This study is part of the Cross-National Survey on Health Behaviour in School-aged Children--a WHO Collaborative Study, which started in 1982. The aim of the study was to describe the oral hygiene habits (toothbrushing and flossing) of 11-year-old schoolchildren in 22 European countries (Austria, Belgium, the Czech Republic, Denmark, Estonia, FInland, France, Germany, Greenland, Hungary, Israel, Latvia, Lithuania, Northern Ireland, Norway, Poland, Russia, Scotland, the Slovak Republic, Spain, Sweden, and Wales) and Canada. The data were collected from standardized anonymous questionnaires in school classrooms during the 1993-1994 school year. At least 1300 school children, representing the whole country, participated in the study in each country. Oral hygiene habits were analyzed according to gender, age, country, school performance, and family economy. The children brushed most favorably in Sweden, Denmark, German, Austria, and Norway (83-73% brushed twice a day). More-than-once-a-day toothbrushing was especially uncommon (from 26 to 33%) among boys in Finland, Lithuania, Russia, Estonia, and Latvia. Toothbrushing frequency differed significantly according to school performance in Canada, the Czech Republic, Scotland, Poland, Northern Ireland, and Wales and between different socio-economic groups in Northern Ireland, Wales, the Czech Republic, Scotland, Poland, and Russia. Use of dental floss was rare. In general, flossing was less frequent among boys than among girls. Daily flossing was most common among Canadian adolescents (25%). In conclusion, there are considerable differences in toothbrushing frequency among children in European countries.

High serum lipopolysaccharide (LPS) activity in normoalbuminuric patients with type 1 diabetes (T1D) predicts the progression of diabetic nephropathy (DN), but the mechanisms behind this remain unclear. We observed that treatment of cultured human podocytes with sera from normoalbuminuric T1D patients with high LPS activity downregulated 3-phosphoinositide-dependent kinase-1 (PDK1), an activator of the Akt cell survival pathway, and induced apoptosis. Knockdown of PDK1 in cultured human podocytes inhibited antiapoptotic Akt pathway, stimulated proapoptotic p38 MAPK pathway, and increased apoptosis demonstrating an antiapoptotic role for PDK1 in podocytes. Interestingly, PDK1 was downregulated in the glomeruli of diabetic rats and patients with type 2 diabetes before the onset of proteinuria, further suggesting that reduced expression of PDK1 associates with podocyte injury and development of DN. Treatment of podocytes in vitro and mice in vivo with LPS reduced PDK1 expression and induced apoptosis, which were prevented by inhibiting the Toll-like receptor (TLR) signaling pathway with the immunomodulatory agent GIT27. Our data show that LPS downregulates the cell survival factor PDK1 and induces podocyte apoptosis, and that blocking the TLR pathway with GIT27 may provide a non-nephrotoxic means to prevent the progression of DN.

Nephrin is a core component of podocyte (glomerular epithelial cell) slit diaphragm and is required for kidney ultrafiltration. Down-regulation or mislocalization of nephrin has been observed in diabetic kidney disease (DKD), characterized by albuminuria. Here, we investigate the role of protein kinase C and casein kinase 2 substrate in neurons 2 (PACSIN2), a regulator of endocytosis and recycling, in the trafficking of nephrin and development of DKD. We observe that PACSIN2 is up-regulated and nephrin mislocalized in podocytes of obese Zucker diabetic fatty (ZDF) rats that have altered renal function. In cultured podocytes, PACSIN2 and nephrin colocalize and interact. We show that nephrin is endocytosed in PACSIN2-positive membrane regions and that PACSIN2 overexpression increases both nephrin endocytosis and recycling. We identify rabenosyn-5, which is involved in early endosome maturation and endosomal sorting, as a novel interaction partner of PACSIN2. Interestingly, rabenosyn-5 expression is increased in podocytes in obese ZDF rats, and, in vitro, its overexpression enhances the association of PACSIN2 and nephrin. We also show that palmitate, which is elevated in diabetes, enhances this association. Collectively, PACSIN2 is up-regulated and nephrin is abnormally localized in podocytes of diabetic ZDF rats. In vitro, PACSIN2 enhances nephrin turnover apparently via a mechanism involving rabenosyn-5. The data suggest that elevated PACSIN2 expression accelerates nephrin trafficking and associates with albuminuria

Equal distribution of health care services has long been a major goal of health policy in the Nordic countries. According to these guidelines, every child is expected to have an examination and treatment at least every second year. The aim of this study was to analyze the trends and, in particular, the socioeconomic differences in dental visits between 1977 and 1995. The data were collected as part of a nationwide research program, the Adolescent Health and Lifestyle Survey, which began in 1977. Every second year a self-administered questionnaire was mailed to a representative sample of 14-, 16- and 18-year-old Finns. The sample sizes in the surveys varied from 2422 to 9556, making a total of 56,605 subjects in the whole study. The response rates in different years varied from 77% to 88%. The percentage of adolescents visiting a dentist increased between 1977 and 1981 and thereafter remained stable. Dental visits seemed to correlate with the occupational and educational status of the parents up to 1983, but not after that. The Finnish primary oral health care policy seems to have gained a major objective by eliminating social inequality in dental service utilization among adolescents.

Loss of podocytes is an early feature of diabetic nephropathy (DN) and predicts its progression. We found that treatment of podocytes with sera from normoalbuminuric type 1 diabetes patients with high lipopolysaccharide (LPS) activity, known to predict progression of DN, downregulated CDK2 (cyclin-dependent kinase 2). LPS-treatment of mice also reduced CDK2 expression. LPS-induced downregulation of CDK2 was prevented in vitro and in vivo by inhibiting the Toll-like receptor (TLR) pathway using immunomodulatory agent GIT27. We also observed that CDK2 is downregulated in the glomeruli of obese Zucker rats before the onset of proteinuria. Knockdown of CDK2, or inhibiting its activity with roscovitine in podocytes increased apoptosis. CDK2 knockdown also reduced expression of PDK1, an activator of the cell survival kinase Akt, and reduced Akt phosphorylation. This suggests that CDK2 regulates the activity of the cell survival pathway via PDK1. Furthermore, PDK1 knockdown reduced the expression of CDK2 suggesting a regulatory loop between CDK2 and PDK1. Collectively, our data show that CDK2 protects podocytes from apoptosis and that reduced expression of CDK2 associates with the development of DN. Preventing downregulation of CDK2 by blocking the TLR pathway with GIT27 may provide a means to prevent podocyte apoptosis and progression of DN.