PubMed Health⌕ Search

Biomedical subjects

M E Shaw

Publications and source records attributed to M E Shaw.

At least 19 recordsLinked to original sources
PubMed2005

Analysis of regional variation in hip and knee joint replacement rates in England using Hospital Episodes Statistics.

OBJECTIVES: Total hip and knee joint replacements are effective interventions for people with severe arthritis, and demand for these operations appears to be increasing as our population ages. This study explores regional variations in health care and inequalities in the provision of these expensive interventions, which are high on the UK Government's health agenda. STUDY DESIGN: The Hospital Episode Statistics (HES) for England were analysed. The HES database holds information on patients who are admitted to National Health Service (NHS) hospitals in England. METHODS: Age-standardized procedure rates were calculated using 5-year age groups with the English mid-year population of 2000 as the reference. Univariate associations between age-standardized operation rates and regional characteristics were assessed using Pearson's correlation coefficient. RESULTS: Age and sex-standardized surgery rates vary by 25-30%. For both hip and knee replacement, rates are highest in the South West and Midlands and lowest in the North West, South East and London regions. In the case of knee replacement, there are also marked differences in the sex ratios between regions. The variable that explained most variation in hip replacement rates was the proportion of older people in the region. In the case of knee replacement, the number of NHS centres offering surgery in the region was the main explanatory variable, with regions with fewer centres having the highest provision rates. CONCLUSION: These data can help to inform planning of services. They suggest that there may be inequities as well as inequalities in the provision of primary joint replacement surgery in England.

Aged↗
PubMed2001

Effects of caging type and animal source on the development of foot lesions in Sprague Dawley rats (Rattus norvegicus).

Retrospective analysis of data from a chronic (2-year) rat (Rattus norvegicus) carcinogenicity study was performed to compare the incidence of foot lesion development relative to cage type and animal supplier. Groups of rats from two different suppliers were housed in wire-bottom or polycarbonate cages. Clinical observations and body weights were collected. Data were analyzed to determine foot lesion occurrence, time to onset of foot lesions, and body weight change over time. Noteworthy abnormalities of the plantar surface of the hind foot (i.e., ulcers or nodular swellings) were more common in heavier rats than in lighter animals of the same sex (but different source), and abnormalities were more common in rats housed in wire cages than polycarbonate cages. However, despite differences in weight, cage type, and supplier, lesions were not found until the rats had been housed for more than 1 year.

Animals↗
PubMed1999

Partial allelotype of schistosomiasis-associated bladder cancer.

In Egypt and other regions of the Middle East where the trematode Schistosoma haematobium is endemic, bladder cancer is the most common adult cancer. Unlike bladder cancers in Western countries, which are predominantly transitional-cell carcinoma (TCC), these schistosomiasis-associated bladder cancers are predominantly squamous-cell carcinoma (SCC). Our aim was to assess a large series of schistosomiasis-associated bladder tumours for genetic alterations commonly found in TCC in the United Kingdom and the United States. We have carried out a partial allelotype of 70 tumours from patients with schistosomiasis. LOH was found on all chromosome arms studied (3p, 4p, 4q, 8p, 9p, 9q, 11p, 11q, 13q, 14q, 17p, 18q). The most frequent regions of LOH were 9p (65%), 17p (58%), 3p (40%), 9q (39%) and 8p (37%). LOH on 17p, where the TP53 gene is located, was more common in Egyptian TCC than in SCC. Similarly, 8p LOH was more common in TCC than SCC. The most striking difference between this group of tumours and TCCs from the United Kingdom and the United States was the high frequency of 9p LOH in the region of the CDKN2 gene (65%) and the relatively low frequency of 9q LOH (39%); 15 of 43 tumours with LOH of at least one marker on chromosome 9 showed LOH of 9p only. This suggests that a 9p gene, possibly CDKN2, may contribute to the development of the majority of schistosomiasis-associated bladder tumours but that genes on 9q play a much less important role.

Adenocarcinoma↗
PubMed1998

Clinical correlations with allelotype in supraglottic squamous cancer.

Frequent allelic loss at a genetically polymorphic locus in tumors is an established marker for the presence of a tumor suppressor gene in the neighboring chromosomal region. This technique can be used to identify novel tumor suppressor genes and to monitor their status before the cloning of the gene itself. We have used the polymerase chain reaction and microsatellite loci on all 39 nonacrocentric autosomal chromosomal arms to identify sites of frequent allelic loss in squamous cell carcinomas of the supraglottic larynx. Our allelotype identified seven chromosomal arms (3p, 5q, 8p, 9p, 9q, 13q, and 17p) likely to contain tumor suppressor genes frequently inactivated during squamous tumorigenesis in the larynx. We tested for associations between allelic losses on these chromosomal arms and the clinical and histopathologic features of these tumors. There were no correlations with either T or N classifications. Allelic loss on chromosomal arm 13q is significantly associated with a number of histopathologic features characteristic of poorly differentiated or histologically aggressive tumors. Allelic loss on this arm also exhibits statistical trends toward association with early tumor recurrence and poor survival. The association with survival was substantiated by a multivariate Cox proportional hazards model.

Alleles↗
PubMed1998

Adolescent breakfast skipping: an Australian study.

Eating breakfast is important for the health and development of children and adolescents. This paper reports on the findings of an Australian survey of 699 thirteen-year-olds concerning the extent of skipping breakfast. Results indicated that approximately 12% of the sample skipped breakfast. Gender was the only statistically significant sociodemographic variable, with females skipping at over three times the rate of males. Skippers were more likely to be dissatisfied with their body shape and to have been on a diet to lose weight than were those who ate breakfast. However, in a follow-up telephone survey, the reasons given for skipping breakfast were almost exclusively lack of time and not being hungry in the morning. While North American school nutrition programs have considered poverty to be a key issue in breakfast skipping, these findings suggest that, for Australian adolescents, skipping breakfast is a matter of individual choice.

Adolescent↗
PubMed1995

Deletion mapping of chromosome 11 in carcinoma of the bladder.

Deletions of the short arm of chromosome 11 have been identified by both cytogenetic and molecular criteria in bladder and other types of solid tumor, indicating the presence of one or more suppressor loci in this region. To localize the 11p deletion target(s) more precisely and to screen for loss of heterozygosity (LOH) on the long arm of the chromosome, 100 bladder tumors were analyzed for LOH on chromosome 11 using restriction fragment length polymorphisms (RFLPs) and microsatellite markers mapped to both 11p and 11q. Thirty-four tumors were found to have LOH at 1 or more loci. Of these, 17 had LOH restricted to 11p, 13 had LOH of both 11p and 11q, and 4 had LOH of 11q only. Eight tumors showed LOH at all informative loci indicating probable loss of an entire copy of chromosome 11. A common region of deletion was defined on 11p between D11S922 (11p15.5) and D11S569 (11p15.1-15.2). This region does not include the HRAS or WT1 loci (at 11p15.5 and 11p13, respectively). Seventeen tumors had LOH on 11q, 4 of which had LOH on 11q only. The common region of deletion on 11q was between FGF3 and D11S490 (11q13-q23.2). Two tumors showed LOH on both 11p and 11q with a clear region of retention of heterozygosity between, indicating the existence of two deletion targets on chromosome 11.

Alleles↗
PubMed1995

p16 (CDKN2) is a major deletion target at 9p21 in bladder cancer.

The p16 gene has been identified as a candidate tumour suppressor gene at 9p21, a region commonly deleted in bladder cancer. We screened 140 bladder tumours and 16 cell lines for deletions and sequence variants of p16. Eight cell lines showed homozygous deletion of p16 and two had small sequence variations. All 13 tumours with small defined deletions of 9p21, 18/31 (58%) of tumours with monosomy 9 and 9/91 (10%) of tumours with no chromosome 9 loss of heterozygosity had homozygous deletion of p16. No tumour-specific sequence variants were identified. Deletion mapping revealed a nested set of deletions focused on p16. Six deletions involved p16 but not the related and adjacent gene p15 and one tumour had an intragenic deletion of p16. All other deletions involved both p16 and p15. We conclude that p16 represents the major target for deletion at 9p21 in bladder cancer.

Base Sequence↗
PubMed1994

Frequent loss of heterozygosity for Rb, TP53, and chromosome arm 3p, but not NME1 in squamous cell carcinomas of the supraglottic larynx.

BACKGROUND: The inactivation of some tumor suppressor genes classically manifests itself through the loss of heterozygosity at nearby genetic mapping markers. Inactivation of these genes appears to have diagnostic/prognostic significance in some types of tumors. Molecular genetic tools based on suppressor inactivation might, therefore, have great utility in treatment planning. METHODS: The polymerase chain reaction and highly informative microsatellite markers were used to compare DNA derived from matched sets of tumor and normal tissue samples from 37 supraglottic laryngeal squamous cell carcinomas. Tumor samples were microdissected free of contaminating normal tissue to maximize the detection of allelic loss. Polymerase chain reaction products were fractionated by denaturing gel electrophoresis and were visualized by autoradiography. RESULTS: Allelic losses were frequent at TP53 (56% of the tumors), the retinoblastoma gene (Rb, 59%), and the p13-14 region of chromosome 3 (64%). In contrast, the putative metastasis suppressor, NME1 (also known as NM23), was lost infrequently (7%). NME1 allelic loss did not correlate with the presence of lymph node metastases in these patients. CONCLUSIONS: The high frequencies of allelic loss at TP53, Rb, and 3p13-14 suggest that these suppressors play a major role in laryngeal carcinogenesis. In sharp contrast, the low frequency of loss at NME1 and its equal distribution in nodal metastasis-positive and -negative patients suggests that inactivation of this gene by allelic loss probably does not play a role in the development of regional metastases from these tumors. Allelic loss in 3p13-14 was found in tumors of all histopathologic grades.

Base Sequence↗
PubMed1994

Allelotype of human bladder cancer.

To identify common regions of deletion in human bladder tumors, we have screened 83 cases of transitional cell carcinoma for loss of heterozygosity (LOH) on all autosomal chromosome arms. Seventy-two restriction fragment length polymorphism, variable number of tandem repeats, and minisatellite markers and 18 microsatellite markers were used to obtain a minimum of 50% informative results for each chromosome arm. A mean of 29.6 informative results per patient was obtained from 39 chromosome arms studied, representing information for 76% of chromosome arms. The most frequent losses were apparent monosomies of chromosome 9 (9p, 51%; 9q, 57%). Other frequent losses were on chromosomes 11p (32%), 17p (32%), 8p (23%), 4p (22%), and 13q (15%). LOH of 4p has not been reported previously in bladder carcinoma. The frequency of LOH on all other chromosome arms was < 12%. LOH on chromosome 8p showed a significant association with both high tumor grade and stage, and LOH on 13q showed a significant association with high tumor grade. Fractional allelic loss was calculated for all tumors and had a mean of 0.125 and a median of 0.110. A significant association was found between increased fractional allelic loss and higher tumor grade. An association was also found between LOH of chromosomes 8p and 9q and values for fractional allelic loss > or = the median value. No associations were found between LOH on different pairs of chromosome arms.

Alleles↗
PubMed1993

Preliminary mapping of the deleted region of chromosome 9 in bladder cancer.

Inactivation of a suppressor gene by deletion of chromosome 9 is a candidate initiating event in bladder carcinogenesis. We have used 13 polymorphic markers spanning the length of chromosome 9 in order to map the region of deletion in human bladder carcinomas. In the majority of tumors loss of heterozygosity was found at all informative sites along the chromosome, indicating deletion of the entire chromosome. Nine tumors had selective deletions of chromosome 9. Mapping of the deleted region in these tumors suggests that the target gene is located between D9S22 at 9q22 and D9S18 at 9p12-13.

Chromosome Deletion↗
PubMed1993

98.6 degrees F.

Explore the source record for details and available documents.

Body Temperature↗
PubMed1993

Initiation of bladder cancer may involve deletion of a tumour-suppressor gene on chromosome 9.

Although many genetic lesions including suppressor gene inactivation have been identified in sporadic tumours, the identity of the common initiating or early genetic events in most cases remains obscure. We have analysed tumour and leucocyte DNA from a series of 252 primary human bladder tumours of all grades and stages for deletions of chromosome 9. Probes from four polymorphic loci were used to detect loss of heterozygosity (LOH) in tumour specimens. Fifty-nine per cent of tumours from patients informative at one or more of these loci showed LOH. A comparison of LOH for markers on 9p and 9q indicated that proximal 9p or 9q is the likely site for a candidate bladder tumour-suppressor gene. Most strikingly, LOH was observed not only in tumours of high grade or stage but also in > 50% of grade 1 and 2 superficial (pTa) tumours. This is the first change to be identified at significant frequency in such tumours. Inactivation of a tumour-suppressor gene on chromosome 9 may therefore be an early genetic event in the development of bladder cancer.

Chromosome Deletion↗
PubMed1993

Deletion mapping of chromosome 8 in cancers of the urinary bladder using restriction fragment length polymorphisms and microsatellite polymorphisms.

We have used a combination of restriction fragment length polymorphism (RFLP) markers and highly informative microsatellite polymorphisms to map a common region of deletion on chromosome 8p in cancers of the urinary bladder. Analysis of loss of heterozygosity (LOH) using microsatellite polymorphisms was shown to be at least as sensitive as detection of RFLPs by Southern blotting. A total of 110 tumours was analysed for loss of heterozygosity (LOH) on 8p and 8q; 109 patients were informative for at least one marker on each chromosome arm and 29 tumours (26%) showed LOH of chromosome 8 markers, 26 of which (25%) showed LOH on 8p. Sixteen tumours (14%) showed LOH on 8q. Thirteen of these also had LOH on 8p. Of the 29 tumours with LOH, five had LOH at all informative loci, indicating loss of an entire copy of chromosome 8. An association was found between high tumour grade and stage and chromosome 8 LOH. Fifty-three per cent of grade 3 muscle-invasive tumours showed LOH compared with 11% of grade 1 non-invasive tumours (0.01 < P < 0.025 and 0.025 < P < 0.05 for grade and stage respectively). Deletion mapping of tumours with chromosome 8 LOH suggests the presence of a suppressor gene(s) for urothelial cancer within a region defined by the loci NEFL and PLAT (8p21-q11.2). If there is a common target for deletions in bladder and those in hepatocellular and colorectal tumours reported previously, this defines a common region of deletion at 8p21.3.

Base Sequence↗
PubMed1987

Effects of exposure to NO2 on dome formation in alveolar epithelial cell monolayers.

Primary cultured monolayers of rat Type II pneumocytes were used to investigate the effects of NO2 on alveolar epithelial barrier properties. Such monlayers form fluid-filled domes which are thought to result from active solute transport from medium to substratum, with water following passively. Using dome formation as a transport marker, 5-day-old cultures were directly exposed to 30 ppm NO2 in 5% CO2/air at 25 degrees C by cyclically tilting culture plates from side to side such that both halves of the monolayer were exposed during each cycle. Exposures consisted of 10 cycles of 4 min each (2 min per side), for a cell exposure time of 20 min. Control plates were simultaneously exposed to 5% CO2/air under identical conditions. Twenty-four hours after exposure, NO2-exposed monolayers exhibited significant decreases in dome density and individual dome volume as compared to controls. By 48 hr postexposure, differences between NO2-exposed and control values were less but remained significant. Control monolayers were essentially unaffected by exposure to 5% CO2/air. These results show that short-term sublethal exposures to NO2 produce a decrease in dome formation in Type II alveolar epithelial cell monolayers. This finding is most likely due to a decrease in the active transepithelial sodium transport rate and/or an increase in the permeability of cell membranes or tight junctions.

Animals↗
PubMed1987

Effects of nitrogen dioxide on alveolar epithelial barrier properties.

This study analyzed the effects of nitrogen dioxide (NO2) on alveolar epithelial permeability and transport properties. Primary cultured monolayers of rat Type II pneumocytes, cultured on both nonporous and porous surfaces, were used as models of isolated alveolar epithelium for in vitro exposure to nitrogen dioxide. The effects of nitrogen dioxide exposure for monolayers cultured on nonporous substrata were monitored by observing the changes in the net volume of fluid under the monolayer; for cells cultured on porous substrata, alterations in tissue bioelectric properties were noted. As a first step, primary cultured monolayers of rat Type II pneumocytes plated on nonporous plastic Petri dishes were used to investigate the effects of nitrogen dioxide on alveolar epithelial barrier properties. Such monolayers form fluid filled domes that are thought to result from active solute transport from medium to substratum, with water following passively. We used dome formation as a transport marker. Five-day-old cultures were directly exposed to 30 ppm NO2 in 5 percent CO2 in air at 25 degrees C, by cyclically tilting culture plates from side to side, so that both halves of the monolayer were exposed during each cycle. Exposures consisted of 10 cycles of four minutes each (two minutes per side), for a cell exposure time of 20 minutes. Control plates were simultaneously exposed to 5 percent CO2 in air under identical conditions. One day after the exposure, nitrogen dioxide-exposed monolayers exhibited significant decreases in dome density and individual dome volume, compared to the controls. By 48 hours post-exposure, differences between nitrogen dioxide-exposed and control monolayers were less, but remained significant. These results showed that short-term sublethal exposures to nitrogen dioxide produce a decrease in dome formation in Type II alveolar epithelial cell monolayers. This finding is most likely due to a decrease in the active transepithelial sodium transport rate, or an increase in the permeability of cell membranes or tight junctions, or both. Addition of vitamin E-containing liposomes to the culture media 24 hours pre-exposure did not affect the nitrogen dioxide-induced decrease in dome formation, indicating that under these circumstances no protective effect was provided by the antioxidant.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1979

Managing in style.

Explore the source record for details and available documents.

Administrative Personnel↗