Biomedical subjects

J L Wright

Publications and source records attributed to J L Wright.

At least 73 records · Page 4Linked to original sources

PubMed1998

A critical assessment of high-earning orthodontists in the General Dental Services of England and Wales (1990-1991)

Cases from the Dental Practice Board's 2 per cent random sample of completed cases which had been treated by orthodontic practitioners with high gross earnings, were compared to all the cases within the sample from other practitioners. They were assessed using the PAR index and IOTN. High earning orthodontists treated slightly more cases with lower objective need for treatment, but treated no more cases 'Unnecessarily' than other practitioners. They used more fixed appliances, and had marginally better levels of residual need for treatment at finish, although this was at least partially explained by lower levels at start. Generally, their standards were not substantially different to other practitioners. Appliance type had a marked effect on outcome, as did levels of malocclusion and need for treatment at start. Both groups of practitioners performed similarly (better) with dual arch fixed appliances: however, overall standards could only be described as mediocre. There is no justification to single out high earning orthodontists for special scrutiny. However, it may be beneficial if the system of remuneration in the General Dental Services could be modified to give more positive incentive to quality, rather than simply quantity of treatments.

Analysis of Variance↗

PubMed1998

Isolation of Enterobacter intermedium from the gallbladder of a patient with cholecystitis.

We describe the isolation and identification of Enterobacter intermedium from the gallbladder of a patient with cholecystitis. There have been only four documented isolations of this organism from humans; it normally occurs in surface water and unpolluted soils. The identification was initially made by a MicroScan Walk/Away system with a Neg Combo 18 conventional identification-susceptibility panel. The organism is susceptible to the aminoglycosides and imipenem but resistant to the cephalosporins and ciprofloxacin.

Anti-Bacterial Agents↗

PubMed1998

Comparison of the uptake of fine and ultrafine TiO2 in a tracheal explant system.

To examine the relationship between particle uptake by pulmonary epithelial cells and particle size, we exposed rat tracheal explants to fine particles (FPs; 0.12 micron) or ultrafine particles (UFPs; 0.021 micron) of titanium dioxide for 3 or 7 days. By electron microscopy, particles were found in the epithelium at both time points, but in the subepithelial tissues, they were found only at 7 days. The volume proportion of both FPs and UFPs in the epithelium increased from 3 to 7 days; it was greater for UFPs at 3 days but was greater for FPs at 7 days. The volume proportion of particles in the subepithelium at 7 days was equal for both dusts, but the ratio of epithelial to subepithelial volume proportion was approximately 2:1 for FPs and 1:1 for UFPs. Mean volume of individual particle aggregates was similar for both dusts at 3 days but was markedly smaller for FPs at 7 days. These observations suggest that the behavior of particles of different size is complex: UFPs persist in the tissues as relatively large aggregates, whereas the size of FP aggregates becomes smaller over time. UFPs appear to enter the epithelium faster, and once in the epithelium, a greater proportion of them is translocated to the subepithelial space compared with FPs. However, if it is assumed that the volume proportion is representative of particle number, the number of particles reaching the interstitial space is directly proportional to the number applied; i.e., overall, there is no preferential transport from lumen to interstitium by size.

Animals↗

PubMed1998

Biosynthesis of domoic acid by the diatom Pseudo-nitzschia multiseries.

The biosynthesis of the neurotoxin domoic acid (DA) in the diatom Pseudo-nitzschia multiseries was investigated using 13C- and 14C-labelled precursors. The labelling pattern determined by NMR spectroscopy following incorporation of [1,2-13C2]-acetate showed enrichment of every carbon of DA. The enrichment levels were consistent with a biosynthetic pathway involving two different intermediate precursor units. Addition of labelled acetate either early or late during exponential growth gave similar patterns and levels of incorporation. Analysis of the labelling pattern indicated that DA is biosynthesised by condensation of an isoprenoid intermediate with another intermediate derived from the tricarboxylic acid (TCA) cycle. The absence of deuterium at C2 in DA following incorporation of [2-13C, 2H3]-acetate is consistent with alpha-ketoglutarate or a derivative as the TCA cycle-derived intermediate. The different incorporation efficiencies of acetate into the putative precursor intermediates suggest that either each unit is biosynthesized in a different part of the diatom cell, or that the isoprene chain is not assembled by the usual acetate-mevalonate pathway. The latter proposal is supported by the complete absence of deuterium retention in the isoprenoid-derived portion following incorporation of [2-13C, 2H3]-acetate.

Acetates↗

PubMed1998

The use of myofunctional appliances in the UK: a survey of British orthodontists.

A questionnaire was sent out to members of the British Orthodontic Society in an attempt to establish how myofunctional appliances are currently used in the UK and to attempt to explain the differences between provider groups. This article reports the findings of this survey and that, of all the appliances currently available, British orthodontists prefer to use the Twin Block appliance. Furthermore, most of the sample questioned felt that the laboratory cost of many myofunctional appliances meant their provision under the General Dental Service was not practical.

Analysis of Variance↗

PubMed1998

Antioxidant gene expression in rat lung after exposure to cigarette smoke.

To investigate the effects of cigarette smoke on the expression of genes encoding intracellular antioxidant species, we exposed rats to whole cigarette smoke or air (control) daily for 1, 2, 7, or 14 days. After sacrifice, RNA was extracted from one lung and expression of mRNA for catalase (CAT), manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZnSOD), glutathione peroxidase (GPX), and metallothionein (MT) was determined by Northern blots and dot blots. The anatomical distribution of expression of these genes was determined by in situ hybridization studies on sections of the contralateral lung. We found that expression of both MnSOD and MT was significantly increased (to levels 70 to 400% greater than in controls) at days 1 and 2 and returned to control levels by day 7. GPX expression was slightly but significantly increased at days 7 and 14 in smoke-exposed animals. CuZnSOD and CAT expression did not change from control levels. In control lungs, MnSOD was expressed in all cell types, with the highest expression seen in bronchial epithelial cells; a notable finding was a mosaic pattern of expression in the bronchial epithelium, with contiguous areas of bronchial epithelium composed of cells expressing MnSOD at high levels (hot spots), compared with the adjacent epithelium. In smoke-exposed lungs, the hot spots became less prominent after 1 and 2 days of exposure to smoke, but after 7 and 14 days the distribution of MnSOD expression was similar in control and smoke-exposed animals. CAT, CuZnSOD, GPX, and MT also showed widespread expression in the lung by in situ hybridization; GPX, CuZnSOD and MT were all most highly expressed in bronchial epithelium, whereas CAT expression levels were similar in all cell types. In contrast to MnSOD, expression of CAT, CuZnSOD, GPX, and MT was uniform within the bronchial epithelium, and the distribution of expression was the same in control and smoke-exposed animals at all time points. We conclude that most of these antioxidant enzymes and scavengers show prominent bronchial expression but that MnSOD shows a unique pattern, with intense hot spots in the epithelium of the small airways. This pattern is similar to the phenomenon of clonal heterogeneity described in other tissues but not previously reported in the lung. We conclude that cigarette smoke, like other forms of oxidant attack, transiently increases expression of MnSOD, and up-regulation of MnSOD expression appears to occur particularly in bronchial epithelial cells, which normally express MnSOD at relatively low levels. MT expression is also transiently increased by smoke whereas GPX expression increases after prolonged (7 to 14 days) exposure to cigarette smoke.

Animals↗

PubMed1998

Data elements for emergency department systems, release 1.0 (DEEDS): a summary report. DEEDS Writing Committee.

Variations in the way that data are entered in emergency department record systems impede the use of ED records for direct patient care and deter their reuse for many other legitimate purposes. To foster more uniform ED data, the Centers for Disease Control and Prevention's National Center for Injury Prevention and Control is coordinating a public-private partnership that has developed recommended specifications for many observations, actions, instructions, conclusions, and identifiers that are entered in ED records. The partnership's initial product, Data Elements for Emergency Department Systems, Release 1.0 (DEEDS), is intended for use by individuals and organizations responsible for ED record systems. If the recommended specifications are widely adopted, then problems--such as data incompatibility and high costs of collecting, linking, and using data--can be substantially reduced. The collaborative effort that led to DEEDS, Release 1.0 sets a precedent for future review and revision of the initial recommendations.

Emergency Service, Hospital↗

PubMed1997

Clinical guidelines for dentistry: will they be useful?

OBJECTIVE: To review the literature on the development and effectiveness of clinical guidelines. DESIGN: Literature review of relevant publications following a Medline search. Publications that reported studies investigating effectiveness of guidelines were confined to randomised controlled trials. CONCLUSIONS: If guidelines are to be effective they should be (i) based on high levels of scientific evidence, (ii) developed with input from the dentists who will be using them and (iii) presented in a satisfactory manner. Importantly, the effectiveness of the guidelines should be rigorously evaluated.

Decision Making↗

PubMed1997

Effects of an intratumoral injection of human recombinant tumor necrosis factor-alpha on cerebrovascular permeability and leukocytic infiltration in a rat glioma model.

The pro-inflammatory and blood-brain barrier (BBB) effects of intratumoral (IT) injection of human recombinant tumor necrosis factor-alpha (rTNF-alpha) were studied in the Fischer rat RT-2 glioma model. Animals received a single stereotaxic injection of either 6 x 10(4) U rTNF-alpha or excipient (vehicle) into the center of an intracerebrally implanted glioma. In order to demonstrate any effects rTNF-alpha might have on the BBB, studies were conducted using endogenous IgG (150 kD) as a tracer. Forty-eight hours following injection of excipient, a margin of peritumoral IgG extravasation was observed while rats treated with 6 x 10(4) U rTNF-alpha showed a dense and extensive IgG extravasation involving both hemispheres. Histological examination revealed that an IT rTNF-alpha injection induced leukocytic adherence, neutrophilic cuffing and infiltration throughout the lesion from 12 to 72 h after injection. These histological observations were supported by quantification of cerebral myeloperoxidase (MPO) levels which indicated a significant increase in neutrophils over the excipient recipients at 4 and 12 h. These MPO levels contrasted with our earlier studies in normal rats which revealed no significant difference in tissue MPO levels following injection of excipient or rTNF-alpha. In addition, when MPO levels in tumor models and normal rats receiving TNF were compared, a significantly greater presence of neutrophils was seen in tumor models at 12 h post-TNF injection. We believe that the increased inflammatory response seen in a progressing glioma compared to normal brain may be the result of decreased resistance to leukocytic infiltration due to increased vascular surface area, the lack of infiltration-resistant perivascular basement membrane, and/or increased extracellular space.

Animals↗

PubMed1997

Comparative toxicity of the diarrhetic shellfish poisons, okadaic acid, okadaic acid diol-ester and dinophysistoxin-4, to the diatom Thalassiosira weissflogii.

Quantitative structure-activity relationships were determined for the diarrhetic shellfish poisoning (DSP) toxins, okadaic acid (OA), OA diol-ester and dinophysistoxin-4 (DTX-4), using a sensitive bioassay procedure with the diatom Thalassiosira weissflogii. OA diol-ester was found to be nearly as toxic as OA. This result contradicted the accepted idea that only the free acid toxins, such as DTX-1 and OA, are potent phosphatase inhibitors. Postassay analyses using liquid chromatography-mass spectrometry (LC-MS) of cultures incubated with OA diol-ester showed that the ester had partially decomposed to OA, which explained some but not all of the observed toxicity. The formation of OA during the bioassay raised the possibility that cells exposed to inactive DSP toxin esters could metabolically activate them. This was examined in an additional experiment which showed that the hydrolysis of both DTX-4 and OA diol-ester was spontaneous and apparently not mediated by the presence of T. weissflogii cells. However, cells of T. weissflogii challenged with OA diol-ester rapidly metabolized most of the toxin to a more water-soluble product. From interpretation of mass spectral data obtained using ion-spray LC-MS, the metabolite was identified as an oxygenated diol-ester of OA, implying that it was the product of a monooxygenase-detoxification pathway. It is postulated that OA diol-ester, as a lipid-soluble, uncharged molecule with a propensity to hydrolyse to OA, may facilitate the transfer of OA across cell walls and membranes.

Animals↗

PubMed1997

Factors affecting the outcome of orthodontic treatment within the general dental service.

Previous studies have suggested large differences in the outcome of orthodontic treatment as measured by the PAR index in two adjacent regions of England. The aim of this prospective study was to identify any factors contributing to the mean PAR score reduction in the North Western region and the Mersey region. Forty-one practitioners submitted 375 sets of start models and 250 end of treatment models. The study ran for 36 months. There were no significant differences detected in the type of malocclusion treated or in outcome of treatment between the two regions with respect to the PAR and IOTN indices. This study did, however, clearly demonstrate that qualified orthodontic practitioners were achieving significantly better results with fixed appliances that practitioners with no orthodontic qualification who used fixed appliances.

Adolescent↗

PubMed1997

Site of methacholine reactivity in the peripheral airways: analysis using lung explants.

We used a recently developed lung explant technique to investigate the partitioning of airway contractility in the bronchioles of normoresponsive and hyperresponsive rats. Specifically, we addressed the questions 1) whether airway response to methacholine varied with airway size and 2) whether airways from rats known to be innately hyperresponsive to methacholine (Fisher) would have responses different from normoresponsive rats (Sprague-Dawley). We found that, in both strains of rats, contraction to methacholine occurred primarily in the medium- and larger-sized bronchioles (airways of diameter > 0.32 mm) and that, at the higher methacholine concentrations, the Fisher rats had greater degrees of contraction than did the Sprague-Dawley rats. These results suggest that the increased airway responsiveness seen in Fisher rats is due to an intrinsic increase in responsiveness (increased contractility) of their airways, which may be related to amount of smooth muscle, rather than an increase in airway sensitivity to methacholine. They do not, however, completely rule out the possibility of in vivo species-dependent differences in airway-parenchymal interactions.

Airway Resistance↗

PubMed1997

Endothelin-A receptor antagonist BQ-610 blocks cigarette smoke-induced mitogenesis in rat airways and vessels.

To ascertain whether endothelin may play a role in cigarette smoke-induced cell proliferation in the airways and arterial vasculature of the lung, we exposed groups of seven Sprague-Dawley rats to either room air (control) plus saline infusion, an intravenous infusion of the selective endothelin A antagonist BQ-610 (control BQ-610), the smoke of 10 cigarettes (smoke only), or the smoke of 10 cigarettes after intravenous BQ-610 infusion (smoke + BQ-610). Cell proliferation was quantified by determining the percentage of cell nuclei labeled by 5-bromo-2'-deoxyuridine. We separately evaluated the cells in the epithelium and wall components of the bronchioles, and endothelium and wall components of the peribronchiolar and perialveolar ductular arteries. We found that cigarette smoke produced significant cell proliferation in the airway epithelium and wall, in the peribronchiolar arterial endothelial compartment, and in both the endothelial and wall compartments of the perialveolar ductular arteries. Pretreatment with BQ-610 reduced the peribronchiolar arterial endothelial and the perialveolar ductular arterial wall proliferation to control lev- els and reduced but did not totally abrogate the smoke-in- duced proliferation of the airway epithelial, airway wall, and perialveolar ductular arterial endothelial compartments. We conclude that cigarette smoke-induced cell proliferation of the airways and pulmonary arterial vessels is at least partially mediated through stimulation of the endothelin-A receptors.

Animals↗

PubMed1997

Guinea pig pulmonary hypertension caused by cigarette smoke cannot be explained by capillary bed destruction.

Chronic exposure to cigarette smoke is known to produce pulmonary hypertension in humans and in animal models, but the etiology of this process is controversial. To evaluate whether alterations in the structure of the pulmonary capillary bed or the peribronchiolar arterioles could be correlated with the pulmonary arterial pressure (Ppa), we examined the pulmonary vasculature in guinea pigs that had developed pulmonary hypertension after being exposed to cigarette smoke for 6 mo. The smoke-exposed animals had a significant increased Ppa compared with the control (air-exposed) animals (14.4 +/- 2.4 vs. 9.9 +/- 0.9 cmH2O). In the smoke-exposed animals, there was an increased percentage of muscularized peribronchiolar arterioles (33.5 +/- 5.8% smoke exposed vs. 56.1 +/- 5.8% control), and the capillary diameter and density were significantly decreased in both the center and periphery of the lobule (center diameter 8.8 +/- 1.9, periphery diameter 10.0 +/- 2.0 microns, center density 79 +/- 5, and periphery density 84 +/- 4 in smoked exposed vs. center diameter 7.7 +/- 1.9, periphery diameter 8.6 +/- 2.0 microns, center density 73 +/- 6, and periphery density 77 +/- 6 in controls). Neither group showed any correlation between these values and the Ppa. We conclude that although chronic exposure to cigarette smoke produces alteration of the capillary bed and pulmonary arterioles secondary to emphysematous air-space enlargement, these structural findings cannot explain the increase in Ppa. It appears that pulmonary hypertension due to chronic cigarette smoke exposure is a result of a primary alteration of capillary or muscular arteriolar vascular structure but instead may be secondary to alterations of the dynamic properties of the vascular bed with subsequent increase in vascular resistance.

Animals↗

PubMed1997

A longitudinal analysis of pulmonary function in rats during a 12 month cigarette smoke exposure.

We wanted to examine the longitudinal effects of chronic cigarette smoke exposure, and to determine whether the chronic alterations in pulmonary function induced by long-term cigarette smoke exposure in an animal model could be predicted by initial or early alterations in function. A group of Sprague Dawley rats was exposed to the smoke of 7 cigarettes x day(-1) for 5 days x week(-1) during a total period of 12 months. Lung volume, flow-volume curves and pressure-volume curves were recorded at baseline, and after 2, 4, 8 and 12 months of smoke exposure. A control group of rats was subjected to the same regimen of testing, but was not exposed to smoke. Thirteen rats completed the study in the smoke-exposed group and seven rats in the control group. We found that chronic exposure to cigarette smoke produced early abnormalities in pulmonary function, with the forced expiratory volume in one second/forced vital capacity (FEV1/FVC) ratio showing an acceleration of ageing effect, particularly between 4 and 8 months of exposure. In this model, although the two groups had significantly different airflow after 12 months, the initial values in each group were remarkably similar, and we could not identify any pulmonary function test which had predictive value. We conclude that longitudinal studies of cigarette smoke exposure in this rat model allow better characterization of the nature and time course of the effects of smoking on the lung.

Animals↗

PubMed1996

Resuscitating the pediatric patient.

Cardiopulmonary resuscitation in the pediatric patient population is a rare and often terminal event. This article addresses the anticipatory approach to the sick child with a focus on recognizing illness before resuscitation becomes necessary. An appreciation of the unique developmental, anatomic, and physiologic differences in children in terms of their relation to the assessment of illness is emphasized. Definitive interventions for the child who progresses to extremis also are described.

Adolescent↗

PubMed1996

Isolation and structure of prorocentrolide B, a fast-acting toxin from Prorocentrum maculosum.

A new toxin, prorocentrolide B (1), has been isolated following bioassay-guided fractionation of a BuOH extract of the tropical dinoflagellate, Prorocentrum maculosum Faust. This compound produces a rapid toxic response in the mouse bioassay, a type of activity not accounted for by other diarrhetic shellfish poisoning toxins produced by P. maculosum. The structure 1 was established by NMR and MS and is similar to prorocentrolide (2), a toxin from a strain of Prorocentrum lima. NMR data and the modeling program ConGen have been used to establish the relative stereochemistry of some individual ether ring systems and the hexahydroisoquinoline ring.

Animals↗

PubMed1996

Morphologic determinants of airway responsiveness in chronic smokers.

Nonspecific bronchial hyperresponsiveness (NSBH) occurs in asthmatics and in smokers who have airway obstruction. NSBH may be caused by different mechanisms in these conditions. We hypothesized that NSBH in smokers was a consequence of the structural changes that occur in chronic obstructive pulmonary disease (COPD) and lead to airway obstruction. We measured nonspecific bronchial responsiveness, assessed by PC20, in 77 smokers who had mild to moderate airflow obstruction prior to lung resection for a pulmonary nodule. We related airway responsiveness to baseline airway function (FEV1 % predicted), to functional (PLmax, PL90, and P-V curve shape) and morphometric (alveolar attachments) markers of lung elasticity as well as to thickening in small airways. Airway wall thickness, internal and external to the outer border of smooth muscle was quantified by plotting the square root of airway wall area versus a marker of airway size, airway internal perimeter (Pi). PC20 was significantly related to FEV1% predicted and PLmax. and when these functional parameters were controlled for, PC20 was also inversely related to airway wall thickness. There was also a trend for the most responsive patients to have fewer alveolar attachments per millimeter on the external perimeter of the airway walls. These data suggest that exaggerated nonspecific airway narrowing in COPD is secondary to structural changes caused by the disease.

Aged↗