Dolomite [CaMg(CO 3 ) 2 ] forms in numerous geological settings, usually as a diagenetic replacement of limestone, and is an important component of petroleum reservoir rocks, rocks hosting base metal deposits and fresh water aquifers. Dolomite is a rhombohedral carbonate with a structure consisting of an ordered arrangement of alternating layers of Ca 2+ and Mg 2+ cations interspersed with CO 2À 3 anion layers normal to the c-axis. Dolomite has R 3 symmetry, lower than the (CaCO 3 ) R 3c symmetry of calcite primarily due to Ca-Mg ordering. High-magnesium calcite also has R 3c symmetry and differs from dolomite in that Ca 2+ and Mg 2+ ions are not ordered. High-magnesium calcite with near-dolomite stoichiometry (%50 mol% MgCO 3 ) has been observed both in nature and in laboratory products and is referred to in the literature as protodolomite or very high-magnesium calcite. Many dolomites display some degree of cation disorder (Ca 2+ on Mg 2+ sites and vice versa), which is detectable using transmission electron microscopy and X-ray diffractometry. Laboratory syntheses at high temperature and pressure, as well as studies of natural dolomites show that factors affecting dolomite ordering, stoichiometry, nucleation and growth include temperature, alkalinity, pH, concentration of Mg and Ca, Mg to Ca ratio, fluid to rock ratio, mineralogy of the carbonate being replaced, and surface area available for nucleation. In spite of numerous attempts, dolomite has not been synthesized in the laboratory under near-surface conditions. Examination of published X-ray diffraction data demonstrates that assertions of dolomite synthesis in the laboratory under near-ambient conditions by microbial mediation are unsubstantiated. These laboratory products show no evidence of cation ordering and appear to be very high-magnesium calcite. Elevated-temperature and elevated-pressure experiments demonstrate that dolomite nucleation and growth always are preceded by very high-magnesium calcite formation. It remains to be demonstrated whether microbial-mediated growth of very high-magnesium calcite in nature provides a precursor to dolomite nucleation and growth analogous to reaction paths in high-temperature experiments.

Microarray gene expression profiling is able to predict the prognosis of stage II colon cancer patients. The present study also illustrates the usefulness of resampling techniques for honest performance assessment of microarray-based PPs.

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Three peritidal carbonate crusts and associated intercrust sediments (total thickness of ∼30cm; aged <3000 years BP) on Ambergris Cay, Belize, contain 32–100% calcian dolomite (δx=72·5% dolomite) ranging in composition from 40 to 46 mol% MgCO3 (δx=43·3). Dolomite replaced high Mg calcite foraminiferal muds penecontemporaneously with sedimentation, forming partially dolomitized sediments and lithified crusts. Dolomitization probably occurred in normal to moderately evaporated seawater and is apparently continuing at the present. Detailed scanning electron microscope analysis shows a linear increase in mean dolomite crystal size with depth; 0·4 μm near the top of the section to 1·0 μm near the base of the dolomitized section. This size increase is not accompanied by any significant decrease in porosity. Crystal size distributions appear to be log‐normal and become increasingly broad and flat with depth. Rietveld X‐ray pattern‐fitting structure refinements indicate increasing Ca and Mg concentrations on their respective sites (cation ordering) as a function of increasing depth. Most of the ordering occurs within the first 15 cm of the surface. Stoichiometry does not increase with depth indicating no relationship between the Ca/Mg ratio and cation ordering. Strong geochemical trends were observed down‐section in the dolomite, including: (1) increasing Mn content (44 to 274 ppm), and (2) decreasing δ13C values (−0·9 to −5·5‰ PDB). Oxygen isotope values range from δ18O = 1·3‰ PDB in the upper part of the section to 2·6‰ PDB in the lower part of the section and are interpreted to represent two distinct groups of values rather than a continuous trend. Down‐section dolomite crystal size increase and shapes of crystal size distributions are consistent with recrystallization via a surface energy‐driven dissolution‐reprecipitation process (Ostwald ripening). The observed trends in carbon isotopes and Mn content probably result from geochemical re‐equilibration during recrystallization and reflect reducing conditions and an isotopically light, organically derived, carbon source. Oxygen isotope compositions probably reflect relict original dolomite values and are a result of decreasing evaporation due to rising sea level.

BackgroundThe prostate gland represents a multifaceted system in which prostate epithelia and stroma have distinct physiological roles. To understand the interaction between stroma and glandular epithelia, it is essential to delineate the gene expression profiles of these two tissue types in prostate cancer. Most studies have compared tumor and normal samples by performing global expression analysis using a mixture of cell populations. This report presents the first study of prostate tumor tissue that examines patterns of differential expression between specific cell types using laser capture microdissection (LCM).MethodsLCM was used to isolate distinct cell-type populations and identify their gene expression differences using oligonucleotide microarrays. Ten differentially expressed genes were then analyzed in paired tumor and non-neoplastic prostate tissues by quantitative real-time PCR. Expression patterns of the transcription factors, WT1 and EGR1, were further compared in established prostate cell lines. WT1 protein expression was also examined in prostate tissue microarrays using immunohistochemistry.ResultsThe two-step method of laser capture and microarray analysis identified nearly 500 genes whose expression levels were significantly different in prostate epithelial versus stromal tissues. Several genes expressed in epithelial cells (WT1, GATA2, and FGFR-3) were more highly expressed in neoplastic than in non-neoplastic tissues; conversely several genes expressed in stromal cells (CCL5, CXCL13, IGF-1, FGF-2, and IGFBP3) were more highly expressed in non-neoplastic than in neoplastic tissues. Notably, EGR1 was also differentially expressed between epithelial and stromal tissues. Expression of WT1 and EGR1 in cell lines was consistent with these patterns of differential expression. Importantly, WT1 protein expression was demonstrated in tumor tissues and was absent in normal and benign tissues.ConclusionsThe prostate represents a complex mix of cell types and there is a need to analyze distinct cell populations to better understand their potential interactions. In the present study, LCM and microarray analysis were used to identify novel gene expression patterns in prostate cell populations, including identification of WT1 expression in epithelial cells. The relevance of WT1 expression in prostate cancer was confirmed by analysis of tumor tissue and cell lines, suggesting a potential role for WT1 in prostate tumorigenesis.

Most sporadically occurring renal tumors include a functional loss of the tumor suppressor VHL. Development of VHL-deficient renal cell carcinoma (RCC) relies upon activation of the hypoxia-inducible factor HIF-2α, a master transcriptional regulator of genes that drive diverse processes including angiogenesis, proliferation and anaerobic metabolism. In determining the critical functions for HIF-2α expression in RCC cells, the NADPH oxidase NOX4 has been identified, but the pathogenic contributions of NOX4 to RCC have not been evaluated directly. Here we report that NOX4 silencing in VHL-deficient RCC cells abrogates cell branching, invasion, colony formation and growth in a murine xenograft model RCC. These alterations were phenocopied by treatment of the superoxide scavenger, TEMPOL, or by overexpression of manganese superoxide dismutase or catalase. Notably, NOX4 silencing or superoxide scavenging was sufficient to block nuclear accumulation of HIF-2α in RCC cells. Our results offer direct evidence that NOX4 is critical for renal tumorigenesis and they show how NOX4 suppression and VHL re-expression in VHL-deficient RCC cells are genetically synonymous, supporting development of therapeutic regimens aimed at NOX4 blockade.

Treatment for head and neck cancer precipitates a myriad of distressing symptoms, Patients may be isolated both physically and socially and may lack the self-efficacy to report problems and participate as partners in their care. The goal of this project was to design a telehealth intervention to address such isolation, develop patient self-efficacy, and improve symptom management during the treatment experience. Participatory action research and a review of the literature were used to develop electronically administered symptom management algorithms addressing all major symptoms experienced by patients undergoing treatment for head and neck cancers, Daily questions and related messages were then programmed into an easy-to-use telehealth messaging device, the Health Buddy®. Clinician and patient acceptance, feasibility, and technology issues were measured. Using participatory action research is an effective means for developing electronic algorithms acceptable to both clinicians and patients. The use of a simple tele-messaging device as an adjunct to symptom management is feasible, affordable, and acceptable to patients. This telehealth intervention provides support and education to patients undergoing treatment for head and neck cancers.

The early growth response gene 1, EGR1, is an important transcriptional regulator and acts as the convergent point between a variety of extracellular stimuli and activation of target genes. Unlike other tumor types, prostate tumors express high levels of EGR1 relative to normal tissues. However, the mechanism of EGR1 regulation in prostate tumor cells is unknown. As EGR1 expression and epidermal growth factor (EGF) signaling are frequently upregulated in prostate tumors, we tested the hypothesis that EGF induces EGR1 expression in prostate cancer cells. Using RT-PCR to quantify EGR1 transcripts, we found that EGF induced EGR1 expression in a dose-and time-dependent manner and the ERK pathway inhibitor, PD98059, abrogated the EGF-mediated EGR1 response in LNCaP and PC3 cells. Analysis of the EGR1 promoter using deletion constructs identified an EGF-responsive region in the proximal promoter (-771 to -245 bp) containing 3 potential serum response element (SRE) sites. In vivo chromatin immunoprecipitation assays demonstrated that Elk-1 binding at the SRE sites of the EGR1 promoter was enhanced by EGF treatment in PC3 cells. Overexpression of Elk-1 was sufficient to activate the EGF-responsive region of EGR1 promoter in PC3 cells and, similarly, a dominant-negative Elk-1 suppressed EGR1 promoter activity. Taken together, these results demonstrate for the first time that EGR1 expression in PC3 cells is mediated through an EGF-ERK-Elk-1 signaling cascade.