PDAT Research Articles

Analysis of potential substrate binding sites of PDAT in Arabidopsis thaliana and Saccharomyces cerevisiae

Analysis of potential substrate binding sites of PDAT in Arabidopsis thaliana and Saccharomyces cerevisiae

A scientific forecast on dental research output within the next 20 years using exponential smoothing algorithm

Introduction: To report a scientific forecast of the number of published dental articles in the next 20 years. Materials and Methods: On October 12, 2016, to find all dental articles, PubMed was searched via the query “1800/1/1”[PDAT]: “2015/12/31”[PDAT] AND jsubsetd [text]. Relevant limitations were applied to find dental clinical trials, review articles, and free full-text dental articles. Consequently, all PubMed records were exported to a CSV file. To forecast the future dental research output using existing time-based data, the Exponential Triple Smoothing algorithm was used, which is an advanced machine learning algorithm. Data were analyzed by Microsoft Office Excel 2016. Results: Seventy-five (1940–2015) years of human attempts to publish dental articles were explored and 572490 records were found, from which 27244 (4.75%) articles were free full-text, 19238 (3.36%) were clinical trials, and 31853 (5.56%) were reviews. Researchers will publish 19195 dental articles in 2036, among which 917 (4.77%) articles will be clinical trials, 1474 (7.67%) will be review articles, and 5482 (28.55%) will be free full-text articles. Conclusion: Changes may be because of the quantity of research funds. The number of all types of dental articles will increase with an acceptable rate over the next 20 years. Of more interest, the number of free full-text articles will grow more rapidly than other article types.

Oxidative stress increases the expression of the angiotensin-II receptor type 1 in mouse peritoneal macrophages.

Angiotensin II (Ang II) has been shown to accelerate atherogenesis, and the cellular Ang II type 1 (AT(1))-receptor mediates most of Ang II-induced pro-atherogenic effects. In this study we have examined the effect of macrophage oxidative stress on cellular AT(1)-receptor expression. Mouse peritoneal macrophages (MPM) from apolipoprotein-E deficient (E(0)) mice at increasing ages (1 6 months) demonstrated an age-dependent increase in cellular lipid-peroxides (PD) content. In parallel, the AT(1)-receptor mRNA and protein levels both increased by up to 3.7-fold and 1.7-fold, respectively, in MPM from 6-month old mice compared with 1-month old mice. Vitamin E supplementation to E(0) mice significantly decreased the MPM PD content and macrophage AT(1)-receptor mRNA expression compared with placebo-treated mice. The role of oxidative stress in the cellular expression of AT(1)-receptors was further demonstrated by manipulation of macrophage glutathione content. Buthionine-sulfoximine, a glutathione synthesis inhibitor, increased MPM PD content and AT(1)-receptor mRNA expression, whereas L-2-oxothiazolidine-4-carboxylic acid, that contributes to glutathione synthesis, reduced macrophage PD and AT(1)-receptor mRNA expression. Incubation of MPM with oxidised low-density lipoproteins (LDL) led to a significant, dose-dependent and time-dependent increase in macrophage AT(1)-receptor mRNA and protein expression, compared with control cells. In contrast, native LDL or acetylated LDL did not significantly affect macrophage AT(1)-receptor mRNA expression. In conclusion, our findings suggest that oxidative stress in macrophages induces AT(1)-receptor expression. This phenomenon can stimulate the interaction of Ang II with macrophages and hence accelerate macrophage foam cell formation and early atherogenesis.