Stunting represents growth failure resulting from poor nutrition and health during the pre- and postnatal periods. Initiatives since 1980 have steadily reduced malnutrition and consequent retardation of child growth, but 1 of 3 preschool children worldwide remains stunted. Countries have varied substantially in progress achieved in reducing stunting. This study aimed to understand which underlying (i.e., proximal) and basic (i.e., distal) national factors have been most important in explaining this variation among countries, and the relation between the 2 sets of factors. Eighty-five developing countries with at least 2 surveys for stunting >4 y apart were included from the WHO Global Database on Child Growth. The analytic data set with independent variables from several sources was constructed to match closely by year for each country to initial and final stunting data. Full-information maximum likelihood estimated multiple linear regression models while accounting for missing data in independent variables. The final model explained 65.5% of the variance of change in stunting, and included both underlying and basic variables: initial and change in immunization rate, initial and change in safe water rate, initial female literacy rate, initial government consumption, initial income distribution, and the initial proportion of the economy devoted to agriculture. Although factors that were important for reducing stunting in the past may not necessarily be the ones that are important in the future, these results suggest that it possible for substantial progress to be made in reducing the current high prevalence of stunting by investing in both long-term development and in specific interventions.

PurposeChronic low-grade inflammation may induce chronic kidney disease in patients with type 2 diabetes. This study investigated the relation between inflammatory biomarkers and chronic kidney disease in patients with type 2 diabetes, which has not yet been reported in Asian populations.Materials and MethodsA cross-sectional study was performed in 543 patients recruited from diabetic clinics for an ongoing, prospective study. Multivariate logistic regression was used to evaluate the association between inflammatory biomarkers and the presence of chronic kidney disease (estimated glomerular filtration rate < 60 mL/min per 1.73 m2 by the simplified Modification of Diet in Renal Disease equation using plasma creatinine).ResultsThe risk of chronic kidney disease increased in the highest quartiles of C-reactive protein (CRP) [multivariate odds ratio (OR) = 3.73; 95% CI = 1.19-1.70] and tumor necrosis factor-α (multivariate OR = 4.45; 95% CI = 1.63-12.11) compared to the lowest quartiles after adjustments for age, sex, zinc intake, and other putative risk factors for chronic kidney disease.ConclusionOur results suggest that CRP and tumor necrosis factor-α may be independent risk factors for chronic kidney disease in patients with type 2 diabetes. A causal mechanism of this association should be evaluated in a follow-up study of Korean patients with type 2 diabetes.

Genetic information such as DNA sequences has been limited to fully explain mechanisms of gene regulation and disease process. Epigenetic mechanisms, which include DNA methylation, histone modification and non-coding RNAs, can regulate gene expression and affect progression of disease. Although studies focused on epigenetics are being actively investigated in the field of medicine and biology, epigenetics in dental research is at the early stages. However, studies on epigenetics in dentistry deserve attention because epigenetic mechanisms play important roles in gene expression during tooth development and may affect oral diseases. In addition, understanding of epigenetic alteration is important for developing new therapeutic methods. This review article aims to outline the general features of epigenetic mechanisms and describe its future implications in the field of dentistry.

BackgroundThis study aimed to investigate the microshear bond strength of universal bonding adhesives to leucite-reinforced glass-ceramic.MethodsLeucite-reinforced glass-ceramic blocks were polished and etched with 9.5% hydrofluoric acid for 1 min. The specimens were assigned to one of four groups based on their surface conditioning (n = 16): 1) NC: negative control with no further treatment; 2) SBU: Single Bond Universal (3M ESPE); 3) ABU: ALL-BOND Universal (Bisco); and 4) PC: RelyX Ceramic Primer and Adper Scotchbond Multi-Purpose Adhesive (3M ESPE) as a positive control. RelyX Ultimate resin cement (3M ESPE) was placed on the pretreated ceramic and was light cured. Eight specimens from each group were stored in water for 24 h, and the remaining eight specimens were thermocycled 10,000 times prior to microshear bond strength evaluation. The fractured surfaces were examined by stereomicroscopy and scanning electron microscopy (SEM).ResultsAfter water storage and thermocycling, the microshear bond strength values decreased in the order of PC > SBU and ABU > NC (P < 0.05). Thermocycling significantly reduced the microshear bond strength, regardless of the surface conditioning used (P < 0.05). Cohesive failure in the ceramic and mixed failure in the ceramic and resin cement were observed in the fractured specimens. The percentage of specimens with cohesive failure after 24 h of water storage was: NC (50%), SBU (75%), ABU (75%), and PC (87%). After thermocycling, the percentage of cohesive failure in NC decreased to 25%; however, yet the percentages of the other groups remained the same.ConclusionsAlthough the bond strength between resin and hydrofluoric acid-etched glass ceramic was improved when universal adhesives were used, conventional surface conditioning using a separate silane and adhesive is preferable to a simplified procedure that uses only a universal adhesive for cementation of leucite-reinforced glass-ceramic.

MOK, a pharmacopuncture medicine consisting of 10 herbs, has a long history as treatment for various inflammatory conditions. To investigate the mechanisms of action of MOK, its anti-inflammatory and antioxidative effects were assessed in RAW 264.7 macrophages stimulated by lipopoly-saccharide (LPS). RAW 264.7 cells were treated with different concentrations of MOK extract for 30 min prior to stimulation with or without LPS for the indicated times. Nitric oxide (NO) production was measured using Griess reagent, while the mRNA levels of inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and the antioxidant enzymes Mn superoxide dismutase and heme oxygenase-1, were determined using reverse transcription-polymerase chain reaction analysis. Western blotting was used to determine the protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, superoxide dismutase (SOD)2, catalase (CAT) and heme oxygenase-1 (HO-1), and the phosphorylation of mitogen-activated protein kinases (MAPKs), including ERK1/2, JNK and p38. Western blotting and immunocytochemistry were used to observe the nuclear expression of nuclear factor (NF)-κB p65. Additionally, reactive oxygen species (ROS) and prostaglandin (PG)E2 production were determined using the ROS assay and an enzyme immunoassay. With MOK treatment, there was a notable decrease in NO and PGE2 production induced by LPS in RAW 264.7 cells by downregulation of iNOS and COX-2 mRNA and protein expression. Furthermore, with MOK treatment, there was a decrease in the mRNA expression levels of TNF-α, IL-1β and IL-6, as well as in the phosphorylation of ERK, JNK and p38 MAPK, by blocking the nuclear translocation of NF-κB p65 in LPS-stimulated cells. In addition, MOK treatment led to an increase in the antioxidant enzymes SOD, CAT and HO-1 in LPS-stimulated cells, with a concomitant decrease in ROS generation. These results indicate that the inflammatory responses in activated macrophages are inhibited by MOK through downregulation of the transcription levels of inflammatory mediators and inhibition of the MAPK/NF-κB pathway. Moreover, MOK protects against oxidative damage by upregulating the expression of antioxidant enzymes and generating ROS scavengers.

A methylene chloride soluble fraction of the fruits of Cudrania tricuspidata significantly inhibited the mouse brain monoamine oxidase (MAO). Three known prenylated isoflavones were isolated and identified by activity-guided fractionation. Gancaonin A (1), 4'-O-methylalpinumisoflavone (2), and alpinumisoflavone (3) inhibited MAO activity in a concentration-dependent manner with IC50 values of 19.4, 23.9, and 25.8 microM, respectively. Of these, gancaonin A (1) showed a selective and potent inhibitory effect against MAO-B (IC50 0.8 microM) than MAO-A (IC50 >800 microM). The kinetic analysis using Lineweaver-Burk plots indicated that gancaonin A (1) competitively inhibited MAO-B.

Four new prenylated xanthones, cudratricusxanthones J-M (1-4), were isolated from the CH2Cl2-soluble extract of the root bark of Cudrania tricuspidata, along with four known prenylated xanthones, isocudraxanthone K (5), cudraxanthone C (6), cudratricusxanthone A (7), and cudraxanthone L (8), and three known prenylated flavonoids, cudraflavone A (9), cudraflavanone A (10), and cudraflavone B (11). The structures of compounds 1-4 were elucidated using spectroscopic methods. Cudratricusxanthone A (7), cudraflavanone A (10), and cudraflavone B (11) showed moderate inhibitory effects on mouse brain monoamine oxidase (MAO) with IC50 values of 88.3, 89.7, and 80.0 microM, respectively.

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