Validation of the WHOQOL-Bref instrument in Brazilian sign language (Libras).

PURPOSE: The recognition of the Brazilian Sign Language (Libras) as the official language of the Brazilian deaf, in 2002, reaffirms the linguistic and cultural particularities of the deaf population. Therefore, there is a lack of a validated instrument for assessing the Quality of Life of deaf people using Libras. With authorization from the World Health Organization (WHO), a version of the WHOQOL-Bref in Libras was developed, called WHOQOL-Bref/Libras. However, its psychometric properties have not been examined as yet. Therefore, the purpose of this work is to perform the psychometric validation of the WHOQOL-Bref/Libras. METHODS: WHOQOL-Bref/Libras and a sociodemographic questionnaire were applied to 311 deaf people from the five Brazilian regions. To assess temporal stability, the questionnaire was readministered to 52 deaf people, over an interval of 2 weeks. RESULTS: WHOQOL-Bref/Libras demonstrated satisfactory psychometric values for reliability, discriminant and construct validity, temporal stability, and internal consistency. Cronbach's alpha coefficient showed satisfactory values for each of the WHOQOL-Bref domains: Physical health (0.641), Psychological (0.705), Environment (0.710), and Overall-Bref domains (0.873). The WHOQOL-Bref/Libras is the appropriate option to assess the quality of life of deaf people who communicate through Libras. CONCLUSION: WHOQOL-Bref/Libras had a satisfactory psychometric performance; therefore, it is a valid option that will provide autonomous participation for the deaf in quality of life investigations.

Association between dental caries activity, quality of life and obesity in Brazilian adolescents.

OBJECTIVES: The impact of oral conditions on quality of life in overweight/obesity needs to be elucidated. The aim of this study was to evaluate the association between dental caries activity, quality of life and obesity in Brazilian adolescents. MATERIALS AND METHODS: This study was conducted at public schools in Brazil, on a sample of 202 adolescents, 12 years of age. For anthropometric evaluation, the body mass index (BMI)-for-age was used. In oral examinations, the Decayed, Missing, Filled teeth (DMFT), significant caries (SiC) and dental caries activity (DCA) indices were used (κ > 0.94). The Child-Oral Impacts on Daily Performance (Child-OIDP) index was applied. The sample was divided into two groups: O (overweight/obese; n = 101) and N (normal weight; n = 101). For data analysis, chi-square, odds ratio (OR), Wilcoxon and Pearson correlation tests were used (P < 0.05). RESULTS: The DMFT scores were 1.67 and 2.12 and the SiC scores were 3.85 and 4.26 for groups O and N, respectively. BMI-for-age was significantly related to DCA (OR = 0.579; P < 0.000) and to SiC (OR = 0.649; P = 0.024). There were differences between the groups in eating, cleaning mouth, emotional status, smiling, studying and the overall Child-OIDP (P < 0.05). Positive associations between the impacts on eating, cleaning mouth and smiling were found (P < 0.05). DMFT values showed significant correlation with the emotional status performance in group O and the DCA was positively correlated with performance at school in group O (P < 0.05). CONCLUSION: Obesity, dental caries and quality of life were not correlated. Adolescents with normal weight presented a low perception of the impact of oral conditions on quality of life; however, it seemed to affect psychological aspects in their daily performances. Providing adolescents with nutritional assistance may prevent obesity and dental caries, and improve their quality of life.

An epidemiological scoring system for tooth wear and dental erosive wear.

BACKGROUND: The prevalence and severity of tooth wear and dental erosion is rising in children and there is no consensus about an index to be employed. AIM: To assess the reliability of an epidemiological scoring system dental wear index (DWI) to measure tooth wear and dental erosive wear. DESIGN: An epidemiological cross-sectional survey was conducted to evaluate and compare tooth wear and dental erosion using the dental wear index and erosion wear index (EWI). The study was conducted with randomised samples of 2,371 children aged between 4 years and 12 years selected from the State of São Paulo, Brazil. Records were used for calculating tooth wear and dental erosion; the incisal edge and canine cusp were excluded. RESULTS: As the schoolchildren's ages increased the severity of primary tooth wear increased in canines (P = 0.0001, OR = 0.34) and molars (P = 0.0001, OR = 2.47) and erosion wear increased in incisal/occlusal (P = 0.0001, OR = 5.18) and molars (P = 0.0001, OR = 2.47). There was an increased prevalence of wear in the permanent teeth of older schoolchildren, particularly on the incisal/occlusal surfaces (P = 0.0001, OR = 7.03). CONCLUSION: The prevalence of tooth wear and dental erosion increased as age increased in children. The epidemiological scoring system Dental Wear Index is able to measure both tooth wear and dental erosive wear. This index should be used to monitor the progression of non-carious lesions and to evaluate the levels of disease in the population.

Restrição ao uso de tabaco e a prevenção do câncer bucal / Restriction of tobacco use and the prevention of oral cancer

A Organização Mundial da Saúde relata que a epidemia mundial de tabagismo é uma das maiores ameaças à saúde pública dos tempos modernos. O objetivo deste estudo foi relacionar a adoção de medidas restritivas ao uso do tabaco e suas implicações na prevenção ao câncer bucal, por meio de revisão crítica. As evidencias científicas apontam que o uso de tabaco é considerado como causa primária de muitos problemas e doenças bucais, dentre às quais se destacam o câncer bucal, doença periodontal, perdas dentárias e defeitos congênitos. No Brasil e no mundo os principais documentos que regulam a disposição, uso e estratégias de combate aotabaco são relacionados à legislação vigente, documentos internacionais e aos estudos epidemiológicos. Conclui-se que a prevenção ao câncer bucal está relacionada à conscientização das populações quanto aos malefícios causados por hábitos deletérios, como o uso de tabaco, à adoção de práticas saudáveis, bem como se evidencia a necessidade de desenvolvimento de ações abrangentes para o controle do câncer, nos diferentes níveis de atuação e a adoção de medidas mais amplas de restrição ao uso de tabaco pelos diversossetores da sociedade.

The World Health Organization reports that the worldwide epidemic of smoking is the major threat to the public health of modern times. The objective of this study was to relate the adoption of restrictive measures to tobacco use and its implications in the prevention of oral cancer, through critical review. The scientific evidence suggests that the use of tobacco is considered as the primary cause of many problems and oraldiseases, among which are the oral cancer, periodontal disease, tooth loss and congenital defects. In Brazil and the world the main documents regulating the provision, use and strategies to combat tobacco use are related to legislation, international documents and the epidemiological studies. It is concluded that prevention of oral cancer is related to awareness of people about the harm caused by deleterious habits such as use of tobacco, the adoption of healthy practices, and as well as highlighting the need for development ofcomprehensive actions to control the cancer, the different levels of performance and the adoption of furthermeasures to restrict the use of tobacco by the different sectors of society.

Short-term memory formation and long-term memory consolidation are enhanced by cellular prion association to stress-inducible protein 1.

Cellular prion protein (PrP(C)) is a cell surface glycoprotein that interacts with several ligands such as laminin, NCAM (Neural-Cell Adhesion Molecule) and the stress-inducible protein 1 (STI1). PrP(C) association with these proteins in neurons mediates adhesion, differentiation and protection against programmed cell death. Herein, we used an aversively motivated learning paradigm in rats to investigate whether STI1 interaction with PrP(C) affects short-term memory (STM) formation and long-term memory (LTM) consolidation. Blockage of PrP(C)-STI1 interaction with intra-hippocampal infusion of antibodies against PrP(C) or STI1 immediately after training impaired both STM and LTM. Furthermore, infusion of PrP(C) peptide 106-126, which competes for PrP(C)-STI1 interaction, also inhibited both forms of memory. Remarkably, STI1 peptide 230-245, which includes the PrP(C) binding site, had a potent enhancing effect on memory performance, which could be blocked by co-treatment with the competitive PrP(C) peptide 106-126. Taken together, these results demonstrate that PrP(C)-STI1 interaction modulates both STM and LTM and suggests a potential use of ST11 peptide 230-245 as a pharmacological agent.

The interaction between prion protein and laminin modulates memory consolidation.

Cellular prion protein (PrPc) has a pivotal role in prion diseases. PrPc is a specific receptor for laminin (LN) gamma1 peptide and several lines of evidence indicate that it is also involved in neural plasticity. Here we investigated whether the interaction between PrPc and LN plays a role in rat memory formation. We found that post-training intrahippocampal infusion of PrPc-derived peptides that contain the LN binding site (PrPc163-182 and PrPc173-192) or of anti-PrPc or anti-LN antibodies that inhibit PrPc-LN interaction impaired inhibitory avoidance memory retention. The amnesic effect of anti-PrPc antibodies and PrPc173-192 peptide was reversed by co-infusion of a LN gamma1 chain-derived peptide containing the PrPc-binding site, suggesting that PrPc-LN interaction is indeed crucial for memory consolidation. In addition, PrPc173-192 peptide and anti-PrPc or anti-LN antibodies also inhibited the activation of hippocampal cAMP-dependent protein kinase A (PKA) and extracellular regulated kinase (ERK1/2), two kinases that mediate the up-regulation of signaling pathways needed for consolidation of inhibitory avoidance memory. Our findings show that, through its interaction with LN, hippocampal PrPc plays a critical role in memory processing and suggest that this role is mediated by activation of both PKA and ERK1/2 signaling pathways.

Stress-inducible protein 1 is a cell surface ligand for cellular prion that triggers neuroprotection.

Prions are composed of an isoform of a normal sialoglycoprotein called PrP(c), whose physiological role has been under investigation, with focus on the screening for ligands. Our group described a membrane 66 kDa PrP(c)-binding protein with the aid of antibodies against a peptide deduced by complementary hydropathy. Using these antibodies in western blots from two-dimensional protein gels followed by sequencing the specific spot, we have now identified the molecule as stress-inducible protein 1 (STI1). We show that this protein is also found at the cell membrane besides the cytoplasm. Both proteins interact in a specific and high affinity manner with a K(d) of 10(-7) M. The interaction sites were mapped to amino acids 113-128 from PrP(c) and 230-245 from STI1. Cell surface binding and pull-down experiments showed that recombinant PrP(c) binds to cellular STI1, and co-immunoprecipitation assays strongly suggest that both proteins are associated in vivo. Moreover, PrP(c) interaction with either STI1 or with the peptide we found that represents the binding domain in STI1 induce neuroprotective signals that rescue cells from apoptosis.

Cellular prion protein transduces neuroprotective signals.

To test for a role for the cellular prion protein (PrP(c)) in cell death, we used a PrP(c)-binding peptide. Retinal explants from neonatal rats or mice were kept in vitro for 24 h, and anisomycin (ANI) was used to induce apoptosis. The peptide activated both cAMP/protein kinase A (PKA) and Erk pathways, and partially prevented cell death induced by ANI in explants from wild-type rodents, but not from PrP(c)-null mice. Neuroprotection was abolished by treatment with phosphatidylinositol-specific phospholipase C, with human peptide 106-126, with certain antibodies to PrP(c) or with a PKA inhibitor, but not with a MEK/Erk inhibitor. In contrast, antibodies to PrP(c) that increased cAMP also induced neuroprotection. Thus, engagement of PrP(c) transduces neuroprotective signals through a cAMP/PKA-dependent pathway. PrP(c) may function as a trophic receptor, the activation of which leads to a neuroprotective state.