Differential effects of nanoselenium doping on healthy and cancerous osteoblasts in coculture on titanium

In the present study, selenium (Se) nanoclusters were grown through heterogeneous nucleation on titanium (Ti) surfaces, a common orthopedic implant material. Normal healthy osteoblasts (bone-forming cells) and cancerous osteoblasts (osteosarcoma) were cultured on the Se-doped surfaces having three different coating densities. For the first time, it is shown that substrates with Se nanoclusters promote normal osteoblast proliferation and inhibit cancerous osteoblast growth in both separate (mono-culture) and coculture experiment. This study suggests that Se surface nanoclusters can be properly engineered to inhibit bone cancer growth while simultaneously promoting the growth of normal bone tissue

Chronicles of Oklahoma

Article describes the planning, construction, and founding process of Southwestern Normal School in Weatherford, Oklahoma, as well as its growth, expansion, and eventual destruction

Protostars in the Elephant Trunk Nebula

The optically-dark globule IC 1396A is revealed using Spitzer images at 3.6, 4.5, 5.8, 8, and 24 microns to be infrared-bright and to contain a set of previously unknown protostars. The mid-infrared colors of the 24 microns detected sources indicate several very young (Class I or 0) protostars and a dozen Class II stars. Three of the new sources (IC 1396A: gamma, delta, and epsilon) emit over 90% of their bolometric luminosities at wavelengths greater than 3 microns, and they are located within ~0.02 pc of the ionization front at the edge of the globule. Many of the sources have spectra that are still rising at 24 microns. The two previously-known young stars LkHa 349 a and c are both detected, with component c harboring a massive disk and component a being bare. Of order 5% of the mass of material in the globule is presently in the form of protostars in the 10^5 to 10^6 yr age range. This high star formation rate was likely triggered by radiation from a nearby O star.Comment: Spitzer first ApJS special issue (in press

CD44+CD24− prostate cells are early cancer progenitor/stem cells that provide a model for patients with poor prognosis

Recent evidence supports the hypothesis that cancer stem cells are responsible for tumour initiation and formation. Using flow cytometry, we isolated a population of CD44+CD24− prostate cells that display stem cell characteristics as well as gene expression patterns that predict overall survival in prostate cancer patients. CD44+CD24− cells form colonies in soft agar and form tumours in NOD/SCID mice when as few as 100 cells are injected. Furthermore, CD44+CD24− cells express genes known to be important in stem cell maintenance, such as BMI-1 and Oct-3/4. Moreover, we can maintain CD44+CD24− prostate stem-like cells as nonadherent spheres in serum-replacement media without substantially shifting gene expression. Addition of serum results in adherence to plastic and shifts gene expression patterns to resemble the differentiated parental cells. Thus, we propose that CD44+CD24− prostate cells are stem-like cells responsible for tumour initiation and we provide a genomic definition of these cells and the differentiated cells they give rise to. Furthermore, gene expression patterns of CD44+CD24− cells have a genomic signature that is predictive of poor patient prognosis. Therefore, CD44+CD24− LNCaP prostate cells offer an attractive model system to both explore the biology important to the maintenance and differentiation of prostate cancer stem cells as well as to develop the therapeutics, as the gene expression pattern in these cells is consistent with poor survival in prostate cancer patients

Disk and Envelope Structure in Class 0 Protostars: II. High Resolution Millimeter Mapping of the Serpens Sample

We present high-resolution CARMA 230 GHz continuum imaging of nine deeply embedded protostars in the Serpens Molecular Cloud, including six of the nine known Class 0 protostars in Serpens. This work is part of a program to characterize disk and envelope properties for a complete sample of Class 0 protostars in nearby low-mass star forming regions. Here we present CARMA maps and visibility amplitudes as a function of uv-distance for the Serpens sample. Observations are made in the B, C, D, and E antenna configurations, with B configuration observations utilizing the CARMA Paired Antenna Calibration System. Combining data from multiple configurations provides excellent uv-coverage (4-500 klam), allowing us to trace spatial scales from 1e2 to 1e4 AU. We find evidence for compact disk components in all of the observed Class 0 protostars, suggesting that disks form at very early times (t<0.2 Myr) in Serpens. We make a first estimate of disk masses using the flux at 50 klam, where the contribution from the envelope should be negligible, assuming an unresolved disk. The resulting disk masses range from 0.04 Msun to 1.7 Msun, with a mean of approximately 0.2 Msun. Our high resolution maps are also sensitive to binary or multiple sources with separations > 250 AU, but significant evidence of multiplicity on scales <2000 AU is seen in only one source.Comment: Accepted to the Astrophysical Journal Supplement

Identification of Genes Required for Neural-Specific Glycosylation Using Functional Genomics

Glycosylation plays crucial regulatory roles in various biological processes such as development, immunity, and neural functions. For example, α1,3-fucosylation, the addition of a fucose moiety abundant in Drosophila neural cells, is essential for neural development, function, and behavior. However, it remains largely unknown how neural-specific α1,3-fucosylation is regulated. In the present study, we searched for genes involved in the glycosylation of a neural-specific protein using a Drosophila RNAi library. We obtained 109 genes affecting glycosylation that clustered into nine functional groups. Among them, members of the RNA regulation group were enriched by a secondary screen that identified genes specifically regulating α1,3-fucosylation. Further analyses revealed that an RNA–binding protein, second mitotic wave missing (Swm), upregulates expression of the neural-specific glycosyltransferase FucTA and facilitates its mRNA export from the nucleus. This first large-scale genetic screen for glycosylation-related genes has revealed novel regulation of fucTA mRNA in neural cells

A Protein Inventory of Human Ribosome Biogenesis Reveals an Essential Function of Exportin 5 in 60S Subunit Export

A systematic search for human ribosome biogenesis factors shows conservation of many aspects of eukaryotic ribosome synthesis with the well-studied process in yeast and identifies an export route of 60S subunits that is specific for higher eukaryotes

Expression Profiling of Major Histocompatibility and Natural Killer Complex Genes Reveals Candidates for Controlling Risk of Graft versus Host Disease

Background: The major histocompatibility complex (MHC) is the most important genomic region that contributes to the risk of graft versus host disease (GVHD) after haematopoietic stem cell transplantation. Matching of MHC class I and II genes is essential for the success of transplantation. However, the MHC contains additional genes that also contribute to the risk of developing acute GVHD. It is difficult to identify these genes by genetic association studies alone due to linkage disequilibrium in this region. Therefore, we aimed to identify MHC genes and other genes involved in the pathophysiology of GVHD by mRNA expression profiling. Methodology/Principal Findings: To reduce the complexity of the task, we used genetically well-defined rat inbred strains and a rat skin explant assay, an in-vitro-model of the graft versus host reaction (GVHR), to analyze the expression of MHC, natural killer complex (NKC), and other genes in cutaneous GVHR. We observed a statistically significant and strong up or down regulation of 11 MHC, 6 NKC, and 168 genes encoded in other genomic regions, i.e. 4.9%, 14.0%, and 2.6% of the tested genes respectively. The regulation of 7 selected MHC and 3 NKC genes was confirmed by quantitative real-time PCR and in independent skin explant assays. In addition, similar regulations of most of the selected genes were observed in GVHD-affected skin lesions of transplanted rats and in human skin explant assays. Conclusions/Significance: We identified rat and human MHC and NKC genes that are regulated during GVHR in skin explant assays and could therefore serve as biomarkers for GVHD. Several of the respective human genes, including HLA-DMB, C2, AIF1, SPR1, UBD, and OLR1, are polymorphic. These candidates may therefore contribute to the genetic risk of GVHD in patients

DNA repair: the culprit for tumor-initiating cell survival?

The existence of “tumor-initiating cells” (TICs) has been a topic of heated debate for the last few years within the field of cancer biology. Their continuous characterization in a variety of solid tumors has led to an abundance of evidence supporting their existence. TICs are believed to be responsible for resistance against conventional treatment regimes of chemotherapy and radiation, ultimately leading to metastasis and patient demise. This review summarizes DNA repair mechanism(s) and their role in the maintenance and regulation of stem cells. There is evidence supporting the hypothesis that TICs, similar to embryonic stem (ES) cells and hematopoietic stem cells (HSCs), display an increase in their ability to survive genotoxic stress and injury. Mechanistically, the ability of ES cells, HSCs and TICs to survive under stressful conditions can be attributed to an increase in the efficiency at which these cells undergo DNA repair. Furthermore, the data presented in this review summarize the results found by our lab and others demonstrating that TICs have an increase in their genomic stability, which can allow for TIC survival under conditions such as anticancer treatments, while the bulk population of tumor cells dies. We believe that these data will greatly impact the development and design of future therapies being engineered to target and eradicate this highly aggressive cancer cell population