The design of a learning environment based on the theory of multiple intelligence and the study its effectiveness on the achievements, attitudes and retention of students

AbstractMultiple intelligences theory (MIT) which takes into account students’ individual differences has an important role in the teaching and learning process. In this study a novel learning environment based on MIT which takes students’ interests and needs into an account has been developed. Many activities were carried out depending on students’ intelligence types. The effects of different activities on students’ achievements, attitudes toward chemistry and retention of knowledge in periodical features’ variety at the 10th class were measured and compared. The comparison between experimental group, which was instructed through MIT learning strategies and materials, and control group thought by traditional methods was observed. The research was applied in the first semester of 2009-2010 education years. The study carried out on 75 high school students in Izmir. The application of the study was lasted for 8 weeks containing methods and tests’ practices. Following MIT assessment survey, achievement test and attitude scales were used to analyze its effectiveness. Based on the theories and literature data, an instructional material included concept maps, puzzles, stories, classical music in background, group games, and photos about periodic features’ variety as an alternative to traditional written material. As a result of statistical analysis there were significant differences between achievement post-test and attitudes post-test towards chemistry course of control and experimental groups. Consequently, instructional methods needed to be varied so students could use their intellectual strengths to better understand topics, increase their intrinsic motivation, intervention and encourage active student engagement to improve learning at middle school level

Genetic inflammatory factors predict restenosis after percutaneous coronary interventions

Background - Restenosis is a negative effect of percutaneous coronary intervention (PCI). No clinical factors are available that allow good risk stratification. However, evidence exists that genetic factors are important in the restenotic process as well as in the process of inflammation, a pivotal factor in restenosis. Association studies have identified genes that may predispose to restenosis, but confirmation by large prospective studies is lacking. Our aim was to identify polymorphisms and haplotypes in genes involved in inflammatory pathways that predispose to restenosis. Methods and Results - The GENetic DEterminants of Restenosis ( GENDER) project is a multicenter prospective study, including 3104 consecutive patients after successful PCI. Forty-eight polymorphisms in 34 genes in pathways possibly involved in the inflammatory process were analyzed. The 16Gly variant of the beta(2)-adrenergic receptor gave an increased risk of target vessel revascularization (TVR). The rare alleles of the CD14 gene (- 260T/T), colony-stimulating factor 2 gene (117Thr/Thr), and eotaxin gene (- 1328A/A) were associated with decreased risk of TVR. However, through the use of multiple testing corrections with permutation analysis, the probability of finding 4 significant markers by chance was 12%. Conclusions - Polymorphisms in 4 genes considered involved in the inflammatory reaction showed an association with TVR after PCI. Our results may contribute to the unraveling of the restenotic process. Given the explorative nature of this analysis, our results need to be replicated in other studies

Tumor necrosis factor-alpha plays an important role in restenosis development

Genetic factors appear to be important in the restenotic process after percutaneous coronary intervention (PCI), as well as in inflammation, a pivotal factor in restenosis. TNF alpha, a key regulator of inflammatory responses, may exert critical influence on the development of restenosis after PCI. The GENetic DEterminants of Restenosis (GENDER) project included 3104 patients who underwent a successful PCI. Systematic genotyping for six polymorphisms in the TNF alpha gene was performed. The role of TNF alpha in restenosis was also assessed in ApoE*3-Leiden mice, TNF alpha knockout mice, and by local delivery of a TNF alpha biosynthesis inhibitor, thalidomide. The -238G-1031T haplotype of the TNF alpha gene increased clinical and angiographic risk of restenosis (P = 0.02 and P = 0.002, respectively). In a mouse model of reactive stenosis, arterial TNF alpha mRNA was significantly time-dependently up-regulated. Mice lacking TNF alpha or treated locally with thalidomide showed a reduction in reactive stenosis (P = 0.01 and P = 0.005, respectively). Clinical and preclinical data indicate that TNF alpha plays an important role in restenosis. Therefore, TNF alpha genotype may be used as a risk marker for restenosis and may contribute to individual patient screening prior to PCI in clinical practice. Inhibition of TNF alpha may be an anti-restenotic target strategy

Interleukin 10:a new risk marker for the development of restenosis after percutaneous coronary intervention

Genetic factors appear to be important in the process of restenosis after percutaneous coronary intervention (PCI), as well as in inflammation, a pivotal factor in restenosis. An important mediator in the inflammatory response is interleukin (IL)-10. Our aim was to study whether genetic variants in IL-10 predispose to the risk of restenosis. The GENetic DEterminants of Restenosis (GENDER) study included 3104 patients treated with successful PCI. Target vessel revascularization (TVR) was chosen as primary end point. Genotyping of the -2849G/A, -1082G/A, -592C/A and +4259A/G polymorphisms of the IL-10 gene was performed by MassArray platform. After adjusting for clinical variables, three polymorphisms significantly increased the risk of restenosis (-2849AA: relative risk (RR), 1.7, 95% confidence interval (CI), 1.2-2.5; -1082AA: RR, 1.4, 95% CI, 1.1-1.8 and +4259GG: RR, 2.0, 95% CI, 1.4-2.8). To further exclude possible involvement of neighboring genes due to LD in the IL-10 locus, additional polymorphisms were genotyped. The results reveal that association of the IL-10 gene with restenosis is independent of flanking genes. Our findings demonstrate that IL-10 is associated with restenosis and therefore support the hypothesis that anti-inflammatory genes also may be involved in developing restenosis. Furthermore, they may provide a new targeting gene for drug-eluting stents