Aquaporin 5 Interacts with Fluoride and Possibly Protects Against Caries

Aquaporins (AQP) are water channel proteins and the genes coding for AQP2, AQP5, and AQP6 are clustered in 12q13. Since AQP5 is expressed in serous acinar cells of salivary glands, we investigated its involvement in caries. DNA samples from 1,383 individuals from six groups were studied. Genotypes of eight single nucleotide polymorphisms covering the aquaporin locus were tested for association with caries experience. Interaction with genes involved in enamel formation was tested. The association between enamel microhardness at baseline, after creation of artificial caries lesion, and after exposure to fluoride and the genetic markers in AQP5 was tested. Finally, AQP5 expression in human whole saliva, after exposure to fluoride in a mammary gland cell line, which is known to express AQP5, and in Wistar rats was also verified. Nominal associations were found between caries experience and markers in the AQP5 locus. Since these associations suggested that AQP5 may be inhibited by levels of fluoride in the drinking water that cause fluorosis, we showed that fluoride levels above optimal levels change AQP5 expression in humans, cell lines, and rats. We have shown that AQP5 is involved in the pathogenesis of caries and likely interact with fluoride.Fil: Anjomshoaa, Ida. University of Pittsburgh; Estados UnidosFil: Briseño Ruiz, Jessica. University of Pittsburgh; Estados UnidosFil: Deeley, Kathleen. University of Pittsburgh; Estados UnidosFil: Poletta, Fernando Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas "Norberto Quirno". CEMIC-CONICET.; ArgentinaFil: Mereb, Juan C.. Provincia de Río Negro. Ministerio de Salud. Hospital de Área El Bolsón ; ArgentinaFil: Leite, Aline L.. Universidade de Sao Paulo; BrasilFil: Barreta, Priscila A. T.. Universidade de Sao Paulo; BrasilFil: Silva, Thelma L.. Universidade de Sao Paulo; BrasilFil: Dizak, Piper. University of Pittsburgh; Estados UnidosFil: Ruff, Timothy. University of Pittsburgh; Estados UnidosFil: Patir, Asli. İstanbul Medipol Üniversitesi; TurquíaFil: Koruyucu, Mine. İstanbul Üniversitesi; TurquíaFil: Abbasoğlu, Zerrin. Yeditepe Üniversitesi; TurquíaFil: Casado, Priscila L.. Universidade Federal Fluminense; BrasilFil: Brown, Andrew. University of Pittsburgh; Estados UnidosFil: Zaky, Samer H.. University of Pittsburgh; Estados UnidosFil: Bayram, Merve. İstanbul Medipol Üniversitesi; TurquíaFil: Küchler, Erika C.. University of Pittsburgh; Estados UnidosFil: Cooper, Margaret E.. University of Pittsburgh; Estados UnidosFil: Liu, Kai. University of Pittsburgh; Estados UnidosFil: Marazita, Mary L.. University of Pittsburgh; Estados UnidosFil: Tanboğa, İlknur. Marmara Üniversitesi; TurquíaFil: Granjeiro, José M.. Universidade Federal Fluminense; Brasil. Instituto Nacional de Metrologia, Qualidade e Tecnologia; BrasilFil: Seymen, Figen. İstanbul Üniversitesi; TurquíaFil: Castilla, Eduardo Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas "Norberto Quirno". CEMIC-CONICET.; Argentina. Fundación Oswaldo Cruz; BrasilFil: Orioli, Iêda M.. Universidade Federal do Rio de Janeiro; BrasilFil: Sfeir, Charles. University of Pittsburgh; Estados UnidosFil: Owyang, Hongjiao. Marmara Üniversitesi; TurquíaFil: Rabelo Buzalaf, Marilia Afonso. Universidade de Sao Paulo; BrasilFil: Vieira, Alexandre R.. University of Pittsburgh; Estados Unido

Role of estrogen related receptor beta (ESRRB) in DFN35B hearing impairment and dental decay

BACKGROUND: Congenital forms of hearing impairment can be caused by mutations in the estrogen related receptor beta (ESRRB) gene. Our initial linkage studies suggested the ESRRB locus is linked to high caries experience in humans. METHODS: We tested for association between the ESRRB locus and dental caries in 1,731 subjects, if ESRRB was expressed in whole saliva, if ESRRB was associated with the microhardness of the dental enamel, and if ESRRB was expressed during enamel development of mice. RESULTS: Two families with recessive ESRRB mutations and DFNB35 hearing impairment showed more extensive dental destruction by caries. Expression levels of ESRRB in whole saliva samples showed differences depending on sex and dental caries experience. CONCLUSIONS: The common etiology of dental caries and hearing impairment provides a venue to assist in the identification of individuals at risk to either condition and provides options for the development of new caries prevention strategies, if the associated ESRRB genetic variants are correlated with efficacy.Fil: Weber, Megan L.. University of Pittsburgh; Estados UnidosFil: Hsin, Hong Yuan. University of Pittsburgh; Estados UnidosFil: Kalay, Ersan. Karadeniz Technical University; TurquíaFil: Brožková, Dana Š. Charles University; República Checa. University Hospital Motol; República ChecaFil: Shimizu, Takehiko. Nihon University. School of Dentistry; JapónFil: Bayram, Merve. Medipol Istanbul University; TurquíaFil: Deeley, Kathleen. University of Pittsburgh; Estados UnidosFil: Küchler, Erika C.. University of Pittsburgh; Estados UnidosFil: Forella, Jessalyn. University of Pittsburgh; Estados UnidosFil: Ruff, Timothy D.. University of Pittsburgh; Estados UnidosFil: Trombetta, Vanessa M.. University of Pittsburgh; Estados UnidosFil: Sencak, Regina C.. University of Pittsburgh; Estados UnidosFil: Hummel, Michael. University of Pittsburgh; Estados UnidosFil: Briseño Ruiz, Jessica. University of Pittsburgh; Estados UnidosFil: Revu, Shankar K.. University of Pittsburgh; Estados UnidosFil: Granjeiro, José M.. Universidade Federal Fluminense; BrasilFil: Antunes, Leonardo S.. Universidade Federal Fluminense; BrasilFil: Antunes, Livia A.. Universidade Federal Fluminense; BrasilFil: Abreu, Fernanda V.. Universidade Federal Fluminense; BrasilFil: Costabel, Marcelo C.. Universidade Federal do Rio de Janeiro; BrasilFil: Tannure, Patricia N.. Veiga de Almeida University; Brasil. Salgado de Oliveira University; BrasilFil: Koruyucu, Mine. Istanbul University; TurquíaFil: Patir, Asli. Medipol Istanbul University; TurquíaFil: Poletta, Fernando Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Mereb, Juan C.. Estudio Colaborativo Latino Americano de Malformaciones Congénitas; ArgentinaFil: Castilla, Eduardo Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Orioli, Iêda M.. Universidade Federal do Rio de Janeiro; BrasilFil: Marazita, Mary L.. University of Pittsburgh; Estados UnidosFil: Ouyang, Hongjiao. University of Pittsburgh; Estados UnidosFil: Jayaraman, Thottala. University of Pittsburgh; Estados UnidosFil: Seymen, Figen. Istanbul University; TurquíaFil: Vieira, Alexandre R.. University of Pittsburgh; Estados Unido

Enamel Formation Genes Influence Enamel Microhardness Before and After Cariogenic Challenge

There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes may contribute to caries. For the present study, we used DNA samples collected from 1,831 individuals from various population data sets. Single nucleotide polymorphism markers were genotyped in selected genes (ameloblastin, amelogenin, enamelin, tuftelin, and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Associations with caries experience can be detected but they are not necessarily replicated in all population groups and the most expressive results was for a marker in AMELX (p = 0.0007). To help interpret these results, we evaluated if enamel microhardness changes under simulated cariogenic challenges are associated with genetic variations in these same genes. After creating an artificial caries lesion, associations could be seen between genetic variation in TUFT1 (p = 0.006) and TUIP11 (p = 0.0006) with enamel microhardness. Our results suggest that the influence of genetic variation of enamel formation genes may influence the dynamic interactions between the enamel surface and the oral cavity. © 2012 Shimizu et al

Método para la calibración de modelos estocásticos de flujo y transporte en aguas subterráneas, para el diseño de redes de monitoreo de calidad del agua /

 tesis que para obtener el grado de Doctorado en Ingeniería (Ingeniería Civil), presenta Jessica Vanessa Briseño Ruiz ; tutora principal de tesis Graciela del Socorro Herrera Zamarrón316 páginas : ilustracionesDoctorado en Ingeniería (Ingeniería Civil) Universidad Nacional Autónoma de México, 2012 Programa de Posgrado en Ingenierí

Método para el diseño óptimo de redes de monitoreo de los niveles del agua subterránea

Para estimar la disponibilidad del agua subterránea y su evolución es indispensable medir los niveles del agua subterránea por periodos largos de tiempo. Sin embargo, los recursos económicos son una limitante en la recopilación de suficientes datos que permitan estimar con certeza la evolución de dichos niveles. Por este motivo se requiere de métodos para el diseño de redes de monitoreo de los niveles del agua subterránea que faciliten utilizar los recursos económicos disponibles para el monitoreo de manera efectiva. El método de Herrera y Pinder (Herrera, 1998) para el diseño óptimo de redes de monitoreo de la calidad del agua subterránea, aplicado por Herrera et al. (2001), y también por Herrera y Pinder (2005), tiene varias ventajas. Por un lado, permite seleccionar tanto posiciones como tiempos de monitoreo en forma óptima; además, con la información obtenida de la red de monitoreo, permite hacer estimaciones en espacio y tiempo, y utiliza un modelo de flujo y transporte, el cual sintetiza el conocimiento de las características del acuífero, de la dinámica del flujo subterráneo y de la problemática de calidad del agua subterránea que se tenga, así como del conocimiento de las leyes de la física. En este trabajo, una modificación de esta metodología se prueba por primera vez para el diseño de redes de monitoreo de los niveles del agua subterránea. Se presenta un caso sintético en el que la red se diseña para un solo tiempo, suponiendo que el flujo está en estado estacionario. Los resultados presentados indican que la metodología propuesta por Herrera y Pinder para el diseño de redes de monitoreo tiene buenas perspectivas para aplicarse exitosamente al diseño de redes de monitoreo de los niveles del agua

Role of TRAV Locus in Low Caries Experience

Submitted by sandra infurna ([email protected]) on 2016-01-14T10:57:58Z No. of bitstreams: 1 eduardo_castilla3_etal_IOC_2013.pdf: 1589582 bytes, checksum: da12596860deef9b52fce978ae3bf565 (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-01-14T12:11:08Z (GMT) No. of bitstreams: 1 eduardo_castilla3_etal_IOC_2013.pdf: 1589582 bytes, checksum: da12596860deef9b52fce978ae3bf565 (MD5)Made available in DSpace on 2016-01-14T12:11:08Z (GMT). No. of bitstreams: 1 eduardo_castilla3_etal_IOC_2013.pdf: 1589582 bytes, checksum: da12596860deef9b52fce978ae3bf565 (MD5) Previous issue date: 2013University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.Nihon University of Dentistry at Matsudo. Department of Pediatric Dentistry. Matsudo Chiba, Japan.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.ECLAMC (Latin American Collaborative Study of Congenital Malformations). CEMIC (Center for Medical Education and Clinical Research), Buenos Aires, Argentina / ECLAMC at INAGEMP-CNPq (National Institute of Population Medical Genetics) . Fundação Oswaldo Cruz. Departamento de Genética. Rio de Janeiro, RJ, Brasil.Pontifícia Universidade Católica do Paraná (PUCPR). Centro de Ciências Biológicas e da Saúde. Curitiba, PR, Brasil.Pontifícia Universidade Católica do Paraná (PUCPR). Centro de Ciências Biológicas e da Saúde. Curitiba, PR, Brasil.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.Universidade Federal do Rio de Janeiro. Departamento de Odontologia Pediátrica e Ortodontia. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense. Instituto de Biologia. Unidade de Pesquisa Clínica. Niterói, RJ, Brasil.Universidade Federal Fluminense. Instituto de Biologia. Unidade de Pesquisa Clínica. Niterói, RJ, Brasil.Istanbul Medipol University. Department of Pedodontics. Istanbul, Turkey.Istanbul University. Department of Pedodontics. Istanbul, Turkey.ECLAMC at Hospital de Area El Bolsón. Río Negro, Argentina.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Texas Health Science Center. Medical School. Pediatric Research Center. School of Dentistry. Department of Endodontics. Houston, Texas, USA.University of Texas Health Science Center. Medical School. Pediatric Research Center. School of Dentistry. Department of Endodontics. Houston, Texas, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.Istanbul University. Department of Pedodontics. Istanbul, Turkey.Universidade Federal do Rio de Janeiro. Departamento de Odontologia Pediátrica e Ortodontia. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense. Instituto de Biologia. Unidade de Pesquisa Clínica. Niterói, RJ, Brasil / INMETRo. Duque de Caxias, RJ, Brasil.Pontifícia Universidade Católica do Paraná (PUCPR). Centro de Ciências Biológicas e da Saúde. Curitiba, PR, Brasil.ECLAMC at INAGEMP-CNPq (National Institute of Population Medical Genetics) in. Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biologia. Departamento de Genética. Rio de Janeiro, RJ, Brasil.ECLAMC (Latin American Collaborative Study of Congenital Malformations). CEMIC (Center for Medical Education and Clinical Research), Buenos Aires, Argentina / ECLAMC at INAGEMP-CNPq (National Institute of Population Medical Genetics) . Fundação Oswaldo Cruz. Departamento de Genética. Rio de Janeiro, RJ, Brasil.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA / University of Pittsburgh. Department of Human Genetics, and Clinical and Translational Science. Center for Craniofacial and Dental Genetics. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA / University of Pittsburgh. School of Dental Medicine, and Clinical and Translational Science. Department of Pediatric Dentistry. Center for Craniofacial and Dental Genetics. Pittsburgh, PA, USA.Caries is the most common chronic, multifactorial disease in the world today; and little is still known about the genetic factors influencing susceptibility. Our previous genome- wide linkage scan has identified five loci related to caries susceptibility: 5q13.3, 13q31.1, 14q11.2, 14q 24.3, and Xq27. In the present study, we fine mapped the 14q11.2 locus in order to identify genetic contributors to caries susceptibility. Four hundred seventy-seven subjects from 72 pedigrees with similar cultural and behavioral habits and limited access to dental care living in the Philippines were studied. An additional 387 DNA samples from unrelated individuals were used to determine allele frequencies. For replication purposes, a total of 1,446 independent subjects from four different populations were analyzed based on their caries experience (low versus high). Fortyeight markers in 14q11.2 were genotyped using TaqMan chemistry. Transmission disequilibrium test was used to detect overtransmission of alleles in the Filipino families, and chi-square, Fisher’s exact and logistic regression were used to test for association between low caries experience and variant alleles in the replication data sets. We finally assessed the mRNA expression of TRAV4 in the saliva of 143 study subjects. In the Filipino families, statistically significant associations were found between low caries experience and markers in TRAV4. We were able to replicate these results in the populations studied that were characteristically from underserved areas. Direct sequencing of 22 subjects carrying the associated alleles detect one missense mutation (Y30R) that is predicted to be probably damaging. Finally, we observed higher expression in children and teenagers with low caries experience, correlating with specific alleles in TRAV4. Our results suggest TRAV4 may have a role in protecting against caries

Correlations of enamel microhardness values in the several experimental points.

<p>Statistically significant correlations are presented in bold font.</p

Definitions of caries experience based on age and DMFT (Decayed, Missing due to caries, Filled Teeth) scores used in the Filipino families.

a<p>DMFT cut-offs were modified from the World Health Organization (World Health Organization, 2003),</p>b<p>Standard deviation.</p

Previously reported associations between enamel formation genes and caries susceptibility.

*<p>In the presence of <i>Streptococcus mutans</i>.</p>#<p>Only is less severely affected cases.</p

Demographics and caries experience of the replication study populations.

a<p>Decayed, Missing due to caries, Filled Teeth.</p>b<p>Standard deviation.</p>c<p>High and low caries experience was defined based on criteria 1 on <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0045022#pone-0045022-t001" target="_blank">Table 1</a>.</p