Properties of Veneer and Veneer-Based Products from Genetically Improved White Spruce Plantations

This study examined the suitability of genetically improved fast-growing and short-rotation plantations for veneer-based products. The materials came from a 36-year-old white spruce (Picea glauca) half-sib progeny/provenance trial located in two regions (sites) of Quebec. A total of 270 sample trees were collected for the study, 130 trees from St-Ignace in the Gaspé Region and 140 trees from Valcartier near Quebec City. Veneer from the Valcartier site had a mean wood density of 0.353 g/cm3 and a mean modulus of elasticity (MOE) of 9.48 GPa (1.375 million psi). Veneer from the St-Ignace site had a mean wood density of 0.345 g/cm3] and a mean MOE of 8.05 GPa (1.167 million psi). The differences in veneer wood density and MOE between the two sites were statistically significant. Compared to other Canadian species commonly used for veneer products, the genetically improved fast-growing and short-rotation white spruce yielded considerably lower veneer stiffness.The plantation-grown white spruce veneer from both sites was knotty. Ninety-eight percent of the veneer was classified as visual grade C. The visually graded veneer would be suitable for sheathing grade plywood. With proper stress grading, 14% of the white spruce veneer was suitable for 12.41 GPa (1.8 million psi) grade laminated veneer lumber (LVL), and another 24% of the veneer was suitable for a lower 10.34 GPa (1.5 million psi) grade of LVL, or as core plies for LVL manufacture. The remaining 62% of the stress-graded veneer was suitable for sheathing grade plywood

Atomic Electrons in Strong Magnetic Fields: Transition from Elliptical to Helical Behavior.

The behavior of an atomic electron in a static magnetic field strong enough to correspond to the transition regime is examined. The field strength is characterized by the parameter L^, the effective component of angular momentum. A Floquet-Mathieu analysis shows that the bifurcation of classical trajectories into elliptical and helical families is related to the 2:1 resonance which occurs at L^=L^T. Quantum mechanics gives an avoided crossing at L^T; we examine the nature of the wave functions as L^ passes through the resonance. Semiclassical calculations accurately reproduce the quantum eigenvalues and produce trajectories which underlie the quantum wave functions. The avoided crossing is expressed in semiclassical terms as a switch between elliptical and helical families. The bifurcation of the classical motion means that, at the primitive semiclassical level, some states may be missed and others may be generated in both elliptical and helical representations

CD44 modulates Smad1 activation in the BMP-7 signaling pathway

Bone morphogenetic protein 7 (BMP-7) regulates cellular metabolism in embryonic and adult tissues. Signal transduction occurs through the activation of intracellular Smad proteins. In this paper, using a yeast two-hybrid screen, Smad1 was found to interact with the cytoplasmic domain of CD44, a receptor for the extracellular matrix macromolecule hyaluronan. Coimmunoprecipitation experiments confirmed the interaction of Smad1 with full-length CD44—interactions that did not occur when CD44 receptors truncated within the cytoplasmic domain were tested. Chondrocytes overexpressing a truncated CD44 on a background of endogenous full-length CD44 no longer exhibited Smad1 nuclear translocation upon BMP-7 stimulation. Further, pretreatment of chondrocytes with Streptomyces hyaluronidase to disrupt extracellular hyaluronan–cell interactions inhibited BMP-7–mediated Smad1 phosphorylation, nuclear translocation of Smad1 or Smad4, and SBE4–luciferase reporter activation. These results support a functional link between the BMP signaling cascade and CD44. Thus, changes in hyaluronan–cell interactions may serve as a means to modulate cellular responsiveness to BMP

Age-Related Differences in Susceptibility to Carcinogenesis: A Quantitative Analysis of Empirical Animal Bioassay Data

In revising cancer risk assessment guidelines, the U.S. Environmental Protection Agency (EPA) analyzed animal cancer bioassay data over different periods of life. In this article, we report an improved analysis of these data (supplemented with some chemical carcinogenesis observations not included in the U.S. EPA’s original analysis) and animal bioassay studies of ionizing radiation. We use likelihood methods to avoid excluding cases where no tumors were observed in specific groups. We express dosage for animals of different weights on a metabolically consistent basis (concentration in air or food, or per unit body weight to the three-quarters power). Finally, we use a system of dummy variables to represent exposures during fetal, preweaning, and weaning–60-day postnatal periods, yielding separate estimates of relative sensitivity per day of dosing in these intervals. Central estimate results indicate a 5- to 60-fold increased carcinogenic sensitivity in the birth–weaning period per dose ÷ (body weight(0.75)-day) for mutagenic carcinogens and a somewhat smaller increase—centered about 5-fold—for radiation carcinogenesis per gray. Effects were greater in males than in females. We found a similar increased sensitivity in the fetal period for direct-acting nitrosoureas, but no such increased fetal sensitivity was detected for carcinogens requiring metabolic activation. For the birth–weaning period, we found an increased sensitivity for direct administration to the pups similar to that found for indirect exposure via lactation. Radiation experiments indicated that carcinogenic sensitivity is not constant through the “adult” period, but the dosage delivered in 12- to 21-month-old animals appears a few-fold less effective than the comparable dosage delivered in young adults (90–105 days of age)

Misuse of “Power” and other mechanical terms in sport and exercise science research

In spite of the Système International d’Unitès (SI) that was published in 1960, there continues to be widespread misuse of the terms and nomenclature of mechanics in descriptions of exercise performance. Misuse applies principally to failure to distinguish between mass and weight, velocity and speed, and especially the terms "work" and "power." These terms are incorrectly applied across the spectrum from high-intensity short-duration to long-duration endurance exercise. This review identifies these misapplications and proposes solutions. Solutions include adoption of the term "intensity" in descriptions and categorisations of challenge imposed on an individual as they perform exercise, followed by correct use of SI terms and units appropriate to the specific kind of exercise performed. Such adoption must occur by authors and reviewers of sport and exercise research reports to satisfy the principles and practices of science and for the field to advance

New methods for finding common insertion sites and co-occurring common insertion sites in transposon- and virus-based genetic screens

Insertional mutagenesis screens in mice are used to identify individual genes that drive tumor formation. In these screens, candidate cancer genes are identified if their genomic location is proximal to a common insertion site (CIS) defined by high rates of transposon or retroviral insertions in a given genomic window. In this article, we describe a new method for defining CISs based on a Poisson distribution, the Poisson Regression Insertion Model, and show that this new method is an improvement over previously described methods. We also describe a modification of the method that can identify pairs and higher orders of co-occurring common insertion sites. We apply these methods to two data sets, one generated in a transposon-based screen for gastrointestinal tract cancer genes and another based on the set of retroviral insertions in the Retroviral Tagged Cancer Gene Database. We show that the new methods identify more relevant candidate genes and candidate gene pairs than found using previous methods. Identification of the biologically relevant set of mutations that occur in a single cell and cause tumor progression will aid in the rational design of single and combinatorial therapies in the upcoming age of personalized cancer therapy

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

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

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment