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Biomedical subjects

D R Taylor

Publications and source records attributed to D R Taylor.

At least 37 records · Page 2Linked to original sources
PubMed2000

Craniofacial form and obstructive sleep apnea in Polynesian and Caucasian men.

STUDY OBJECTIVES: This aim of this study was to determine the relative contributions of craniofacial form and anthropometric factors to obstructive sleep apnea (OSA) in two different racial groups, both markedly obese and with a similar mean respiratory disturbance index (RDI). DESIGN: A cross-sectional study of New Zealand Maori (Polynesian) and European (Caucasian) men with RDI> or =15, using lateral and postero-anterior cephalometric radiography. SETTING: N/A. PATIENTS OR PARTICIPANTS: N/A. MEASUREMENTS AND RESULTS: Measurements of facial and cranial width, length and height, airway size, stature, weight, body mass index (BMI), neck circumference, RDI, and age were obtained. The Polynesian men had, on average, a greater neck circumference than the Caucasian men. There were no significant differences in age, weight, BMI or RDI between the two groups. The Polynesian men also had broader craniofacial skeletons, larger and more prognathic mandibles, greater neck extension, and some larger airway dimensions than the Caucasian men. In the Polynesian men, the width of the bony nasal aperture was positively associated with RDI, and mandibular prognathism was negatively associated with RDI. In contrast, in the Caucasian men only neck circumference was positively associated with RDI, while the retropalatal airway was negatively associated with RDI. CONCLUSIONS: The results indicate that OSA in these two racially distinct groups is due to different etiological factors. Small reductions in mandibular prognathism and a wider bony nasal aperture were major factors associated with OSA in Polynesians. On the other hand, in the Caucasian group OSA was associated with a larger neck circumference and a reduced retropalatal airway size.

Anthropometry↗
PubMed2000

Intrinsic constraint on plasmablast growth and extrinsic limits of plasma cell survival.

B cells recruited into splenic antibody responses grow exponentially, either in extrafollicular foci as plasmablasts, or in follicles where they form germinal centers. Both responses yield plasma cells. Although many splenic plasma cells survive <3 d, some live much longer. This study shows that early plasma cell death relates to a finite capacity of the spleen to sustain plasma cells rather than a life span endowed by the cell's origin or the quality of antibody it produces. Antibody responses were compared where the peak numbers of plasma cells in spleen sections varied between 100 and 5,000 cells/mm(2). In each response, plasmablast clones divided some five times, with the peak numbers of plasma cells produced relating directly to the number of B cells recruited into the response. The spleen seems to have the capacity to sustain between 20 and 100 plasma cells/mm(2). When this number is exceeded, there is a loss of excess cells. Immunoglobulin variable region gene sequencing, and 5-bromo-2'-deoxyuridine pulse-chase studies indicate that long-lived splenic plasma cells are a mixture of cells derived from the extrafollicular and germinal center responses and cells derived from virgin and memory B cells. Only a proportion has switched immunoglobulin class.

Animals↗
PubMed2000

Hepatitis C virus: evasion of the interferon-induced antiviral response.

Hepatitis C virus (HCV) is an emerging virus of great medical significance. A low drug-response rate and a high frequency of persistent infection have caused HCV to reach pandemic proportions. Many infected individuals go on to develop liver cirrhosis and hepatocellular carcinoma, and HCV is now the leading reason for liver transplants in the United States. Differences in genotype response to interferon therapy suggests that one or more viral genes may participate in evasion of the interferon-mediated cellular antiviral response. This review focuses on the viral genes that interact with the host cell to evade the interferon response and on the insights that these interactions may provide into HCV pathogenesis.

Antiviral Agents↗
PubMed2000

Gastric pneumatosis following cardiac surgery.

Infiltration of the stomach wall by air, first described by Fraenkel in 1889 [3], is a very rare condition. We describe the first reported case of gastric pneumatosis occurring in a child with complex congenital heart disease after cardiac surgery.

Enteral Nutrition↗
PubMed2000

Identification of endogenous gibberellins in strawberry, including the novel gibberellins GA123, GA124 and GA125.

Extracts of carboxylic acids from immature fruits of strawberry (Fragaria x ananassa Duch. cv. Elsanta) were analysed for gibberellins by combined gas chromatography-mass spectrometry. The following previously characterised gibberellins were identified by comparison of their mass spectra and Kovats retention indices (KRIs) with those of standards or published data: GA1, GA3, GA5, GA8, GA12, GA17, GA19, GA20, GA29, GA44, GA48, GA49, GA53, GA77, GA97, GA111 and GA112. Evidence for endogenous 1-epi GA61 (GA119) and 11alpha-OH-GA12 was also obtained. In addition, a number of putative GAs were detected. Of these, three were shown to be 12alpha-hydroxy-GA53, 12alpha-hydroxy-GA44, and 12alpha-hydroxy-GA19 by comparison with authentic compounds prepared by rational synthesis, and have been allocated the descriptors GA123, GA124 and GA125, respectively.

Fruit↗
PubMed2000

Hepatitis C virus and interferon resistance.

Interferon plays a critical role in the host's natural defense against viral infections and in their treatment. It is the only therapy for hepatitis C virus (HCV) infection; however, many virus isolates are resistant. Several HCV proteins have been shown to possess properties that enable the virus to evade the interferon-mediated cellular antiviral responses.

Animals↗
PubMed2000

The respiratory effects of cannabis dependence in young adults.

AIM: To evaluate the relationship between cannabis dependence and respiratory symptoms and lung function in young adults, while controlling for the effects of tobacco smoking. SETTING AND PARTICIPANTS: Nine hundred and forty-three young adults from a birth cohort of 1037 subjects born in Dunedin, New Zealand in 1972/1973 were studied at age 21. MEASUREMENTS: Standardized respiratory symptom questionnaires were administered. Spirometry and methacholine challenge tests were undertaken. Cannabis dependence was determined using DSM-III-R criteria. Descriptive analyses and comparisons between cannabis-dependent, tobacco-smoking and non-smoking groups were undertaken. Adjusted odds ratios for respiratory symptoms, lung function and airway hyper-responsiveness (PC20) were measured. FINDINGS: Ninety-one subjects (9.7%) were cannabis-dependent and 264 (28.1%) were current tobacco smokers. After controlling for tobacco use, respiratory symptoms associated with cannabis dependence included: wheezing apart from colds, exercise-induced shortness of breath, nocturnal wakening with chest tightness and early morning sputum production. These were increased by 61%, 65%, 72% (all p < 0.05) and 144% (p < 0.01) respectively, compared to non-tobacco smokers. The frequency of respiratory symptoms in cannabis-dependent subjects was similar to tobacco smokers of 1-10 cigarettes/day. The proportion of cannabis-dependent study members with an FEV1/FVC ratio of < 80% was 36% compared to 20% for non-smokers (p = 0.04). These outcomes occurred independently of co-existing bronchial asthma. CONCLUSION: Significant respiratory symptoms and changes in spirometry occur in cannabis-dependent individuals at age 21 years, even although the cannabis smoking history is of relatively short duration.

Adolescent↗
PubMed2000

Bronchodilator tolerance and rebound bronchoconstriction during regular inhaled beta-agonist treatment.

There is uncertainty about the development of airway tolerance to beta-agonists and the phenomenon of rebound bronchoconstriction on beta-agonist withdrawal. We have recently completed a study of the regular terbutaline and budesonide treatment in asthma. We report our observations on the effect of starting and stopping terbutaline treatment on morning and evening peak flows. The study was a randomized four-way, double-dummy, cross-over comparison of regular inhaled terbutaline (500-1000 microg four times daily), budesonide, combined treatment and matching placebo. Each treatment was given for 6 weeks following a 4 week single-blind placebo washout. Ipratropium was used for symptom relief. No other asthma medication was permitted during either the treatment or wash-out periods. Evaluable data were obtained from 52 subjects for both placebo and terbutaline treatment. Changes in mean morning and evening peak flows during terbutaline treatment were compared to the baseline peak flows during the last 2 weeks of the preceding washout. The peak flow changes on stopping terbutaline were also analysed. Mean morning peak flow was not significantly different during terbutaline treatment when compared to either baseline or placebo treatment. Evening peak flows were significantly higher during terbutaline treatment [mean increase 23.1 l min(-1) (95% CI = 18.8, 27.4)]. Analysis of the peak flow changes on a day-by-day basis revealed an initial increase in morning peak flows for the first 2 days of treatment of 19.2 and 13.41 min(-1) [increases of 25.0 and 17.31 min(-1) in comparison with the corresponding values during placebo (P<0.01)] followed by a return to baseline. The increase in evening peak flows was also greater for the first 2 days of treatment than for the remainder of the treatment period (P<0.01). On ceasing terbutaline treatment there was a fall in mean morning peak flow below the baseline on the following morning of 21.6 l min(-1) (P<0.05 compared to placebo). The temporary increase in morning peak flows and greater than expected rise in evening peak flows for the first 2 days of treatment suggest the development of tolerance to the bronchodilator effect of terbutaline. Similarly, the fall in morning peak flows on treatment withdrawal suggests rebound bronchoconstriction. These effects are likely to be mediated by downregulation of the beta-receptor during treatment. The clinical significance of these changes is uncertain in view of the stability of overall asthma control during terbutaline treatment, but sudden withdrawal of beta-agonist treatment could conceivably lead to a deterioration in asthma control.

Administration, Inhalation↗
PubMed2000

Asthma exacerbations during long term beta agonist use: influence of beta(2) adrenoceptor polymorphism.

BACKGROUND: Polymorphisms of the beta(2) adrenoceptor influence receptor function in vitro and asthma phenotypes in vivo. However, their importance in determining responses to inhaled beta agonist treatment has not been clearly defined. METHODS: In a retrospective analysis of previously published data we have examined relationships between polymorphisms at codons 16 and 27 of the beta(2) adrenoceptor and clinical outcomes in a randomised, placebo controlled, crossover trial of regularly scheduled salbutamol and salmeterol in 115 patients with mild to moderate asthma. Genotyping was obtained for positions 16 and 27 in 108 and 107 patients, respectively. For position 16, 17 patients (16%) were homozygous Arg-Arg, 40 (37%) were heterozygous Arg-Gly, and 51 (47%) were homozygous Gly-Gly. RESULTS: Within the homozygous Arg-16 group major exacerbations were more frequent during salbutamol treatment than with placebo (1.91 (95% CI 1.07 to 3.12) per year versus 0.81 (95% CI 0.28 to 1.66) per year; p = 0.005). No significant treatment related differences occurred for heterozygous Arg-Gly patients (salbutamol 0.11 (95% CI 0.01 to 0.40), placebo 0.54 (95% CI 0.26 to 1.00) exacerbations per year) or homozygous Gly-16 patients (salbutamol 0.38 (95% CI 0.17 to 0.73), placebo 0.30 (95% CI 0.12 to 0.61) exacerbations per year). No adverse changes occurred for any position 16 subgroup with salmeterol. There was no significant relationship between position 27 genotypes and treatment related outcomes. CONCLUSION: Homozygous Arg-16 patients are susceptible to clinically important increases in asthma exacerbations during chronic dosing with the short acting beta(2) agonist salbutamol.

Adolescent↗
PubMed2000

The influence of polymorphism at position 16 of the beta2-adrenoceptor on the development of tolerance to beta-agonist.

Polymorphism at position 16 of the beta2-adrenoceptor alters receptor down-regulation in vitro. Our aim was to compare the development of tolerance to beta-agonist in homozygous Gly-16 patients with patients harboring the "wild" genotype (homozygous Arg-16) during regular treatment with salmeterol. In a prospective, randomized, double-blind, placebo-controlled, cross-over study, 20 subjects with mild to moderate asthma (10 Gly-16, 10 Arg-16) received 2 weeks of treatment with inhaled salmeterol 100 microg b.i.d. Thereafter, dose responses to inhaled salbutamol were constructed for forced expiratory volume in 1 sec (FEV1), heart rate, QTc interval, serum potassium and glucose, and finger tremor. The protective effect of salbutamol against adenosine monophosphate (AMP) challenge was also measured. Salmeterol resulted in a significant reduction in the area under curve (AUC) for FEV1 (p = 0.01), heart rate (p = 0.01), QTc interval (p = 0.01), and tremor (p = 0.05), and in the maximum responses for FEV1 (p = 0.05), heart rate (p = 0.02), and glucose (p = 0.02). The protective effect of salbutamol against AMP was reduced by 3.61 doubling doses (p < 0.001). However, differences between Gly-16 and Arg-16 patients were small and nonsignificant. Thus, although tolerance is influenced in vitro by polymorphism of the beta2-adrenoceptor, the magnitude of between-genotype differences in vivo is unlikely to be significant.

Adrenergic beta-Agonists↗
PubMed1999

Excessive use of inhaled salbutamol: the potential benefits of dose-reduction. A case report.

Inhaled, short-acting, beta-agonist medications are widely used in the treatment of asthma. It is recommended in current asthma management guidelines that these medications should only be used "as required" for relief of asthma symptoms. Despite this, there are still a number of asthmatic patients who are using excessive amounts. In occasional patients this may be detrimental to the control of asthma. We report the case of a 43-year-old, steroid-dependent asthmatic, with unstable asthma, using salbutamol up to 30 times a day. Following reduction of her beta-agonist use she had a dramatic improvement in her asthma control and was able to successfully stop her oral steroids.

Administration, Inhalation↗
PubMed1999

Hepatitis C virus RNA polymerase and NS5A complex with a SNARE-like protein.

Hepatitis C virus (HCV) NS5A is a phosphoprotein that possesses a cryptic trans-activation activity. To investigate its potential role in viral replication, we searched for the cellular proteins interacting with NS5A protein by yeast two-hybrid screening of a human hepatocyte cDNA library. We identified a newly discovered soluble N-ethylmaleimide-sensitive factor attachment protein receptor-like protein termed human vesicle-associated membrane protein-associated protein of 33 kDa (hVAP-33). In vitro binding assay and in vivo coimmunoprecipitation studies confirmed the interaction between hVAP-33 and NS5A. Interestingly, hVAP-33 was also shown to interact with NS5B, the viral RNA-dependent RNA polymerase. NS5A and NS5B bind to different domains of hVAP-33: NS5A binds to the C-terminus, whereas NS5B binds to the N-terminus of hVAP-33. Immunofluorescent staining showed a significant colocalization of hVAP-33 with both NS5A and NS5B proteins. hVAP-33 contains a coiled-coil domain followed by a membrane-spanning domain at its C-terminus. Cell fractionation analysis revealed that hVAP-33 is predominantly associated with the ER, the Golgi complex, and the prelysosomal membrane, consistent with its potential role in intracellular membrane trafficking. These interactions provide a mechanism for membrane association of the HCV RNA replication complex and further suggest that NS5A is a part of the viral RNA replication complex.

Animals↗
PubMed1999

Inhibition of the interferon-inducible protein kinase PKR by HCV E2 protein.

Most isolates of hepatitis C virus (HCV) infections are resistant to interferon, the only available therapy, but the mechanism underlying this resistance has not been defined. Here it is shown that the HCV envelope protein E2 contains a sequence identical with phosphorylation sites of the interferon-inducible protein kinase PKR and the translation initiation factor eIF2alpha, a target of PKR. E2 inhibited the kinase activity of PKR and blocked its inhibitory effect on protein synthesis and cell growth. This interaction of E2 and PKR may be one mechanism by which HCV circumvents the antiviral effect of interferon.

Cell Line↗
PubMed1999

Bronchoprotective and bronchodilator effects of single doses of (S)-salbutamol, (R)-salbutamol and racemic salbutamol in patients with bronchial asthma.

OBJECTIVES: The drug salbutamol is used as a 50: 50 racemic mixture of its two enantiomers, (R)- and (S)-salbutamol. Previous studies suggest that the (R)-enantiomer is active, and the (S)-enantiomer is either inert or may be responsible for adverse effects. The aim of the study was to measure the protection given against methacholine (MCh) and adenosine monophosphate (AMP) by (R)-, (S)- and rac-salbutamol and their bronchodilator effects. METHODS: A double-blind, placebo-controlled, four-way cross-over study was performed in subjects with mild to moderate asthma. There were three groups: AMP30 (n = 10), MCh30 (n = 13) and MCh180 (n = 10). The groups received AMP or MCh challenges at either 30 min or 180 min after each of four pretreatments: 100 microg (S)-salbutamol, 100 microg (R)-salbutamol, 200 microg rac-salbutamol or placebo (normal saline), each administered via nebuliser. Spirometry was measured at 30, 60, 90, 120, 150 and 180 min in the MCh180 group. RESULTS: (R)- and rac-salbutamol showed equivalent bronchoprotective effects at 30 min. PC20AMP increased by 3.22 (1.86) and 3.41 (2.15) doubling doses (P < 0.001) and PC20MCh increased by 2.86 (1.09) and 2.75 (0.89) (P < 0.001) respectively. (S)-salbutamol caused no equivalent effect. There was no significant effect at 180 min. No hyper-responsiveness occurred after treatment with (S)-salbutamol. The mean increase in forced expiratory volume in 1 s (FEV1) was 12.4% (6.8%) with (R)- and 12.0%(7.7%) with rac-salbutamol at 90 min. No significant change in FEV1 occurred with (S)-salbutamol. CONCLUSIONS: These results confirm other recent findings that the bronchoprotective and bronchodilator effects of salbutamol are attributable to its (R)-enantiomer. No adverse effects were noted after single doses of (S)-salbutamol.

Adenosine Monophosphate↗
PubMed1999

Characterization of microbial communities using randomly amplified polymorphic DNA (RAPD).

Similarity among a number of aquatic microbial communities was examined using randomly amplified polymorphic DNA (RAPD), a common polymerase chain reaction (PCR)-based DNA fingerprinting technique. After amplification of whole-community DNA extracts, the PCR products were resolved by agarose gel electrophoresis and the band patterns compared to determine percent similarity. Twelve different primers were used to amplify approximately 100 fragments (total) from each DNA sample; the bands were scored as present or absent and the similarity between each sample was determined using Jaccard's coefficient. From this information. dendrograms were constructed and a bootstrapping procedure was used to assess how well supported the tree topologies were. Principal component analyses were also conducted as a means of visualizing the relationships among samples. Results obtained for two different experimental systems (a pair of tidal creeks and several wells in a shallow groundwater aquifer) correlated well with the temporal and spatial variations in environmental regime at the sites confirming that arbitrarily primed PCR-based DNA fingerprinting techniques such as RAPD are useful means of discriminating among microbial communities and estimating community relatedness. Moreover, this approach has several advantages over other DNA-based procedures for whole-community analysis; it is less laborious and uses smaller quantities of DNA, making it amenable to sample-intensive monitoring, and it does not depend on culturing or the use of selective PCR primers.

Bacteria↗
PubMed1999

Tolerance to beta-agonists during acute bronchoconstriction.

Previous reports suggest that regular use of beta-agonists does not lead to tolerance to their bronchodilator effects. However, most studies have been conducted in stable asthma. This study investigates whether bronchodilator tolerance can be demonstrated during acute bronchoconstriction. Thirty-four asthmatic subjects were treated with 6 weeks inhaled terbutaline (1 mg q.i.d.), budesonide (400 microg, b.i.d.), both drugs or placebo in a randomized, double-blind, cross-over study. After each treatment methacholine was administered to induce a 20% fall in the forced expiratory volume in one second (FEV1). The response to inhaled salbutamol 100, 100, 200 microg at 5 min intervals) was then measured. Dose-response curves were compared using an analysis of covariance. Pre-methacholine FEV1, the highest pre-methacholine FEV1, the fall in FEV1 induced by methacholine and the logarithm of the provocative dose of methacholine required to induce the 20% fall in FEV1 (PD20) were used as covariates. There was a significantly reduced response to salbutamol after 6 weeks terbutaline treatment: the mean (95% confidence intervals (CI)) area under the dose-response curve was reduced by 36% (24, 47) compared to placebo (p<0.0001). The reduction in bronchodilator response was not affected by concomitant treatment with budesonide. Significant tolerance to the bronchodilator effect of inhaled beta-agonists may be demonstrated when tested during acute bronchoconstriction. Continuous treatment with inhaled beta-agonists may lead to a reduced response to emergency beta-agonist treatment during asthma exacerbations.

Acute Disease↗