SEARCH · Search PubMed

Results for “ASSOCIATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources

PubMed2002

A comparative study of odontogenic keratocysts associated with and not associated with an impacted mandibular third molar.

OBJECTIVE: The purpose of this study was to compare odontogenic keratocysts associated with and not associated with an impacted mandibular third molar. STUDY DESIGN: Panoramic radiographs of odontogenic keratocysts associated with impacted mandibular third molars (15 cysts, associated group) were compared with radiographs of odontogenic keratocysts not associated with impacted mandibular third molars (25 cysts, nonassociated group). The radiographic images were analyzed with reference to the patients' age and sex. RESULTS: The mean age of patients in the associated group was lower than that of patients in the nonassociated group. The mean area of the cysts in the associated group was larger than that of those in the nonassociated group. The patients' ages did not significantly correlate to the areas of either kind of cyst. CONCLUSIONS: The odontogenic keratocysts in the associated group had a tendency toward rapid growth in the patients' youth.

Adolescent↗

PubMed1999

Snt309p modulates interactions of Prp19p with its associated components to stabilize the Prp19p-associated complex essential for pre-mRNA splicing.

The SNT309 gene was identified via a mutation that causes lethality of cells in combination with a prp19 mutation. We showed previously that Snt309p is a component of the Prp19p-associated complex and that Snt309p, like Prp19p, is associated with the spliceosome immediately after or concomitantly with dissociation of U4 from the spliceosome. We show here that extracts prepared from the SNT309-deleted strain (DeltaSNT309) were defective in splicing but could be complemented by addition of the purified Prp19p-associated complex. Isolation of the Prp19p-associated complex from DeltaSNT309 extracts indicated that the complex was destabilized in the absence of Snt309p and dissociated on affinity chromatography, suggesting a role of Snt309p in stabilization of the Prp19p-associated complex. Addition of the affinity-purified Prp19p-Snt309p binary complex to DeltaSNT309 extracts could reconstitute the Prp19p-associated complex. Genetic analysis further suggests that Snt309p plays a role in modulating interactions of Prp19p with other associated components to facilitate formation of the Prp19p-associated complex. A model for how Snt309p modulates such interactions is proposed.

Cell Division↗

PubMed2001

Assembly of tapasin-associated MHC class I in the absence of the transporter associated with antigen processing (TAP).

The assembly of MHC class I molecules is regulated by a multi-protein complex in the endoplasmic reticules (ER) termed the loading complex. Tapasin is suggested to be one of the molecules forming this complex on the basis of its interaction with both the transporter associated with antigen processing (TAP) and MHC class I molecules. To address whether TAP is indispensable for the processing of the assembly of tapasin-associated MHC class I molecules, we studied the association of MHC class I molecules with tapasin, the assembly of tapasin-associated MHC class I with peptides and the peptide-mediated dissociation of MHC class I from tapasin in TAP-mutant T2 cells. In the absence of TAP, MHC class I heavy chain and beta(2)-microglobulin dimers were found to be properly associated with tapasin. The stable MHC class I dimer was required for its association with tapasin in the ER. In the absence of TAP, tapasin retained MHC class I molecules much longer in the ER than in the presence of TAP. This low off-rate of MHC class I from tapasin was due to the absence of high-affinity peptides in the ER of TAP-mutant cells but not to the absence of TAP per se. The introduction of peptides into permeabilized microsomes of TAP-mutant cells led to effective loading of the peptides onto tapasin-associated MHC class I and to the subsequent dissociation of MHC class I from tapasin. These results demonstrate that regulation of the assembly of tapasin-associated MHC class I is independent of the interaction of tapasin with TAP, but is dependent upon the peptides transported by TAP.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2004

Risk factors and outcomes associated with a short umbilical cord.

OBJECTIVE: To identify risk factors and outcomes associated with a short umbilical cord. METHODS: We conducted a population-based case-control study using linked Washington State birth certificate-hospital discharge data for singleton live births from 1987 to 1998 to assess the association between maternal, pregnancy, delivery, and infant characteristics and short umbilical cord. Cases (n = 3565) were infants diagnosed with a short umbilical cord. Controls (n = 14260) were randomly selected from among births without a diagnosis of short umbilical cord. RESULTS: Case mothers were less likely to be overweight (body mass index 25 or more, odds ratio [OR] 0.7; 95% confidence interval [CI] 0.6, 0.8) and more likely to be primiparous (OR 1.4; 95% CI 1.3, 1.6). Case infants were more likely to be female (OR 1.3; 95% CI 1.2, 1.4), have a congenital malformation (OR 1.6; 95% CI 1.4, 1.8), and be small for their gestational age (risk ratio [RR] 1.6; 95% CI 1.4, 1.9). A short cord was associated with increased risk for maternal labor and delivery complications, including retained placenta (RR 1.6; 95% CI 1.2, 2.3) and operative vaginal delivery (RR 1.4; 95% CI 1.3, 1.5). Adverse fetal and infant outcomes in cases included fetal distress (RR 1.8; 95% CI 1.6, 2.1) and death within the first year of life among term infants (RR 2.4; 95% CI 1.2, 4.6). CONCLUSION: Modifiable risk factors associated with the development of a short cord were not identified. Case mothers and infants are more likely to experience labor and delivery complications. Term case infants had a 2-fold increased risk of death, which suggests closer postpartum monitoring of these infants.

Adult↗

PubMed2002

Conserved region CR2 of Epstein-Barr virus nuclear antigen leader protein is a multifunctional domain that mediates self-association as well as nuclear localization and nuclear matrix association.

Self-association of viral proteins is important for many of their functions, including enzymatic, transcriptional, and transformational activities. Epstein-Barr virus (EBV) nuclear antigen leader protein (EBNA-LP) contains various numbers of W1W2 repeats and a unique carboxyl-terminal Y1Y2 domain. It was reported that EBNA-LP associates with a variety of cellular proteins and plays a critical role in EBV-induced transformation. We report here that EBNA-LP self-associates in vivo and the domain responsible for the homotypic association is a multifunctional domain mediating nuclear localization, nuclear matrix association, and EBNA-2-dependent coactivator function of the protein. Our conclusions are based on the following observations. (i) EBNA-LP interacts with itself or its derivatives in the yeast two-hybrid system. (ii) A purified chimeric protein consisting of glutathione S-transferase fused to EBNA-LP specifically formed complexes with EBNA-LP transiently expressed in COS-7 cells. (iii) When Flag epitope-tagged EBNA-LP with either one or two W1W2 repeats and EBNA-LP containing four W1W2 repeats were coexpressed in COS-7 cells, the latter was specifically coimmunoprecipitated with the former. (iv) Mutational analyses of EBNA-LP with deletion mutants revealed that the region between codons 19 and 39 (relative to the first amino acid residue of the W2 domain) is essential for self-association of the protein. The mapped region almost completely overlaps with CR2 and CR3, regions conserved among a subset of primate gamma-herpesviruses and critical for EBNA-2-dependent coactivator function. Amino acid substitutions in CR2 alone abolished the ability of the protein to self-interact. This laboratory previously reported that CR2 is also responsible for nuclear localization and nuclear matrix association (A. Yokoyama, Y. Kawaguchi, I. Kitabayashi, M. Ohki, and K. Hirai, Virology 279:401-413, 2001). (v) Sucrose gradient sedimentation showed that amino acid substitutions in CR2 reduced the ability of the protein to form protein complexes in B cells. These results suggest that self-association of EBNA-LP may be important for its various functions and interactions of the protein with multiple cellular proteins.

Amino Acid Sequence↗

PubMed2006

Polymorphisms of the low-density lipoprotein receptor-related protein 5 (LRP5) gene are associated with obesity phenotypes in a large family-based association study.

BACKGROUND: The low-density lipoprotein receptor-related protein 5 (LRP5) gene, essential for glucose and cholesterol metabolism, may have a role in the aetiology of obesity, an important risk factor for diabetes. PARTICIPANTS AND METHODS: To investigate the association between LRP5 polymorphisms and obesity, 27 single-nucleotide polymorphisms (SNPs), spacing about 5 kb apart on average and covering the full transcript length of the LRP5 gene, were genotyped in 1873 Caucasian people from 405 nuclear families. Obesity (defined as body mass index (BMI) >30 kg/m(2)) and three obesity-related phenotypes (BMI, fat mass and percentage of fat mass (PFM)) were investigated. RESULTS: Single markers (12 tagging SNPs and 4 untaggable SNPs) and haplotypes (5 blocks) were tested for associations, using family-based designs. SNP4 (rs4988300) and SNP6 (rs634008) located in block 2 (intron 1) showed significant associations with obesity and BMI after Bonferroni correction (SNP4: p<0.001 and p = 0.001, respectively; SNP6: p = 0.002 and 0.003, respectively). The common allele A for SNP4 and minor allele G for SNP6 were associated with an increased risk of obesity. Significant associations were also observed between common haplotype A-G-G-G of block 2 with obesity, BMI, fat mass and PFM with global empirical values p<0.001, p<0.001, p = 0.003 and p = 0.074, respectively. Subsequent sex-stratified analyses showed that the association in the total sample between block 2 and obesity may be mainly driven by female subjects. CONCLUSION: Intronic variants of the LRP5 gene are markedly associated with obesity. We hypothesise that such an association may be due to the role of LRP5 in the WNT signalling pathway or lipid metabolism. Further functional studies are needed to elucidate the exact molecular mechanism underlying our finding.

Adult↗

PubMed2026

FMT alleviates multidrug-resistant Salmonella enterica-induced diarrhea and is associated with loss of IncHI2A-associated resistance determinants in mice.

INTRODUCTION: Multidrug-resistant (MDR) Salmonella enterica (S. enterica) poses a serious threat to animal and public health because of increasingly limited treatment options. Fecal microbiota transplantation (FMT) is a potential microbiota-based intervention; however, its effects on MDR Salmonella infection and pathogen-associated antibiotic resistance gene (ARG) dynamics remain unclear. METHODS: A murine diarrhea model was established using the clinical MDR S. enterica isolate P174, and infected mice were treated with FMT. Clinical symptoms, intestinal pathology, transcriptional inflammatory responses, gut microbiota composition, and ARG profiles of recovered Salmonella isolates were evaluated. Whole-genome sequencing was used to characterize resistance determinants, and the stability of ARGs and IncHI2A backbone markers was further assessed during 19 in vitro passages. RESULTS: FMT reduced diarrhea, promoted body weight recovery, and alleviated intestinal tissue injury and inflammatory cell infiltration. Colonic expression of Tnf, Il1b, and Il6 decreased, whereas Il10 expression increased. FMT was also associated with partial recovery of gut microbial diversity, increased relative abundances of Lactobacillus, Bifidobacterium, and other commensal anaerobic taxa, and reduced Salmonella abundance. Whole-genome sequencing showed that bla OXA-1, floR, oqxA, and oqxB were co-localized on an IncHI2A-associated plasmid sequence. Loss of these resistance determinants increased over time in isolates recovered from FMT-treated mice, whereas no loss of the four ARGs or the IncHI2A backbone markers repB and parB was detected during 19 in vitro passages. Among isolates showing simultaneous loss of all four ARGs, nearly all also lacked detectable repB and parB, whereas isolates with partial ARG loss retained both markers. These patterns were consistent with both backbone-associated loss and resistance-region deletion or rearrangement. Most ARG-loss isolates showed reduced antimicrobial resistance. DISCUSSION: FMT alleviated MDR S. enterica-induced intestinal disease and was associated with partial recovery of gut microbiota characteristics and increased instability and loss of IncHI2A-associated resistance determinants in vivo. These findings suggest a potential association between intestinal microbial ecological changes and altered maintenance patterns of resistance-associated genetic elements in MDR S. enterica.

Salmonella enterica↗

PubMed2005

Associative and categorical relations in the associative memory illusion.

What kinds of associations underlie the associative memory illusion? In Experiment 1, lists composed of horizontal, or coordinate, free associates elicited false recognition of critical lures much more often than did lists composed of vertical, or subordinate, category instances. Experiment 2 replicated this result, and showed that the difference between free associates and category instances was not an artifact of differential levels of forward or backward associative strength. Associative structure plays an important role in the associative memory illusion: The illusion is strongest when the critical lure lies at the same level of categorization as the studied items.

Analysis of Variance↗

PubMed2003

Immunotherapy for IgM anti-Myelin-Associated Glycoprotein paraprotein-associated peripheral neuropathies.

BACKGROUND: Serum monoclonal anti-Myelin Associated Glycoprotein antibodies may be pathogenic in some patients with IgM paraprotein and demyelinating neuropathy. Immunotherapies aimed at reducing the level of these antibodies might be expected to be of benefit in the treatment of the neuropathy. Many potential therapies have been described in small trials, uncontrolled studies and case reports. OBJECTIVES: To examine the efficacy of any form of immunotherapy in reducing disability and impairment resulting from IgM anti-Myelin Associated Glycoprotein paraprotein-associated demyelinating peripheral neuropathy. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group register (August 2002) and MEDLINE (January 1966 - August 2002) and EMBASE (January 1980 - August 2002) for controlled trials, checked the bibliographies to identify other controlled trials and contacted authors and other experts in the field. SELECTION CRITERIA: Types of studies: randomised or quasi-randomised controlled trials. TYPES OF PARTICIPANTS: patients of any age with anti-Myelin Associated Glycoprotein antibody associated demyelinating peripheral neuropathy with monoclonal gammopathy of undetermined significance of any severity. Types of interventions: any type of immunotherapy. Types of outcome measures: Primary: improvement in the Neuropathy Disability Score or Modified Rankin Scale six months after randomisation Secondary: Neuropathy Disability Score and/or the Modified Rankin Score 12 months after randomisation. Ten metre walk time, subjective clinical scores and electrophysiological parameters at six and 12 months after randomisation. IgM paraprotein levels and anti-Myelin Associated Glycoprotein antibody titres six months after randomisation. Adverse effects of treatments. DATA COLLECTION AND ANALYSIS: We identified six randomised controlled trials of which five were included after discussion between the authors. One author extracted the data and the other checked them. No missing data could be obtained from authors. MAIN RESULTS: The five eligible trials used four of the many available immunotherapy treatments. Only two had comparable interventions and outcomes but these were only short-term studies. There were no significant benefits of the treatments used in the predefined outcomes. However intravenous immunoglobulin showed benefits in terms of improved Modified Rankin Scale at two weeks and 10 metre walk time at four weeks. Serious adverse effects of intravenous immunoglobulin are known to occur from observational studies but none were encountered in these trials. REVIEWER'S CONCLUSIONS: There is inadequate reliable evidence from trials of immunotherapies in anti-Myelin Associated Glycoprotein paraproteinaemic neuropathy to recommend any particular immunotherapy treatment. Intravenous immunoglobulin is relatively safe and may produce some short-term benefit. Large well designed randomised trials are required to assess the efficacy of promising new therapies.

Demyelinating Diseases↗

PubMed2006

Immunotherapy for IgM anti-myelin-associated glycoprotein paraprotein-associated peripheral neuropathies.

BACKGROUND: Serum monoclonal anti-myelin associated glycoprotein antibodies may be pathogenic in some people with IgM paraprotein and demyelinating neuropathy. Immunotherapies aimed at reducing the level of these antibodies might be expected to be beneficial. OBJECTIVES: To examine the efficacy of any form of immunotherapy in reducing disability and impairment resulting from IgM anti-myelin associated glycoprotein paraprotein-associated demyelinating peripheral neuropathy. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Register (March 2005), MEDLINE (January 1966 to March 2005) and EMBASE (January 1980 to March 2005) for controlled trials. We also checked bibliographies and contacted authors and experts in the field. SELECTION CRITERIA: We included randomised or quasi-randomised controlled trials of participants of any age treated with any type of immunotherapy for anti-myelin-associated glycoprotein antibody associated demyelinating peripheral neuropathy with monoclonal gammopathy of undetermined significance of any severity. Our primary outcome measure was change in the Neuropathy Impairment Scale or Modified Rankin Scale at six months after randomisationSecondary outcome measures were: Neuropathy Impairment Scale or the Modified Rankin Score at 12 months after randomisation; ten-metre walk time, subjective clinical scores and electrophysiological parameters at six and 12 months after randomisation; IgM paraprotein levels and anti-myelin associated glycoprotein antibody titres at six months after randomisation and adverse effects of treatments. DATA COLLECTION AND ANALYSIS: We identified eight possible trials. Of these, five randomised controlled trials were included after discussion between the authors. One author extracted and the other checked the data. No missing data could be obtained from trial authors. MAIN RESULTS: The five eligible trials (97 participants) tested intravenous immunoglobulin, interferon-alpha or plasma exchange. Only two, of intravenous immunoglobulin, had comparable interventions and outcomes but both were short-term. There were no significant benefits of the treatments used in the outcomes predefined for this review, but not all the predefined outcomes were used in every included trial. Intravenous immunoglobulin showed benefits in terms of improvement in Modified Rankin Scale at two weeks and 10-metre walk time at four weeks. Serious adverse effects of intravenous immunoglobulin are known to occur from observational studies but none were encountered in these trials. AUTHORS' CONCLUSIONS: There is inadequate reliable evidence from trials of immunotherapies in anti-myelin associated glycoprotein paraproteinaemic neuropathy to recommend any particular immunotherapy treatment. Intravenous immunoglobulin is relatively safe and may produce some short-term benefit. Large well-designed randomised trials of at least six to 12 months duration are required to assess existing or novel therapies.

Demyelinating Diseases↗

PubMed2002

Role of the rodent hippocampus in paired-associate learning involving associations between a stimulus and a spatial location.

The ability of rats with control or hippocampal lesions to learn an object-place, odor-place, or object-odor paired-associate task was assessed in a cheeseboard maze apparatus. The data indicate that rats with hippocampal lesions were significantly impaired, compared with controls, in learning both the object-place and the odor-place paired-associate tasks. However, rats with hippocampal lesions learned the object-odor paired-associate task as readily as did controls. The data suggest that the rodent hippocampus is involved in paired-associate learning when a stimulus must be associated with a spatial location. However, the hippocampus is not involved in paired-associate learning when the association does not involve a spatial component.

Animals↗

PubMed2003

Learned associability and associative change in human causal learning.

The Mackintosh (1975) model of associative learning specifies that processing of both the cues presented on a trial and the outcome of that trial will interact to determine the amount of associative change undergone by a given cue. Experiments looking at the distribution of associative change among the elements of a reinforced compound in animal conditioning studies indicate that processing of the outcome of a trial does indeed influence associative change. The work reported here investigates the distribution of associative change among the elements of a reinforced compound in a human causal judgement paradigm, and it indicates that processing of the cues presented on a trial also plays a role in determining associative change (in terms of changes in the associability of cues as a result of experience). Taken in combination, these results provide good support for Mackintosh (1975) and the characterizations of both cue and outcome processing that it offers.

Adult↗

PubMed1985

Cytoskeletal architecture and immunocytochemical localization of microtubule-associated proteins in regions of axons associated with rapid axonal transport: the beta,beta'-iminodipropionitrile-intoxicated axon as a model system.

Axons from rats treated with the neurotoxic agent beta,beta'-iminodipropionitrile (IDPN) were examined by quick-freeze, deep-etch electron microscopy. Microtubules formed bundles in the central region of the axons, whereas neurofilaments were segregated to the periphery. Most membrane-bounded organelles, presumably including those involved in rapid axonal transport, were associated with the microtubule domain. The high resolution provided by quick-freeze, deep-etch electron microscopy revealed that the microtubules were coated with an extensive network of fine strands that served both to cross-link the microtubules and to interconnect them with the membrane-bounded organelles. The strands were decorated with granular materials and were irregular in dimension. They appeared either singly or as an extensive anastomosing network in fresh axons. The microtubule-associated strands were observed in fresh, saponin-extracted, or aldehyde-fixed tissue. To explore further the identity of the microtubule-associated strands, microtubules purified from brain tissue and containing the high molecular weight microtubule-associated proteins MAP 1 and MAP 2 were examined by quick-freeze, deep-etch electron microscopy. The purified microtubules were connected by a network of strands quite similar in appearance to those observed in the IDPN axons. Control microtubule preparations consisting only of tubulin and lacking the MAPs were devoid of associated strands. To learn which of the MAPs were present in the microtubule bundles in the axon, sections of axons from IDPN-treated rats were examined by immunofluorescence microscopy using antibodies to MAP 1A, MAP 1B, MAP 2, and tubulin. Anti-MAP 2 staining was only marginally detectable in the IDPN-treated axons, consistent with earlier observations. Anti-MAP 1A and anti-MAP 1B brightly stained the IDPN-treated axons, with the staining exclusively limited to the microtubule domains. Furthermore, thin section-immunoelectron microscopy using colloidal gold-labeled second antibodies revealed that both anti-MAP 1A and anti-MAP 1B stained fuzzy filamentous structures between microtubules. In view of earlier work indicating that rapid transport is associated with the microtubule domain in the IDPN-treated axon, it now appears that MAP 1A and MAP 1B may play a role in this process. We believe that MAP 1A and MAP 1B are major components of the microtubule-associated fibrillar matrix in the axon.

Animals↗

PubMed1997

Association of syntaxin 3 and vesicle-associated membrane protein (VAMP) with H+/K(+)-ATPase-containing tubulovesicles in gastric parietal cells.

H+/K(+)-ATPase is the proton pump in the gastric parietal cell that is responsible for gastric acid secretion. Stimulation of acid secretion is associated with a reorganization of the parietal cells resulting in the incorporation of H+/K(+)-ATPase from a cytoplasmic membrane pool, the tubulovesicle compartment, into the apical canalicular membrane. To better characterize the role of membrane trafficking events in the morphological and physiological changes associated with acid secretion from parietal cells, we have characterized the expression and localization of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) in these cells. Each of the six different SNARE proteins examined [syntaxins 1 through 4 of 25-kDa synaptosome-associated protein, and vesicle-associated membrane protein] were found to be expressed in parietal cells. Furthermore, two of these SNAREs, vesicle-associated membrane protein and syntaxin 3, were associated with H+/K(+)-ATPase-containing tubulovesicles while the remainder were excluded from this compartment. The expression of syntaxin 1 and synaptosome-associated protein of 25 kDa in parietal cells, two SNAREs previously thought to be restricted to neuroendocrine tissues, suggests that parietal cells may utilize membrane trafficking machinery that is similar to that utilized for regulated exocytosis in neurons. Furthermore, the localization of syntaxin 3, a putative target membrane SNARE, to the tubulovesicle compartment indicates that syntaxin 3 may have an alternative function. These observations support a role for intracellular membrane trafficking events in the regulated recruitment of H+/K(+)-ATPase to the plasma membrane after parietal cell stimulation.

Animals↗

PubMed2003

Apoptosis regulation differs between ulcerative colitis-associated and sporadic colonic tumors. Association with survivin and bcl-2.

To clarify kinetics in ulcerative colitis (UC)-associated lesions, cell proliferation, apoptosis, and expression of apoptosis-inhibitory proteins were studied. Ki-67 labeling and survivin and bcl-2 expression were examined immunohistochemically in 22 low-grade dysplasias (LGDs), 25 high-grade dysplasias (HGDs), and 13 adenocarcinomas associated with UC, and for comparison in 21 sporadic adenomas with LGD, 22 sporadic adenomas with HGD, and 21 invasive adenocarcinomas. Apoptosis was studied with nick-end labeling and immunohistochemical analysis of single-stranded DNA. In UC-associated LGDs, Ki-67--positive cells were more frequent in the lower than the upper half of the crypt, related to bcl-2 expression, while in sporadic adenomas such cells were more common in the upper half. No difference in apoptosis was found between UC-associated LGDs and sporadic adenomas with LGD or between UC-associated HGDs and sporadic adenomas with HGD. However, UC-associated carcinomas exhibited a lower apoptotic count than their sporadic invasive counterparts. This seemed related to higher survivin expression without a significant difference between the 2 types of invasive lesions regarding bcl-2 levels. Apoptosis is less frequent in UC-associated than in sporadic invasive colon carcinomas, this being linked to elevated survivin expression. The control of apoptosis may be different in the 2 types of tumorigenesis.

Adenoma↗

PubMed2025

Genome wide association study reveals novel associations with face morphology.

Genome-wide association studies (GWAS) on the Middle Eastern population, including the United Arab Emirates (UAE), have been relatively limited. The present study aims to investigate genotype-face morphology associations in the UAE population through Genome Wide Association Studies (GWAS). Phenotypic data (44 face measurements) from 172 Emiratis was obtained through three-dimensional (3D) scanning technology and an automatic face landmarking technique. GWAS analysis revealed associations of 19 genetic loci with six face features, 14 of which are novel. The GWAS analysis revealed 11 significant relationships between 44 face parameters and 242 SNPs, exceeding the GWAS significance threshold. These phenotypes were previously associated with body height, craniofacial defects, and facial characters. The most significant associations of these genetic variations were related to six main facial features which were facial convexity, left orbital protrusion, mandibular contour, nasolabial angle D, inferior facial angle B, and inferior facial angle A. To the best of our knowledge, this is the first GWAS study to investigate the association of SNP variations with face morphology in the Middle Eastern population.

Humans↗

PubMed2002

Association between parents' preferences and perceptions of barriers to vaccination and the immunization status of their children: a study from Pediatric Research in Office Settings and the National Medical Association.

OBJECTIVES: To assess the association between parents' perceptions of various barriers to vaccination and their preferences regarding specific strategies designed to reduce missed vaccination opportunities and the immunization status of their children and to estimate the overall contribution of the perception of barriers on underimmunization among children who are vaccinated in pediatricians' offices. METHODS: As part of a nationwide study on the immunization status of children followed by practicing pediatricians, parents of children who were 8 to 35 months of age and seen consecutively at 177 participating practice sites completed a survey on health beliefs regarding the vaccination process. In addition to demographic information, parents were asked to identify the most difficult thing about obtaining immunizations, as well as their preferences regarding the maximum number of vaccine injections that should be administered to their child at 1 visit and for receiving a needed immunization during an office visit for a mild illness. Immunization data on study children were abstracted from the practice medical record, and specific survey responses for each parent were compared with the immunization status of his or her child at 8 months of age using chi2 tests. For parental health beliefs associated with immunization status by bivariate analyses, the relative risks for underimmunization and population-attributable risk percentages of each belief were calculated after potentially confounding variables were adjusted for. RESULTS: Immunization data were collected on 13 520 children; 13 516 parents responded to at least 1 question regarding vaccination health beliefs. Two thirds of the responding parents indicated that their child should receive no more than 2 immunizations at 1 visit. However, there was no difference in the preferred maximum number of vaccines between parents of children who were fully immunized at 8 months of age and those of underimmunized children. Similarly, there was no difference in a stated preference for receiving a needed immunization during an illness visit. Overall, 74% of respondents indicated that there was "nothing" difficult about obtaining vaccines for their children. The most commonly cited barrier was concern about the side effects of vaccines, identified by 22.6% of parents. However, this barrier was not associated with immunization status. Each of the remaining barriers-including the confusing vaccination schedule, expense of vaccines, the inconvenience of the vaccination process, having a child who was often too ill to receive vaccines, religious objections, and other identified barriers-was statistically associated with immunization status, with adjusted relative risks for underimmunization ranging from 1.42 to 3.04. However, because each of these barriers was identified as important by <5% of parents, the population-attributable risk percentage for each was < or =2.5%. Overall, it was estimated that parental perception of barriers associated with immunization status accounts for 8.0% of the underimmunization observed among children who are vaccinated in the offices of primary care pediatricians. CONCLUSIONS: Parental preferences regarding vaccination practices designed to reduce missed opportunities were not associated with the immunization status of their children. Although several barriers to vaccination were associated with immunization status, individual barriers were identified by a small minority of parents. Overall, parental perceptions of barriers to vaccination do not seem to be a significant cause of underimmunization in this population of children.

Attitude to Health↗

PubMed2006

Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: the American Academy of Neurology affirms the value of this guideline.

BACKGROUND AND PURPOSE: This guideline provides an overview of the evidence on various established and potential stroke risk factors and provides recommendations for the reduction of stroke risk. METHODS: Writing group members were nominated by the committee chair on the basis of each writer's previous work in relevant topic areas and were approved by the American Heart Association Stroke Council's Scientific Statement Oversight Committee. The writers used systematic literature reviews (covering the time period since the last review published in 2001 up to January 2005), reference to previously published guidelines, personal files, and expert opinion to summarize existing evidence, indicate gaps in current knowledge, and when appropriate, formulate recommendations based on standard American Heart Association criteria. All members of the writing group had numerous opportunities to comment in writing on the recommendations and approved the final version of this document. The guideline underwent extensive peer review before consideration and approval by the AHA Science Advisory and Coordinating Committee. RESULTS: Schemes for assessing a person's risk of a first stroke were evaluated. Risk factors or risk markers for a first stroke were classified according to their potential for modification (nonmodifiable, modifiable, or potentially modifiable) and strength of evidence (well documented or less well documented). Nonmodifiable risk factors include age, sex, low birth weight, race/ethnicity, and genetic factors. Well-documented and modifiable risk factors include hypertension, exposure to cigarette smoke, diabetes, atrial fibrillation and certain other cardiac conditions, dyslipidemia, carotid artery stenosis, sickle cell disease, postmenopausal hormone therapy, poor diet, physical inactivity, and obesity and body fat distribution. Less well-documented or potentially modifiable risk factors include the metabolic syndrome, alcohol abuse, drug abuse, oral contraceptive use, sleep-disordered breathing, migraine headache, hyperhomocysteinemia, elevated lipoprotein(a), elevated lipoprotein-associated phospholipase, hypercoagulability, inflammation, and infection. Data on the use of aspirin for primary stroke prevention are reviewed. CONCLUSIONS: Extensive evidence is available identifying a variety of specific factors that increase the risk of a first stroke and providing strategies for reducing that risk.

Brain Ischemia↗