Small mammal community maintains stability through compensatory dynamics after restoration of a ponderosa pine forest

Ecosystem stability has been of increasing interest in the past several decades as it helps predict the consequences of anthropogenic disturbances on ecosystems. Species may exhibit stability through compensation, with greatly fluctuating populations year to year but a consistent density response over time. Stability is increased when species with similar functional roles compensate for one another by responding differently to environmental change. In restoration projects, the objective is to restore stability by altering ecosystem composition, structure, and function to resemble natural (‘‘reference’’) conditions. We assessed the success of ecological restoration treatments by examining the structural and functional responses of the small mammal community before and after treatment, and compared to reference conditions. We used Royle density models to examine the responses of eight species of small mammals to restoration (thinning) treatments in ponderosa pine forests to determine if the community maintained total density, biomass, and function (represented by ectomycorrhizal fungi dispersion) after disturbance. Community composition differed in each of 6 years following treatment, but total density and biomass remained constant, suggesting the community is a stable prey base for predators. In addition, goldenmantled ground squirrels (Spermophilus lateralis) and gray-collared chipmunks (Tamias cinereicollis) appeared to play a similar role in dispersing ectomycorrhizal fungi across different forest structures. Both total species density and biomass were greater after thinning than in unthinned stands, and were similar to reference stands. These results suggest that although species composition changes from year to year after disturbance, restoration treatments can maintain ecosystem stability in terms of small mammal community-level properties

The state of gender diversity in medical physics

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154924/1/mp14035.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154924/2/mp14035_am.pd

Systematic Review – Final: How do thinning and burning treatments in southwestern conifer forests in the United States affect wildlife density and population performance?

The aim of this review is to examine whether thinning and burning treatments in conifer forests in the southwestern United States affect wildlife distribution, abundance, and population performance

Revisiting fetal dose during radiation therapy: evaluating treatment techniques and a custom shield [JACMP, 17(5), 2016]

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/139980/1/acm212191_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/139980/2/acm212191.pd

SafetyNet: streamlining and automating QA in radiotherapy

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135420/1/acm20387-sup-0002.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/135420/2/acm20387.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/135420/3/acm20387-sup-0003.pd

Improving treatment plan evaluation with automation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135377/1/acm20016.pd

Revisiting fetal dose during radiation therapy: evaluating treatment techniques and a custom shield

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135233/1/acm20001i.pd

Locus-specific epigenetic remodeling controls addiction- and depression-related behaviors

Chronic exposure to drugs of abuse or stress regulates transcription factors, chromatin-modifying enzymes and histone post-translational modifications in discrete brain regions. Given the promiscuity of the enzymes involved, it has not yet been possible to obtain direct causal evidence to implicate the regulation of transcription and consequent behavioral plasticity by chromatin remodeling that occurs at a single gene. We investigated the mechanism linking chromatin dynamics to neurobiological phenomena by applying engineered transcription factors to selectively modify chromatin at a specific mouse gene in vivo. We found that histone methylation or acetylation at the Fosb locus in nucleus accumbens, a brain reward region, was sufficient to control drug- and stress-evoked transcriptional and behavioral responses via interactions with the endogenous transcriptional machinery. This approach allowed us to relate the epigenetic landscape at a given gene directly to regulation of its expression and to its subsequent effects on reward behavior

A Selective HDAC 1/2 Inhibitor Modulates Chromatin and Gene Expression in Brain and Alters Mouse Behavior in Two Mood-Related Tests

Psychiatric diseases, including schizophrenia, bipolar disorder and major depression, are projected to lead global disease burden within the next decade. Pharmacotherapy, the primary – albeit often ineffective – treatment method, has remained largely unchanged over the past 50 years, highlighting the need for novel target discovery and improved mechanism-based treatments. Here, we examined in wild type mice the impact of chronic, systemic treatment with Compound 60 (Cpd-60), a slow-binding, benzamide-based inhibitor of the class I histone deacetylase (HDAC) family members, HDAC1 and HDAC2, in mood-related behavioral assays responsive to clinically effective drugs. Cpd-60 treatment for one week was associated with attenuated locomotor activity following acute amphetamine challenge. Further, treated mice demonstrated decreased immobility in the forced swim test. These changes are consistent with established effects of clinical mood stabilizers and antidepressants, respectively. Whole-genome expression profiling of specific brain regions (prefrontal cortex, nucleus accumbens, hippocampus) from mice treated with Cpd-60 identified gene expression changes, including a small subset of transcripts that significantly overlapped those previously reported in lithium-treated mice. HDAC inhibition in brain was confirmed by increased histone acetylation both globally and, using chromatin immunoprecipitation, at the promoter regions of upregulated transcripts, a finding consistent with in vivo engagement of HDAC targets. In contrast, treatment with suberoylanilide hydroxamic acid (SAHA), a non-selective fast-binding, hydroxamic acid HDAC 1/2/3/6 inhibitor, was sufficient to increase histone acetylation in brain, but did not alter mood-related behaviors and had dissimilar transcriptional regulatory effects compared to Cpd-60. These results provide evidence that selective inhibition of HDAC1 and HDAC2 in brain may provide an epigenetic-based target for developing improved treatments for mood disorders and other brain disorders with altered chromatin-mediated neuroplasticity.Stanley Medical Research InstituteNational Institutes of Health (U.S.) (R01DA028301)National Institutes of Health (U.S.) (R01DA030321

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts