The NIH's Funding to US Dental Institutions from 2005 to 2014.

This study examines funding from the National Institutes of Health (NIH) to US dental institutions between 2005 and 2014 based on publicly available data from the NIH Research Portfolio Online Reporting Tools. Over the 10-y span, 56 US dental institutions received approximately $2.2 billion from 20 Institutes, Centers, and Offices at the NIH. The National Institute of Dental and Craniofacial Research (NIDCR) is the largest NIH supporter of dental institutions, having invested 70% of the NIH total, about $1.5 billion. The NIDCR is also the primary supporter of research training and career development, as it has invested $177 million, which represents 92% of the total NIH investment of $192 million. Over the past 10 y, about half of the NIDCR's extramural award dollars have gone to dental schools, while the NIH has invested about 1%. There has been an approximately 10% net decrease in extramural dollars awarded to dental institutions over the past decade; however, given the year-to-year variability in support to dental institutions, it is unclear if this net decline reflects a long-term trend. In addition, there was an overall reduction in the extramural dollars awarded by the NIDCR and by the NIH. For example, from 2005 to 2014, the total NIDCR budget for extramural research decreased by roughly 4%, which represents a decrease of $20 million to dental institutions. After adjusting for inflation, the decline in funding to dental institutions from the NIDCR and NIH was approximately 30%. Although the NIDCR and NIH continue to invest in dental institutions, if the current decline were to continue, it could negatively affect the research conducted at dental institutions. Therefore, we discuss opportunities for dental institutions to increase NIDCR and NIH support and improve their capacity for research, research training, and career development.

Regulation of histone acetylation in the hippocampus of chronically stressed rats: a potential role of sirtuins.

The hippocampus is a brain region that is particularly susceptible to structural and functional changes in response to chronic stress. Recent literature has focused on changes in gene transcription mediated by post-translational modifications of histones in response to stressful stimuli. Chronic variable stress (CVS) is a rodent model that mimics certain symptoms of depression in humans. Given that stress exhibits distinct effects on the cells of the sub-regions of the hippocampus, we investigated changes in histone acetylation in the CA1, CA3, and dentate gyrus (DG) of the hippocampus in response to CVS. Western blotting revealed a significant decrease in acetylation of histone 4 (H4) at Lys12 in CA3 and DG of CVS animals compared to control animals. Furthermore, phospho-acetyl H3 (Lys9/Ser10) was also decreased in the CA3 and DG regions of the hippocampus of CVS animals. In addition, since histone deacetylases (HDACs) contribute to the acetylation state of histones, we investigated the effects of two HDAC inhibitors, sodium butyrate, a class I and II global HDAC inhibitor, and sirtinol, a class III sirtuin inhibitor, on acetylation of histone 3 (H3) and H4. Application of HDAC inhibitors to hippocampus slices from control and CVS animals revealed increased histone acetylation in CVS animals, suggesting that levels of histone deacetylation by HDACs were higher in the CVS animals compared to control animals. Interestingly, histone acetylation in response to sirtinol was selectively increased in the slices from the CVS animals, with very little effect of sirtuin inhibitors in slices from control animals. In addition, sirtuin activity was increased specifically in CA3 and DG of CVS animals. These results suggest a complex and regionally-specific pattern of changes in histone acetylation within the hippocampus which may contribute to stress-induced pathology.