Maxwell-Boltzmann Distribution of M 3+-F− Interstitial Pairs in Fluorite-Type Lattices

Maxwell-Boltzmann distribution curves for M3+-F− interstitials in fluorite-type lattices have been calculated and compared with spectroscopic data. The dominant sites, in the order of their relative importance for low concentrations and T\u3c700 K, are the C4v(1, 0, 0), Cs(2, 1, 0), C3v(1, 1, 1), Cs(1, 2, 2), Cs(1, 1, 3), and Cs(2, 3, 0) sites. The dominant presence of the third-nearest-neighbor monoclinic Cs(2, 1, 0) pair, which has not been reported previously, is predicted by our calculations. In view of this result, the electron spin resonance data on U3+ in CaF2 reported by Mahlab, Volterra, Low, and Yariv, which these authors interpreted in terms of the fifth-nearest-neighbor site, have been shown to arise actually from the prominent presence of the third-nearest-neighbor Cs(2, 1, 0) site

Canonical Distribution Law and KCl: Sm2+ Fluorescence: The C2v Paradox

A combination of critical experiments has been carried out in order to elucidate the recent conclusions of Bradbury and Wong, who attributed all the dominant KCl: Sm2+ fluorescence lines to the nearest-neighbor C2v(1,1,0)Sm2+−K+ vacancy site. In an extensive investigation into the radiationless quenching, characteristic lifetimes, excitation spectra, and Zeeman polarization of KCl: Sm2+ fluorescence lines, all the prominent lines are unequivocally attributed to a distribution of three different Sm2+ - K+ vacancy sites. In addition, 18 weak lines are shown to originate from dimeric cluster and O2− compensated sites. The paradoxical C2v interpretations of Bradbury and Wong are shown to be based on incorrect premises, inadequate experimentation, and confusion in the identity of samples with different dopant concentrations

Crystalline ionic solutions

Systems of crystalline ionic solutions containing impurity cations and associated compensation defects are described. Interactions between aliovalent ions and compensation defects give rise to configuration partition functions which predict a distribution in ion-defect pair separation distances at low temperatures. At elevated temperatures such ion-defect pairs dissociate, and the concept of pair formation more appropriately gives way to the concept of pair correlation functions. The relative sizes of the aliovalent ion and the host ion which it replaces are seen to exert a pronounced effect on pair distribution. Salient features of the theory are applied to the KCl: Sr2+, NaCl: Mn2+, NaCl: Sr2+, LiCl: Mn2+ and (alkaline-earth halide): (rareearth)3+ systems. While the high-temperature treatment lends itself to comparisons with the Debye-Hückel theory for electrolytes, the low-temperature pair distribution theory is shown to be valid chiefly because of the specific nature of the crystalline ionic solutions

Reactions in Crystalline Lattices: Chemistry of Lower Valence States of Lanthanides

Reduction of rare-earth (RE) ions to lower valence states in ionic crystals is described in terms of the equilibrium distribution theory for the (alkali halide):RE2+ and (alkaline-earth halide):RE3+ systems. Thermoluminescence glow curves of radiation-reduced CaF2:RE3+ systems reveal that the reoxidation of the divalent ions apparently occurs through thermal excitation of an f electron to the d bands. The additive reduction of RE2+ to the monovalent state in alkali halides yields striking results: While Sm1+ ions in KCl obtained by gamma radiation give rise to broad-band optical spectra which were attributed to 4f66s1 --> 4f56s2 transitions, those obtained through high-temperature additive treatment with liquid K give rise to narrow-line spectra that are not easily interpreted. These results illustrate well the major differences between the radiation reduction and additive reduction processes

Expression profiling identifies genes involved in emphysema severity

Chronic obstructive pulmonary disease (COPD) is a major public health problem. The aim of this study was to identify genes involved in emphysema severity in COPD patients

MS4A1 Dysregulation in Asbestos-Related Lung Squamous Cell Carcinoma Is Due to CD20 Stromal Lymphocyte Expression

Asbestos-related lung cancer accounts for 4–12% of lung cancers worldwide. We have previously identified ADAM28 as a putative oncogene involved in asbestos-related lung adenocarcinoma (ARLC-AC). We hypothesised that similarly gene expression profiling of asbestos-related lung squamous cell carcinomas (ARLC-SCC) may identify candidate oncogenes for ARLC-SCC. We undertook a microarray gene expression study in 56 subjects; 26 ARLC-SCC (defined as lung asbestos body (AB) counts >20AB/gram wet weight (gww) and 30 non-asbestos related lung squamous cell carcinoma (NARLC-SCC; no detectable lung asbestos bodies; 0AB/gww). Microarray and bioinformatics analysis identified six candidate genes differentially expressed between ARLC-SCC and NARLC-SCC based on statistical significance (p<0.001) and fold change (FC) of >2-fold. Two genes MS4A1 and CARD18, were technically replicated by qRT-PCR and showed consistent directional changes. As we also found MS4A1 to be overexpressed in ARLC-ACs, we selected this gene for biological validation in independent test sets (one internal, and one external dataset (2 primary tumor sets)). MS4A1 RNA expression dysregulation was validated in the external dataset but not in our internal dataset, likely due to the small sample size in the test set as immunohistochemical (IHC) staining for MS4A1 (CD20) showed that protein expression localized predominantly to stromal lymphocytes rather than tumor cells in ARLC-SCC. We conclude that differential expression of MS4A1 in this comparative gene expression study of ARLC-SCC versus NARLC-SCC is a stromal signal of uncertain significance, and an example of the rationale for tumor cell enrichment in preparation for gene expression studies where the aim is to identify markers of particular tumor phenotypes. Finally, our study failed to identify any strong gene candidates whose expression serves as a marker of asbestos etiology. Future research is required to determine the role of stromal lymphocyte MS4A1 dysregulation in pulmonary SCCs caused by asbestos

Genes and Gene Ontologies Common to Airflow Obstruction and Emphysema in the Lungs of Patients with COPD

Chronic obstructive pulmonary disease (COPD) is a major public health problem with increasing prevalence worldwide. The primary aim of this study was to identify genes and gene ontologies associated with COPD severity. Gene expression profiling was performed on total RNA extracted from lung tissue of 18 former smokers with COPD. Class comparison analysis on mild (n = 9, FEV1 80–110% predicted) and moderate (n = 9, FEV1 50–60% predicted) COPD patients identified 46 differentially expressed genes (p<0.01), of which 14 genes were technically confirmed by quantitative real-time-PCR. Biological replication in an independent test set of 58 lung samples confirmed the altered expression of ten genes with increasing COPD severity, with eight of these genes (NNMT, THBS1, HLA-DPB1, IGHD, ETS2, ELF1, PTGDS and CYRBD1) being differentially expressed by greater than 1.8 fold between mild and moderate COPD, identifying these as candidate determinants of COPD severity. These genes belonged to ontologies potentially implicated in COPD including angiogenesis, cell migration, proliferation and apoptosis. Our secondary aim was to identify gene ontologies common to airway obstruction, indicated by impaired FEV1 and KCO. Using gene ontology enrichment analysis we have identified relevant biological and molecular processes including regulation of cell-matrix adhesion, leukocyte activation, cell and substrate adhesion, cell adhesion, angiogenesis, cell activation that are enriched among genes involved in airflow obstruction. Exploring the functional significance of these genes and their gene ontologies will provide clues to molecular changes involved in severity of COPD, which could be developed as targets for therapy or biomarkers for early diagnosis

A mission control architecture for robotic lunar sample return as field tested in an analogue deployment to the Sudbury impact structure

A Mission Control Architecture is presented for a Robotic Lunar Sample Return Mission which builds upon the experience of the landed missions of the NASA Mars Exploration Program. This architecture consists of four separate processes working in parallel at Mission Control and achieving buy-in for plans sequentially instead of simultaneously from all members of the team. These four processes were: Science Processing, Science Interpretation, Planning and Mission Evaluation. Science Processing was responsible for creating products from data downlinked from the field and is organized by instrument. Science Interpretation was responsible for determining whether or not science goals are being met and what measurements need to be taken to satisfy these goals. The Planning process, responsible for scheduling and sequencing observations, and the Evaluation process that fostered inter-process communications, reporting and documentation assisted these processes. This organization is advantageous for its flexibility as shown by the ability of the structure to produce plans for the rover every two hours, for the rapidity with which Mission Control team members may be trained and for the relatively small size of each individual team. This architecture was tested in an analogue mission to the Sudbury impact structure from June 6-17, 2011. A rover was used which was capable of developing a network of locations that could be revisited using a teach and repeat method. This allowed the science team to process several different outcrops in parallel, downselecting at each stage to ensure that the samples selected for caching were the most representative of the site. Over the course of 10 days, 18 rock samples were collected from 5 different outcrops, 182 individual field activities - such as roving or acquiring an image mosaic or other data product - were completed within 43 command cycles, and the rover travelled over 2,200 m. Data transfer from communications passes were filled to 74%. Sample triage was simulated to allow down-selection to 1kg of material for return to Earth

Otx2 Gene Deletion in Adult Mouse Retina Induces Rapid RPE Dystrophy and Slow Photoreceptor Degeneration

International audienceBACKGROUND: Many developmental genes are still active in specific tissues after development is completed. This is the case for the homeobox gene Otx2, an essential actor of forebrain and head development. In adult mouse, Otx2 is strongly expressed in the retina. Mutations of this gene in humans have been linked to severe ocular malformation and retinal diseases. It is, therefore, important to explore its post-developmental functions. In the mature retina, Otx2 is expressed in three cell types: bipolar and photoreceptor cells that belong to the neural retina and retinal pigment epithelium (RPE), a neighbour structure that forms a tightly interdependent functional unit together with photoreceptor cells. METHODOLOGY/PRINCIPAL FINDINGS: Conditional self-knockout was used to address the late functions of Otx2 gene in adult mice. This strategy is based on the combination of a knock-in CreERT2 allele and a floxed allele at the Otx2 locus. Time-controlled injection of tamoxifen activates the recombinase only in Otx2 expressing cells, resulting in selective ablation of the gene in its entire domain of expression. In the adult retina, loss of Otx2 protein causes slow degeneration of photoreceptor cells. By contrast, dramatic changes of RPE activity rapidly occur, which may represent a primary cause of photoreceptor disease. CONCLUSIONS: Our novel mouse model uncovers new Otx2 functions in adult retina. We show that this transcription factor is necessary for long-term maintenance of photoreceptors, likely through the control of specific activities of the RPE