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Biomedical subjects

J Condon

Publications and source records attributed to J Condon.

At least 19 recordsLinked to original sources
PubMed2004

Estimation of infection prevalence from correlated binomial samples.

Infection prevalence in a population often is estimated from grouped binary data expressed as proportions. The groups can be families, herds, flocks, farms, etc. The observed number of cases generally is assumed to have a Binomial distribution and the estimate of prevalence is then the sample proportion of cases. However, the individual binary observations might not be independent--leading to overdispersion. The goal of this paper was to demonstrate random-effects models for the estimation of infection prevalence from data which are correlated and in particular, to illustrate a nonparametric random-effects model for this purpose. The nonparametric approach is a relatively recent addition to the random-effects class of models and does not appear to have been discussed previously in the veterinary epidemiology literature. The assumptions for a logistic-regression model with a nonparametric random effect were outlined. In a demonstration of the method on data relating to Salmonella infection in Irish pig herds, the nonparametric method resulted in the classification of herds into a small number of distinct prevalence groups (i.e. low, medium and high prevalence) and also estimated the relative frequency of each prevalence category in the population. We compared the estimates from a logistic model with a nonparametric distribution for the random effects with four alternative models: a logistic-regression model with no random effects, a marginal model using a generalised estimating equation (GEE) and two methods of fitting a Normally distributed random effect (the GLIMMIX macro and the NLMIXED procedure both in SAS). Parameter estimates from random-effects models are not readily interpretable in terms of prevalences. Therefore, we outlined two methods for calculating population-averaged estimates of prevalence from random-effects models: one using numerical integration and the other using Monte Carlo simulation.

Animals↗
PubMed2000

Are women with polycystic ovary syndrome resistant to activated protein C?

OBJECTIVE: This study was performed to test the hypothesis that an increased prevalence of activated protein C (APC) resistance in women with polycystic ovary syndrome (PCOS) puts them at increased risk of miscarriage and thrombosis. DESIGN: Case control study. SETTING: A district general hospital in the United Kingdom. PATIENT(S): Forty-one women with PCOS and 25 controls. INTERVENTION(S): Clinical histories, ultrasound scans, and venepunctures. MAIN OUTCOME MEASURE(S): Diagnosis of PCOS or control, clinical histories, APC resistance according to an activated partial thromboplastin time-based assay. RESULT(S): There was no significant difference in the proportion of women with APC resistance in both groups (three women in the PCOS group [7%] vs. one woman in the control group [4%]). The prevalence of APC resistance in the entire study population was 6.5%. In the PCOS group, 29% (12/41) gave a positive family history of thrombosis compared with 8% (2/25) in the control group. None of the women with a positive family history of thrombosis had abnormal antithrombin 111, protein C, or protein S levels. CONCLUSION(S): This study suggests that women with PCOS may have the same prevalence of APC resistance as the background population and that APC resistance may not put them at a higher risk of thrombosis or miscarriage compared with the case of the general population.

Abortion, Spontaneous↗
PubMed2000

Identification of a novel hybrid glycophorin gene encoding GP.Hop.

BACKGROUND: The GP.Hop (Mi.IV) phenotype expresses the MNS low-incidence antigens Mur, Hop, TSEN, MINY, and MUT. Because serologically similar MNS phenotypes expressing some or all of these antigens were shown to be carried by hybrid GP(B-A-B) proteins, it was proposed that a similar protein would be found for GP.Hop. The identification of a second GP.Hop propositus (ES) initiated a study to determine the molecular basis of this phenotype. STUDY DESIGN AND METHODS: Serologic tests and immunoblotting analysis with glycophorin-specific antibodies were performed. GYPB, the gene encoding the GPB protein, was cloned and sequenced after reverse transcription PCR amplification of total RNA isolated from ES. GYPB-specific primers encompassing GYPB pseudoexon 3, intron 3, and exon 4 were also used to clone and sequence genomic DNA from ES and MH, the original GP.Hop proband. RESULTS: Serologic and immunochemical data confirmed that ES's RBCs carried antigens associated with the GP.Hop phenotype. Sequencing of ES's cDNA demonstrated the presence of genes predicted to encode s-specific GPB and an S-specific GP(B-A-B) hybrid in which the 3' end of GYPB pseudoexon 3 had been replaced by a short nucleotide sequence from exon 3 of the GPA gene (GYPA). The hybrid nucleotide sequence contained sequence motifs previously shown to be required for the expression of the Mur, Hop, TSEN, MINY, and MUT, which is consistent with their presence as detected serologically. Genomic DNA analysis found that the crossover point in GYPB pseudoexon 3 was identical in ES and MH. CONCLUSIONS: The GP.Hop phenotype is produced by a hybrid GP(B-A-B) protein caused by a DNA insertion of GYPA into GYPB. The composition of the hybrid protein is GPB(1-26)-GPpsiB(27-50)-GPA(51-58)-GPB(S)(59-103).

Amino Acid Sequence↗
PubMed2000

Factors impacting on shared care working relationships between practice nurses and general practitioners: a literature review.

Practice nurses have worked in general practice for many years yet little is known or published in Australia about their work. Recent health care reforms in Australia, particularly the establishment of the Divisions of General Practice and various best-practice innovations linked to the National GP Strategy have seen an increase in the role of practice nurses. Despite this GPs in Australia are cautious about the role of practice nurses. Much of this caution arises from reform in general practice in Britain particularly the establishment of fund-holding for general practice. This article reviews the literature on practice nurses in Britain and Australia within the framework of the health reforms in general practice in both countries.

Adult↗
PubMed2000

The role of the practice nurse. An exploratory study.

AIM: There is little research on the role of the practice nurse in Australia. However, there is some evidence that practice nurses are no longer primarily receptionists, but rather function as nurses. This article reports on a small qualitative study that set out to identify areas of effective shared care between general practitioners and practice nurses. METHOD: Semistructured interviews were conducted with general practitioners and practice nurses in eight general practices. A general practitioner who did not employ a practice nurse and a general practitioner and two nurse practitioners at a Community Health Centre were also interviewed. RESULTS: It was found that general practitioners and practice nurses have established effective working relationships that enhance patient care. Shared care was not found, except to some extent in the area of wound care. CONCLUSION: Most GPs and practice nurses interviewed believed that the current funding model, requiring GPs to sight all patients before a fee can be claimed, restricts the potential use of practice nurses' expertise, for example with patients returning for routine blood tests or blood pressure monitoring, or wound dressing. A change to the current model would have implications for the education and accreditation of practice nurses.

Australia↗
PubMed1998

Expression of type 2 11beta-hydroxysteroid dehydrogenase and corticosteroid hormone receptors in early human fetal life.

In adult life, the type 2 isozyme of 11beta-hydroxysteroid dehydrogenase (11betaHSD2) protects the mineralocorticoid receptor (MR) from glucocorticoid by inactivating cortisol to cortisone. 11betaHSD2 activity has been reported in human fetal tissues, where glucocorticoids may impair fetal growth yet are also required for normal fetal development. Using digoxigenin-labeled complementary ribonucleic acid (RNA) probes and an in-house 11betaHSD2 antiserum, we have analyzed the expression of 11betaHSD2, MR, and glucocorticoid receptor (GR) in human fetal tissues of gestational age 6-17 weeks (n=15). 11BetaHSD2 expression was absent at gestational age 6+ weeks, but was expressed in abundance in many fetal tissues between 8-12 weeks. At this time, 11betaHSD2 colocalized with GR messenger RNA (mRNA) expression in metanephros, gut, muscle, spinal cord and dorsal root ganglia, periderm, sex chords of testis, and adrenal. In particular within fetal kidney, intense expression of 11betaHSD2 and GR mRNA was observed over Bowman's capsule and the vascular tufts of developing glomeruli as they migrated from the surface of the kidney to the inner cortex. Only lung and adrenal medullary rests demonstrated high levels of GR mRNA but low levels of 11betaHSD2. 11BetaHSD2 mRNA and immunoreactivity staining patterns were similar, with the exception of the fetal adrenal, where mRNA was localized to the outer definitive zone but immunoreactivity was localized to the inner fetal zone. Colocalization of 11betaHSD2 (and GR mRNA) with MR mRNA was observed principally within epithelial cells of collecting ducts, particularly after 16 weeks gestation when the pattern of distribution of 11betaHSD2 became more adult in nature. High levels of MR mRNA were observed within developing bone. The data indicate that 11betaHSD2 in fetal life principally modulates ligand access to the GR in most fetal tissues, notably glomeruli and tubules in the developing kidney, testis, and periderm, and this may be have ramifications for fetal sodium homeostasis and differentiation. The development of tissues previously shown to have a critical requirement for glucocorticoids, such as lung and adrenal medulla, is facilitated by the expression of GR mRNA, but not 11betaHSD2. The expression of MR mRNA in high abundance in bone suggests a role for corticosteroids in human bone development, and the low/absent expression of 11betaHSD2 at this site suggests that it is functionally acting as a GR.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1997

Ontogeny and sexual dimorphic expression of mouse type 2 11beta-hydroxysteroid dehydrogenase.

11beta-hydroxysteroid dehydrogenase (11beta-HSD) catalyzes the interconversion of cortisol to hormonally inactive cortisone (corticosterone (B) to 11-dehydrocorticosterone (A) in rodents), and as such is established as a pre-receptor signalling pathway for corticosteroid hormone action. To further evaluate the role of this enzyme in adult and fetal life we have characterized two isoforms of 11beta-HSD in mouse tissues. Mouse 'liver' or type 1 11beta-HSD is a bi-directional dehydrogenase/oxo-reductase (K(m) for B 1.9 microM, K(m) for A 0.73 microM). Oxo-reductase activity utilized only NADPH as a co-factor, whilst dehydrogenase activity increased with both NAD or NADP. Mouse 'kidney' or 11beta-HS3D2 activity was NAD-dependent with a K(m) for B of 0.11 microM. Dexamethasone was not a substrate. Using an in-house mouse 11beta-HSD2 cDNA and NAD-dependent activity studies, 11 beta-HSD2 was expressed in epithelial cells of colon, renal collecting ducts, ovary, and adrenal, but was absent in liver, spleen, testis and heart. With the exception of gonadal tissues, activity and mRNA levels were consistently higher in adult male versus female tissues. In fetal kidney and colon there was absent/low levels of 11beta-HSD2 expression from fetal day 15 to term (day 19/20). Placental 11beta-HSD2 mRNA and activity were highest on fetal day 13/14 and fell progressively to undetectable levels by term. Two isoforms of 11beta-HSD are present in mouse tissues in accordance with other mammalian species. The sexual-dimorphic expression 11 beta-HSD2 in kidney and colon may reflect male-female differences in sodium homeostasis, and the absent expression of 11 beta-HSD2 in late gestation may facilitate glucocorticoid-dependent maturation of mouse fetal tissues.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1997

The development of the Louis MACRO (Mother and Child Risk Observation) forms: assessing parent-infant-child risk in the presence of maternal mental illness.

OBJECTIVE: The theoretical framework and psychometric properties of the MACRO (Mother and Child Risk Observation) 1 and 2 forms (age 0 to 4 year) are presented. The MACRO forms provide ratings on five domains--three related to parenting, two on infant (or child) characteristics and maternal mental state. Case vignettes illustrate their clinical utility. METHOD: Ratings on the MACRO of 110 mother-infant and 85 mother-toddler consecutive admissions to a South Australian psychiatric in-patient mother-infant unit provided data on internal consistency, interrater, and test-retest reliability. RESULTS: Internal consistency was between .79 and .95 for all MACRO domains. Item-total correlations were between .39 and .90 with the exception of one item. Social Support. Distributions of item scores indicated acceptable discrimination. Interrater reliability was .79 or above for all domains. Test-retest reliability after 7 days was .71 or above. CONCLUSIONS: Preliminary psychometric investigations of the MACRO was favorable. Should further validity investigations prove satisfactory, the MACRO will provide a valuable clinical and research tool. The MACRO offers a convenient framework for assessing risk and interpreting the impact of maternal mental illness upon children within a context that permits consideration of factors such as illness severity, parenting practices, and child contribution to outcome.

Adolescent↗
PubMed1997

Detection of immunoglobulin G (IgG) and IgM antibodies to Toxoplasma gondii: evaluation of four commercial immunoassay systems.

A comparative evaluation of the following commercial immunoassays for the determination of antibodies to Toxoplasma gondii was performed: Behring Diagnostics OPUS Toxo G and Toxo M, Abbott Diagnostics IMX Toxo-IgG 2.0 and Toxo-IgM, Sanofi Diagnostics Pasteur Platelia Toxo IgG and Toxo IgM, and bioMérieux Vitek VIDAS Toxo IgG and IgM. Of 676 specimens that were tested for Toxoplasma-specific immunoglobulin G (IgG) antibodies, 26% were reactive by all methods while 8% displayed some discrepancy. Of 718 specimens that were tested for Toxoplasma-specific IgM antibodies, 3% were reactive by all methods while 10% displayed some discrepancy. Analysis of discrepant specimens revealed performance shortcomings with all IgM-specific assays. The impact of such shortcomings is magnified in a population with a low prevalence of toxoplasmosis.

Animals↗
PubMed1997

Differential expression of nuclear 11beta-hydroxysteroid dehydrogenase type 2 in mineralocorticoid receptor positive and negative tissues.

Corticosteroid hormone action is controlled at a pre-receptor level by the activity of two isoforms of 11beta-hydroxysteroid dehydrogenase (11beta-HSD), catalyzing the interconversion of hormonally active cortisol to inactive cortisone. In particular 11beta-HSD2 protects the mineralocorticoid receptor (MR) from glucocorticoid excess, enabling aldosterone to interact with the MR. We have analyzed the subcellular localization of 11beta-HSD2 in relation to the expression of the MR in human colon and placenta. 3H-aldosterone binding studies confirmed expression of the MR in human colon but not term placental trophoblast. Enzyme activity studies and Western blot analyses carried out on subcellular fractions confirmed the presence of 11beta-HSD2 in microsomes. In colon, but not placenta, 11beta-HSD2 was also localized to the microsome-free, nuclear fraction. Protection upon the MR by 11beta-HSD2 in "classical" mineralocorticoid target tissues such as colon can be subserved at both a nuclear and extra-nuclear level. Tissue specific factors are responsible for the subcellular localization of 11beta-HSD2 and we postulate that one such factor may be the MR itself.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1996

Evaluation of monoclonal anti-D reagents using D variant cells.

Monoclonal anti-D antibodies submitted to the Third Monoclonal International Workshop were evaluated against a number of D variant cells using standard serological techniques. The monoclonal antibodies were able to discriminate between the cells of Categories Va, VI and DFR but not Category III cells. Cells within each category did not give any aberrant results. The Rh:33 cells behaved as normal Rh(D) positive cells.

Antibodies, Monoclonal↗
PubMed1996

Adrenal 11 beta-hydroxysteroid dehydrogenase.

11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyzes the interconversion of cortisol (F) to inactive cortisone (E) in man (corticosterone (B) to 11-dehydrocorticosterone (A) in rodents) and plays a crucial role in regulating corticosteroid hormone action. Two isoforms of this enzyme have been characterized; a low affinity NADP(H)-dependent enzyme (11 beta-HSD1) and a high affinity NAD-dependent dehydrogenase (11 beta-HSD2). We have analysed the expression of 11 beta-HSD in the rodent and human adrenal gland and have investigated its role with respect to glucocorticoid-mediated catecholamine biosynthesis. Our studies indicated higher expression of 11 beta-HSD2 mRNA in male versus female intact mouse adrenal. Both 11 beta-HSD isoforms were detected in intact male rat adrenal homogenates. For the 11 beta-HSD1 isoform, NADPH-dependent oxo-reductase activity exceeded that of NADP-dependent dehydrogenase activity (188 versus 98 pmol/mg.protein.hr). In situ hybridisation studies indicated specific localisation of 11 beta-HSD1 mRNA to cells at the corticomedullary junction. 11 beta-HSD2 mRNA was uniformly distributed across the cortex and was low/absent in the medulla. Administration of glycyrrhizic acid in vivo (> 100 mg/kg for 4 days) resulted in inhibition of 11 beta-HSD1 mRNA and activity and a decrease in mRNA levels for the glucocorticoid-dependent enzyme, phenylethanolamine N-methyltransferase, whilst levels of the glucocorticoid-independent enzyme, tyrosine hydroxylase were unchanged. No 11 beta-HSD expression was observed in the rat phaeochromocytoma cell line, PC12 cells, nor in human normal adrenal gland or phaeochromocytoma specimens. There are marked species and sex differences in the expression of 11 beta-HSD isoforms within the adrenal. The role of 11 beta-HSD within the adrenal gland remains obscure, but at least in the rat, the expression of the reductase enzyme, 11 beta-HSD1, to the corticomedullary junction may serve to maintain high medullary glucocorticoid concentrations required for catecholamine biosynthesis.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1994

Outcome prediction in childhood acute lymphoblastic leukaemia by molecular quantification of residual disease at the end of induction.

Methods to detect and quantify minimal residual disease (MRD) after chemotherapy for acute lymphoblastic leukaemia (ALL) could improve treatment by identifying patients who need more or less intensive therapy. We have used a clone-specific polymerase chain reaction to detect rearranged immunoglobulin heavy-chain gene from the leukaemic clone, and quantified the clone by limiting dilution analysis. MRD was successfully quantified, by extracting DNA from marrow slides, from 88 of 181 children with ALL, who had total leucocyte counts below 100 x 10(9)/L at presentation and were enrolled in two clinical trials, in 1980-84 and 1985-89. Leukaemia was detected in the first remission marrow of 38 patients, in amounts between 6.7 x 10(-2) and 9.9 x 10(-7) cells; 26 of these patients relapsed. Of 50 patients with no MRD detected, despite study of 522-496,000 genomes, only 6 relapsed. The association between MRD detection and outcome was significant for patients in each trial. In the first trial, patients relapsed at all levels of detected MRD, whereas in the later trial, in which treatment was more intensive and results were better, the extent of MRD was closely related to the probability of relapse (5 of 5 patients with > 10(-3) MRD, 4 of 10 with 10(-3) to 2 x 10(-5), 0 of 3 with levels below 2 x 10(-5), and 2 of 26 with no MRD detected). Early quantification of leukaemic cells after chemotherapy may be a successful strategy for predicting outcome and hence individualizing treatment in childhood ALL, because the results indicate both in-vivo drug sensitivity of the leukaemia and the number of leukaemic cells that remain to be killed by post-induction therapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

The Mental Adjustment to HIV scale: measurement and dimensions of response to AIDS/HIV disease.

Attitudes of people with HIV disease towards HIV have seldom been measured. However, a well-established scale to measure attitudes toward cancer in those with the disease, the 38-item Mental Adjustment to Cancer (MAC) scale was modified to assess adjustment to HIV disease. We administered the scale to 107 Australian men with HIV infection, of whom 36 had an AIDS-defining condition, who were patients at an ambulatory care facility and in a research study. The data were factor analyzed using a method identical to that used in the development of the MAC scale to determine the latent dimensions of attitudes toward HIV/AIDS. The Mental Adjustment to HIV scale (MAH) factor analysis revealed five factors: Helplessness-Hopelessness, Fighting Spirit, and Denial-Avoidance as in the original MAC scale, plus a Fatalism subscale which also measured Preoccupation, and a new subscale, which measured Belief in Influencing the Course of the Disease. Together, these five factors accounted for half of the variance. These data suggest that while there are similarities between mental attitude to cancer and mental attitude to HIV in the latent dimensions of the questionnaire items, there are also some differences. Most significant is the belief in people with HIV disease in being able to personally influence the course of the illness, and the combination of Preoccupation with Fatalism. The five subscales of the MAH scale had Cronbach's alpha reliabilities between 0.80 and 0.55. The MAH appears to be a useful way to measure total attitudes and subscale scores of people with HIV infection, including AIDS, to their disease.

Acquired Immunodeficiency Syndrome↗
PubMed1994

The association between spouse-reported Type A behaviour pattern and coronary heart disease.

This paper describes further validation of the Spouse-Report Type A Behaviour Pattern Questionnaire. In a case controlled study of 61 cardiac patients versus 61 community controls, the questionnaire was found to discriminate statistically between a group of patients with proven coronary heart disease and a group of matched healthy controls on the anger/hostility subscale and total Type A score. No relationship between Type A score and coronary heart disease severity was found. Possible explanations for these findings are examined.

Adult↗
PubMed1993

Hostility and anger measures in coronary heart disease.

Recent research addressing the link between psychological factors and risk of coronary heart disease (CHD) has focused on the areas of hostility and anger and produced sometimes contradictory results. This study makes use of four questionnaire measures of hostility and anger, which were administered to matched groups with and without CHD. Quicker experiences of anger with greater verbal expression best predicted CHD. The difficulties in teasing out the relative contributions of emotional expression, experience and personality using available questionnaires are discussed.

Adult↗