PubMed Health⌕ Search

Biomedical subjects

E Crowley

Publications and source records attributed to E Crowley.

15 recordsLinked to original sources
PubMed2006

Dental caries and enamel fluorosis among the fluoridated population in the Republic of Ireland and non fluoridated population in Northern Ireland in 2002.

BACKGROUND: An all Ireland/North South survey of Oral Health was carried out in 2001/2002. AIMS: To compare levels of dental caries and enamel fluorosis among children and adolescents in the fluoridated Republic of Ireland (RoI) with those in the non fluoridated North of Ireland (NI). METHODOLOGY: Cross sectional oral health survey of a representative, random, stratified sample of 5-, 8-, 12- and 15-year-olds in Rol and in NI (N = 19,950). WHO examination criteria with the addition of visible, non cavitated dentine caries were used for recording caries. Fluorosis was measured using Dean's Index. RESULTS: In the RoI, the mean d(3c)mft / D(3c)MFT for 5-, 8-, 12-, and 15-year-olds with full domestic water fluoridation (n = 9,975), was 1.0, 0.3, 1.1 and 2.1 respectively. The corresponding means in non fluoridated NI (n = 1,475) were 1.8, 0.3, 1.5 and 3.6 respectively. (p < 0.0001, NS, p < 0.0005 and p < 0.0001). The prevalence of enamel fluorosis has increased in RoI since 1984, 23% and 36% of 8- and 15-year olds respectively in fluoridated areas had Dean's Index scores at the questionable or greater level in 2002 compared with 6% and 5% respectively in 1984. CONCLUSIONS: In 2002 apart from 8-year-olds, caries levels were lower amongst children resident in fluoridated communities in RoI than amongst corresponding age groups in non-fluoridated NI. Caries has declined in fluoridated and non fluoridated groups in both jurisdictions since the early 1960s. In RoI fluorosis levels were higher amongst lifetime residents of fluoridated communities and have increased since 1984.

Adolescent↗
PubMed2005

Parents' preference as to whether they would like to accompany their child when receiving dental treatment--results from a national survey.

BACKGROUND AND DESIGN: parental accompaniment of children during dental treatment has always been a contentious issue. One of the factors that should be considered is the preference of the parents. The aim of this paper is to report the preference of parents of eight-year-old schoolchildren in Ireland in relation to accompanying their child during dental procedures and is part of the National Survey of Children's Dental Health in Ireland, which was conducted between October 2001 and June 2002. The survey had a cross sectional design and parents of children (average age 8.4 years) selected for dental examination were asked to complete a questionnaire. RESULTS: 3629 completed questionnaires were obtained from parents of eight-year-old children giving a response rate of 68 per cent. Sixty-seven per cent of parents expressed a preference to accompany their child during dental treatment, while nine per cent expressed a preference not to accompany their child. The sex of the child (p = 0.33) or the fact that the parents were holders of a medical card (surrogate for disadvantage) (p = 0.08) did not affect parents' preference. However, parents of a single child had a higher preference (78 per cent) for accompanying their child than did parents with greater than one child in the family unit (66 per cent) (p = 0.0009). CONCLUSION: If given the choice, the majority of parents would prefer to accompany their child when receiving dental treatment.

Adult↗
PubMed2004

Dental caries and enamel fluorosis among the fluoridated and non-fluoridated populations in the Republic of Ireland in 2002.

BACKGROUND: A national survey of oral health of children and adolescents was carried out in the Republic of Ireland (RoI) in 2001/2002. AIMS: To compare the prevalence of caries between child and adolescent residents in fluoridated and non-fluoridated communities in the RoI whilst controlling for disadvantage. To compare caries levels amongst disadvantaged and non-disadvantaged groups with and without water fluoridation. To report the changes in caries levels between the 1960s and 2002 in RoI. To report the changes in dental fluorosis levels between 1984 and 2002. METHODOLOGY: Cross sectional oral health survey of a representative, random, stratified sample of 17,851 5-, 8-, 12- and 15-year-old children and adolescents in RoI. WHO examination criteria with the addition of visible, non-cavitated dentine caries were used for recording caries. Fluorosis was measured using Dean's Index. RESULTS: In the RoI the mean dmft/DMFT scores for 5-, 8-, 12-, and 15-year-olds were 1.2, 0.3, 1.1 and 2.3. For those with domestic water fluoridation since birth the scores were 1.0, 0.3, 1.1 and 2.1 respectively. In non-fluoridated areas of RoI the mean dmft/DMFT scores for 5-, 8-, 12-, and 15-year-olds was 1.7, 0.3, 1.3 and 3.2, respectively. For 5-, 12- and 15-year-old age groups dental caries levels were lower amongst children with fluoridated domestic water supplies (all p<0.0001). The prevalence of dental fluorosis has increased in RoI since 1984. 23% and 36% of 8- and 15-year olds respectively in fluoridated areas had Dean's Index scores at the questionable or greater level in 2002, compared with 6% and 5% respectively in 1984. CONCLUSIONS: Caries levels are lower among children with fluoridated domestic water supplies. Decay levels are much lower in 2002 than they were in 1984 and in the 1960s. The oral health of the less well off is worse than that of the rest of the population. The prevalence of dental fluorosis is higher amongst children and adolescents with fluoridated water supplies. Comparisons with 1984 data show an increase in the prevalence of fluorosis since that time.

Adolescent↗
PubMed2002

Outcomes of patients with chronic renal insufficiency in the bypass angioplasty revascularization investigation.

BACKGROUND: Although severe chronic kidney disease (CKD) is an independent predictor of mortality among patients with coronary artery disease, the impact of mild CKD on morbidity and mortality has not been fully defined. METHODS AND RESULTS: Morbidity and mortality for the 3608 patients with multivessel coronary artery disease enrolled in the Bypass Angioplasty Revascularization Investigation randomized trial and registry were compared on the basis of the presence and absence of CKD, defined as a preprocedure serum creatinine level of >1.5 mg/dL. Seventy-six patients had CKD. Patients with renal insufficiency were older and more likely to have a history of diabetes, hypertension, and other comorbidities. Among patients undergoing PTCA, patients with CKD had a greater frequency of in-hospital death and cardiogenic shock (P<0.05 and 0.01, respectively). There was a trend toward a larger proportion of patients with CKD experiencing angina at 5 years (P=0.079). Patients with CKD had more cardiac admissions (P=0.003 and <0.0001 for patients undergoing PTCA and CABG, respectively) and a shorter time to subsequent CABG after initial revascularization than patients without CKD (P=0.01). CKD was associated with a higher risk of death at 7 years, both of all causes (relative risk 2.2, P<0.001) and of cardiac causes (relative risk 2.8, P<0.001). CONCLUSIONS: CKD is associated with an increased risk of recurrent hospitalization, subsequent CABG, and mortality. This increased risk of death is independent of and additive to the risk associated with diabetes.

Angina Pectoris↗
PubMed2002

Polymerase eta and p53 jointly regulate cell survival, apoptosis and Mre11 recombination during S phase checkpoint arrest after UV irradiation.

Xeroderma pigmentosum variant (XPV) cells lack the damage-specific polymerase eta and undergo a protracted arrest at the S phase checkpoint(s) following UV damage. The S phase checkpoints encompass several qualitatively different processes, and stimulate downstream events that are dependent on the functional state of p53. Primary fibroblasts with wild-type p53 arrest in S, and require a functional polymerase eta (pol eta) to carry out bypass replication, but do not recruit recombination factors for recovery. XPV cells with non-functional p53, as a result of transformation by SV40 or HPV16 (E6/E7), recruit the hMre11/hRad50/Nbs1 complex to arrested replication forks, coincident with PCNA, whereas normal transformed cells preferentially use the pol eta bypass replication pathway. The formation of hMre11 foci implies that arrested replication forks rapidly undergo a collapse involving double strand breakage and rejoining. Apoptosis occurs after UV only in cells transformed by SV40, and not in normal or XPV fibroblasts or HPV16 (E6/E7) transformed cells. Conversely, ultimate cell survival in XPV cells was much less in HPV16 (E6/E7) transformed cells than in SV40 transformed cells, indicating that apoptosis was not a reliable predictor of cell survival. Inhibition of p53 transactivation by pifithrin-alpha or inhibition of protein synthesis by cycloheximide did not induce hMre11 foci or apoptosis in UV damaged fibroblasts. Inhibition of kinase activity with wortmannin did not increase killing by UV, unlike the large increase seen with caffeine. Since HPV16 (E6/E7) transformed XPV cells were highly UV sensitive and not further sensitized by caffeine, it appears likely that caffeine sensitization proceeds through a p53 pathway. The S phase checkpoints are therefore, a complex set of different checkpoints that are coordinated by p53 with the capacity to differentially modulate cell survival, apoptosis, bypass replication and hMre11 recombination.

Acid Anhydride Hydrolases↗
PubMed2001

DNA polymerase eta undergoes alternative splicing, protects against UV sensitivity and apoptosis, and suppresses Mre11-dependent recombination.

Polymerase eta (pol eta) is a low-fidelity DNA polymerase that is the product of the gene, POLH, associated with the human XP variant disorder in which there is an extremely high level of solar-induced skin carcinogenesis. The complete human genomic sequence spans about 40 kb containing 10 coding exons and a cDNA of 2.14 kb; exon I is untranslated and is 6 kb upstream from the first coding exon. Using bacterial artificial chromosomes (BACs), the gene was mapped to human chromosome band 6p21 and mouse band 17D. The gene is expressed in most tissues, except for very low or undetectable levels in peripheral lymphocytes, fetal spleen, and adult muscle; exon II, however, is frequently spliced out in normal cells and in almost half the transcripts in the testis and fetal liver. Expression of POLH in a multicopy episomal vector proved nonviable, suggesting that overexpression is toxic. Expression from chromosomally integrated linear copies using either an EF1-alpha or CMV promoter was functional, resulting in cell lines with low or high levels of pol eta protein, respectively. Point mutations in the center of the gene and in a C-terminal cysteine and deletion of exon II resulted in inactivation, but addition of a terminal 3 amino acid C-terminal tag, or an N- or C-terminal green fluorescent protein, had no effect on function. A low level of expression of pol eta eliminated hMre11 recombination and partially restored UV survival, but did not prevent UV-induced apoptosis, which required higher levels of expression. Polymerase eta is therefore involved in S-phase checkpoint and signal transduction pathways that lead to arrest in S, apoptosis, and recombination. In normal cells, the predominant mechanism of replication of UV damage involves pol eta-dependent bypass, and Mre11-dependent recombination that acts is a secondary, backup mechanism when cells are severely depleted of pol eta.

Alternative Splicing↗
PubMed2001

Celecoxib-induced Sweet's syndrome.

Sweet's syndrome and related neutrophilic dermatoses have been associated with a variety of medications. Celecoxib is a new cyclo-oxygenase-2 inhibitor recently approved for arthritis. We describe a 57-year-old man who experienced tender pustulopapular lesions on the dorsal aspects of the hands, neck, and legs 1 week after starting celecoxib. Histopathologic examination of the lesion showed a diffuse dermal neutrophilic infiltrate, edema of the papillary dermis, spongiform pustules, and no leukocytoclastic vasculitis. These findings were consistent with Sweet's syndrome. Without realizing a possible association, the patient rechallenged himself with a second course of the medication, which resulted in a rapid exacerbation of his lesions. After discontinuing the medication for the second time, the patient has had complete clearing of his lesions. To our knowledge, this is the first report of Sweet's syndrome associated with this new class of nonsteroidal anti-inflammatory drugs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Tyrosine phosphorylation and cytoskeletal tension regulate the release of fibroblast adhesions.

We have investigated the mechanisms by which fibroblasts release their adhesions to the extracellular matrix substrata using a permeabilized cell system in which the adhesions remain relatively stable. A large number of different molecules were assayed for their effect on focal adhesion stability using immunofluorescence with antibodies against different focal adhesion constituents. ATP uniquely stimulates a rapid breakdown of focal adhesions, and at high ATP concentrations (> 5 mM), many cells are released from the dish. The remaining cells appear contracted with talin, alpha-actinin, and vinculin localized diffusely throughout the cell. Integrin containing tracks of variable intensity outline the regions where cells had resided before they detached from the substratum. At lower ATP concentrations (0.5-5 mM) the cells remain spread; however the focal adhesion components, including integrin, show an array of phenotypes ranging from diffusely localized throughout the cell to a localization in small, thin focal adhesions. Okadaic acid, a serine, threonine phosphatase inhibitor, enhances the contracted phenotype, even at low concentrations (0.5 mM) of ATP. The localization of focal adhesion components is different in okadaic acid-treated cells. In highly contracted cells, integrin is present in tracks where the cells resided before the contraction; however focal adhesions are no longer apparent. Talin, vinculin, and alpha-actinin localize in trabecular networks toward the periphery of the cell. Interestingly, phosphotyrosine staining as well as nascent, intracellular integrin precedes the recruitment of focal adhesion constituents into the trabecular network. The ATP-stimulated focal adhesion breakdown appears to operate through two mechanisms. First, ATP stimulates the tyrosine phosphorylation of several cytoskeletally associated proteins. These tyrosine phosphorylations correlated well with focal adhesion breakdown. Furthermore, addition of a recombinant, constitutively active tyrosine phosphatase inhibits both the tyrosine phosphorylations and the breakdown of the focal adhesions. None of the major tyrosine phosphoproteins are FAK, integrin, tensin, paxillin, or other phosphoproteins implicated in focal adhesion assembly. The second mechanism is cell contraction. High ATP concentrations, or lower ATP concentrations in the presence of okadaic acid induce cell contraction. Inhibiting the contraction by addition of a heptapeptide IRICRKG, which blocks the actin-myosin interaction, also inhibits focal adhesion breakdown. Neither the peptide nor the phosphatase inhibits focal adhesion breakdown under all conditions suggesting that both tension and tyrosine phosphorylations mediate the release of adhesions.

Adenosine Triphosphate↗
PubMed1990

The alpha 1/beta 1 and alpha 6/beta 1 integrin heterodimers mediate cell attachment to distinct sites on laminin.

This study was undertaken to determine the roles of individual alpha/beta 1 integrin heterodimers in promoting cellular interactions with the different attachment-promoting domains of laminin (LN). To do this, antibodies to the integrin beta 1 subunit or to specific integrin alpha subunits were tested for effects on cell attachment to LN, to elastase fragments E1-4 and E1, derived from the short arms and core of LN's cruciform structure, and to fragment E8 derived from the long arm of this structure. The human JAR choriocarcinoma cells used in this study attached to LN and to fragments E1 and E8. Attachment to E1-4 required a much higher substrate coating concentration, suggesting that it is a poor substrate for JAR cell attachment. The ability of cells to attach to different LN domains suggested the presence of more than one LN receptor. These multiple LN receptors were shown to be beta 1 integrin heterodimers because antibodies to the integrin beta 1 subunit inhibited attachment of JAR cells to LN and its three fragments. To identify the individual integrin alpha/beta 1 heterodimers that mediate interactions with these LN domains, mAbs specific for individual beta 1 heterodimers in human cells were used to study JAR cell interactions with LN and its fragments. An anti-alpha 6/beta 1-specific mAb, GoH3, virtually eliminated cell attachment to E8 and partially inhibited attachment to E1 and intact LN. Thus the major alpha 6/beta 1 attachment domain is present in fragment E8. An alpha 1/beta 1-specific mAb (S2G3) strongly inhibited cell attachment to collagen IV and partially inhibited JAR attachment to LN fragment E1. Thus, the alpha 1/beta 1 heterodimer is a dual receptor for collagen IV and LN, interacting with LN at a site in fragment E1. In combination, the anti-alpha 1- and anti-alpha 6-specific antibodies completely inhibited JAR cell attachment to LN and fragment E1. Thus, the alpha 1/beta 1 and alpha 6/beta 1 integrin heterodimers each function as LN receptors and act together to mediate the interactions of human JAR choriocarcinoma cells with LN.

Antibodies, Monoclonal↗
PubMed1989

Melanoma cell adhesion to basement membrane mediated by integrin-related complexes.

During invasion and metastasis, tumor cells use a variety of surface adhesion receptors to attach to and invade basement membranes and interstitial stroma. We examined the role of the cell surface integrin-like complex in the attachment of the invasive murine B16-BL6 melanoma cell line to basement membrane. Polyclonal antibodies prepared against integrin-related complexes isolated from hamster BHK cells (anti-ECMR) or mouse erythroleukemia cells (anti-mouse FnR) inhibited the attachment of B16 cells to complex basement membrane matrices and to substrates coated with purified extracellular matrix components (fibronectin, laminin, and type IV collagen). The expression of integrin-like receptors on the surface of B16 cells was confirmed by selective immunoprecipitation of radiolabeled and solubilized membrane proteins with the antibodies. Both antibodies also reacted with an integrin-related fibronectin-binding receptor complex purified by ligand affinity chromatography on fibronectin-Sepharose columns. The anti-integrin antibodies failed to react with the Mr 68,000 laminin-binding protein, suggesting that their inhibition of cell attachment to laminin and complex basement membrane was not due to contaminating antibodies against the Mr 68,000 laminin receptor. The results indicate that the integrin receptor complexes on B16-BL6 cells either interact directly with a diverse set of extracellular-matrix-associated components or somehow modulate the activity and function of other receptors. Thus integrins may have an important role in tumor cell invasion of tissue barriers.

Animals↗
PubMed1989

Signal transduction through the fibronectin receptor induces collagenase and stromelysin gene expression.

We have investigated the effects of ligation of the fibronectin receptor (FnR) on gene expression in rabbit synovial fibroblasts. Monoclonal antibodies to the FnR that block initial adhesion of fibroblasts to fibronectin induced the expression of genes encoding the secreted extracellular matrix-degrading metalloproteinases collagenase and stromelysin. That induction was a direct consequence of interaction with the FnR was shown by the accumulation of mRNA for stromelysin and collagenase. Monoclonal antibodies to several other membrane glycoprotein receptors had no effect on metalloproteinase gene expression. Less than 2 h of treatment of the fibroblasts with anti-FnR in solution was sufficient to trigger the change in gene expression, and induction was blocked by dexamethasone. Unlike other inducers of metalloproteinase expression, including phorbol diesters and growth factors, addition of the anti-FnR in solution to cells adherent to serum-derived adhesion proteins or collagen produced no detectable change in cell shape or actin microfilament organization. Inductive effects were potentiated by cross-linking of the ligand. Fab fragments of anti-FnR were ineffective unless cross-linked or immobilized on the substrate. Adhesion of fibroblasts to native fibronectin did not induce metallo-proteinases. However, adhesion to covalently immobilized peptides containing the arg-gly-asp sequence that were derived from fibronectin, varying in size from hexapeptides up to 120 kD, induced collagenase and stromelysin gene expression. This suggests that degradation products of fibronectin are the natural inductive ligands for the FnR. These data demonstrate that signals leading to changes in gene expression are transduced by the FnR, a member of the integrin family of extracellular matrix receptors. The signaling of changes in gene expression by the FnR is distinct from signaling involving cell shape and actin cytoarchitecture. At least two distinct signals are generated: the binding of fibronectin-derived fragments and adhesion-blocking antibodies to the FnR triggers events different from those triggered by binding of the native fibronectin ligand. Because the genes regulated by this integrin are for enzymes that degrade the extracellular matrix, these results suggest that information transduced by the binding of various ligands to integrins may orchestrate the expression of genes regulating cell behavior in the extracellular environment.

Animals↗
PubMedDate not supplied

Neonatal lupus erythematosus: an unusual congenital presentation with cutaneous atrophy, erosions, alopecia, and pancytopenia.

Neonatal lupus erythematosus (NLE) is a rare disorder believed to be caused by the transplacental passage of specific autoantibodies from the mother to the fetus. Affected infants typically present with either characteristic skin lesions developing in the first month or later in life or congenital heart block. We report a very unusual case of NLE that was characterized by congenital skin atrophy, erosions, alopecia, and profound pancytopenia. Ro, La, and RNP antibodies were absent, and the diagnosis was made because of light microscopic and immunofluorescent findings. This case emphasizes that NLE can have widespread congenital skin involvement and suggests that at least some cases are mediated by antibodies other than Ro, La, and RNP.

Alopecia↗
PubMedDate not supplied

Medial collateral ligament knee sprains in college football. Brace wear preferences and injury risk.

In this prospective, multiinstitutional analysis of medial collateral ligament sprains in college football players, we categorized 987 previously uninjured study subjects according to frequency of wearing preventive knee braces, studied the patterns by which 47 of 100 injuries occurred to unbraced knees, and identified several extrinsic, sport-specific risk factors shared for both braced and unbraced knees. The attendance, brace wear choice, position, string, and session of each participant were recorded daily; medial collateral ligament sprains were reported whenever tissue damage was confirmed. Both the likelihood of wearing braces and risk of injury without them was highly dependent on session (games/practices), position group (line, linebacker/tight end, skill), and string group (players/nonplayers). Subjects wearing braces often faced a high injury risk to their unbraced knees, a finding compatible with the opinion that braces were a necessary evil, best worn when concern over danger of injury outweighed desire for speed and agility. It is concluded that to avoid misinterpretations due to the confounding influence of brace wear selection bias, accurate investigation of daily brace wear patterns is required. Then, before considing the impact of preventive knee braces, a repartitioning of the data base is essential to assure that only similar groups will be compared.

Athletic Injuries↗
PubMedDate not supplied

Medial collateral ligament knee sprains in college football. Effectiveness of preventive braces.

This is the second of 2 articles on a 3-year investigation of medial collateral ligament sprains of the knee to assess the effectiveness of prophylactic knee braces in NCAA Division I college football players. Position, string, type of session, and daily brace wear were recorded. The injury rates for braced and unbraced knees were used to create an incidence density ratio. The data were stratified and simultaneously controlled for position, string, and session and evaluated for their statistical significance. The 987 Big Ten players generated 155,772 knee exposures over the study period (50% braced). Noticeable differences existed in the rates of injury for the braced and unbraced knees in almost every position during practices, depending on player or nonplayer status. When the influential factors of position, string, and session are considered, there is a consistent but not statistically significant tendency for the players wearing preventive knee braces to experience a lower injury rate than for their unbraced counterparts. For starters and substitutes in the line positions, as well as the linebackers and tight ends, there was a consistent trend toward a lower injury rate in both practices and games. The braced players in the skill positions (backs/kickers), at least during games, exhibited a higher injury rate.

Athletic Injuries↗