Physiological Responses of Big Sagebrush to Different Types of Herbage Removal
Desert Sagebrush Type
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CitationCook, C. W., & Stoddart, L. A. (1960). Physiological responses of big sagebrush to different types of herbage removal. Journal of Range Management, 13(1), 14-16.
PublisherSociety for Range Management
JournalJournal of Range Management
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PREDICTING HYDRAULIC RESPONSE: COMPARISON OF TEXTURAL AND RESPONSE CLUSTERING APPROACHES TO SOIL CLASSIFICATIONFerre, Ty P. A.; Rice, Amy Katherine; Ferre, Ty P. A.; Schaap, Marcel; Tuller, Markus; Zreda, Marek (The University of Arizona., 2009)Traditional soil classification methods invoke physical differences based on particle size to group soils into textural classes. Resulting groupings are used to make predictions about soil attributes and processes of interest including hydrologic response. My hypothesis is that more useful classification schemes will be created by starting with response and applying an inverse approach to generate soil groupings. I propose an alternative classification scheme based on these hypotheses, using techniques of cluster analysis. The resulting system has high predictive capacity with simplicity comparable to the U.S. Dept. of Agriculture soil textural triangle or other similar classification diagrams. I conclude that: classification is most appropriate when carried out on process and objective specific bases; there is a physical meaning to cluster-based groupings, which allows for more appropriate segregation of response as compared to textural groupings; using clusters, a small number of samples can be used to characterize the range of response.
Biological specificity of CDK4/6 inhibitors: dose response relationship, <i>in vivo</i> signaling, and composite response signatureKnudsen, Erik S.; Hutcheson, Jack; Vail, Paris; Witkiewicz, Agnieszka K.; Univ Arizona, Ctr Canc; Univ Arizona, Dept Med; Univ Arizona, Dept Pathol (IMPACT JOURNALS LLC, 2017-06-10)Recently developed potent and selective CDK4/6 inhibitors fall into two classes based on structure and toxicity profiles in clinical studies. One class, exemplified by palbociclib and ribociclib, exhibits neutropenia as a dose-limiting toxicity and requires discontinuous dosing. In contrast, the structurally distinct CDK4/6 inhibitor abemaciclib is dosed continuously, and has diarrhea and fatigue as dose-limiting toxicities. In preclinical models, palbociclib has been extensively studied and induces cell cycle inhibition in an RB-dependent manner. Thus far, abemaciclib has been less extensively evaluated. We found that abemaciclib cell cycle inhibitory activity is RB-dependent at clinically achievable concentrations. Abemaciclib elicited potent suppression of RB/E2F regulated genes associated with prognosis in ER-positive breast cancer. However, unlike palbociclib, at 250nM-1 mu M doses abemaciclib induced cell death in RB-deficient cell lines. This response was associated with a rapidlyinduced multi-vacuolar phenotype indicative of lysosomal membrane permeabilization that could be ameliorated with chloroquine. This event was not a reflection of inhibition of other CDK family members, but could be recapitulated with CBX4945 that inhibits casein and DYRK/HIPK kinases. To determine if these "off-target" features of abemaciclib were observed in vivo, mice harboring matched RB-positive and negative xenografts were treated with palbociclib and abemaciclib. In vivo, all of the apparent activity of abemaciclib was RB-dependent and strongly elicited suppression of cell cycle regulatory genes in a fashion markedly similar to palbociclib. Using gene expression data from cell lines and tumors treated with abemaciclib and palbociclib a composite signature of response to CDK4/6 inhibition was developed that included many genes that are individually required for tumor cell proliferation or viability. These data indicate that while abemaciclib and palbociclib can exert distinct biological and molecular effects, there are common gene expression features that could be broadly utilized in measuring the response to CDK4/6 inhibition.