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A J Anderson

Publications and source records attributed to A J Anderson.

At least 55 records · Page 3Linked to original sources
PubMed1997

Early diagnostic efficiency of cardiac troponin I and Troponin T for acute myocardial infarction.

OBJECTIVE: To compare the early diagnostic efficiency of the cardiac troponin I (cTn-I) level with that of the cardiac troponin T (cTn-T) level, as well as the creatine kinase (CK), CK-MB, and myoglobin levels, for acute myocardial infarction (AMI) in patients without an initially diagnostic ECG presenting to the ED within 24 hours of the onset of their symptoms. METHODS: A prospective, observational, cohort study was performed involving chest pain patients admitted to a large urban community hospital. Participants were consecutive consenting ED chest pain patients > or = 30 years of age. Exclusions included duration of symptoms > 24 hours, inability to complete data collection, receipt of CPR, and ST-segment elevation on the initial ECG. Measurements included levels of cTn-I, cTn-T, CK, CK-MB, and myoglobin at the time of presentation and 1, 2, 6, and 12-24 hours after presentation as well as presenting ECG and clinical follow-up. Confirmation of the diagnosis of AMI was based on World Health Organization criteria. RESULTS: Of the 177 patients included in the study, 27 (15%) were diagnosed as having AMIs. The sensitivities of all 5 biochemical markers for AMI were poor at the time of ED presentation (3.7-33.3%) but rose significantly over the study period. The sensitivity of cTn-T was significantly better than that of cTn-I over the initial 2 hours, but both markers' sensitivities were low (< 60%) during this time frame. The cTn-I was significantly more specific for AMI than was the cTn-T, but not significantly better than CK-MB or myoglobin. Likelihood ratio analysis showed that the biochemical markers with the highest positive likelihood ratios for AMI during the first 2 hours following ED presentation were myoglobin and CK-MB. From 6 through 24 hours, the positive likelihood ratios for cTn-I, CK-MB, and myoglobin were superior to those of CK and cTn-T. CONCLUSIONS: cTn-I, CK-MB, and myoglobin are significantly more specific for AMI than are CK and cTn-T. Myoglobin is the biochemical marker having the highest combination of sensitivity, specificity, and negative predictive value for AMI within 2 hours of ED presentation. Neither cTn-I nor cTn-T offers significant advantages over myoglobin and CK-MB in the early (< or = 2 hours) initial screening for AMI. The cardiac troponins are of benefit in identifying AMI > or = 6 hours after presentation.

Biomarkers↗
PubMed1997

Cloning and mutational analysis of the gene for the stationary-phase inducible catalase (catC) from Pseudomonas putida.

Pseudomonas putida, a bacterium that colonizes plant roots and enhances plant growth, produces three isozymes of catalase (A, B, and C) in stationary-phase cells. A catalase probe, generated by PCR analysis of P. putida genomic DNA with oligomers based on typical catalase sequences, hybridized to a genomic clone that expressed catalase C in Escherichia coli. The catC gene from this clone had a 2,133-bp open reading frame with a high level of identity to the stationary-phase-specific E. coli katE. Chromosomal mutants of P. putida deficient in catalase C, obtained by gene interruption with a luxAB-npt cassette, demonstrated enhanced catC transcription in stationary-phase cells and, upon exposure to phenol, in logarithmic-phase cells. The catalase C-deficient cells were not impaired in their ability to colonize roots of bean or wheat plants grown under sterile conditions.

Amino Acid Sequence↗
PubMed1996

DNA damage and apoptosis in Alzheimer's disease: colocalization with c-Jun immunoreactivity, relationship to brain area, and effect of postmortem delay.

Many neurons in Alzheimer's disease (AD) exhibit terminal deoxynucleotidyl transferase (TdT) labeling for DNA strand breaks with a distribution suggestive of apoptosis. We have shown previously that immunoreactivity for c-Jun is elevated in AD and found in association with neuronal pathology. In addition, cultured neurons undergoing beta-amyloid-mediated apoptosis exhibit a selective and prolonged induction of c-Jun. Consequently, we conducted double-labeling experiments to examine whether c-Jun is associated with DNA strand breaks in AD tissue; we observed a strong colocalization between these markers. As would be predicted based on the distribution of AD pathology, we also found that TdT labeling was prominent in the entorhinal cortex, but absent or at very low levels in cerebellum. Furthermore, we confirmed that postmortem delay (PMD) does not affect TdT labeling within the limits used for tissue used in this study. However, in contrast to previous studies, we report an increase in TdT labeling with more extended PMDs. Finally, gel electrophoresis of genomic DNA isolated from AD and control cases failed to reveal evidence for either an apoptotic or a necrotic mechanism of cell death in AD, possibly because of a low number of cells actually undergoing cell death at any given time. Our findings support the hypothesis that DNA damage labeled using TdT reflects neuronal vulnerability and cell loss associated with AD pathology, and that at least a portion of the cells labeled with this technique is undergoing apoptosis. Furthermore, in agreement with in vitro findings, these results suggest a relationship between the expression of c-Jun and neuronal risk and/or cell death in AD.

Aged↗
PubMed1996

Up-regulation of Bcl-2 is associated with neuronal DNA damage in Alzheimer's disease.

Cell death and neurofibrillary tangle formation are prominent features of Alzheimer's disease (AD). It has been suggested that DNA damage may reflect neuronal vulnerability. In this context, the Ced homologue Bcl-2 is able to repress a number of cell death programs. Recently we found both numerous nuclei exhibiting DNA damage within neurons in the AD brain and increases in Bcl-2 immunoreactivity. In this study, we examined the relationship between Bcl-2 expression and nuclear DNA damage or tangle formation. Nuclei exhibiting DNA damage were associated with an up-regulation of Bcl-2 expression, whereas tangle-bearing neurons were associated with a down-regulation of Bcl-2 expression.

Aged↗
PubMed1996

Cross-linking of concanavalin A receptors on cortical neurons induces programmed cell death.

The loss of neurons by programmed cell death is a normal feature of the nervous system during development and has recently been implicated as a major mechanism of cell death in neurodegenerative diseases. In some cases, programmed cell death is induced by the activation of membrane receptors and is referred to as activation-induced programmed cell death. Activation-induced programmed cell death has been previously described in cells from the immune system, in which the activation of receptors by receptor clustering leads to programmed cell death. To determine whether activation-induced programmed cell death occurs in neurons, Concanavalin A was used to cross-link membrane receptors on cortical neurons. Concanavalin A-induced neuronal death was dose dependent and effective at concentrations previously shown to induce activation-induced programmed cell death in lymphocytes. Programmed cell death was attenuated when Concanavalin A-specific binding to neurons was blocked with methyl alpha-D-mannopyranoside. Succinyl Concanavalin A, which bound to Concanavalin A receptors but was ineffective at cross-linking them, did not induce programmed cell death. Concanavalin A-induced neuronal death exhibited many of the hallmarks associated with programmed cell death, such as membrane blebbing, nuclear condensation and margination, and internucleosomal DNA cleavage. In addition, neurons exposed to Concanavalin A displayed a rapid, robust, and persistent increase in the immediate early gene protein c-Jun. A similar increase in c-Jun precedes programmed cell death induced by beta-amyloid in neurons, and under some conditions an increase in c-Jun has been shown to be required for programmed cell death to occur in neurons. Increased expression of c-jun and other immediate early genes has also been correlated with activation-induced programmed cell death in lymphocytes. These observations suggest that Concanavalin A induces activation-induced programmed cell death in neurons via signals produced from the cross-linking of receptors on neuronal membranes. These results also raise the possibility that beta-amyloid induces programmed cell death in a similar manner, by causing the cross-linking of receptors on neuronal membranes. This mechanism may be relevant to neuronal programmed cell death that occurs during development and neurodegeneration.

Animals↗
PubMed1995

Sequence of a gene encoding periplasmic Pseudomonas syringae ankyrin.

A gene encoding ankyrin (Ank) was isolated from a genomic library of the plant pathogen Pseudomonas syringae pathovar syringae strain 61 (Pss61). The gene encodes an 183-amino-acid (aa) polypeptide which has homology to the 33-aa repeat domain of mammalian Ank and Ank homologs from other bacteria, animals and plants.

Amino Acid Sequence↗
PubMed1995

Structures of the two polymers present in the lipopolysaccharide of Burkholderia (Pseudomonas) cepacia serogroup O4.

Like several other strains of Burkholderia (Pseudomonas) cepacia, the reference strain for serogroup O4 in the French typing scheme [Heidt, A., Monteil, H. & Richard, C. (1983) J. Clin. Microbiol. 18, 738-740] produces a lipopolysaccharide containing two distinct polymers. Attempts to separate the polymers chromatographically were unsuccessful, but the periodate-resistant major polymer could be isolated by application of the Smith degradation technique to the mixture. By means of chemical and NMR spectroscopic analysis, the following structure could be assigned to the repeating unit of the major polymer: -->3)-alpha-D-Galp-(1-->3)-beta-D-Galp-(1-->3)-beta-D-GalpNAc-(1-->. The following structure of the repeating unit of the minor polymer was established from similar studies of its degradation product, resulting from the oxidation of L-rhamnose (Rha), and of the original mixture: -->3)-alpha-D-GalpNAc-(1-->3)-beta-D-GalpNAc-(1-->4)-alpha-L-Rhap- (1-->. Individually, the polymers have recently been found in related strains of B. cepacia. The minor polymer was identified as the O-antigen in serotype A of a Canadian typing scheme [Beynon, L. M. & Perry, M. B. (1993) Biochem. Cell Biol. 71, 417-420], and the major polymer in serotype C of a Japanese typing scheme [Paramonov, N. A., Shashkov, A. S., Knirel, Y. A., Soldatkina, M. A. & Zakharova, I. Y. (1994) Bioorg. Khim. 20, 984-993]. In the case of the O4 strain studied here, both polymers were produced under a variety of growth conditions.

Biopolymers↗
PubMed1995

Characterization of atrioventricular nodal behavior and ventricular response during atrial fibrillation before and after a selective slow-pathway ablation.

BACKGROUND: The presence of atrioventricular nodal dual-pathway physiology in patients with atrioventricular nodal reentrant tachycardia (AVNRT) provides an opportunity to characterize the effect of a selective slow-pathway ablation on the ventricular rate during atrial fibrillation (AF). This may have important clinical implications for the nonpharmacological management of AF with a rapid ventricular rate. METHODS AND RESULTS: Selective radiofrequency catheter ablation of the atrioventricular nodal slow pathway was performed with a stepwise approach in patients with documented sustained AVNRT. The AV nodal conduction properties and refractoriness and the ventricular rate during induced AF were assessed at baseline and under autonomic blockade before and after a selective slow-pathway ablation in 18 patients (mean age, 34 +/- 8 years). Sustained AVNRT was induced with a mean cycle length of 339 +/- 58 ms. A slow-pathway ablation was successfully achieved with 5 +/- 4 applications of radiofrequency energy. The shortest cycle length of 1:1 AV conduction and the AV nodal effective refractory period significantly prolonged after ablation (367 +/- 53 versus 403 +/- 55 ms, P < .0001, and 258 +/- 55 versus 292 +/- 74 ms, P < .05, respectively). Selective slow-pathway ablation significantly prolonged the mean (526 +/- 93 versus 612 +/- 107 ms, P < .0001), the shortest (378 +/- 59 versus 423 +/- 73 ms, P < .0001), and the longest (826 +/- 150 versus 969 +/- 226 ms, P < .01) cycle lengths of the ventricular response to AF. Significant slowing of the ventricular rate during AF occurred in 13 patients (72%), including all eight patients in whom AV nodal dual-pathway physiology was abolished. Five patients did not have a significant change in the ventricular rate during AF; a persistent dual AV nodal pathway physiology was demonstrable in four of these patients. Loss of dual-pathway physiology after ablation had a sensitivity of 77%, specificity of 80%, and positive predictive value of 91% for slowing the ventricular rate during AF. CONCLUSIONS: In patients undergoing a slow-pathway ablation for control of AVNRT, selective slow-pathway ablation may cause a significant decrease in the ventricular rate during AF. These effects are primarily due to the prolongation of AV nodal conduction properties and refractory period of the residual AV nodal transmission system. These findings may have important therapeutic implications for the nonpharmacological treatment of AF, particularly in patients with underlying dual AV nodal physiology.

Adult↗
PubMed1995

Localization of insulin-like growth factor-I immunoreactivity in larval and juvenile barramundi (Lates calcarifer).

Antisera to mammalian IGFs cross-react with several fish species, suggesting a long phylogenetic history of IGF-like peptides and their functional importance to all vertebrates. In this study, the tissue distribution of IGF-I-immunoreactivity (IGF-I-IR) was studied at various larval and juvenile stages of the life cycle of barramundi (Lates calcarifer). It was shown that the distribution of IGF-I-IR in this species was tissue-specific and age-dependent. In newly hatched larvae, presumptive musculature in the trunk and the pectoral fin rudiments reacted positively for IGF-I. As specimen age increased, however, IGF-I-IR in these tissues became less evident. In the retinas of barramundi 42 hr and older, a distinct band of IGF-I-IR was consistently detected between the presumptive outer nuclear and bacillary layers. Examination of sections from specimens 9 days and older revealed strong reactivity for IGF-I in a large proportion of renal tubule epithelial cells. In sections from larvae 13 to 28 days old, diffuse cytoplasmic IGF-I-IR was identified in cells lining the gill structures. At these same developmental stages, IGF-I reactive cells were also observed in the islets of Langerhans. In young juveniles (22 to 28 days posthatching), sparsely scattered clusters of neurons in the lower brain were observed which exhibited granular IGF-I-IR in perikarya. In all instances reported, IGF-I-IR in barramundi tissue was abolished by replacing antisera with normal rabbit serum or by preabsorption of antisera with purified IGF-I peptide, indicating the specificity of the reactions obtained. The distribution patterns of IGF-I-IR in barramundi tissues were broadly consistent with the reported distributions of IGF-I-like peptides and transcripts in other teleost species. The findings of this study are in general agreement with the hypothesis that IGF-I-like peptides may be involved in the regulation of tissue growth, differentiation, and function during early barramundi development.

Aging↗
PubMed1995

A potential role for apoptosis in neurodegeneration and Alzheimer's disease.

Previous studies have shown that beta-amyloid (A beta) peptides are neurotoxic. Recent data suggest that neurons undergoing A beta-induced cell death exhibit characteristics that correspond to the classical features of apoptosis, suggesting that these cells may initiate a program of cell death. This chapter explores the criteria and precautions that must be applied to evaluate mechanisms of cell death in vitro and in vivo, discusses the evidence supporting an apoptotic mechanism of cell death in response to A beta in cultured neurons, and describes potential correlations for these findings in the Alzheimer's disease brain. In addition, cellular signaling pathways that may be associated with apoptosis in response to A beta are examined, and support for apoptosis as a mechanism of cell death for other neurodegeneration-inducing stimuli (e.g., oxidative injury) is described. The connection of multiple stimuli that induce neuronal cell death to an apoptotic mechanism suggests that apoptosis could play a central role in neurodegeneration in the brain.

Alzheimer Disease↗
PubMed1995

Characterization of a potassium channel toxin from the Caribbean Sea anemone Stichodactyla helianthus.

A peptide toxin, ShK, that blocks voltage-dependent potassium channels was isolated from the whole body extract of the Caribbean sea anemone Stichodactyla helianthus. It competes with dendrotoxin I and alpha-dendrotoxin for binding to synaptosomal membranes of rat brain, facilities acetylcholine release at an avian neuromuscular junction and suppresses K+ currents in rat dorsal root ganglion neurones in culture. Its amino acid sequence is R1SCIDTIPKS10RCTAFQCKHS20MKYRLSFCRK30TCGTC35. There is no homology with other K+ channel-blocking peptides, except for BgK from the sea anemone Bunodosoma granulifera. ShK and BgK appear to be in a different structural class from other toxins affecting K+ channels.

Amino Acid Sequence↗
PubMed1995

Differential induction of immediate early gene proteins in cultured neurons by beta-amyloid (A beta): association of c-Jun with A beta-induced apoptosis.

beta-Amyloid (A beta) is a 39-42 amino acid that is the primary component of plaques in Alzheimer's disease (AD). Previous studies from our laboratory and others have shown that A beta induces neurodegeneration via apoptosis in vitro, suggesting that A beta may also initiate an apoptotic pathway of cell death in AD. Apoptosis has been suggested to proceed by a gene-directed program in several systems. Accordingly, we have investigated whether A beta-mediated apoptosis is associated with the induction of genes that may regulate or play a role in cell death in vitro. Immediate early genes (IEGs) respond to cellular stimuli and participate in cellular signaling pathways. The protein products of some IEGs, e.g., c-jun, are capable of forming dimers and acting as transcriptional regulatory proteins, and have been implicated in apoptosis in both nonneuronal and neuronal cells. In this study, we report a selective and abnormally sustained induction of c-Jun in cultured hippocampal neurons treated with A beta. In addition, we describe the lack of induction of c-Jun in neurons that are relatively resistant to A beta-mediated toxicity, and a correspondence between immunoreactivity for c-Jun and changes in nuclear morphology that are indicative of apoptosis. These data demonstrate that c-Jun is induced in cultured neurons that undergo A beta-mediated apoptosis and suggest that c-Jun may participate in a cell death program in these neurons.

Amyloid beta-Peptides↗
PubMed1995

Cloning and characterization of the katB gene of Pseudomonas aeruginosa encoding a hydrogen peroxide-inducible catalase: purification of KatB, cellular localization, and demonstration that it is essential for optimal resistance to hydrogen peroxide.

Pseudomonas aeruginosa is an obligate aerobe that is virtually ubiquitous in the environment. During aerobic respiration, the metabolism of dioxygen can lead to the production of reactive oxygen intermediates, one of which includes hydrogen peroxide. To counteract the potentially toxic effects of this compound, P. aeruginosa possesses two heme-containing catalases which detoxify hydrogen peroxide. In this study, we have cloned katB, encoding one catalase gene of P. aeruginosa. The gene was cloned on a 5.4-kb EcoRI fragment and is composed of 1,539 bp, encoding 513 amino acids. The amino acid sequence of the P. aeruginosa katB was approximately 65% identical to that of a catalase from a related species, Pseudomonas syringae. The katB gene was mapped to the 71- to 75-min region of the P. aeruginosa chromosome, the identical region which harbors both sodA and sodB genes encoding both manganese and iron superoxide dismutases. When cloned into a catalase-deficient mutant of Escherichia coli (UM255), the recombinant P. aeruginosa KatB was expressed (229 U/mg) and afforded this strain resistance to hydrogen peroxide nearly equivalent to that of the wild-type E. coli strain (HB101). The KatB protein was purified to homogeneity and determined to be a tetramer of approximately 228 kDa, which was in good agreement with the predicted protein size derived from the translated katB gene. Interestingly, KatB was not produced during the normal P. aeruginosa growth cycle, and catalase activity was greater in nonmucoid than in mucoid, alginate-producing organisms. When exposed to hydrogen peroxide and, to a greater extent, paraquat, total catalase activity was elevated 7- to 16-fold, respectively. In addition, an increase in KatB activity caused a marked increase in resistance to hydrogen peroxide. KatB was localized to the cytoplasm, while KatA, the "housekeeping" enzyme, was detected in both cytoplasmic and periplasmic extracts. A P. aeruginosa katB mutant demonstrated 50% greater sensitivity to hydrogen peroxide than wild-type bacteria, suggesting that KatB is essential for optimal resistance of P. aeroginosa to exogenous hydrogen peroxide.

Aerobiosis↗
PubMed1995

Newly identified psychiatric illness in one general practice: 12-month outcome and the influence of patients' personality.

BACKGROUND: Relatively little is known about the natural history and outcome of psychological problems in patients who present to general practitioners. Only a small proportion of such patients are seen by specialists. Clinical experience suggests that patient personality is one of the factors influencing outcome in patients diagnosed as having psychiatric illness. AIM: This study set out to examine prospectively the progress and 12-month outcome of patients with newly identified psychiatric illness, and the association of patients' personality with outcome. METHOD: One hundred and seventy one patients with clinically significant psychiatric illness attending one practice in a Scottish new town were followed up prospectively (96 presented with psychological symptoms and 75 with somatic symptoms), and were compared with a group of 127 patients with chronic physical illness. Patients were assessed in terms of psychiatric state, social problems and personality using both computer-based and pencil and paper tests in addition to clinical assessments at each consultation during the follow-up year and structured interview one year after recruitment. RESULTS: Most of the improvement in psychiatric state scores on the 28-item general health questionnaire occurred in the first six months of the illness. Of the 171 patients with psychiatric illness 34% improved quickly and remained well, 54% had an intermittent course but had improved at 12-month follow up while 12% pursued a chronic course without improvement. The mean number of consultations in the follow-up year was 8.4 for patients presenting with psychological symptoms, 7.2 for those presenting with somatic symptoms and 6.6 for patients with chronic physical illness. The Eysenck N score proved a strong predictor of the outcome of new psychiatric illness. CONCLUSION: Only one in three patients with newly identified psychiatric illness improved quickly and and remained well, reflecting the importance of continuing care of patients with psychological problems. This study has confirmed the feasibility of simple personality testing in everyday practice and shown a link between Eysenck N score and the outcome of new psychiatric illness. The predictive value of the Eysenck N score in general practice requires further research.

Adolescent↗
PubMed1994

Immunohistochemical evidence for apoptosis in Alzheimer's disease.

Recently, in vitro studies conducted in our laboratory and others have suggested that apoptosis may have a role in the neuronal cell death associated with Alzheimer's disease (AD). To evaluate this hypothesis, the hippocampi and entorhinal cortices of AD, aged control, and surgical biopsy tissue were examined using the ApopTag system for the detection of DNA fragmentation and DNA strains to reveal nuclear morphology. Numerous neuronal nuclei displaying distinct morphological characteristics of apoptosis were present within tangle-bearing neurons as well as non-tangle-bearing neurons in AD brain, whereas few or no such nuclei were detected in control brain. Our in vivo results support the hypothesis that apoptosis may be one mechanism leading neuronal cell death in AD.

Aged↗
PubMed1994

Structure of the O9 antigen from Burkholderia (Pseudomonas) cepacia.

The O9 antigen of Burkholderia (Pseudomonas) cepacia has the following disaccharide repeating-unit: -->4)-alpha-D-Glcp-(1-->3)-alpha-L-Rhap-(1--> The same unit is present in the O antigens of Serratia marcescens strain S1254 and serogroup O4 (predominantly acetylated at O-2 of rhamnose in the latter case).

Burkholderia cepacia↗
PubMed1994

Increased immunoreactivity for Jun- and Fos-related proteins in Alzheimer's disease: association with pathology.

The protein products of the Jun and Fos immediate early gene (IEG) families are cooperative transcriptional regulatory factors implicated in regulating the expression of many genes. The levels of a variety of proteins such as the amyloid precursor protein and basic fibroblast growth factor are altered in Alzheimer's disease (AD), thus the events regulating these changes are of interest. Both of these genes contain an activator protein-1 consensus sequence which may be responsive to regulation by immediate early genes. In order to evaluate the potential involvement of IEGs in AD pathology, we have examined Jun- and Fos-related protein immunoreactivity in control and AD brain. Specifically, we investigated the correspondence of immunoreactivity for Jun and Fos proteins with immunoreactivity for paired helical filament-1 (PHF-1), a marker for neurofibrillary tangles which recognizes abnormally phosphorylated tau, glial fibrillary acidic protein (GFAP), and thioflavine staining in double-labeling experiments. An intensification of both Jun and Fos immunoreactivity was observed in AD cases; in addition, both Jun and Fos immunoreactivity were colocalized with PHF-1 in some neurons in AD brain. Jun and Fos immunoreactivity were also colocalized with GFAP-positive astrocytes distributed in the cortex of AD and control cases, and surrounding thioflavine-stained plaques in AD brain. These observations suggest that members of the Jun and Fos IEG families may play a role in AD pathology.

Aged↗