Development and validation of a questionnaire assessing eating pleasure dimensions in the adult French-speaking population of the province of Québec, Canada.

The purpose of this study was to develop and validate a questionnaire assessing eating pleasure dimensions in the adult French-speaking population of the province of Québec, Canada. We developed the Eating Pleasure Questionnaire, a 53-item questionnaire. An expert panel evaluated the content validity, and a pre-test was performed with 30 French-speaking Quebecers (15 men and 15 women, mean age = 46 years) to evaluate the face validity. A sample of 300 Quebecers (150 men and 150 women, mean age = 36 years) completed the online questionnaire for validation. The structure of the questionnaire was examined using exploratory factor analysis (EFA). Internal consistency was evaluated with Cronbach's alpha coefficients. Test-retest reliability was assessed using intra class correlation coefficients (ICC) and construct validity, using Pearson's correlations. Evaluation of content validity and face validity led to the clarification of the instructions, the suppression of two items, the addition of two items and some reformulations. The EFA showed a 7-factor structure: 1- health/ideological food choice motives, 2- sensory experiences and individual preferences, 3- social experiences, 4- mindful eating, 5- emotional/situational eating and reward, 6- food preparation process and 7- new experiences. Cronbach's alpha values for the seven factors ranged from 0.67 to 0.86. The total scale Cronbach's alpha was 0.91, which suggests a good internal consistency. The questionnaire appears reliable with ICC ranging from 0.66 to 0.87. It also showed a good construct validity, with expected positive associations with food well-being (how people link food to well-being), intrinsic motivation, and the pleasure orientation (the importance of obtaining pleasure from food). Overall, these analyses suggest that the Eating Pleasure Questionnaire is valid to evaluate eating pleasure dimensions in our population.

Can eating pleasure be a lever for healthy eating? A systematic scoping review of eating pleasure and its links with dietary behaviors and health.

The aims of this review were to map and summarize data currently available about 1) key dimensions of eating pleasure; 2) associations of eating pleasure, and its key dimensions, with dietary and health outcomes and 3) the most promising intervention strategies using eating pleasure to promote healthy eating. Using the scoping review methodology, a comprehensive search of the peer-reviewed literature (Medline, PsycInfo, Embase, ERIC, Web of Science, CINAHL, ABI/Inform global and Sociology Abstract) and of the grey literature (ProQuest Dissertations & Theses and Google) was carried out by two independent reviewers. We included 119 of the 28,908 studies found. In total, 89 sub-dimensions of eating pleasure were grouped into 22 key dimensions. The most frequently found related to sensory experiences (in 50.9% of the documents), social experiences (42.7%), food characteristics besides sensory attributes (27.3%), food preparation process (19.1%), novelty (16.4%), variety (14.5%), mindful eating (13.6%), visceral eating (12.7%), place where food is consumed (11.8%) and memories associated with eating (10.9%). Forty-five studies, mostly cross-sectional (62.2%), have documented links between eating pleasure and dietary and/or health outcomes. Most studies (57.1%) reported favorable associations between eating pleasure and dietary outcomes. For health outcomes, results were less consistent. The links between eating pleasure and both dietary and health outcomes varied according to the dimensions of eating pleasure studied. Finally, results from 11 independent interventions suggested that strategies focusing on sensory experiences, cooking and/or sharing activities, mindful eating, and positive memories related to healthy food may be most promising. Thus, eating pleasure may be an ally in the promotion of healthy eating. However, systematically developed, evidence-based interventions are needed to better understand how eating pleasure may be a lever for healthy eating.

Evidence for association between the HLA-DQA locus and abdominal aortic aneurysms in the Belgian population: a case control study.

BACKGROUND: Chronic inflammation and autoimmunity likely contribute to the pathogenesis of abdominal aortic aneurysms (AAAs). The aim of this study was to investigate the role of autoimmunity in the etiology of AAAs using a genetic association study approach with HLA polymorphisms. METHODS: HLA-DQA1, -DQB1, -DRB1 and -DRB3-5 alleles were determined in 387 AAA cases (180 Belgian and 207 Canadian) and 426 controls (269 Belgian and 157 Canadian) by a PCR and single-strand oligonucleotide probe hybridization assay. RESULTS: We observed a potential association with the HLA-DQA1 locus among Belgian males (empirical p = 0.027, asymptotic p = 0.071). Specifically, there was a significant difference in the HLA-DQA1*0102 allele frequencies between AAA cases (67/322 alleles, 20.8%) and controls (44/356 alleles, 12.4%) in Belgian males (empirical p = 0.019, asymptotic p = 0.003). In haplotype analyses, marginally significant association was found between AAA and haplotype HLA-DQA1-DRB1 (p = 0.049 with global score statistics and p = 0.002 with haplotype-specific score statistics). CONCLUSION: This study showed potential evidence that the HLA-DQA1 locus harbors a genetic risk factor for AAAs suggesting that autoimmunity plays a role in the pathogenesis of AAAs.

HLA-DQA is associated with abdominal aortic aneurysms in the Belgian population.

Chronic inflammation and autoimmunity likely contribute to the pathogenesis of abdominal aortic aneurysms (AAAs). The aim of this study was to investigate the role of autoimmunity in the etiology of AAAs using a genetic association study approach with human leukocyte antigen (HLA) polymorphisms (HLA-DQA1, -DQB1, -DRB1 and -DRB3-5 alleles) in 387 AAA cases and 426 controls. We observed an association with the HLA-DQA1 locus among Belgian males, and found a significant difference in the HLA-DQA1*0102 allele frequencies between AAA cases and controls. In conclusion, this study showed potential evidence that the HLA-DQA1 locus harbors a genetic risk factor for AAAs suggesting that autoimmunity plays a role in the pathogenesis of AAAs.

Sequential molecular and cellular events during neoplastic progression: a mouse syngeneic ovarian cancer model.

Studies performed to identify early events of ovarian cancer and to establish molecular markers to support of early detection and the development of chemopreventive regimens have been hindered by a lack of adequate cell models. Taking advantage of the spontaneous transformation of mouse ovarian surface epithelial (MOSE) cells in culture, we isolated and characterized distinct transitional stages of ovarian cancer as the cells progressed from a premalignant nontumorigenic phenotype to a highly aggressive malignant phenotype. Transitional stages were concurrent with progressive increases in proliferation, anchorage-independent growth capacity, in vivo tumor formation, and aneuploidy. During neoplastic progression, our ovarian cancer model underwent distinct remodeling of the actin cytoskeleton and focal adhesion complexes, concomitant with downregulation and/or aberrant subcellular localization of two tumor-suppressor proteins E-cadherin and connexin-43. In addition, we demonstrate that epigenetic silencing of E-cadherin through promoter methylation is associated with neoplastic progression of our ovarian cancer model. These results establish critical interactions between cellular cytoskeletal remodeling and epigenetic silencing events in the progression of ovarian cancer. Thus, our MOSE model provides an excellent tool to identify both cellular and molecular changes in the early and late stages of ovarian cancer, to evaluate their regulation, and to determine their significance in an immunocompetent in vivo environment.

Tight junction proteins claudin-3 and claudin-4 are frequently overexpressed in ovarian cancer but not in ovarian cystadenomas.

PURPOSE: Claudin proteins represent a large family of integral membrane proteins crucial for tight junction (TJ) formation and function. Claudins have been shown to be up-regulated in various cancers and have been suggested as possible biomarkers and targets for cancer therapy. Because claudin-3 and claudin-4 have been proposed to be expressed in epithelial ovarian cancer, we have performed a detailed analysis of CLDN3 and CLDN4 expression in a panel of ovarian tumors of various subtypes and cell lines. We also investigated whether high expression of claudin-3 and claudin-4 was associated with TJ function in ovarian cancer cells. EXPERIMENTAL DESIGN: RNA was obtained from a panel of 39 microdissected epithelial ovarian tumors of various histological subtypes for real-time reverse transcription-PCR analysis. In addition, a total of 70 cases of ovarian carcinomas, ovarian cysts, and normal ovarian epithelium from a tissue array were analyzed by immunohistochemistry. Finally, a panel of cell lines was used for Western analysis of claudin expression and TJ permeability studies. RESULTS: Although expressed at low levels in some normal human tissues, including the ovary, CLDN3 and CLDN4 are highly up-regulated in epithelial ovarian cancers of all subtypes. Immunohistochemical analyses using our ovarian tissue array confirmed the high level of expression of claudin-3 and claudin-4 in the majority of ovarian carcinomas, including many tumors exhibiting cytoplasmic staining. Ovarian cystadenoma did not frequently overexpress these proteins, suggesting that the expression of these proteins is associated with malignancy. In ovarian cancer cell lines, claudin-3 and claudin-4 expression was not associated with functional TJs as measured by transepithelial electrical resistance. CONCLUSIONS: These results show that CLDN3 and CLDN4 are frequently up-regulated in ovarian tumors and cell lines and may represent novel markers for this disease. Overexpression of these genes in ovarian cancer also suggests interesting scenarios for the involvement of TJ in tumorigenesis. A better knowledge of the mechanisms underlying ovarian tumorigenesis will likely result in the development of novel approaches for the diagnosis and therapy of this deadly disease.

Human papillomavirus (HPV) transcripts in malignant inverted papilloma are from integrated HPV DNA.

OBJECTIVES: The objectives of the study were to detect human papillomavirus (HPV) sequences in nasal inverted papilloma (IP) lesions and to determine whether HPV is involved in the progression of IP to sinonasal squamous cell carcinoma (SCC). STUDY DESIGN: A retrospective study was performed on 14 patients diagnosed with IP within the last 12 years. Three of these 14 patients developed SCC. METHODS: Eighteen formalin-fixed, paraffin-embedded tissue blocks were obtained for these 14 patients. After DNA extraction, polymerase chain reaction (PCR) was performed, followed by hybridization using HPV 6, 11, 16, 18, 31, 33, 35, 45, and 52 specific DNA probes, in an attempt to identify HPV type in each specimen. After RNA extraction, the integration status of the HPV genome was evaluated based on the relative abundance of E7 and E5 viral transcripts, assessed by quantitative real-time PCR. RESULTS: HPV sequences were detected in samples from 3 of the 14 patients with IP. Of the three patients with SCC, HPV sequences were detected in two patients, whereas one patient was negative for the oligoprobes tested. Of the 11 patients diagnosed only with IP, 1 patient was positive for HPV DNA (HPV type 11). This difference in HPV positivity between IP and SCC was not statistically significant (P = .09, Fisher's Exact test, two tailed). Viral transcripts were detected in both patients with SSC who were HPV positive. Because HPV early transcripts are polycistronic, loss of 3' transcript sequences (E5) and retention of 5' sequences (E7) indicates integration. One of the SSC containing HPV 18 sequences showed a E7/E5 ratio of 776:1. The other SSC showed E7 transcripts and an absence of E5 transcripts CONCLUSION: HPV transcripts were present in SCC positive for HPV, and the relative level of E7 to E5 transcripts indicates integration of the viral genome. These findings are suggestive of HPV having an active role in the lesion. More extensive studies are needed to determine the exact role of HPV in IP and progression to SCC.

Integration of human papillomavirus type 11 in recurrent respiratory papilloma-associated cancer.

OBJECTIVES/HYPOTHESIS: The main objective was to demonstrate that human papillomavirus (HPV) type 11 is an aggressive virus that plays a significant role in the development of laryngeal cancer in patients with a history of recurrent respiratory papillomatosis (RRP). We have done so by preliminary investigation into the molecular mechanism underlying the malignant transformation of RRP to invasive squamous cell carcinoma. STUDY DESIGN: An experimental, nonrandomized, retrospective study using tissue specimens from nine patients with a history of RRP that progressed to laryngeal or bronchogenic cancer was performed. METHODS: DNA and RNA were extracted from 20 formalin-fixed, paraffin-embedded specimens from six patients with a history of early onset RRP and laryngeal cancer and from three patients with early onset RRP and bronchogenic cancer. Polymerase chain reaction (PCR) was performed on DNA to determine the HPV type in each specimen. Reverse-transcriptase PCR specific for virus transcripts was performed on RNA to determine whether the viral genome was integrated into the host genome. RESULTS: HPV-11 but not HPV-6, 16, or 18 was found in all of the laryngeal and bronchogenic cancers in patients with a history of early onset RRP in this study. RNA, sufficiently intact for examination, was obtained from seven patients. Analysis of HPV 11 transcripts revealed integration of the viral genome in three of seven patients. CONCLUSIONS: HPV type 6 and 11 are considered "low-risk" viruses and are not associated with genital cancers, as are HPV types 16 and 18. However, our data suggests that HPV type 11 is an aggressive virus in laryngeal papilloma that should be monitored in patients with RRP.

HLA-DQ alleles in white and African American patients with juvenile-onset recurrent respiratory papillomatosis.

OBJECTIVE: To determine HLA-DQalpha and -DQbeta1 allele associations in juvenile-onset recurrent respiratory papillomatosis (RRP) for risk, disease course, and human papillomavirus type. DESIGN: A nonrandomized controlled study was performed on DNA extracted from papilloma specimens of children with a history of RRP, and from peripheral blood of African American and white children without RRP. The frequencies of DQalpha and DQbeta1 alleles were compared between patients and ethnically matched controls. SUBJECTS: Records of 48 children treated for RRP at Children's Hospital of Michigan in Detroit (26 African American and 22 white) were reviewed. Control subjects consisted of 80 African American and 80 white children seen at the hospital for conditions other than RRP. RESULTS: African American and white patients with DQbeta1*050X (not *0501, *0502, *0503, *0504, or *0505) were at higher risk to develop RRP than controls (P =.01 and.03, respectively). DQbeta1*0402 was protective for African Americans (P =.01). Whites with DQalpha*0102 were at risk for RRP (P =.03). This allele was associated with disease remission in African Americans (P =.03). DQalpha*0101/0104 conferred protection in whites (P =.047). No association was seen for allele frequency and human papillomavirus type. Whites with haplotype DQalpha*0501/DQbeta1*0201 were at high risk for RRP (P =.002). No relationships were seen for African Americans or whites between haplotype frequencies and disease course or human papillomavirus type. CONCLUSIONS: HLA-DQalpha and -DQbeta1 alleles occur at different frequencies in African American and white children with RRP than controls. Specific alleles influence risk for RRP. Allele and haplotype frequencies have some influence on disease course, but were independent of human papillomavirus type.

The Bali STD/AIDS study: human papillomavirus infection among female sex workers.

Female sex workers in low priced brothel areas in Denpasar, Bali, Indonesia participated in an intervention study designed to promote condom use and sexually transmitted disease (STD)/AIDS prevention. The intervention provided educational sessions for sex workers, STD treatment for sex workers, condom distribution, and media for clients. The brothel areas were divided into high and low areas for programme effort. The high effort areas received a more intensive behavioural intervention than the low effort areas. A clinic was available for STD treatment in both areas. Behavioural surveys and STD testing were used to evaluate the programmes. About 600 were evaluated for several STDs and completed personal interviews at enrolment and at six-month intervals during the 18-month study. About 50% of women were new to the study at each round. Human papillomavirus (HPV) testing of cervical swabbed specimens, using polymerase chain reaction methodology, was performed at the beginning of the study and 18 months later. Human papillomavirus infection was initially high in these women (38.3%) and declined to 29.7% after 18 months (P <0.01). The prevalence of HPV infection declined with age (P <0.01). HPV infection was associated with a number of STD symptoms that were reported in personal interviews. These associations were stronger in the first time period. Infection with Neisseria gonorrhoeae was associated with HPV infection at baseline (P =0.03). HPV infection declined in the study area with the more intensive educational programme (P <0.01). The prevalence of HPV infection declined over time and was associated with study area and age of woman.

Risk for Cervical Intraepithelial Neoplasia in Systemic Lupus Erythematosus is not Related to Disease Severity.

INTRODUCTION: Cervical intraepithelial neoplasia (CIN) is increased in women with systemic lupus erythematosus (SLE). Cervical neoplasia is caused by human papilloma virus (HPV) infection which persists and causes malignant transformation of infected cervical cells. Women with lupus have impaired immune systems which can facilitate HPV persistence. We hypothesized that women with SLE who developed CIN would be younger, have more severe disease and received more immunosuppressive treatment. To test this hypothesis, a case-control study was conducted focusing on two key variables, SLE disease severity and immunosuppressive treatment, which we believed would be the major determinants of CIN development in SLE. METHODS: A case control analysis was performed to compare the clinical characteristics of SLE women with cervical neoplasia (cases) to SLE women without cervical neoplasia (controls). Formalin fixed blocks of neoplastic cervical tissue were obtained from 113 women with SLE and tissue histology confirmed by 2 pathologists. Clinical data was obtained by retrospective chart reviews. Logistic regression was used to evaluate for any significant differences in clinical variables between the cases and the controls. Two sets of controls were used for comparison with a 2:1 match for each control group to cases group. RESULTS: Using matched controls adjusting for age and race, logistic regression analysis showed no significant difference between cases and controls for any of the clinical variables. In particular, there were no significant differences between cases vs. matched and vs. unmatched controls for factors related to SLE (disease severity, use of immunosuppressive drugs), chronic metabolic diseases (hypertension, diabetes) and HPV risk factors (marital status, smoking, gravidity parity). CONCLUSION: The key finding of this study is that SLE patients who develop CIN are not clinically different from SLE patients who do not develop CIN. Thus, lupus disease severity and immunosuppressive treatment were not susceptibility factors for CIN in our female lupus cohort.

Dynamic gene expression in the human cerebral cortex distinguishes children from adults.

In comparison with other primate species, humans have an extended juvenile period during which the brain is more plastic. In the current study we sought to examine gene expression in the cerebral cortex during development in the context of this adaptive plasticity. We introduce an approach designed to discriminate genes with variable as opposed to uniform patterns of gene expression and found that greater inter-individual variance is observed among children than among adults. For the 337 transcripts that show this pattern, we found a significant overrepresentation of genes annotated to the immune system process (pFDR ~/= 0). Moreover, genes known to be important in neuronal function, such as brain-derived neurotrophic factor (BDNF), are included among the genes more variably expressed in childhood. We propose that the developmental period of heightened childhood neuronal plasticity is characterized by more dynamic patterns of gene expression in the cerebral cortex compared to adulthood when the brain is less plastic. That an overabundance of these genes are annotated to the immune system suggests that the functions of these genes can be thought of not only in the context of antigen processing and presentation, but also in the context of nervous system development.

Human papillomavirus, cervical cancer and women's knowledge.

BACKGROUND: Human papillomavirus (HPV) is the major risk factor for cervical cancer. METHODS: We implemented a retrospective case-series study to discern HPV knowledge accuracy among women diagnosed with and treated for cervical cancer. Cases (n=1174), identified from the Pathology database, were diagnosed and treated for cervical cancer at the same institution. Data were collected using self-administered questionnaires and by reviewing medical records. RESULTS: A total of 328 (27.9%) women returned the completed forms. Only 19% of the respondents had identified HPV as the primary risk factor for cervical cancer. Environmental pollutants, radiation exposure, poor dietary habits, excessive physical activity and family history of cervical cancer were listed as risk factors among many others. Multivariate analysis was performed to determine variables that were best associated with HPV knowledge accuracy. Age and education were the two variables that were statistically associated with the outcome. Younger and more educated women who participated in this study were more likely to know about the association between HPV infection and the risk of cervical cancer. CONCLUSIONS: Cervical cancer risk factor knowledge, especially knowledge about HPV is low, even among women with the history of cervical cancer. Younger and more educated women are more likely to have HPV and cervical cancer knowledge accuracy. The importance of personal health practices and the focus on health education should be equally emphasized to achieve successful cancer prevention through vaccination.

E6 and E7 oncogene expression by human papilloma virus (HPV) and the aggressive behavior of recurrent laryngeal papillomatosis (RLP).

Recurrent laryngeal papillomatosis (RLP), a chronic disease associated with human papilloma virus (HPV), requires serial surgical procedures for debulking, resulting in debilitating long-term dysphonia, laryngeal scarring, and rarely malignant degeneration. Human papilloma virus 11 tumors have been widely accepted as more aggressive than HPV 6 tumors; however, the clinical course has been difficult to predict at disease onset, and the biologic mediators of proliferation have not been well characterized. A retrospective case review of 43 patients (4 months to 10 years at diagnosis) was performed on children treated for recurrent laryngeal papillomatosis. Patient charts were reviewed for demographic information, age at RLP diagnosis, approximate frequency of surgical intervention, and absolute number of surgical procedures performed. Human papilloma virus subtyping was performed. Expression analysis of the HPV-encoded E6 and E7 oncogenes was performed by reverse-transcriptase polymerase chain reaction. Fourteen patients had subtype 11 (33%) and 29 patients had subtype 6 (67%). As expected, HPV 11 patients showed a more aggressive clinical course than HPV 6 patients. However, 38% of patients with subtype 6 (11 patients) followed a clinical course that mirrored the more severe subtype 11 patients. These patients expressed the disease at a younger age (P < 0.0002) and showed higher levels of E6 and E7 oncogenes compared to the patients with the more indolent course. Although HPV subtype and early onset of RLP are well characterized prognostic factors, our study documents the significance of E6 and E7 oncogene expression as potential biologic mediators of proliferation and thereby clinical behavior.