A facile one-pot synthesis of N-La codoped TiO2 porous materials with bio-hierarchical architectures and enhanced photocatalytic activity

Bio-hierarchical TiO2-based porous structures (denoted as morph-TiO2) with N and La co-doping (denoted as N-La-morph-TiO2) are successfully synthesized via a facile one-pot reaction by using butterfly wings as bio-template and surfactant as co-template. Due to the novel dual-template strategy, the well-aligned 3D bio-hierarchical porous structures in combination with N-La codoping not only modify the band structure of TiO2 to make it more responsive to visible light, but also increase the surface area and lead TiO2 to have enhanced photocatalytic activity for methyl orange (MO) degradation under UV and/or visible light illumination as compared with P25 TiO2 and pristine TiO2. The optimized N-La-morph-TiO2 nanostructures present a narrow pore size distribution with an average pore diameter of 8.7 nm and a high specific surface area (196 m2 g−1), which is nearly four times that of P25 TiO2. The enhanced photocatalytic activity is attributed to the combination of the doped inorganic elements, the fine hierarchical and well-aligned porous nanostructures as analyzed by SEM, TEM, XPS, BET, UV–vis absorption and photodegradation tests. The promotional mechanisms and principles reported in this work are believed to have great significance in heterogeneous photocatalysis

Overexpression of Elafin in Ovarian Carcinoma Is Driven by Genomic Gains and Activation of the Nuclear Factor κB Pathway and Is Associated with Poor Overall Survival12

Ovarian cancer is a leading cause of cancer mortality in women. The aim of this study was to elucidate whether whey acidic protein (WAP) genes on chromosome 20q13.12, a region frequently amplified in this cancer, are expressed in serous carcinoma, the most common form of the disease. Herein, we report that a trio of WAP genes (HE4, SLPI, and Elafin) is overexpressed and secreted by serous ovarian carcinomas. To our knowledge, this is the first report linking Elafin to ovarian cancer. Fluorescence in situ hybridization analysis of primary tumors demonstrates genomic gains of the Elafin locus in a majority of cases. In addition, a combination of peptidomimetics, RNA interference, and chromatin immunoprecipitation experiments shows that Elafin expression can be transcriptionally upregulated by inflammatory cytokines through activation of the nuclear factor κB pathway. Importantly, using a clinically annotated tissue microarray composed of late-stage, high-grade serous ovarian carcinomas, we show that Elafin expression correlates with poor overall survival. These results, combined with our observation that Elafin is secreted by ovarian tumors and is minimally expressed in normal tissues, suggest that Elafin may serve as a determinant of poor survival in this disease

Mesenchymal gene program-expressing ovarian cancer spheroids exhibit enhanced mesothelial clearance.

Metastatic dissemination of ovarian tumors involves the invasion of tumor cell clusters into the mesothelial cell lining of peritoneal cavity organs; however, the tumor-specific factors that allow ovarian cancer cells to spread are unclear. We used an in vitro assay that models the initial step of ovarian cancer metastasis, clearance of the mesothelial cell layer, to examine the clearance ability of a large panel of both established and primary ovarian tumor cells. Comparison of the gene and protein expression profiles of clearance-competent and clearance-incompetent cells revealed that mesenchymal genes are enriched in tumor populations that display strong clearance activity, while epithelial genes are enriched in those with weak or undetectable activity. Overexpression of transcription factors SNAI1, TWIST1, and ZEB1, which regulate the epithelial-to-mesenchymal transition (EMT), promoted mesothelial clearance in cell lines with weak activity, while knockdown of the EMT-regulatory transcription factors TWIST1 and ZEB1 attenuated mesothelial clearance in ovarian cancer cell lines with strong activity. These findings provide important insights into the mechanisms associated with metastatic progression of ovarian cancer and suggest that inhibiting pathways that drive mesenchymal programs may suppress tumor cell invasion of peritoneal tissues

Mesenchymal gene program-expressing ovarian cancer spheroids exhibit enhanced mesothelial clearance.

Metastatic dissemination of ovarian tumors involves the invasion of tumor cell clusters into the mesothelial cell lining of peritoneal cavity organs; however, the tumor-specific factors that allow ovarian cancer cells to spread are unclear. We used an in vitro assay that models the initial step of ovarian cancer metastasis, clearance of the mesothelial cell layer, to examine the clearance ability of a large panel of both established and primary ovarian tumor cells. Comparison of the gene and protein expression profiles of clearance-competent and clearance-incompetent cells revealed that mesenchymal genes are enriched in tumor populations that display strong clearance activity, while epithelial genes are enriched in those with weak or undetectable activity. Overexpression of transcription factors SNAI1, TWIST1, and ZEB1, which regulate the epithelial-to-mesenchymal transition (EMT), promoted mesothelial clearance in cell lines with weak activity, while knockdown of the EMT-regulatory transcription factors TWIST1 and ZEB1 attenuated mesothelial clearance in ovarian cancer cell lines with strong activity. These findings provide important insights into the mechanisms associated with metastatic progression of ovarian cancer and suggest that inhibiting pathways that drive mesenchymal programs may suppress tumor cell invasion of peritoneal tissues

Profiles of Genomic Instability in High-Grade Serous Ovarian Cancer Predict Treatment Outcome

PURPOSE: High-grade serous cancer (HGSC) is the most common cancer of the ovary and is characterized by chromosomal instability. Defects in homologous recombination repair (HRR) are associated with genomic instability in HGSC, and are exploited by therapy targeting DNA repair. Defective HRR causes uniparental deletions and loss of heterozygosity (LOH). Our purpose is to profile LOH in HGSC and correlate our findings to clinical outcome, and compare HGSC and high-grade breast cancers. EXPERIMENTAL DESIGN: We examined LOH and copy number changes using single nucleotide polymorphism array data from three HGSC cohorts and compared results to a cohort of high-grade breast cancers. The LOH profiles in HGSC were matched to chemotherapy resistance and progression-free survival (PFS). RESULTS: LOH-based clustering divided HGSC into two clusters. The major group displayed extensive LOH and was further divided into two subgroups. The second group contained remarkably less LOH. BRCA1 promoter methylation was associated with the major group. LOH clusters were reproducible when validated in two independent HGSC datasets. LOH burden in the major cluster of HGSC was similar to triple-negative, and distinct from other high-grade breast cancers. Our analysis revealed an LOH cluster with lower treatment resistance and a significant correlation between LOH burden and PFS. CONCLUSIONS: Separating HGSC by LOH-based clustering produces remarkably stable subgroups in three different cohorts. Patients in the various LOH clusters differed with respect to chemotherapy resistance, and the extent of LOH correlated with PFS. LOH burden may indicate vulnerability to treatment targeting DNA repair, such as PARP1 inhibitors

Non-growing-season soil respiration is controlled by freezing and thawing processes in the summer monsoon-dominated Tibetan alpine grassland

The Tibetan alpine grasslands, sharing many features with arctic tundra ecosystems, have a unique non-growing-season climate that is usually dry and without persistent snow cover. Pronounced winter warming recently observed in this ecosystem may significantly alter the non-growing-season carbon cycle processes such as soil respiration (R-s), but detailed measurements to assess the patterns, drivers of, and potential feedbacks on R-s have not been made yet. We conducted a 4 year study on R-s using a unique R-s measuring system, composed of an automated soil CO2 flux sampling system and a custom-made container, to facilitate measurements in this extreme environment. We found that in the nongrowing season, (1) cumulative R-s was 82-89g C m(-2), accounting for 11.8-13.2% of the annual total R-s; (2) surface soil freezing controlled the diurnal pattern of R-s and bulk soil freezing induced lower reference respiration rate (R-0) and temperature sensitivity (Q(10)) than those in the growing season (0.40-0.53 versus 0.84-1.32 mu mol CO2 m(-2)s(-1) for R-0 and 2.5-2.9 versus 2.9-5.6 for Q(10)); and (3) the intraannual variation in cumulative R-s was controlled by accumulated surface soil temperature. We found that in the summer monsoon-dominated Tibetan alpine grassland, surface soil freezing, bulk soil freezing, and accumulated surface soil temperature are the day-, season-, and year-scale drivers of the non-growing-season R-s, respectively. Our results suggest that warmer winters can trigger carbon loss from this ecosystem because of higher Q(10) of thawed than frozen soils.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000344797500005&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Environmental SciencesGeosciences, MultidisciplinaryMeteorology & Atmospheric SciencesSCI(E)[email protected]