detect ADEs, but to measure whether they are being reduced. Automated surveillance is much less costly than computerized physicians order entry.

Adverse Drug Reaction Reporting Systems↗

PubMed2006

[Mechanism of carbachol and adenosine action on spontaneous quantal mediator release at frog neuromuscular junction].

Experiments on the frog sartorius muscle showed that nonhydrolisable acetylcholine analog carbachol (CCh) depresses spontaneous quantal mediator release via muscarinic M2 receptors of nerve ending. Adenosine (Ade) acting via inhibitory A1 receptors is another strong spontaneous quantal release modulator. Inhibition of pertussis toxin (PTx)-sensitive G-proteins only partly eliminated CCh and Ade depressive action. It means metabotropic A1 and M2 receptors of the frog nerve ending regulate spontaneous quantal release via activating of both PTx-sensitive and PTx-insensitive inhibitory mechanisms.

Adenosine↗

PubMed1991

Antibody-dependent enhancement and neutralization pattern of sera from SIV-infected or HIV-2-vaccinated rhesus monkeys.

Neutralizing and enhancing activities in sera were detected by using an in vitro infection assay of HUT78 cells. Ten animals were vaccinated with HIV-2ROD recombinant vaccinia viruses and respective purified proteins. Only sera from monkeys vaccinated with env elicited neutralizing antibodies. No antibody-dependent enhancement (ADE) properties were detected in all the tested sera. Six other macaques were infected with SIV-mac251. All of them had detectable ADE properties in their sera. No major neutralizing activity was detected.

AIDS Vaccines↗

PubMed1990

Pathogenesis of dengue: an alternative hypothesis.

This paper presents a novel but entirely hypothetical concept on the pathogenesis of the shock syndrome (DSS) associated with dengue hemorrhagic fever (DHF). Antibody-dependent enhancement (ADE) is widely thought to be central to the development of these clinical entities. Current views on the mechanisms underlying ADE centre on two major lines of thought: 1) Non-neutralizing antibodies to dengue virus (DV) can enhance viral uptake and replication in target cells (monocytes). 2) DHF/DSS are the consequences of enhanced viral replication, paired with immunopathological processes that are evoked by monocyte dysfunction and detrimental reactions caused by activated T-lymphocytes. The present hypothesis proposes, by contrast, a central role for the following processes: 1) Secondary infection of an individual who has sub or non-neutralizing antibody titers against DV leads to a booster antibody response and a steep rise in antibody levels. 2) Antibodies against DV bind to and direct a selective attack of the complement system onto cells expressing viral antigens on their surface. DHF/DSS are the direct and indirect consequences of complement activation on these cells. The advanced hypothesis, which departs from the mainstream of "immune enhancement" concepts, can easily be tested by experimentation.

Antigens, Viral↗

PubMed1986

Thiopental and epinephrine-induced dysrhythmias in dogs anesthetized with enflurane or isoflurane.

Epinephrine-induced dysrhythmias were studied in 19 dogs anesthetized with 1.25 MAC enflurane or isoflurane, or the same preceded by thiopental (20 mg/kg). In 11 (group 1) dogs, thiopental reduced the dose of epinephrine required for production of ventricular ectopy, bigeminy and tachycardia with enflurane, and only ventricular tachycardia with isoflurane (P less than 0.05). Thiopental potentiation of epinephrine-induced dysrhythmias with enflurane lasted 4 hr after induction. In eight (group 2) dogs, the arrhythmic dose (ADE in microgram/ml) and plasma level of epinephrine (PLE in ng/ml) for four or more ventricular extrasystoles in 15 sec were determined in the same animal under each of the four test conditions. ADE and PLE values (X +/- SEM) were, respectively, enflurane, 9.1 +/- 1.0 and 141 +/- 24 (8/8 dogs); enflurane-thiopental, 5.0 +/- 0.6 and 63 +/- 16 (8/8 dogs); isoflurane, 28.3 and 330 (1/7 dogs); and isoflurane-thiopental, 15.2 +/- 2.8 and 265 +/- 59 (5/7 dogs). In addition, thiopental had no effect on plasma epinephrine levels reached during epinephrine infusions with 1.0 (enflurane only), 2.0 (enflurane, isoflurane) and 4.0 micrograms X kg-1 X min-1 (isoflurane only). Nor were epinephrine levels reached during enflurane or enflurane-thiopental different from those reached during isoflurane or isoflurane-thiopental. It is concluded that thiopental potentiates several types of epinephrine-induced ventricular dysrhythmias with enflurane, but only ventricular tachycardia with isoflurane. Furthermore, isoflurane or isoflurane-thiopental were less sensitizing than enflurane or enflurane-thiopental. Finally, neither thiopental nor the anesthetic agents affected plasma epinephrine levels reached during epinephrine infusions lasting 3 min.

Animals↗

PubMed1987

["Illegal" transformation of red adenine-dependent mutants of the yeast Pichia pinus by the pYE(ADE2)2 plasmid].

The red adenine-dependent mutants ade1 of the yeast Pichia pinus blocked in the VI step of adenine biosynthesis (lack of AIR-carboxylase) and ade2 mutants blocked in the VII step of adenine biosynthesis (lack of SAIKAR-synthase) were transformed with the plasmid pYE(ADE2)2 containing ADE2 gene of Saccharomyces cerevisiae encoding AIR-carboxylase. The appearance of white Ade+ clones with the frequency 2-7.10(-8) (which is ten-fold higher than reversion frequency) was only observed in the case of ade2 transformation. Genetic analysis points to connection of the "illegitimate" transformants' appearance with the change in the mutant ade2 locus or in a locus closely linked to the former. Ade+ phenotype was stable during 20 generations of mitotic budding. Southern blotting assay of transformant chromosomal DNA indicates that reconstitution of ade2 defective gene is related with its "correction", owing to integration of pYE(ADE2)2 sequence in the vicinity of the mutant locus.

Adenine↗

PubMed1987

Effect of vitamins on Trichinella pseudospiralis Garkavi, 1972 infection in mice.

The effects of vitamins A, B complex, E, and ADE on the eosinophilia, body weight, number of obtained larvae and distribution of larvae of Trichinella pseudospiralis were examined in mice. The increased eosinophilia started to appear in the majority of infected mice from day 7 p.i., the maximum being around day 21 p.i. The highest values of eosinophilia were observed in the mice after application of vitamin B complex. In spite of considerable individual differences, the greatest decrease in body weight occurred in mice receiving vitamins E and B complex. The greatest numbers of larvae were obtained from mice receiving vitamins E and B complex, which is proportional to the increase in eosinophilia. The numbers of muscle larvae in untreated mice and in those receiving vitamins ADE were approximately the same. The lowest numbers of larvae occurred in mice receiving vitamin A. In all mice groups the greatest numbers of larvae were localized in the left foreleg and diaphragm.

Animals↗

PubMed1988

Effect of vitamins on Trichinella spiralis Owen, 1835 infection in mice.

The effects of vitamins A, B complex, E, and ADE on the body weight, eosinophilia, intensity of infection and distribution of T. spiralis larvae were studied in mice. The greatest loss of weight followed after the application of vitamins B complex and E. An increased eosinophilia appeared in the majority of infected mice since day 7 p.i., reaching the maximum on day 21 p.i. In mice receiving vitamins B complex, A, and ADE, the increased eosinophilia was observed still on day 60 p.i. The highest levels of eosinophilia occurred after the application of vitamins B complex and E, which was directly proportional to the intensity of infection. The lowest intensity of infection was recorded in mice receiving vitamin A. Though there were great differences between individual mice, the greatest number of larvae were localized in the diaphragm and left masseter.

Animals↗

PubMed1988

[Identification of mutations in the asporogenic yeast Candida tropicalis using intrageneric fusion of protoplasts].

The possibility of genetic identification of mutations in asporogenic yeast by the technique of intrageneric fusion of yeast protoplasts of Candida tropicals and Saccharomyces cerevisiae has been demonstrated for Candida tropicals strains G5-9 (Ade- Leu-) and G32-4 (Leu-). The mutations to auxotrophy ade- in the strain G5-9 and leu- in G32-4 of Candida tropicals are allelic to ade2 and leu1 mutations in the genes of Saccharomyces cerevisiae yeast. The allelic character of adenine auxotrophy mutation in Candida tropicals and ade2 mutation in Saccharomyces cerevisiae is confirmed by the absence of AIR-carboxylase activity in cellular extract from the strain G5-9.

Alleles↗

PubMed1988

Localization of denatured enzyme molecules in rat lenses.

Immunohistochemical localization of altered enzyme molecules was detected by the use of antibodies to denatured enzymes (ADE) conjugated with fluorescein. Denatured aldolase, glucose 6-phosphate dehydrogenase and superoxide dismutase are mostly located in the subcortical region and in the nucleus of the rat lens. In the nuclear fibres the enzyme is located near the membrane of the fibres. This study provides additional evidence that altered enzyme molecules accumulate in the lens, and indicates their exact localization. ADE antibody can distinguish between inactive enzyme molecules and active ones, using immunohistochemical techniques.

Animals↗

PubMed1987

[Saccharomyces cerevisiae mutants characterized by increased induced mutagenesis. II. Genetic analysis of mutants].

Induction of forward adenine-dependent (Ade+----Ade-) mutations by HAP was used to analyse genetically yeast mutants with enhanced induced mutagenesis. Three mutations studied in detail segregated as a single mendelian trait and composed independent complementation groups (HIM1, HIM2, HIM3). the him1-1 mutation was centromere-linked, the him3-1 and him2-1 mutations being not. All three mutations did not show any cross-linkage. Uracil-DNA glycosylase activity was determined in crude cell extract from wild type strain and him mutants; no detectable differences were observed.

Adenine↗

PubMed1985

Inhibition of macrophage phagocytosis by methylation inhibitors. Lack of correlation of protein carboxymethylation and phospholipid methylation with phagocytosis.

Adenosine (Ado), deoxyadenosine (dAdo), and adenine arabinoside (AraA) inhibit the phagocytosis of IgG-coated erythrocytes and zymosan by resident and thioglycollate-elicited macrophages (thio-macrophages) in a dose-dependent and reversible manner. 3-Deazaadenosine (3cAdo) and adenine (Ade) also inhibit the phagocytosis by resident macrophages. Homocysteine thiolactonate (Hcy) potentiates the inhibition by Ado and 3cAdo while erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) potentiates the inhibition by Ado, dAdo and AraA. This inhibition has a very rapid onset and the drugs do not interfere with the binding of IgG-coated erythrocytes to macrophages. The combination of Ado, Hcy and EHNA does not appreciably affect the intracellular level of ATP and S-adenosyl-L-methionine (AdoMet) in thio-macrophages but causes accumulations of Ado and S-adenosyl-L-homocysteine (AdoHcy) up to 135 and 145 nmol/mg of protein, respectively. During phagocytosis reversal, Ado is metabolized within 15 min while AdoHcy decreases log-arithmically with a half-life of 50 min. Carboxymethylation and phospholipid methylation, however, resume about 60-90 min after phagocytosis has recovered, and thus cannot function as transmembrane signals for phagocytosis. Other evidence showing the lack of correlation between phagocytosis and carboxymethylation inhibition include 1) Ado + Hcy inhibit carboxymethylation much better than Ado + EHNA (91 versus 75%) in thio-macrophage, but the two combinations show comparable phagocytosis inhibition potency; 2) Ado + Hcy inhibit carboxymethylation almost as well as Ado + Hcy + EHNA, but the latter is a much more effective drug combination for phagocytosis inhibition; 3) Ade and 3cAdo, although inhibiting resident macrophage phagocytosis as well as Ado + EHNA + Hcy, are much weaker carboxymethylation inhibitors; 4) dAdo and AraA potently inhibit phagocytosis but not carboxymethylation. The difference in the apparent methylation levels is not due to changes in the specific activities of AdoMet, which decrease with a half-life of 88 min. Interestingly, after the initial lag phase of about 90 min after the initiation of inhibition reversal, carboxymethylation and phagocytosis increase in parallel. In a log-log plot of carboxymethylation, phospholipid methylation, or phagocytosis versus the intracellular AdoHcy accumulation, a linear relationship is obtained. It is possible that AdoHcy accumulation is responsible for phagocytosis inhibition but inhibits by a mechanism other than interfering with protein and lipid methylations.

Adenine↗

PubMed1983

Chromosomal gene controlling symbiotic nitrogen fixation in Rhizobium meliloti L5-30.

Auxotrophic Rhizobium meliloti strain RM 246 carries two independent mutations: in the biosynthesis of cysteine (cys) and symbiotic nitrogen fixation process (fix). These two mutations were mapped by transduction between his-240 and ade-4 markers. Cotransduction frequencies show the following order of genes: his-240 fix-1 cys-246 ade-4.

Chromosome Mapping↗

PubMed1983

[Translocation of transposons Tn10 and Tn5 in the Yersinia pestis chromosome].

The possibility of translocation of the transposons Tn5 and Tn10 into the genome of Yersinia pestis, with the subsequent mutagenic effect was demonstrated. We revealed transposon harbouring clones at frequency 10(-4) to 10(-2). Derivatives of P1cml clr100ts phage served as vectors. Insertion of Tn10 transposon induced mutations in ilv, ser, arg, pur, pro, leu, nic, tyr, gua genes. The number of the insertion sites on the chromosome obtained for Tn5 was the same, these being arg, ade, pyr, leu, gua, trp, his, pan, ilv. The majority of auxotrophs did not revert. Occasionally, revertants were observed at frequencies 10(-8) to 10(-6). Unlike Escherichia coli, reversion was not accompanied by the loss of transposons. The rearrangements induced by transposons, presumably, near the insertion site, as well as duplications of transposons followed by incorporation of copies into novel sites, led to the appearance of additional defective genes, which made it possible to select various types of polyauxotrophs. Based on reiteration of coinciding double and triple mutant markers, we proposed a linkage group of genes within a segment of Y. pestis chromosome: lys ... tyr - ser - arg - ilv - leu - gua - ade(pur) - pro ... his ... pyr ... trp. The reasons for peculiarities of the behaviour of transposons in Y. pestis bacteria are discussed.

Chromosome Mapping↗

PubMed1984

Halothane-epinephrine arrhythmias and adrenergic responsiveness after chronic imipramine administration in dogs.

The incidence of halothane-epinephrine arrhythmias increases after the short-term administration of imipramine, probably because of enhanced noradrenergic transmission. To determine whether this effect persists after long-term imipramine treatment, we have studied the arrhythmogenicity and adrenergic responsiveness in halothane anesthetized dogs after six weeks of imipramine administration, 150 mg X day-1, orally. The mean (+/- SD) arrhythmogenic dose of epinephrine (ADE) in nine dogs anesthetized with 1.2 MAC halothane was 2.57 (+/- 1.04) micrograms X kg-1 X min-1. The alpha-adrenergic responsiveness, assessed as the dose of phenylephrine that caused a 75% increase in mean arterial pressure (alpha 75), was 5.78 +/- 2.39 micrograms X kg-1 X min-1. The dose of isoproterenol that increased heart rate by 75% (beta 75) was 309 +/- 180 ng X kg-1 X min-1. After imipramine treatment, the ADE (2.63 +/- 1.26), alpha 75 (5.16 +/- 2.05), and beta 75 (386 +/- 266) were not statistically different from the pre-imipramine values (P greater than 0.05), despite a fivefold increase in circulating norepinephrine. We conclude that chronic imipramine does not alter arrhythmogenicity and adrenergic responsiveness, since compensatory mechanisms, at the sympathetic nerve terminal, may revert the initial hyper-responsiveness to normal.

Anesthesia↗