Caries prevalence and tooth loss in Hungarian adult population: results of a national survey

<p>Abstract</p> <p>Background</p> <p>Oral health is basicly important for the well-being of people. Thus, it is strongly suggested to organize epidemiological surveys in order to gain representative data on oral condition of the given population. The purpose of the cross-sectional study was to determine the results on tooth loss and caries prevalence of Hungarian adults in different age groups.</p> <p>Methods</p> <p>Altogether 4606 persons (2923 women, 1683 men) participated in the study who were classified into different age groups: 19 [less than or equal to], 20–24, 35–44, 45–64, 65–74, [greater than or equal to]75 year olds. Probands were selected randomly from the population attending the compulsory lung screening examinations. The participants were examined by calibrated dentists, according to the WHO (1997) criteria. In order to produce representative data, the chosen localities for these examinations covered the capital, the largest towns, the villages, and case weights were used for the statistical evaluation.</p> <p>Results</p> <p>The mean values of DMF-T were found between 11.79±5.68 and 21.90±7.61 These values were significantly higher in women compared to men (p < 0.05). In all age groups the values of M were the highest. Except for the women in the groups of 35–44 and 45–64 year olds, these values showed an increasing tendency both in women and men by age (from 5.50±6.49, and 4.70±4.08 to 21.52±9.07 and 18.41±8.89 respectively). The values of D components reached the highest values in 45–64 year olds (4.54±2.12 and 4.22±2.81, by gender, respectively), then in the older age groups there was a high reduction in these values (in 65–74 year olds: 2.72±1.88 and 1.36±2.48; in 75 or more than 75 year olds: 1.05±1.41 and 1.03±1.76 by gender, respectively). The ratio of D and F values was the highest in the age group of 65–74 year olds (2.12), the lowest ratio could be calculated in 20–34 year olds (0.65).</p> <p>Data showed some decrease in caries experience in 35–44 years of age between 2000 and 2004. The prevalence of persons with 21 or more teeth had been increased from 65.6% to 73.1%. This positive tendency has not been occured in prevalence of edentulousness in this age group: the prevalence of edentulous persons changed from 1.4 to 1.9%. In 65–74 year olds the level of edentulousness became lower, from 25.9 to 14.8% and the prevalence of persons with 21 or more teeth is higher (22.6%) than it was in 2000 (13.0%).</p> <p>Conclusion</p> <p>Present data from Hungary show some slight decrease in caries experience between 35–44 years of age, although this positive tendency has not been occured in prevalence of edentulousness in this age group. A positive tendency could be experienced in the group of 65–74 year olds in edentulousness and in number of teeth, but further efforts are needed to reach a better situation.</p

Synthetic microparticles conjugated with VEGF165 improve the survival of endothelial progenitor cells via microRNA-17 inhibition

Several cell-based therapies are under pre-clinical and clinical evaluation for the treatment of ischemic diseases. Poor survival and vascular engraftment rates of transplanted cells force them to work mainly via time-limited paracrine actions. Although several approaches, including the use of soluble vascular endothelial growth factor (sVEGF)-VEGF165, have been developed in the last 10 years to enhance cell survival, they showed limited efficacy. Here, we report a pro-survival approach based on VEGF-immobilized microparticles (VEGF-MPs). VEGF-MPs prolong VEGFR-2 and Akt phosphorylation in cord blood-derived late outgrowth endothelial progenitor cells (OEPCs). In vivo, OEPC aggregates containing VEGF-MPs show higher survival than those treated with sVEGF. Additionally, VEGF-MPs decrease miR-17 expression in OEPCs, thus increasing the expression of its target genes CDKN1A and ZNF652. The therapeutic effect of OEPCs is improved in vivo by inhibiting miR-17. Overall, our data show an experimental approach to improve therapeutic efficacy of proangiogenic cells for the treatment of ischemic diseases.Soluble vascular endothelial growth factor (VEGF) enhances vascular engraftment of transplanted cells but the efficacy is low. Here, the authors show that VEGF-immobilized microparticles prolong survival of endothelial progenitors in vitro and in vivo by downregulating miR17 and upregulating CDKN1A and ZNF652

GATA2 Mediates Thyrotropin-Releasing Hormone-Induced Transcriptional Activation of the Thyrotropin β Gene

Thyrotropin-releasing hormone (TRH) activates not only the secretion of thyrotropin (TSH) but also the transcription of TSHβ and α-glycoprotein (αGSU) subunit genes. TSHβ expression is maintained by two transcription factors, Pit1 and GATA2, and is negatively regulated by thyroid hormone (T3). Our prior studies suggest that the main activator of the TSHβ gene is GATA2, not Pit1 or unliganded T3 receptor (TR). In previous studies on the mechanism of TRH-induced activation of the TSHβ gene, the involvements of Pit1 and TR have been investigated, but the role of GATA2 has not been clarified. Using kidney-derived CV1 cells and pituitary-derived GH3 and TαT1 cells, we demonstrate here that TRH signaling enhances GATA2-dependent activation of the TSHβ promoter and that TRH-induced activity is abolished by amino acid substitution in the GATA2-Zn finger domain or mutation of GATA-responsive element in the TSHβ gene. In CV1 cells transfected with TRH receptor expression plasmid, GATA2-dependent transactivation of αGSU and endothelin-1 promoters was enhanced by TRH. In the gel shift assay, TRH signal potentiated the DNA-binding capacity of GATA2. While inhibition by T3 is dominant over TRH-induced activation, unliganded TR or the putative negative T3-responsive element are not required for TRH-induced stimulation. Studies using GH3 cells showed that TRH-induced activity of the TSHβ promoter depends on protein kinase C but not the mitogen-activated protein kinase, suggesting that the signaling pathway is different from that in the prolactin gene. These results indicate that GATA2 is the principal mediator of the TRH signaling pathway in TSHβ expression