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Biomedical subjects

C McGowan

Publications and source records attributed to C McGowan.

At least 19 recordsLinked to original sources
PubMed2000

Chest pain and the treatment of psychosocial/emotional distress in CAD patients.

Treatment of psychosocial/emotional distress as a strategy for diminishing chest pain in such patients remains entirely unutilized in standard care. Sixty-three patients with known or suspected CAD were entered in an aggressive lifestyle modification program. Patients completed the Symptom Checklist 90-Revised (SCL90R) at the diagnostic interview session, at 3 and at 12 months. Statistically significant drops were observed on multiple scales of the SCL90R at both 3 and 12 months. An item from the SCL90R was used as a proxy for angina. Multiple measures of emotional distress at baseline were found to correlate with chest pain at baseline, but not a number of traditional cardiovascular risk factors. The chest pain item displayed improvement at both 3 and 12 months. Improvement on all scales of the SCL90R correlated with improvement in chest pain. It may be possible to control chest pain in some CAD patients with psychosocial interventions.

Adaptation, Psychological↗
PubMed2000

Psychosocial and traditional risk factors in early ischaemic heart disease: cross-sectional correlates.

BACKGROUND: Psychosocial/emotional distress has been repeatedly found to be a correlate of the onset/aggravation of ischaemic heart disease. METHODS: Eighty-three patients (63 men and 20 women) with known coronary artery disease who entered an aggressive lifestyle modification programme were administered a clinical/demographic history and the Symptom Checklist 90--Revised at baseline. Several measures of social isolation/alienation (shyness/self-consciousness, feeling lonely, feeling abused and overall) were derived from the the Symptom Checklist 90--Revised. RESULTS: Univariate tests of the association of known cardiovascular risk factors and the Symptom Checklist 90--Revised scales with age at initial diagnosis yielded several significant results for history of hypercholesterolaemia (P = 0.018), history of hypertension (P = 0.030), somatization (P = 0.007), obsessive-compulsive (P = 0.009), depression (P = 0.006), anxiety (P = 0.021), hostility (P = 0.003), paranoia (P = 0.050), psychoticism (P = 0.029), the Global Severity Index (P = 0.007), the Positive Symptom Distress Index (P = 0.005), the Positive Symptom Total Score (P = 0.003) and feeling abused (P = 0.037). Only history of hypertension, history of hypercholesterolaemia and the hostility scale (overall F = 6.08 and P = 0.0009) emerged as unique correlates of age at initial diagnosis in a multiple regression using only the significant univariate predictors. CONCLUSIONS: Psychosocial factors are sufficiently confounded with one another that they lose their predictive value once one is entered in the equation. High scores on the hostility scale were associated with a 5.7 year differential in age at initial diagnosis. The younger a patient is at initial diagnosis, the more likely he/she is to have high levels of emotional distress.

Coronary Disease↗
PubMed1998

Evidence for interspecies gene transfer in the evolution of 2,4-dichlorophenoxyacetic acid degraders.

Small-subunit ribosomal DNA (SSU rDNA) from 20 phenotypically distinct strains of 2,4-dichlorophenoxyacetic acid (2,4-D)-degrading bacteria was partially sequenced, yielding 18 unique strains belonging to members of the alpha, beta, and gamma subgroups of the class Proteobacteria. To understand the origin of 2,4-D degradation in this diverse collection, the first gene in the 2,4-D pathway, tfdA, was sequenced. The sequences fell into three unique classes found in various members of the beta and gamma subgroups of Proteobacteria. None of the alpha-Proteobacteria yielded tfdA PCR products. A comparison of the dendrogram of the tfdA genes with that of the SSU rDNA genes demonstrated incongruency in phylogenies, and hence 2,4-D degradation must have originated from gene transfer between species. Only those strains with tfdA sequences highly similar to the tfdA sequence of strain JMP134 (tfdA class I) transferred all the 2,4-D genes and conferred the 2,4-D degradation phenotype to a Burkholderia cepacia recipient.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1996

Occupational x-ray exposure of anaesthetists.

Lithium fluoride thermoluminescent dosimeter chips were used to measure the radiation dose received by anaesthetists caused by the use of image intensification during a typical 4-week period in an orthopaedic theatre. These were used to estimate an annual dose, for comparison with dose limits, to ascertain if anaesthetists should be included in personnel monitoring services. Doses proved to be below detectable limits; hence anaesthetists are at minimal risk from occupational exposure to radiation. The orthopaedic theatre is believed to use more x-rays than other theatres, so exposure elsewhere should also be undetectable.

Anesthesiology↗
PubMed1995

Characterisation of fast, slow and cardiac muscle tropomyosins from salmonid fish.

Tropomyosin (TM) has been isolated from the cardiac muscle, and fast and slow trunk (myotomal) muscles of the mature salmonid fish Atlantic salmon (Salmo salar) and rainbow trout (Salmo gairdneri). When examined electrophoretically, isoforms of TM were detected which were specific, and exclusive, to each type of muscle. Cardiac and fast muscles contained single and distinct isoforms, while slow muscle contained two distinct isoforms, closely related in terms of apparent M(r), and pI. There was no detectable difference between the same TM type from either salmon or trout. On a variety of gel systems, the cardiac and slow isoforms migrated in close proximity to each other and to rabbit alpha-TM. The fast isoform comigrated with rabbit beta-TM. In developing salmon fry, a more acidic (unphosphorylated) variant of TM was present in addition to, and of similar M(r) to, the fast adult isoform. This TM declined in steady-state level during maturation and was virtually undetected in adult muscle. All of the isolated TMs contained little or no covalently bound phosphate and were blocked at the N-terminus. The amino acids released by carboxypeptidase A, when ordered to give maximal similarity to other muscle TMs, were consistent with the following sequences: fast (LDNALNDMTSI) and cardiac (LDHALNDMTSL). The C-terminal region of the slow TM contained His but was heterogeneous. In viscosity measurements, performed as a function of increasing protein concentration, at low ionic strength (t = 5 degrees C, pH 7.00), fast TM exhibited the highest relative viscosity values. Lower and equivalent levels of polymerisation occurred with the cardiac and slow TMs. Polymerisation of all three isoforms was temperature-dependent, with cardiac TM being least sensitive and fast TM being most sensitive. Determination of the complete coding sequence of adult fast TM confirmed the findings of the carboxypeptidase analysis, but the remainder of the sequence more closely resembled alpha-type TMs than beta-type TMs. Overall, salmon fast TM contains 20 (mostly conservative) substitutions compared to rabbit striated muscle alpha-TM and 40 (mostly conservative) substitutions compared to rabbit striated muscle beta-TM. This demonstrates that electrophoretic mobility is not, in all instances, a suitable method to assess the isomorphic nature of striated muscle TMs.

Amino Acid Sequence↗
PubMed1995

2,4-Dichlorophenoxyacetic acid-degrading bacteria contain mosaics of catabolic genes.

DNA from 32 2,4-dichlorophenoxyacetic acid (2,4-D)-degrading bacteria from diverse locations was probed with the first three genes of the well-known 2,4-D degradation pathway found in Alcaligenes eutrophus JMP134(pJP4). The majority of strains did not show high levels of homology to the first three genes of the 2,4-D degradation pathway, tfdA, -B, and -C. Most strains showed combinations of tfdA-, B-, and C-like elements that exhibited various degrees of homology to the gene probes. Strains having the same genomic fingerprints (as determined by repetitive extragenic palindromic PCR) exhibited the same hybridization pattern regardless of the geographic origin of the strain, with the exception of a strain isolated from Puerto Rico. This strain had the same genomic fingerprint as that of numerous other strains in the collection but differed in its hybridization against the tfdA gene probe. Members of the beta subdivision of the Proteobacteria class, specifically Alcaligenes, Burkholderia, and Rhodoferax species, carried DNA fragments with 60% or more sequence similarity to tfdA of pJP4, and most carried fragments showing at least 60% homology to tfdB. However, many strains did not hybridize with tfdC, although they exhibited chlorocatechol dioxygenase activity. Members of the alpha subdivision of the Proteobacteria class, mostly of the genus Sphingomonas, did not hybridize to either tfdA or tfdC, but some hybridized at low stringency to tfdB. The data suggest that extensive interspecies transfer of a variety of homologous degradative genes has been involved in the evolution of 2,4-D-degrading bacteria.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1994

Selective pulmonary and venous smooth muscle relaxation by furosemide: a comparison with morphine.

Furosemide and morphine reduce pulmonary edema associated with congestive heart failure. It is uncertain whether furosemide or morphine are direct-acting relaxants of arterial and venous smooth muscle. The authors compared the effect of furosemide and morphine on isolated rings of canine pulmonary artery (PA) and vein (PV) and mesenteric, splenic and anterior tibial arteries and their corresponding veins precontracted with norepinephrine or (15S)-hydroxy-11 alpha, 9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid. Furosemide (10-300 microM) selectively relaxed veins by an endothelium-independent mechanism, with its greatest efficacy on the PV. Morphine (10-1000 microM) relaxed both arteries and veins. The mechanism of relaxation by furosemide and morphine was examined in the PV and PA. Morphine-induced relaxation of the PV and PA was dependent on prostanoid release from endothelium and smooth muscle because it was attenuated in endothelium-rubbed and ibuprofen-treated PV and PA but not in blood vessels treated with inhibitors of nitric oxide system/cyclic GMP system (I-NG-nitroarginine and methylene blue). Furosemide-mediated relaxation of the PV was refractory to each of these interventions. Similarly, furosemide- and morphine-induced relaxation of the PV were unaffected by 4-aminopyridine, tetraethylammonium, glibenclamide, dendrodotoxin and apamin and, thereby, were independent of an action on K+ channels. Reduction of extracellular K+ or Cl- attenuated furosemide-mediated relaxation of, and inhibition of 86Rb+ uptake by, PV even in the presence of ouabain. It was concluded that furosemide relaxes veins by an effect on Na+/K+/Cl- cotransport or chloride-mediated refilling of intracellular calcium stores.

Animals↗
PubMed1992

Activation of MPF in fission yeast.

In fission yeast p34cdc2/cyclin is activated at the G2/M boundary by dephosphorylation of Tyr15 of the p34cdc2 subunit. Two protein phosphatases carry out this dephosphorylation event. The major activity is encoded by cdc25, which is a distantly related member of the protein tyrosine phosphatase family. A minor activity is provided by a newly identified fission yeast protein tyrosine phosphatase.

Amino Acid Sequence↗
PubMed1991

cdc25 M-phase inducer.

In this paper, we have described the critical experiments leading to the discovery and analysis of the cdc25 M-phase inducer. We have shown that timing of mitosis is sensitive to the level of cdc25+ expression and that the cellular concentration of p80cdc25 increases as cells approach mitosis. From these observations we conclude that, in S. pombe, rate of accumulation of p80cdc25 plays an important role in determining the timing of mitosis. We postulate that under a given set of conditions, a critical level of p80cdc25 activity is required to undergo mitosis. The actual level that is required can vary depending on ploidy, growth rate, nutritional status of the cell, and perhaps other parameters. These signals may be monitored through the weel pathway leading to tyrosyl phosphorylation of p34cdc2. We have shown that p80cdc25 encodes a phosphate that acts by directly dephosphorylating the Tyr-15 residue of p34cdc2. Our studies strongly indicate that this aspect of the mitotic control network is generally conserved among eukaryotes. It is conceivable, however, that the mode of regulation of cdc25 activity may vary from species to species. Clearly, in S. cerevisiae the cdc25+ homolog, MIH1, in contrast to cdc25+, is not rate-limiting for M-phase onset. It will be important to determine whether the level of cdc25+ homologs in other organisms also oscillates during the cell cycle, or whether their activity is controlled by localization or posttranslational mechanisms, such as phosphorylation. Furthermore, our finding of more than one cdc25+ homolog in a single species suggests an additional level of complexity to the control of M-phase onset by cdc25 in higher eukaryotes that will require further investigation.

Amino Acid Sequence↗
PubMed1989

Influence of vitamin B6 status on aspects of lead poisoning in rats.

The effects of vitamin B6 status and lead (Pb) toxicity on aspects of glutathione (GSH) metabolism in rats were examined in a 2 x 2 factorial experiment. The administration of 2000 ppm Pb as Pb acetate.3H2O significantly (P less than 0.05) increased hepatic GSH levels in rats receiving B6-adequate (+B6) but decreased GSH in rats fed B6-deficient (-B6) diets. The addition of Pb to the +B6 diet also increased hepatic glutathione reductase (GSSG-R) activity. Plasma pyridoxal phosphate (PLP), cystathionine and valine levels were decreased by the -B6 diets independent of the presence of Pb. Plasma arginine, alanine, serine and proline levels were increased by Pb in both -B6 and +B6 groups. Glycine levels were increased in -B6 rats only in the absence of Pb while taurine was decreased by Pb only in +B6 rats. There were significant -B6 x Pb interactions for hepatic GSH, cysteine and GSSG-R as well as plasma valine, glycine and proline. These results suggest an influence of B6 status on Pb-induced changes in hepatic GSH, possibly through its role as a co-factor for enzymes involved in amino acid metabolism.

Amino Acids↗
PubMed1987

Effect of lead toxicity on the organ concentration of glutathione and glutathione-related free amino acids in the chick.

Total non-protein sulfhydryl (NPSH) and glutathione (GSH) concentrations in liver and kidney and GSH-related free amino acid concentrations in liver, kidney and plasma were examined in the chick following intoxication with 2000 ppm dietary lead (Pb). After 3 weeks, NPSH content was significantly (P less than 0.05) increased by Pb in both liver and kidney while only liver GSH was increased by Pb treatment. The concentrations of glutamate, glycine and methionine were elevated in liver by Pb while glycine, cysteine and cystathionine concentrations were increased in the kidney. In plasma, Pb significantly decreased cysteine, taurine and cystathionine concentrations.

Amino Acids↗
PubMed1987

Lead effects in the chick during selenium deficiency.

1. Growing chicks (Gallus domesticus) were fed a selenium-deficient diet supplemented with 0 or 2000 ppm lead (Pb) and 0 or 0.1 ppm selenium (Se). 2. Selenium addition stimulated growth at 0 but not at 2000 ppm Pb, while Pb depressed growth at both levels of Se. 3. Selenium addition stimulated Se-dependent glutathione peroxidase (GSH-Px) activity in liver, but Pb was without effect on GSH-Px activity. 4. Lead addition increased non-protein sulfhydryl (NPSH) concentrations in liver, kidney and thigh muscle. NPSH levels were not altered by Se. 5. The reported antagonism between Pb and Se does not appear to be mediated through effects on GSH-Px or NPSH metabolism.

Aging↗
PubMed1984

Experimental induction of chronic aflatoxicosis in chickens by purified aflatoxin B1 and its reversal by activated charcoal, phenobarbital, and reduced glutathione.

Aflatoxin B1 (AFB1) caused dose-dependent reductions in weight gain and feed consumption when day-old Hubbard X Hubbard broiler type chicks were maintained on a diet contaminated with either 0, 2.5, 5, or 10 ppm purified AFB1 for 8 weeks. Although changes in these parameters were detected at the 2.5 and 5 ppm, the most profound changes were evident at 10 ppm contamination. The concentration of cytochrome P-450 in hepatic microsomes, measured at the end of 8 weeks, also showed dose-dependent decreases. Cytochrome P-450 content in chickens receiving 2.5, 5, and 10 ppm AFB1 was 16, 28, and 65%, respectively, less than the control. Microsomal benzphetamine N-demethylase activity was not inhibited by 2.5 or 5 ppm, but ingestion of 10 ppm AFB1 reduced its activity by more than 40%. Serum glutamic oxalacetic transaminase (SGOT) levels of chickens receiving 10 ppm AFB1 increased by more than 100%, indicating substantial liver damage. However, birds simultaneously receiving 10 ppm AFB1 and activated charcoal (.1% in the feed) or either reduced glutathione (.05%) or phenobarbital (.05%, given intermittently) in their drinking water showed a trend of improvement in feed consumption (less than 10% reversal) and weight gain (less than 28% reversal) over the birds receiving 10 ppm AFB1 alone. The results also indicate that the simultaneous presence of these agents with AFB1 considerably prevented the inhibitory effect of AFB1 on the microsomal cytochrome P-450 and benzphetamine N-demethylase activity. Furthermore, these agents were able to provide moderate protection against AFB1-induced liver injury manifested by elevation of SGOT activity.

Aflatoxin B1↗
PubMed1982

Vascular reactivity during the development of two-kidney, one-clip Goldblatt hypertension in conscious dogs.

This study evaluates the sequential changes in vascular reactivity in conscious dogs during the early and late phases of two-kidney, one-clip Goldblatt hypertension (2-KGH) produced by unilateral renal artery constriction (URAC). The in vivo responses to serotonin (5-HT), norepinephrine (NE), angiotensin II (Ang II), prostacyclin (PGI2), acetylcholine (ACH), and nitroglycerin (GTN) were reproducible and stable throughout the 32-day period of study in dogs subjected to sham URAC. The vascular responses to 5-HT, Ang II, and PGI2 were enhanced day 1 post-URAC, before mean arterial pressure (MAP), cardiac output (CO), or total peripheral resistance (TPR) increased. The magnitude of the enhanced reactivity progressed on days 4 and 32 post-URAC, as hypertension developed. The pressor responses to NE did not change from pre-URAC values until CO and MAP were elevated. The vasodepressor responses to ACH and GTN diminished over a 12-day period post-URAC, in parallel with the change in CO, but prior to any increase in TPR. These data suggest that in dogs with 2-KGH changes in vascular reactivity precede the development of the increased MAP and TPR of hypertension. The lack of uniformity of the onset of the reactivity changes to the different agonists suggests that both intrinsic factors and pressure changes modify the vascular wall in the early and later stages of 2-KGH.

Angiotensin II↗