Evaluating the use of HEIghten critical thinking assessment to monitor critical thinking in dental students.

PURPOSE/OBJECTIVES: Critical thinking and evidence-based dentistry are skills that dental students are required to demonstrate, but monitoring and quantifying progress can be challenging. This study is investigating whether the HEIghten critical thinking assessment (HCTA) could be used as a potential tool, both for use prior to admitting students, and to monitor whether the students' skills improve over their time at dental school. METHODS: Freshman dental students (n = 92) were given the HCTA during their first semester of dental school. Statistical analyses were then performed to examine the association of Dental Admission Test (DAT) scores (overall, perceptual ability, and total science) and Grade Point Average (GPA) (overall and science) on critical thinking scores (total, analytic, and synthetic). RESULTS: There was a significant positive association between GPA, DAT scores and critical thinking scores. CONCLUSIONS: Our results indicate that the HCTA may be a useful tool to enable monitoring of students analytical and synthetic skills throughout their time at dental school.

Suppression of T-cell chemokines by Porphyromonas gingivalis.

Porphyromonas gingivalis is a major pathogen in periodontal disease and is associated with immune dysbiosis. In this study, we found that P. gingivalis did not induce the expression of the T-cell chemokine IP-10 (CXCL10) from neutrophils, peripheral blood mononuclear cells (PBMCs), or gingival epithelial cells. Furthermore, P. gingivalis suppressed gamma interferon (IFN-γ)-stimulated release of IP-10, ITAC (CXCL11), and Mig (CXCL9) from epithelial cells and inhibited IP-10 secretion in a mixed infection with the otherwise stimulatory Fusobacterium nucleatum. Inhibition of chemokine expression occurred at the level of gene transcription and was associated with downregulation of interferon regulatory factor 1 (IRF-1) and decreased levels of Stat1. Ectopic expression of IRF-1 in epithelial cells relieved P. gingivalis-induced inhibition of IP-10 release. Direct contact between P. gingivalis and epithelial cells was not required for IP-10 inhibition. These results highlight the immune-disruptive potential of P. gingivalis. Suppression of IP-10 and other Th1-biasing chemokines by P. gingivalis may perturb the balance of protective and destructive immunity in the periodontal tissues and facilitate the pathogenicity of oral microbial communities.

The Complexity of DEK Signaling in Cancer Progression.

The DNA binding protein and chromatin structural regulator DEK regulate many cellular processes. These include proliferation, differentiation, apoptosis, senescence, DNA repairing and the maintenance of stem cell phenotype. DEK is increasingly recognized as a crucial player in many steps of cancer initiation and progression, and is precisely regulated by abundant promoting and inhibiting factors directly or indirectly. DEK may serve as an architectural modulating protein to regulate the expression and function of multiple human genes in cancer cells. In this article we have reviewed the specificities and complexities of DEK in the regulation of transcription factors and global chromatin, including its biologic roles in malignant cells, and summarized the current research. The possible use of DEK as a diagnostic marker and drug target in the prevention or treatment of tumors is also discussed.

Targeting autophagy as a strategy for drug discovery and therapeutic modulation.

Autophagy is a self-protective mechanism of living cells or organisms under various stress conditions. Studies of human genetics and pathophysiology have implicated that alterations in autophagy affect the context of cellular homeostasis and disease-associated phenotypes. The molecular components of autophagy are currently being explored as new pharmacologic targets for drug development and therapeutic intervention of various diseases. Drugs that restore the normal autophagic pathways have the potential for effectively treating human disorders that depend on aberrations of autophagy. Here, we review the role of autophagy and its alterations in the pathogenesis of diverse diseases, and drug discovery strategies for modulating autophagy for therapeutic benefits as well as possible safety concerns and caveats associated with such approaches.

Friend or foe? Mitochondria as a pharmacological target in cancer treatment.

Mitochondria have acquired numerous functions over the course of evolution, such as those involved in controlling energy production, cellular metabolism, cell survival, apoptosis and autophagy within host cells. Tumor cells can develop defects in mitochondrial function, presenting a potential strategy for designing selective anticancer therapies. Therefore, cancer has been the main focus of recent research to uncover possible mitochondrial targets for therapeutic benefit. This comprehensive review covers not only the recent discoveries of the roles of mitochondria in cancer development, progression and therapeutic implications but also the findings regarding emerging mitochondrial therapeutic targets and mitochondria-targeted agents. Current challenges and future directions for developments and applications of mitochondrial-targeted therapeutics are also discussed.