Geoid Research Articles

Detection of Prostate Cancer using Ensemble based Bi-directional Long Short Term Memory Network

Aim and Background: In recent periods, micro-array data analysis using soft computing and machine learning techniques gained more interest among researchers to detect prostate cancer. Due to the small sample size of micro-array data with a larger number of attributes, traditional machine learning techniques face difficulty detecting prostate cancer. Methodology: The selection of relevant genes exploits useful information about micro-array data, which enhances the accuracy of detection. In this research, the samples are acquired from the gene expression omnibus database, particularly related to the prostate cancer GEO IDs such as GSE 21034, GSE 15484 and GSE 3325/GSE 3998. In addition, ensemble feature optimization technique and Bidirectional Long Short Term Memory (Bi-LSTM) network are employed for detecting prostate cancer from the microarray data of gene expression. Results: The ensemble feature optimization technique includes 4 metaheuristic optimizers that select the top 2000 genes from each GEO IDs, which are relevant to prostate cancer. Next, the selected genes are given to the Bi-LSTM network for classifying the normal and prostate cancer subjects. Conclusion: The simulation analysis revealed that the ensemble based Bi-LSTM network obtained 99.13%, 98.97%, and 94.12% of accuracy on the GEO IDs like GSE 3325/GSE 3998, GSE 21034, and GSE 15484.

Validation of European Gravimetric Geoid models in context of realization of EVRS system in Poland

Validation of European Gravimetric Geoid models in context of realization of EVRS system in Poland

Reduction of ore dilution when mining low-thickness ore bodies by means of artificial maintenance of the mined-out area

Purpose. The research purpose is to study the effectiveness of artificial maintenance of the mined-out space based on the use of cable bolts to reduce the dilution coefficient when mining low-thickness ore bodies. Methods. Geotechnical mapping of the rock mass according to the Q, RMR, RQD and GSI rating classifications is conducted, as well as a linear survey of the fracture system in the hanging wall and footwall rocks is performed using a rock compass and the GEO ID application. Numerical analysis by the limit equilibrium method in the Unwedge software package is applied to determine the safety factor of a mass divided by fractures into wedges. Using a Schmidt test hammer, the uniaxial compressive strength of the mass rocks has been determined. The full-scale studies have been conducted using cable support in the conditions of the Akbakai deposit. Findings. It has been revealed that the footwall rocks are in a stable state, while the safety factor of the hanging wall rocks is 0.98, which requires artificial maintenance using cable bolts. The cable support parameters are calculated taking into account nonuniform distribution of horizontal and vertical stresses in the rock mass. It has been determined that when strengthening the hanging wall with cable bolts in inclined veins with a dip angle of up to 40º, the average ore dilution is 66.1%, and that of previously mined without fastening is 68.7%. In similar experiments in steep-dipping veins with a dip angle of more than 60º, dilution decreases from 62.8 to 48.7%. Originality. It has been revealed that in the conditions of the Akbakai deposit, cable fastening of the hanging wall rocks is effective at an ore deposit dip angle of more than 60º, at which the mined ore dilution coefficient decreases. Practical implications. The research results can be used to increase the stability of hanging wall rocks when mining low-thickness ore bodies with a sublevel caving system.

Low thermal budget epitaxial lift off (ELO) for Ge (111)-on-insulator structure

Germanium-on-insulator (GeOI) structures with a surface orientation of (111) have been successfully fabricated by using low thermal budget epitaxial-lift-off (ELO) technology via direct bonding and selective etching. The material characteristics and transport properties of the Ge(111)OI structure have been systematically investigated through secondary-ion mass spectrometry, Raman spectroscopy, X-ray diffraction, high-resolution transmission electron microscope, and Hall measurement. The transferred Ge (111) layer remained almost intact from the as-grown epitaxial layers, indicating the benefits of ELO technology. The low thermal budget ELO technology demonstrated in this work is promising to integrate Ge channels with different surface orientations on Si (100) substrates for future monolithic 3D applications.

Downregulation of Long Non-coding RNA Nuclear Paraspeckle Assembly Transcript 1 Inhibits MEG-01 Differentiation and Platelet-Like Particles Activity

Platelets are derived from megakaryocytes and play an important role in blood coagulation. By using high throughput sequencing, we have found that the long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) is abundant in platelets (GEO ID: 200097348). However, little is known about its role in regulating megakaryocyte differentiation and platelet activity. This study aims to clarify the effect of NEAT1 on MEG-01 differentiation and platelet-like particle (PLP) activity. NEAT1 in MEG-01 cells was knocked down by siRNA transfection. The adhesion of MEG-01 and PLP to collagen-coated coverslips was observed under a fluorescence microscope. Flow cytometry was used to investigate cell apoptosis, cell cycle, the levels of D41/CD42b on MEG-01 cells and CD62P on PLPs. Quantitative real-time polymerase chain reaction was used to detect NEAT1 and IL-8 expression levels. Western blot was used to measure the protein levels of Bcl-2, Bax, cleaved caspase-3, and IL-8. RNA-binding protein immunoprecipitation was used to detect the interaction of NEAT1 and splicing factor proline/glutamine-rich (SFPQ). Results showed that NEAT1 knockdown decreased the adhesion ability of thrombin-stimulated MEG-01 and PLP. The expression of CD62P on PLPs and CD41/CD42b on MEG-01 cells was inhibited by NEAT1 knockdown. In addition, NEAT1 knockdown inhibited cell apoptosis with increased Bcl2/Bax ratio and decreased cleaved caspase-3, and reduced the percentage of cells in the G0/G1 phase. Meanwhile, NEAT1 knockdown inhibited the expression of IL-8. A strong interaction of NEAT1 and SFPQ, a transcriptional repressor of IL-8, was identified. NEAT1 knockdown reduced the interaction between SFPQ and NEAT1.The results suggest that lncRNA NEAT1 knockdown decreases MEG-01 differentiation, PLP activity, and IL-8 level. The results also indicate that the regulation of NEAT1 on IL-8 may be realized via a direct interaction between NEAT1 and SFPQ.

DOP54 Integrated network analysis using patient-specific single-nucleotide polymorphism profiles uncovers new pathways involved in ulcerative colitis pathogenesis

Abstract Background Genome-wide association studies have deciphered the single nucleotide polymorphisms (SNPs) which are responsible for ulcerative colitis (UC) susceptibility. However, to understand how these SNPs are involved in UC, additional methods are necessary. One such approach is in silico network propagation modelling, which can discover how the effects of SNPs in UC can affect the whole cell. A complementary approach is weighted gene co-expression network analysis (WGCNA), where co-regulated genes are identified using transcriptomic data. Integrating these two methods can shed light on how SNPs are affecting the transcriptome of UC patients. Methods We used immunochip profiles of 941 UC patients and focussed on UC-associated SNPs altering regulatory regions. Based on these regions, we identified affected genes. To understand how their corresponding proteins rewire transcriptional regulation, we predicted the path between these proteins and relevant transcription factors (TF) using the OmniPath signalling network (http://omnipathdb.org). From the TFs, we propagated the signal further to target genes using TFlink (https://tflink.net) and GTRD (http://gtrd.biouml.org). To evaluate the predicted network propagation signal, we conducted WGCNA with transcriptomics data from 46 matching patients’ (GEO ID: GSE48959). To interpret the results, we used Gene Ontology Biological Process annotations of the target genes, and we compared the function and regulation of affected genes and the determined WGCNA modules. Results We found 9 predominant signalling pathways, some already known from other studies to be involved in UC pathogenesis, including NFkB signalling, chemokine signalling, Notch pathway, JAK/STAT signalling. Downstream of these pathways we identified potential key TFs regulate the UC phenotype, for example NFKB1, GATA3, GTF2I. The targets of these TFs were enriched in the WGCNA modules of the patients. The WGCNA modules and the transcriptionally affected genes had enriched processes including cell migration, TGF-β signalling, exocytosis, adaptive T- and B-cell-specific immune responses and tight junctions. We also found myogenetic development specific TFs affected transcriptionally such as MyoD, MEF2A, MEF2D. We are currently validating these results through patient-specific biopsies. Conclusion In silico methods bring us closer to understanding UC pathogenesis. Our results suggest that in a well-defined set of patients, weakened tight junctions and insufficient immune response can lead to dysfunctional epithelial barrier, resulting in poor wound healing in UC. We hope the developed workflow will provide novel diagnostic and therapeutic options in UC.

Multi-Objective Optimized Fuzzy Clustering for Detecting Cell Clusters from Single-Cell Expression Profiles.

Rapid advance in single-cell RNA sequencing (scRNA-seq) allows measurement of the expression of genes at single-cell resolution in complex disease or tissue. While many methods have been developed to detect cell clusters from the scRNA-seq data, this task currently remains a main challenge. We proposed a multi-objective optimization-based fuzzy clustering approach for detecting cell clusters from scRNA-seq data. First, we conducted initial filtering and SCnorm normalization. We considered various case studies by selecting different cluster numbers ( = 2 to a user-defined number), and applied fuzzy c-means clustering algorithm individually. From each case, we evaluated the scores of four cluster validity index measures, Partition Entropy (), Partition Coefficient (), Modified Partition Coefficient (), and Fuzzy Silhouette Index (). Next, we set the first measure as minimization objective (↓) and the remaining three as maximization objectives (↑), and then applied a multi-objective decision-making technique, TOPSIS, to identify the best optimal solution. The best optimal solution (case study) that had the highest TOPSIS score was selected as the final optimal clustering. Finally, we obtained differentially expressed genes (DEGs) using Limma through the comparison of expression of the samples between each resultant cluster and the remaining clusters. We applied our approach to a scRNA-seq dataset for the rare intestinal cell type in mice [GEO ID: GSE62270, 23,630 features (genes) and 288 cells]. The optimal cluster result (TOPSIS optimal score= 0.858) comprised two clusters, one with 115 cells and the other 91 cells. The evaluated scores of the four cluster validity indices, , , , and for the optimized fuzzy clustering were 0.482, 0.578, 0.607, and 0.215, respectively. The Limma analysis identified 1240 DEGs (cluster 1 vs. cluster 2). The top ten gene markers were Rps21, Slc5a1, Crip1, Rpl15, Rpl3, Rpl27a, Khk, Rps3a1, Aldob and Rps17. In this list, Khk (encoding ketohexokinase) is a novel marker for the rare intestinal cell type. In summary, this method is useful to detect cell clusters from scRNA-seq data.

О создании предварительной модели геоида на территорию Республики Кот д’Ивуар

О создании предварительной модели геоида на территорию Республики Кот д’Ивуар

Abstract 3131: Acute myeloid leukemia derived SDF1 repels tumor infiltrating lymphocytes in the bone marrow microenvironment

Abstract Introduction: Acute myeloid leukaemia (AML) is an age-related disease with a median age at diagnosis of 71. Combined with co-morbidities, survival of patients with AML above this age bracket is poor with 90% of older adults dying of their disease. Even in younger patients who achieve remission with chemotherapy, relapse is common and occurs from minimal residual disease sequestered in protective niches in the bone marrow microenvironment (BMM). AML as a disease is highly dependent on the bone marrow microenvironment and accordingly it is envisaged that improved outcomes will come from novel treatment strategies derived from an improved understanding of the biology of AML within the bone marrow and their interaction with the immune cells therein. Objective: Here, we investigate a possible immune evasive mechanism imparted by AML blasts attributed to their localization within the BMM. Methods and Results: Using RNA-seq data generated from bone marrow derived AML (BM-AML) compared to peripheral blood derived AML (PB-AML) (GEO ID: GSE49642, GSE48846) we identified SDF-1 as the most differentially expressed in favour of BM-AML. Further investigation using matched primary clinical samples (BM verses PB) by real-time PCR analysis and ELISA confirmed the in-silico findings. In addition, primary AML engrafted into NSG mice demonstrated high SDF-1 in the BM derived AML blasts compared to AML blasts derived from the spleen. Lentiviral knock-down of SDF-1 in the AML blasts impaired blast engraftment and prolonged survival of the animals. SDF1-mediated migration of T-cell subsets have been previously identified using varying concentrations of SDF1. We therefore, investigated the migration of CD8+ T cells when co-cultured with AML. We show that CD8+ T-cells migrate away from AML when in culture and this fugetaxis is reduced by the knock-down of SDF1 in the blasts. Conclusion: We conclude that SDF-1 is secreted by the AML blasts within the BMM contributing to fugetaxis of CD8+ cells away from the blasts. Implications of these finding suggest a possible immune evasive mechanism by the blasts that can be manipulated to potentiate CD8+ infiltration into the AML bone marrow. Citation Format: Manar S. Shafat, Amina A. Abdul-Aziz, Christopher Marlien, Rachel Piddock, Kristian M. Bowles, Stuart A. Rushworth. Acute myeloid leukemia derived SDF1 repels tumor infiltrating lymphocytes in the bone marrow microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3131.

Abstract 4327: Bone marrow adipocytes drive transcriptional changes in leukemic blasts to enhance their capacity to derive energy from free fatty acid metabolism

Abstract Introduction: Most patients diagnosed with acute myeloid leukaemia [AML] die of their disease and the average age of patients at diagnosis is 72 years. For this reason, new therapeutic strategies with tolerability in the fragile, less fit population is necessary for reducing the mortality rate associated with this disease. The tumor microenvironment is an emerging target in the search for less cytotoxic therapies. We have previously shown that the adipocyte component of the bone marrow (BM) is a key player in blast survival, proliferation and chemotherapy evasion. In this study, we draw focus onto the status of an adipocyte rich environment in the context of leukemia and highlight the key players in regulating leukemic cell metabolism through transport and metabolism of fatty acids. Objective: We hypothesize that the presence of adipocytes within the proximity of AML blasts creates a FA rich environment for increased β - oxidation within the blasts. Methods: We used primary AML blasts and normal CD34+ hematopoietic stem cells (HSC) following informed consent (LRCEref07/H0310/146). Adipocytes were derived from bone marrow stromal cells (BMSC). Differential expression analysis of RNA sequencing data (GEO ID: GSE49642, GSE48846) was used to compare respiratory gene signatures of BM AML blasts, peripheral blood obtained AML and normal CD34+ HSC. Fatty acid binding protein 4 (FABP4) and carnitine palmitoyltransferase 1A (CPT1A) were identified as one of the key genes involved in the lipolysis and oxidation signature differential expression. Oxygen consumption rate (OCR) of adipocyte co-cultured blasts and normal CD34+ were analyzed using Seahorse technology. Lentiviral-knockdown of FABP4 and CPT1A were performed on blasts prior to in vivo xenograft mouse model injection. Results: Leukemic blasts showed increased adipocyte lipolysis stimulation compared with normal CD34+ cells. Moreover, adipocytes increased transcriptional activation of FABP4 and CPT1A in malignant blasts compared to CD34+ HSC. FABP4 inhibitor reduced AML blast survival when cells were cultured with adipocytes which is in contrast to normal CD34+ HSC. Moreover, AML had increased oxygen consumption rate when grown on adipocytes which was inhibited by etomoxir (β - oxidation inhibitor). Finally in-vivo lentiviral mediated knockdown of FABP4 and CPT1A reveled an increased survival of AML xenografts. Conclusion: Our results show that the stimulation of lipolysis and fatty acid oxidative genes that contribute to the genetic signatures of these processes are a malignant blast exclusive profile. Interventions at a molecular level reveal survival favorable outcomes in xenograft models suggesting the need for enhancing strategies which include targeting the FABP4 and CPT1A axis. Our data provide a biologic rationale for exploring future therapies that target the adipocyte/AML interactions. Citation Format: Manar Shafat, Thomas Oellerich, Sebastian Mohr, Stephen Robinson, Dylan Edwards, Rachel Piddock, Amina Abdul-Aziz, Christopher Marlein, Matthew Fenech, Jeremy Turner, Matthew Lawes, Lyubov Zaitseva, Johnathan Watkins, Kristian Bowles, Stuart Rushworth. Bone marrow adipocytes drive transcriptional changes in leukemic blasts to enhance their capacity to derive energy from free fatty acid metabolism [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4327. doi:10.1158/1538-7445.AM2017-4327

KCNJ3 is a new independent prognostic marker for estrogen receptor positive breast cancer patients.

Numerous studies showed abnormal expression of ion channels in different cancer types. Amongst these, the potassium channel gene KCNJ3 (encoding for GIRK1 proteins) has been reported to be upregulated in tumors of patients with breast cancer and to correlate with positive lymph node status. We aimed to study KCNJ3 levels in different breast cancer subtypes using gene expression data from the TCGA, to validate our findings using RNA in situ hybridization in a validation cohort (GEO ID GSE17705), and to study the prognostic value of KCNJ3 using survival analysis. In a total of > 1000 breast cancer patients of two independent data sets we showed a) that KCNJ3 expression is upregulated in tumor tissue compared to corresponding normal tissue (p < 0.001), b) that KCNJ3 expression is associated with estrogen receptor (ER) positive tumors (p < 0.001), but that KCNJ3 expression is variable within this group, and c) that ER positive patients with high KCNJ3 levels have worse overall (p < 0.05) and disease free survival probabilities (p < 0.01), whereby KCNJ3 is an independent prognostic factor (p <0.05). In conclusion, our data suggest that patients with ER positive breast cancer might be stratified into high risk and low risk groups based on the KCNJ3 levels in the tumor.

Gene expression profiling of rice seedlings in response to glutamine treatment

Glutamine, the most abundant free amino acid in humans (Curi et al., 2007 [1]), has many functions. In addition to protein, amino acid, and nucleic acid biosynthesis, glutamine also regulates the expression of genes related to metabolism, cell defense, and signal transduction in humans (Curi et al., 2007 [1]; Brasse-Lagnel et al., 2009 [2]). Glutamine is also one of the major forms of nitrogen in rice (Fukumorita and Chino, 1982 [3]). In addition to metabolic and nutritional effects, glutamine may function as a signaling molecule to regulate gene expression in plants. To this end, we used microarray analysis to identify genes that are rapidly induced by 2.5 mM glutamine in rice roots. The results revealed that glutamine induced the expression of at least 35 genes involved in metabolism, transport, signal transduction, and stress responses within 30 min (Kan et al., 2015 [4]). Here, we provide the details of the experimental procedure associated with our microarray data deposited in NCBI's Gene Expression Omnibus (GEO ID: GSE56770).

Gene expression profiling of DBA/2J mice cochleae treated with l-methionine and valproic acid.

DBA/2J mice, which have homozygous mutations in Cdh23 and Fscn2, are characterized by early onset hearing loss at as early as three-weeks of age (Noben-Trauth et al., 2003 [1]) and are an animal model for progressive hearing loss research. Recently, it has been reported that epigenetic regulatory pathways likely play an important role in hearing loss (Provenzano and Domann, 2007 [2]; Mutai et al., 2009 [3]; Waldhaus et al., 2012 [4]). We previously reported that DBA/2J mice injected subcutaneously with a combination of epigenetic modifying reagents, l-methionine (MET) as methyl donor and valproic acid (VPA) as a pan-histone deacetylases (Hdac) inhibitor, showed a significant attenuation of progressive hearing loss by measuring their auditory brainstem response (ABR) thresholds (Mutai et al., 2015 [5]). Here we present genome wide expression profiling of the DBA/2J mice cochleae, with and without treatment of MET and VPA, to identify the genes involved in the reduction of progressive hearing loss. The raw and normalized data were deposited in NCBI's Gene Expression Omnibus (GEO ID: GSE62173) for ease of reproducibility and reanalysis.

Global transcriptional analysis of short-term hepatic stress responses in Atlantic salmon (Salmo salar) exposed to depleted uranium.

Potential environmental hazards of radionuclides are often studied at the individual level. Sufficient toxicogenomics data at the molecular/cellular level for understanding the effects and modes of toxic action (MoAs) of radionuclide is still lacking. The current article introduces transcriptomic data generated from a recent ecotoxicological study, with the aims to characterize the MoAs of a metallic radionuclide, deplete uranium (DU) in an ecologically and commercially important fish species, Atlantic salmon (Salmo salar). Salmon were exposed to three concentrations (0.25, 0.5 and 1.0 mg/L) of DU for 48 h. Short-term global transcriptional responses were studied using Agilent custom-designed high density 60,000-feature (60 k) salmonid oligonucleotide microarrays (oligoarray). The microarray datasets deposited at Gene Expression Omnibus (GEO ID: GSE58824) were associated with a recently published study by Song et al. (2014) in BMC Genomics. The authors describe the experimental data herein to build a platform for better understanding the toxic mechanisms and ecological hazard of radionuclides such as DU in fish.

Molecular fingerprinting of the podocyte reveals novel gene and protein regulatory networks

A thorough characterization of the transcriptome and proteome of endogenous podocytes has been hampered by low cell yields during isolation. Here we describe a double fluorescent reporter mouse model combined with an optimized bead perfusion protocol and efficient single cell dissociation to yield more than 500,000 podocytes per mouse allowing for global, unbiased downstream applications. Combining mRNA and miRNA transcriptional profiling with quantitative proteomic analyses revealed programs of highly specific gene regulation tightly controlling cytoskeleton, cell differentiation, endosomal transport, and peroxisome function in podocytes. Strikingly, the analyses further predict that these podocyte-specific gene regulatory networks are accompanied by alternative splicing of respective genes. Thus, our 'omics' approach will facilitate the discovery and integration of novel gene, protein, and organelle regulatory networks that deepen our systematic understanding of podocyte biology.

Abstract 10: High expression of GEM and EDNRA is associated with metastasis and poor outcome in patients with advanced bladder cancer.

Abstract At time of diagnosis 25% of all bladder cancers are muscle invasive and require cystectomy, radiotherapy, or chemotherapy. Metastasis is the principal event leading to death of individuals with cancer, and several attempts have been made to identify prognostic biomarkers for metastatic disease. The aim of this study was to compare gene-expression profiles from 10 primary bladder tumors with 12 matched lymph node metastases and eight primary tumors without metastasis to identify markers associated with metastatic disease. All 30 tumors were laser micro-dissected and mRNA expression was measured using Affymetrix U133 +2 GeneChips. MicroRNA expression was measured using TaqMan® MicroRNA Assays from Applied Biosystems. We compared our data to gene expression data from a previously published study with 69 primary bladder tumors to identify potential markers for metastasis (GEO ID: 200031684), and Gene Set Enrichment Analysis (GSEA) was used to test if previously published gene signatures were enriched in our data. We identified 12 genes significantly up-regulated at least two fold in primary tumors with metastasis compared to non-metastatic tumors in both patient cohorts. Of the 12 genes, GEM (GTP binding protein overexpressed in skeletal muscle), EDNRA (Endothelin receptor type A), and PXDN (peroxidasin homolog) were also significantly up regulated in the corresponding lymph node metastases. Validation at the protein level by immunohistochemistry using tissue microarrays containing 417 core biopsies from both primary tumors and lymph node metastasis showed that high expression of GEM (P = 0.032) and EDNRA (P = 0.037) were significantly associated with decreased cancer-specific survival. High EDRNA expression was significantly associated with decreased cancer-specific survival (P = 0.039) while GEM showed no significance (P = 0.15) in multivariate Cox regression analysis. Furthermore, 94% of the lymph nodes showed similar expression as in the primary tumors for EDNRA and 71% for GEM. PXDN expression was not significantly associated with outcome (P = 0.52). GSEA analysis showed that gene-sets involved in DNA double-strand repair was significantly enriched in tumors without metastasis (P = 0.002). Furthermore, a previously reported gene-set identified from comparison of metastases and primary tumors were significantly enriched in the primary tumors with metastasis (P = 0.03). In addition, we found 29 microRNAs to be down regulated in the lymph nodes compared to the primary tumors, and only one was up-regulated. Interestingly, miR-143 and miR-145 were both significantly down regulated in the lymph nodes. They are known to be down-regulated in bladder cancer, and this further down-regulation in the metastases supports the reported tumor suppressor function of these molecules. Additional studies are needed to validate the functions and clinical relevance of GEM and EDNRA. Citation Format: Jens R. Laurberg, Jørgen Jensen, Troels Schepeler, Michael Borre, Torben Ørntoft, Lars Dyrskjøt. High expression of GEM and EDNRA is associated with metastasis and poor outcome in patients with advanced bladder cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 10. doi:10.1158/1538-7445.AM2013-10 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.

The Fennoscandian Geoid Bulge and its Correlation with Land Uplift and Moho Depth

The Fennoscandian Geoid Bulge and its Correlation with Land Uplift and Moho Depth

Impacts of geoid height on large-scale crustal deformation mapping with InSAR observations

An ellipsoidal height datum (e.g. WGS84) is required in SAR Interferometric processing, whilst DEMs are often referenced to a geoid datum (e.g. EMG96). Therefore, geoid height error is introduced due to the inconsistency of height datums in InSAR derived displacement maps. In this paper, the relationship between geoid heights and uncertainties in InSAR displacements is investigated using 27 scenes of Envisat ASAR ScanSAR images and 44 scenes of Image-mode images covering the western Altyn Tagh Fault, northern Tibetan Plateau. A typical error of 8.8 m in SRTM DEM leads to 3mm uncertainty in an InSAR interferogram with a perpendicular baseline of 100m, whilst a geoid height of 20m can result in 10mm uncertainty. Geoid height ranges from one place to another, and are highly correlated with topography. The impacts of geoid height on InSAR displacements increase with perpendicular baselines, but SAR images with a small perpendicular baseline may not be available in some cases. In addition, it may also not always be feasible to use a best-fitting plane to remove the impacts of geoid height. It is thus highly recommended in this paper that DEMs with an ellipsoidal height datum should be employed in interferometric processing, particularly when long-wavelength crustal deformation is targeted.

Effects of germanium doping on the boron‐oxygen complex formation in silicon solar cells

AbstractThe light‐induced degradation (LID) due to the boron–oxygen (B–O) complexes is particularly harmful for solar cells made from the boron‐doped p ‐type Czochralski silicon (Cz‐Si). Many studies focused on this phenomenon and some processes have been proposed to reduce it. Recently, Cz‐Si voluntarily doped with germanium (Ge) was used to inhibit the effect of the B–O complexes activation. We studied here both conventional Cz‐Si (CZ) and Ge‐doped Cz‐Si (GCZ), and compared their sensitivity to the LID. The first result was that solar cells produced with GCZ had the same performances than solar cells made with CZ despite the impurities like iron unintentionally introduced in GCZ by the Ge powder. Then, we found that the degradation under illumination of the efficiency was lower in GCZ only for the solar cells produced from the last solidified part of the ingot (where the Ge content is the highest). These differences were correlated with the amount of interstitial oxygen (Oi) which was found to be lower for the GCZ wafer, possibly due to the formation of Ge–Oi related defects and/or to Ge‐enhanced oxygen precipitation effects. At the cell level, we also compared the kinetics of the LID in both materials and confirmed that the degradation was slower in GCZ. Finally, we showed that the mechanism of lightinduced regeneration (LIR) also occurs in GCZ solar cells, with similar kinetics with respect to conventional Cz‐Si cells (© 2012 WILEY‐VCH Verlag GmbH &amp; Co. KGaA, Weinheim)

Endothelialization and altered hematopoiesis by persistent Etv2 expression in mice

Etv2 is a master gene for the commitment of hematopoietic/endothelial cells and is a potent inducer of endothelial/hematopoietic cells from embryonic stem cells. Etv2 is highly expressed in endothelial/hematopoietic precursors but is downregulated when they are differentiated, indicating that Etv2 should have transient but not constitutive function. However, relatively little attention has been paid to the importance of transient Etv2 expression. To determine whether transient Etv2 expression is essential to normal development and cell differentiation, we generated mice that constitutively express Etv2 from a Cre-activatable ROSA26 locus in endothelial/hematopoietic, somite, or neuronal lineages. Constitutive Etv2 expression caused profound phenotypes in hematopoietic/endothelial cells, with little effect on somite or neuronal lineages. In hematopoietic/endothelial lineages, constitutive Etv2 expression induced by Tie-2 Cre transgene caused abnormal yolk sac vasculature. Prolonged vascular endothelial cadherin expression and decreased B lymphopoiesis were observed in Etv2 expressing vascular endothelial cadherin(+)/CD45(+) cells, indicating that Etv2 forces endothelial program on hematopoietic cells. Etv2 expression in adult hematopoietic cells by Vav-iCre transgene also conferred an endothelial phenotype on hematopoietic stem cells and suppressed hematopoiesis, with erythropoiesis severely affected. We conclude that constitutive Etv2 expression perturbs vascular development and hematopoiesis. While promoting hematopoiesis/vasculogenesis, Etv2 expression should be tightly regulated to achieve normal vascular development and hematopoiesis.