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 739 records · Page 41Linked to original sources

PubMed2002

[Quality management in health care: error prevention and managing errors in medicine].

BACKGROUND: About 3.7% of in-house-treated patients in Switzerland, the USA and Australia are victims of treatment-related health problems which probably are related to avoidable "adverse events" in more than 50% of the occurrences. Reasons are primarily systematic incidents, e.g., organizational deficiencies in the health system and only secondarly individual mistakes. As there are no systematic studies available, it is not proven if those figures can be transferred to the German Health Care System. Here, experts anticipate up to 12.000 proven treatment errors per year. PREVENTION OF AND DEALING WITH ADVERSE EVENTS: Dedicated programs for identification and prevention of adverse events should be implemented--besides systematic quality improvement--to improve professional handling and prevention of adverse events. This consists of a) assessment of the existing problem using existing data bases and/or implementation of mandatory documentation and information routines as well as reporting systems, b) development of sanction-free reporting routines within the legal framework, c) dissemination of behavior-oriented training systems for recognition and prevention of adverse events as well as incentives for the participation in such training systems, d) implementation of automatic routines for prevention of adverse events (e.g., computer-based monitoring of ADE or computer-based reminder systems based on clinical guidelines).

Forecasting↗

PubMed2005

Phylogenetic analysis reveals a novel protein family closely related to adenosine deaminase.

Adenosine deaminase (ADA) is a well-characterized enzyme involved in the depletion of adenosine levels. A group of proteins with similarity to ADA, the adenosine deaminase-related growth factors (ADGF; known as CECR1 in vertebrates), has been described recently in various organisms. We have determined the phylogenetic relationships of various gene products with significant amino acid similarity to ADA using parsimony and Bayesian methods, and discovered a novel paralogue, termed ADA-like (ADAL). The ADGF proteins share a novel amino acid motif, "MPKG," within which the proline and lysine residues are also conserved in the ADAL and ADA subfamilies. The significance of this new domain is unknown, but it is located just upstream of two ADA catalytic residues, of which all eight are conserved among the ADGF and ADAL proteins. This conservation suggests that ADGF and ADAL may share the same catalytic function as ADA, which has been proven for some ADGF members. These analyses also revealed that some genes previously thought to be classic ADAs are instead ADAL or ADGFs. We here define the ADGF, ADAL, ADA, adenine deaminase (ADE), and AMP deaminase (AMPD) groups as subfamilies of the adenyl-deaminase family. The availability of genomic data for the members of this family allowed us to reconstruct the intron evolution within the phylogeny and strengthen the introns-late hypothesis of the synthetic introns theory. This study shows that ADA activity is clearly more complex than once thought, perhaps involving a delicately balanced pattern of temporal and spatial expression of a number of paralogous proteins.

Adenosine Deaminase↗

PubMed1997

Truncated-gene reporter system for studying the regulation of manganese peroxidase expression.

The expression of manganese peroxidase (MnP) in nitrogen-limited cultures of Phanerochaete chrysosporium is regulated by Mn, heat shock (HS), and H2O2 at the level of gene transcription. We have constructed a homologous gene reporter system to further examine the regulation of two mnp genes, mnp1 and mnp2, encoding individual MnP isozymes. Internal deletions of 234 and 359 bp were made within the coding regions of the mnp1 and mnp2 genes, respectively. The truncated mnp genes were subcloned into the shuttle vector pOGI18, which includes the Schizophylum commune ade5 gene as a selectable marker, and transformed into a P. chrysosporium Ade1 auxotrophic mutant. Northern-blot analysis of purified Ade+ transformants demonstrated that both of the truncated mnp genes were regulated in a manner similar to the endogenous mnp genes with respect to nitrogen limitation and induction by Mn, HS, and H2O2.

Basidiomycota↗

PubMed2006

Likelihood ratio tests in behavioral genetics: problems and solutions.

The likelihood ratio test of nested models for family data plays an important role in the assessment of genetic and environmental influences on the variation in traits. The test is routinely based on the assumption that the test statistic follows a chi-square distribution under the null, with the number of restricted parameters as degrees of freedom. However, tests of variance components constrained to be non-negative correspond to tests of parameters on the boundary of the parameter space. In this situation the standard test procedure provides too large p-values and the use of the Akaike Information Criterion (AIC) or the Bayesian Information Criterion (BIC) for model selection is problematic. Focusing on the classical ACE twin model for univariate traits, we adapt existing theory to show that the asymptotic distribution for the likelihood ratio statistic is a mixture of chi-square distributions, and we derive the mixing probabilities. We conclude that when testing the AE or the CE model against the ACE model, the p-values obtained from using the chi(2)(1 df) as the reference distribution should be halved. When the E model is tested against the ACE model, a mixture of chi(2)(0 df), chi(2)(1 df) and chi(2)(2 df) should be used as the reference distribution, and we provide a simple formula to compute the mixing probabilities. Similar results for tests of the AE, DE and E models against the ADE model are also derived. Failing to use the appropriate reference distribution can lead to invalid conclusions.

Analysis of Variance↗

PubMed1991

Heme regulates hepatic 5-aminolevulinate synthase mRNA expression by decreasing mRNA half-life and not by altering its rate of transcription.

Hepatic 5-aminolevulinate (ALA) synthase, the first and rate-limiting enzyme in the heme biosynthetic pathway, is known to be feedback repressed by the end product of the pathway, heme. We investigated whether heme regulates ALA synthase mRNA expression transcriptionally or post-transcriptionally in primary cultures of chick embryo hepatocytes. 2-Propyl-2-isopropylacetamide increased the rate of transcription of the ALA synthase gene, whereas heme or an inhibitor of heme biosynthesis, desferrioximine, had no effect on the drug-induced transcription rate. Heme decreased the half-life of ALA synthase mRNA from approximately 3.5 h to 1.2 as recently reported by Drew and Ades (1989, Biochem. Biophys. Res. Commun. 162, 102-107). We also found that the heme-mediated decrease in mRNA stability was prevented by cycloheximide treatment, suggesting that the heme effect was mediated by a labile protein. These results support a model for hepatic ALA synthase regulation in which inducing drugs directly stimulate ALA synthase gene transcription, whereas heme regulates ALA synthase expression post-transcriptionally by modulating mRNA stability as well as by blocking translocation of ALA synthase enzyme into the mitochondrion.

5-Aminolevulinate Synthetase↗

PubMed1992

Effects of nerve growth factor on cortical and striatal acetylcholine and dopamine release in rats with cortical devascularizing lesions.

The effects of intraventricular nerve growth factor (NGF) or saline treatments on extracellular acetylcholine (ACh), dopamine (DA) and adenosine (Ade) levels in the cortex and striatum of rats with unilateral devascularizing cortical lesions were studied in vivo with microdialysis. The devascularizing cortical lesion produced a decrease in extracellular ACh levels in both cortex and striatum as compared to those in normal rats, while the NGF treatment produced a significant increase in ACh levels in both regions. NGF could even increase cortical ACh levels in normal rats. The cortical lesion produced a decrease in extracellular DA in the cortex, while the NGF treatment appeared to reverse this effect. No significant changes in DA were observed in the striatum. The present study gives evidence that a unilateral cortical devascularizing lesion leads to changes in extracellular ACh and DA levels in cortex and striatum and that these changes could be reversed with intraventricular NGF treatment.

Acetylcholine↗

PubMed1988

Reactions of propylene oxide with 2'-deoxynucleosides and in vitro with calf thymus DNA.

Propylene oxide (PO) is a direct-acting mutagen and rodent carcinogen. We have studied how PO modifies 2'-deoxynucleosides at pH 7.0-7.5 and 37 degrees C for 10 h. PO reacts as an SN2 alkylating agent by forming the following 2-hydroxypropyl (HP) adducts: N6-HP-dAdo (7% yield), 7-HP-Gua (37%) and 3-HP-dThd (4%). Alkylation at N-3 of dCyd resulted in conversion of the adjacent exocyclic imino group at C-4 to an oxygen (hydrolytic deamination) with the formation of a dUrd adduct, 3-HP-dUrd (14%). Ultraviolet spectroscopy and mass spectrometry were used for the structural determination of these adducts. Confirmation of the unexpected 3-HP-dUrd adduct was provided by an accurate mass measurement technique where diagnostic ions in the mass spectra of 3-HP-dUrd were measured to within 0.0005 atomic mass units of the predicted mass. PO was reacted in vitro with calf thymus DNA (pH 7.0-7.5, 37 degrees C, 10 h) and yielded N6-HP-dAdo (1 nmol/mg DNA), 3-HP-Ade (14 nmol/mg DNA), 7-HP-Gua (133 nmol/mg DNA) and 3-HP-dUrd (13 nmol/mg DNA). A mechanism for the hydrolytic deamination of 3-HP-dCyd to 3-HP-dUrd involving the OH on the HP side chain is proposed. This cytosine to uracil conversion may play a role in the mutagenic and carcinogenic activity of this epoxide.

Chemical Phenomena↗

PubMed1984

Arachidonic acid, 12- and 15-hydroxyeicosatetraenoic acids, eicosapentaenoic acid, and phospholipase A2 induce starfish oocyte maturation.

In starfish oocyte maturation (meiosis reinitiation) is induced by the natural hormone 1-methyladenine (1-Me-Ade). This paper shows that arachidonic acid (AA) induces oocyte maturation at concentrations above 0.5 microM. This maturation shares many characteristics with 1-MeAde-induced maturation: same kinetics, same required contact time, same stimulations of protein phosphorylation and sodium influx. Although calcium facilitates the AA-induced but not the 1-MeAde-induced maturation, AA, like 1-MeAde, does not stimulate the uptake of calcium. Calcium does not facilitate the uptake of AA by oocytes. Out of 36 different fatty acids (saturated and unsaturated), only eicosatetraenoic (AA) and eicosapentaenoic acids were found to mimic 1-MeAde. Calcium-dependent phospholipases A2 from bee venom and Naja venom also induce maturation (0.1-1 unit/ml) when added externally to the oocytes. Phospholipase A2 inhibitors (quinacrine, bromophenacylbromide) block maturation; inhibition is reversed by increasing the 1-MeAde concentration and only occurs during the hormone-dependent period. AA is usually metabolized through oxidation by cyclooxygenase or lipoxygenase. Cyclooxygenase inhibitors (acetylsalicylic acid, indomethacin, tolazoline) do not block maturation; prostaglandins E2, D2, F2 alpha, I2, and thromboxane B2 do not induce meiosis reinitiation. On the other hand, lipoxygenase inhibitors (quercetin, butylated hydroxytoluene, and eicosatetraynoic acid) block 1-MeAde-induced maturation; although leukotrienes (A4, B4, C4, D4, E4) have no effects on oocytes, two other lipoxygenase products, 12- and 15-hydroxyeicosatetraenoic acids (and their corresponding hydroperoxy-) induce oocyte maturation (around 1 microM). The possible mode of action of the fatty acids inducing oocyte maturation is discussed.

Animals↗

PubMed1986

Protein phosphorylation and oocyte maturation. II. Inhibition of starfish oocyte maturation by intracellular microinjection of protein phosphatases 1 and 2A and alkaline phosphatase.

Oocyte maturation (meiosis re-initiation) in starfish is induced by the natural hormone 1-methyladenine (1-MeAde). Following hormonal stimulation of the oocyte, an intracellular Maturation Promoting Factor (MPF) appears in the cytoplasm which triggers nuclear envelope breakdown and maturation divisions. Microinjection of pure preparations of the catalytic subunits of protein phosphatases 1 and 2A inhibits 1-MeAde-induced maturation in a dose-dependent manner. Calmodulin-dependent protein phosphatase 2B is inefficient. Maturation induced by mimetics of 1-MeAde, such as dithiothreitol (DTT), methylglyoxal-bis(guanylhydrazone) (MGBG), 8-hydroxyeicosatetraenoic acid (8 HETE) and arachidonic acid (AA) is also inhibited by these protein phosphatases. In all cases inhibition can be reversed by increasing the concentration of 1-Me-Ade or of mimetic. Alkaline phosphatase also inhibits maturation in a dose-dependent way and in a reversible manner. Microinjection of protein phosphatase is still effective when preformed long after the end of the hormone-dependent period, and can even be effective a few minutes before the breakdown of the nuclear envelope. No detectable MPF activity is found in 1-MeAde-treated phosphatase-injected oocytes. However, microinjection of phosphatase 2A simultaneously with MPF (obtained from 1-MeAde-treated donors) does not result in inhibition. These results constitute direct evidence for the necessity of an elevated level of phosphorylated proteins for MPF activity and maturation. The mode of action of 1-MeAde in inducing starfish oocyte maturation is discussed in relation to protein phosphorylation.

Adenine↗

PubMed1986

The endocrine control of reproduction and molt in male and female emperor (Aptenodytes forsteri) and adelie (Pygoscelis adeliae) penguins. I. Annual changes in plasma levels of gonadal steroids and LH.

Changes in plasma LH, testosterone, and estrogens were investigated throughout reproduction and molt in free-living male and female emperor (Aptenodytes forsteri) and adelie (Pygoscelis adeliae) penguins. In both sexes and species, plasma LH and gonadal steroids were severalfold above basal level at the time of arrival on the breeding grounds, suggesting that environmental cues (especially decreasing daylength in emperors) rather than mating and courting primarily stimulate gonadal development and reproduction. In both species a marked increase in plasma LH (both sexes), testosterone (males), and estrogens (females) corresponded with the time of maximum gonadal size, and peak values were obtained at the time of copulation, i.e., in emperors about 10-15 days prior to egg laying. In females, plasma LH and estrogens dropped to low levels between copulation and egg laying. Similarly, following copulation in males plasma testosterone fell to lower levels that in emperors were maintained during incubation and brooding of the non-thermally emancipated chick. Plasma LH levels followed the same trend as testosterone, falling after copulation and falling further prior to molt. Though lower than at copulation, plasma LH was higher in incubating (males) and brooding (males and females) emperors than during rearing of the thermally emancipated chicks, suggesting that plasma LH might be related to incubating, brooding, and territorial behavior. In male and female emperors and in male adelies, plasma gonadal steroids and LH were at basal levels throughout molt.

Animals↗

PubMedDate not supplied

Endogenous myelin basic protein-serum factors (MBP-SFS) and anti-MBP antibodies in a patient with post-herpes simplex virus acute disseminated encephalomyelitis.

The measurement of myelin basic protein serum factors (MBP-SFs) and anti-MBP antibodies in specimens from a patient with post-herpes simplex acute disseminated encephalomyelitis (ADE) is described. Transitory appearance of high affinity anti-MBP antibodies in the absence of detectable MBP-SFs was observed. This pattern was similar to that found previously in acute multiple sclerosis and experimental allergic encephalomyelitis. These findings are consistent with the hypothesis that a possible normal role of MBP-SFs is as neuroautotolerogens, preventing autoreactive lymphocyte clones from damaging myelin.

Acute Disease↗

PubMed1981

Cell-surface glycoprotein synthesis during differentiation of chicken erythroblasts transformed by temperature-sensitive avian erythroblastosis virus.

Chicken erythroblasts transformed by a temperature-sensitive mutant of avian erythroblastosis virus (ts34 AEV) have a greatly increased haemoglobin content (Graf, T., N. Ade and H. Beug: Nature 275, 496-501 (1978)) if allowed to grow for 3-5 days at the non-permissive temperature (41 degrees C), instead of the permissive temperature (35 degrees C) of the virus. Cell-surface molecular changes during this differentiation were investigated by examining the glycoproteins synthesized by a ts34-transformed erythroblast cell line. These cells synthesized a greatly increased amount of a 94,000 molecular weight erythrocyte cell-surface glycoprotein beginning 2-6 h after a shift in growth temperature from 35 degrees to 41 degrees C, consistent with the proposal that such a shift releases these transformed cells from a differentiation block.

Alpharetrovirus↗

PubMed1990

Temporary inhibition of meiosis resumption in vitro by adenylate cyclase stimulation in immature bovine oocytes.

This experiment was designed to analyze the effect of adenylate cyclase stimulation on cumulus-enclosed immature oocytes. More than 1400 selected (complete and unexpanded cumulus) oocytes from follicles 1 to 5 mm in diameter were recovered from ovaries obtained at slaughter and cultured for 24 h in TCM-199+10% fetal calf serum (FCS), with or without the adenylate cyclase stimulator, and in the presence or absence of bovine follicular fluid (BFF, 50%), or in complete BFF. In a second set of experiments, oocytes treated for 24 h were further cultured for a second 24 h with TCM-FCS alone. Oocytes were classified as germinal vesicle (G); intermediate (I; up to Metaphase I); matured (M; Anaphase I to Metaphase II); or degenerated (D), and cumulus expansion was evaluated. Products used were sodium fluoride (NaF), isobutylmethylxanthine (IBMX), adenosine (ADE) and forskolin (FK), all known to stimulate accumulation of cAMP in cells without the involvement of a hormone receptor except for adenosine, which acts as a substrate or as an agonist. The results indicate that NaF (0.01 M), IBMX (0.2 mM), FK (0.1 mM) and complete BFF can significantly reduce the proportion of oocytes reaching the mature state. Combination of NaF or FK to BFF (50%) are also effective at the significant level. Cumulus expansion was always limited when meiotic progress was affected or when adenosine was present in the culture media. When oocytes were cultured for a second 24 h in the control media, only NaF had a significant residual effect, but many oocytes were showing degenerative changes after the second incubation period. This method provides a new means to block oocyte nuclear maturation.

Journal Article↗

PubMed1988

Ruthenium(III) ion complexes with nucleic acid bases and nucleosides.

Complexes of the nucleic bases adenine (ade), guanine (guaH), cytosine (cyt), 2-thio-cytosine (thio-cyt), and the nucleosides adenosine (ado), guanosine (guoH), and inosine (inoH) with ruthenium trichloride have been prepared and characterized by infrared spectroscopy, diffuse reflectance spectra, conductivity, and magnetochemical measurements. On comparison of the infrared spectra of the prepared compounds with previous studies, suggestions are made about the binding site of the metal to the ligand. The complexes have normal magnetic moments close to the spin-only value. The electronic spectra confirms the octahedral structure of the complexes.

Adenine↗

PubMed1989

Macrophage activation and host augmentation against Sendai or herpes simplex virus (HSV) infections with synthetic polypeptides in mice.

Poly-L-Lys (mean mol. wt; 12,000), poly-L-Arg (5000) and poly-L-Orn were found to activate peritoneal macrophages effectively in vivo in 14 synthetic homo polypeptides. The ability of sequential poly(L-Arg-L-X) (5000) to activate macrophages was less than that of poly-L-Arg. Neither (L-Arg)12 nor (L-Arg)6 by themselves activated macrophages, but poly-D-Arg (5000) did, as also did poly-L-Arg; this suggests that the polycationic character of poly-L-Arg plays a role in the activation of macrophages. The intranasal administration of poly-L-Lys, -L-Arg, -L-Orn, -D-Arg, all of which activated macrophages, augmented host resistance against Sendai virus infection in mice. The protection afforded by poly-L-Arg seemed to depend on its mol. wt: the order of protection was poly-L-Arg greater than (L-Arg)12 greater than (L-Arg)6. The intranasal administration of poly-L-Arg 3 days before the infection was effective, while that 1 day before infection was not. There was no difference between the groups in the titer of interferon produced by the infection of Sendai virus given with poly-L-Arg either 3 days before or 1 day before the infection. The administration of poly-L-Arg 3 days before the infection caused a significant decrease of the virus titer in the lung 6 days after the infection when compared with the control or the mice given 1 day before. The intravenous administration of 2-chloroadenosine (2-Cl-Ade), which is a selective inhibitor of macrophages, into the mice which had received poly-L-Arg intranasally 3 days before the infection caused a significant decrease in the survival rate of the mice, indicating that the macrophages activated with poly-L-Arg are likely to be an important element in affording the protection. Subcutaneous administration of poly-L-Arg revealed protective activity against systematic infection with herpes virus-type 1.

2-Chloroadenosine↗

PubMed1987

Effect of testosterone on purine synthesis de novo in rat perineal muscle in vivo.

We examined in vivo the influence of testosterone on purine synthesis de novo, in the levator ani and gastrocnemius muscles of the rat. The hypoxanthine, adenine and guanine contents and the rate of incorporation of [14C]formate into these purine bases were determined in castrated adult and prepubertal rats (groups 1 and 2) both before and after orchiectomy and, in the second case, at different times after testosterone treatment. Substantially similar behavior was found in both groups, with some specific differences. The results showed an increase in the basal levels after castration (except for a dramatic decrease in adenine and a rise in the Gua/Ade molar ratio in prepubertal rats) and a return to basal levels after hormone administration, which was also accompanied by variations in the Gua/Ade molar ratio. The kinetics of purine nucleotide synthesis de novo in vivo and, specifically, of the overall reactions: IMP formation from PRib-PP, IMP----AMP and IMP----GMP, were followed by evaluating the incorporation curves of [14C]formate into hypoxanthine, adenine and guanine. Our results show that testosterone administration enhanced the incorporation rate and gave characteristic patterns: a diphasic cyclic oscillation of the Ade values in adult castrated rats, and single peaks having a specific shape in the other cases. The Gua/Ade labeling ratio was unchanged in castrated rats and increased in both groups during the first 5 days after testosterone treatment, after which values even fell below normal; in most cases, values overlapped the pattern of the Gua/Ade molar ratio. The specific profile of the curves indicated that testosterone initially accelerated the turnover of guanylic acid and in the second phase re-established the normal behavior and ratio of AMP and GMP formation. These results indicate that the 'inosinic branch point' was subject to regulation by testosterone. The profiles of the incorporation curves and of the Gua/Ade ratio were indicative of a primary and secondary response to hormone action.

Adenine↗

PubMed1993

Specific adenosine phosphorylase from hepatopancreas of gastropod Helix pomatia.

1. Specific adenosine phosphorylase from Helix pomatia hepatopancreas was separated from inosine-guanosine phosphorylase and purified 100-165 times; molecular weights were found to be 71,000 and 90,000, respectively. 2. The enzyme is specific for deoxy- and adenosine; it is inactive for 5'-methylthioadenosine and 5-amino-4-imidazole-carboxyamide riboside. Its sensitivity to several inhibitors differs from that of eucaryotic and bacterial purine nucleoside phosphorylases, and is not identical with the sensitivity of the S. mansoni adenosine-splitting enzyme. 3. H. pomatia adenosine phosphorylase differs in its mol. wt and Km values for P(i), ribose 1P, Ado and Ade from adenosine phosphorylase of B. subtilis.

Animals↗

PubMed1990

A pleiotropic mutation affecting purine metabolism in Bacillus subtilis.

A pleiotropic mutation (cpm) which is localized in the vicinity of the spoOA gene is described in Bacillus subtilis. The mutation inhibits spore formation, rendering bacteria auxotrophic for adenine and tyrosine, enhances sensitivity to antibiotics, decreases cell motility, inhibits the ability to grow on pentoses and to maintain bacteriophage multiplication, induces severalfold the activities of alkaline proteinase and alpha-amylase. At the same time, the cpm mutant starts to excrete inosine into the growth medium. This excretion most probably is explained by a 50-fold increase in the activity of inosine monophosphate: 5'-nucleotidase and a 10-fold decrease in the activity of purine nucleoside phosphorylase. The inosine production and Ade- phenotype of the cpm mutant is not accompanied by the change in the activity of succinyl adenosine monophosphate synthetase. The nature of the mutation is discussed.

5'-Nucleotidase↗