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Biomedical subjects

S Eaton

Publications and source records attributed to S Eaton.

At least 73 records · Page 4Linked to original sources
PubMed1998

Comparison of PCR- and hybrid capture-based human papillomavirus detection systems using multiple cervical specimen collection strategies.

This study compared the performances of three human papillomavirus (HPV) detection tests with specimens collected by three alternative procedures. The HPV tests included the Hybrid Capture Tube test (HCT), the microplate-based Hybrid Capture II test (HC II), and the MY09-MY11 L1 consensus primer PCR-based assay. Initial cervical specimens were collected from study subjects with a broom device, and after Papanicolaou smears were made, residual specimens were placed into PreservCyt (PC), a liquid cytology medium. A second specimen was collected from each subject and placed into Digene Specimen Transport Medium (STM). The device for collection of the second specimen alternated with consecutive subjects between a conical cytology brush and a Dacron swab. At the 1.0-pg/ml cutoff, the results of the HC II agreed well with those of the PCR. Specifically, when PCR data were restricted to the types found by the HC II (HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68), there was greater than 90% agreement between the HC II and PCR results with both STM and PC. At a lower cutoff (0.2 pg/ml), HC II-positive results increased further, especially when the test was applied to the PC specimens. However, false-positive HC II results were more often observed at the 0.2-pg/ml cutoff. HC II yielded the highest HPV positivity with specimens placed into PC, followed by specimens collected with a conical brush and placed into STM and, last, by those collected with a Dacron swab and placed into STM. Our results demonstrate the utility of both the STM and PC specimen collection methods and show good agreement between the HC II and PCR.

Adult↗
PubMed1998

The subtle politics of organ donation: a proposal.

Organs available for transplantation are scarce and valuable medical resources and decisions about who is to receive them should not be made more difficult by complicated calculations of desert. Consideration of likely clinical outcome must always take priority when allocating such a precious resource otherwise there is a danger of wasting that resource. However, desert may be a relevant concern in decision-making where the clinical risk is identical between two or more potential recipients of organs. Unlikely as this scenario is, such a decision procedure makes clear the interdependence of organ recipient and organ donor and hints at potential disadvantages for those who are willing to accept but unwilling to donate organs (free-riders). A combined opting-out and preference system weakens many of the objections to opting-out systems and may make the decision to donate organs on behalf of their deceased relatives easier for families.

Ethics, Medical↗
PubMed1998

Smith-Lemli-Opitz syndrome: a variable clinical and biochemical phenotype.

We have reviewed all known UK cases of Smith-Lemli-Opitz syndrome. Among 49 cases with proven 7-dehydrocholesterol reductase deficiency, half had been terminated or had died in infancy. The minimum incidence is 1 in 60,000. The frequent occurrence of hypospadias may account for 71% of recognised cases being male. Important common features which emerged include short thumbs, severe photosensitivity, aggressive behaviour, and atrioventricular septal defect. The typical facial appearance becomes less obvious with age and 20% of cases did not have 2/3 toe syndactyly. Biochemical measurements of serum 7-dehydrocholesterol did not correlate with clinical severity.

Adult↗
PubMed1998

The Fresno Asthma Project: a model intervention to control asthma in multiethnic, low-income, inner-city communities.

The Fresno Asthma Project targeted the entire low-income, inner-city, multiethnic population of Fresno, California. For 36 months following a 6-month planning phase, continuing education was provided to a high proportion of physicians, pharmacists, nurses/respiratory therapists, emergency medical technicians, school personnel, and allied health professionals involved in asthma care in Fresno, including virtually all those providing care/services to the target population. Small group patient education was made available and provided in age- and culturally appropriate formats to patients/families in clinics, hospitals, and schools. General and ethnic media and a Speakers Bureau were used to raise public awareness of asthma as a serious but controllable health problem. This community intervention model is particularly appropriate to multiethnic communities. It is relatively low cost (total direct costs were $140,000 per year), uses existing educational resources, and appears to have minimized counterproductive competition. Although morbidity and mortality trend data are not yet available to monitor program impact, penetration into the target community has been substantial: community physicians refer patients to asthma classes, asthma educator training is ongoing through the local American Lung Association chapter, hospitals and managed care systems serving low- income/MediCal patients offer asthma classes, and public schools and HeadStart are institutionalizing asthma awareness and self-management classes.

Adult↗
PubMed1997

Planar polarization of Drosophila and vertebrate epithelia.

Our understanding of the actin and microtubule rearrangements that generate planar polarity in Drosophila and in vertebrate epithelia has been extended by recent discoveries. Three different Rho family proteins have been shown to mediate polarization in the wing and the eye of Drosophila. In vertebrates, the importance of myosin VIIa has been uncovered by mutations that cause defects in planar polarization in the ear. Advances in our understanding of the Frizzled pathway, which coordinates planar polarization in Drosophila, are moving the field closer to understanding the links between signal transduction and polarized cytoskeletal reorganization.

Animals↗
PubMed1997

Multiple biochemical effects in the pathogenesis of alcoholic fatty liver.

The pathogenesis of alcoholic fatty liver is unknown, but several causes have been proposed based on biochemical findings. These include the metabolism of alcohol leading to a shift in the cytosolic [NAD+]/ [NADH] ratio to reduction, which in turn causes a direct inhibition of beta-oxidation and enhanced triacylglycerol formation via the [glycerol-3-phosphate]/[dihydroxyacetone phosphate] ratio. There are also chronic effects of ethanol on hepatic enzyme activities. Thus, increased activity of phosphatidate phosphohydrolase, an increased amount of fatty acid binding protein, decreased secretion of very low-density lipoprotein and impairment of the respiratory chain as a result of decreased protein synthesis or decreased amounts of ubiquinone could all lead to fat accumulation and steatosis. The interplay of each of these with nutritional and genetic factors would then lead to the heterogeneity of the severity and characteristics of the steatosis observed in human alcoholics.

Ethanol↗
PubMed1996

Mammalian mitochondrial beta-oxidation.

The enzymic stages of mammalian mitochondrial beta-oxidation were elucidated some 30-40 years ago. However, the discovery of a membrane-associated multifunctional enzyme of beta-oxidation, a membrane-associated acyl-CoA dehydrogenase and characterization of the carnitine palmitoyl transferase system at the protein and at the genetic level has demonstrated that the enzymes of the system itself are incompletely understood. Deficiencies of many of the enzymes have been recognized as important causes of disease. In addition, the study of these disorders has led to a greater understanding of the molecular mechanism of beta-oxidation and the import, processing and assembly of the beta-oxidation enzymes within the mitochondrion. The tissue-specific regulation, intramitochondrial control and supramolecular organization of the pathway is becoming better understood as sensitive analytical and molecular techniques are applied. This review aims to cover enzymological and organizational aspects of mitochondrial beta-oxidation together with the biochemical aspects of inherited disorders of beta-oxidation and the intrinsic control of beta-oxidation.

Acyl-CoA Dehydrogenases↗
PubMed1996

The effect of respiratory chain impairment of beta-oxidation in rat heart mitochondria.

Cardiac ischaemia leads to an inhibition of beta-oxidation flux and an accumulation of acyl-CoA and acyl-carnitine esters in the myocardium. However, there remains some uncertainty as to which esters accumulate during cardiac ischaemia and therefore the site of inhibition of beta-oxidation [Moore, Radloff, Hull and Sweely (1980) Am. J. Physiol. 239, H257-H265; Latipää (1989) J. Mol. Cell. Cardiol. 21, 765-771]. When beta-oxidation of hexadecanoyl-CoA in state III rat heart mitochondria was inhibited by titration of complex III activity, flux measured as 14CO2 release, acid-soluble radioactivity or as acetyl-carnitine was progressively decreased. Low concentrations of myxothiazol caused reduction of the ubiquinone pool whereas the NAD+/NADH redox state was less responsive. Measurement of the CoA and carnitine esters generated under these conditions showed that there was a progressive decrease in the amounts of chain-shortened saturated acyl esters with increasing amounts of myxothiazol. The concentrations of 3-hydroxyacyl and 2-enoyl esters, however, were increased between 0 and 0.2 microM myxothiazol but were lowered at higher myxothiazol concentrations. More hexadecanoyl-CoA and hexadecanoyl-carnitine were present with increasing concentrations of myxothiazol. We conclude that 3-hydroxyacyl-CoA dehydrogenase and acyl-CoA dehydrogenase activities are inhibited by reduction of the ubiquinone pool, and that this explains the confusion over which esters of CoA and carnitine accumulate during cardiac ischaemia. Furthermore these studies demonstrate that the site of the control exerted by the respiratory chain over beta-oxidation is shifted depending on the extent of the inhibition of the respiratory chain.

Acetylcarnitine↗
PubMed1996

Wnt signal transduction: more than one wat to skin a (beta-)cat?

Genetic and biochemical studies have suggested that signal transduction by the Wnt pathway is very different to the familiar protein-kinase cascade of the Ras pathway. Among the more intriguing findings is that beta-catenin, a component of intercellular adhesive junctions, is a central component in the Wnt signalling pathway. Recent studies suggest ways in which beta-catenin might serve as a focal point for regulation of adhesion, gene expression and cell proliferation.

Journal Article↗
PubMed1996

beta-Oxidation in human alcoholic and non-alcoholic hepatic steatosis.

1. The CoA and carnitine ester intermediates of mitochondrial beta-oxidation have not previously been quantified in liver disease, although there is some evidence that beta-oxidation is inhibited in alcoholic fatty liver. Mitochondria were isolated from needle liver biopsies from normal subjects, from patients with alcoholic fatty liver and patients with fatty liver of other aetiologies, incubated with 60 mumol/l [U-14C]hexadecanoate and the resultant CoA and carnitine esters were measured. 2. Although there was no significant difference in beta-oxidation flux between the patient groups, there was a significant rise in the proportion of 3-hydroxyacyl-CoA and 2-enoyl-CoA esters in patients with alcoholic fatty liver compared with normal subjects, and in patients with non-alcoholic fatty liver, suggesting an inhibition at the level of 3-hydroxyacyl-CoA dehydrogenase activity. 3. In alcoholic patients this difference could not be accounted for on the basis of the measured activity of short and long-chain 3-hydroxyacyl-CoA dehydrogenases, and it is suggested that either an inhibition of complex I activity or diminished amounts of ubiquinone are likely to be responsible for the observed accumulation of CoA and carnitine esters, which may contribute to the accumulation of triacylglycerols in alcoholic steatosis. In fatty liver of other aetiologies, short- and long-chain 3-hydroxyacyl-CoA dehydrogenase activities were decreased.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1996

Roles for Rac1 and Cdc42 in planar polarization and hair outgrowth in the wing of Drosophila.

The wing of Drosophila melanogaster is covered by an array of distally pointing hairs. A hair begins as a single membrane outgrowth from each wing epithelial cell, and its distal orientation is determined by the restriction of outgrowth to a single distal site on the cell circumference (Wong, L., and P. Adler. 1993. J. Cell Biol. 123:209-211.). We have examined the roles of Cdc42 and Rac1 in the formation of wing hairs. We find that Cdc42 is required for localized actin polymerization in the extending hair. Interfering with Cdc42 activity by expression of a dominant negative protein abolishes both localized actin polymerization and hair outgrowth. In contrast, Rac1 is important for restricting the site at which hairs grow out. Cells expressing the dominant negative Rac1N17 fail to restrict outgrowth to a single site and give rise to multiple wing hairs. This polarity defect is associated with disturbances in the organization of junctional actin and also with disruption of an intricate microtubule network that is intimately associated with the junctional region. We also find that apical junctions and microtubules are involved in structural aspects of hair outgrowth. During hair formation, the apical microtubules that point distally elongate and fill the emerging wing hair. As the hair elongates, junctional proteins are reorganized on the proximal and distal edges of each cell.

Actin Cytoskeleton↗