Where There Is No History: How to Create Trust and Connection in Learning for Transformation in Water Governance

Trust is often seen as an important element in settings of knowledge sharing and the co-creation of knowledge for dealing with transformations in water governance. However, seemingly similar conversations during a co-creation workshop in Uppsala resulted in both trust and distrust, and thereby influenced consequent possibilities for the co-creation of knowledge. Therefore, this article focuses on how trust influences knowledge sharing and how knowledge sharing influences trust. We use a case study approach to analyze the Uppsala co-creation workshop — part of the Climate Change Adaptation and Water Governance (CADWAGO) project — by comparing 25 conversations, making use of theories on swift trust and trust dynamics. We found four different conversation patterns (1) sending; (2) defending; (3) misunderstanding; and (4) connecting. The first three patterns influenced trust negatively and did not lead to knowledge sharing, whereas pattern four showed trust development and co-creation of knowledge. From our comparative analyses, we conclude that trust starts to emerge when there is mutual openness and empathy visible in turn-taking patterns. More specifically, trust emerges when communication styles allow for recognition and exploring underlying needs and wishes, resulting in a more dynamic dialogue, further trust development, and connection between actors. Our list of conversation patterns is provisional but we argue that understanding how different kinds of interactions can lead to trust or distrust is crucial to understanding why and how learning takes place—insights that are essential for fostering learning and transformations in water governance

Ecological and socioeconomic impacts of invasive alien species in island ecosystems

Minimizing the impact of invasive alien species (IAS) on islands and elsewhere requires researchers to provide cogent information on the environmental and socioeconomic consequences of IAS to the public and policy makers. Unfortunately, this information has not been readily available owing to a paucity of scientific research and the failure of the scientific community to make their findings readily available to decision makers. This review explores the vulnerability of islands to biological invasion, reports on environmental and socioeconomic impacts of IAS on islands and provides guidance and information on technical resources that can help minimize the effects of IAS in island ecosystems. This assessment is intended to provide a holistic perspective on island-IAS dynamics, enable biologists and social scientists to identify information gaps that warrant further research and serve as a primer for policy makers seeking to minimize the impact of IAS on island systems. Case studies have been selected to reflect the most scientifically-reliable information on the impacts of IAS on islands. Sufficient evidence has emerged to conclude that IAS are the most significant drivers of population declines and species extinctions in island ecosystems worldwide. Clearly, IAS can also have significant socioeconomic impacts directly (for example human health) and indirectly through their effects on ecosystem goods and services.These impacts are manifest at all ecological levels and affect the poorest, as well as richest, island nations. The measures needed to prevent and minimize the impacts of IAS on island ecosystems are generally known. However, many island nations and territories lack the scientific and technical information, infrastructure and human and financial resources necessary to adequately address the problems caused by IAS. Because every nation is an exporter and importer of goods and services, every nation is also a facilitator and victim of the invasion of alien species.Wealthy nations therefore need to help raise the capacity of island nations and territories to minimize the spread and impact of IAS

Annotation and query of tissue microarray data using the NCI Thesaurus

<p>Abstract</p> <p>Background</p> <p>The Stanford Tissue Microarray Database (TMAD) is a repository of data serving a consortium of pathologists and biomedical researchers. The tissue samples in TMAD are annotated with multiple free-text fields, specifying the pathological diagnoses for each sample. These text annotations are not structured according to any ontology, making future integration of this resource with other biological and clinical data difficult.</p> <p>Results</p> <p>We developed methods to map these annotations to the NCI thesaurus. Using the NCI-T we can effectively represent annotations for about 86% of the samples. We demonstrate how this mapping enables ontology driven integration and querying of tissue microarray data. We have deployed the mapping and ontology driven querying tools at the TMAD site for general use.</p> <p>Conclusion</p> <p>We have demonstrated that we can effectively map the diagnosis-related terms describing a sample in TMAD to the NCI-T. The NCI thesaurus terms have a wide coverage and provide terms for about 86% of the samples. In our opinion the NCI thesaurus can facilitate integration of this resource with other biological data.</p

In-Situ Characterization of Dynamic Morphological and Phase Changes of Selenium-doped Germanium Using a Single Particle Cell and Synchrotron Transmission X-ray Microscopy

The dynamic information of lithium-ion battery active materials obtained from coin cell-based in-situ characterizations might not represent the properties of the active material itself because many other factors in the cell could have impacts on the cell performance. To address this problem, a single particle cell was developed to perform the in-situ characterization without the interference of inactive materials in the battery electrode as well as the X-ray-induced damage. In this study, the dynamic morphological and phase changes of selenium-doped germanium (Ge0.9Se0.1) at the single particle level were investigated via synchrotron-based in-situ transmission X-ray microscopy. The results demonstrate the good reversibility of Ge0.9Se0.1 at high cycling rate that helps understand its good cycling performance and rate capability. This in-situ and operando technique based on a single particle battery cell provides an approach to understanding the dynamic electrochemical processes of battery materials during charging and discharging at the particle level

Multiple Tumor Suppressor Pathways Negatively Regulate Telomerase

AbstractTelomerase expression is repressed in most somatic cells but is observed in stem cells and a high percentage of human cancers and has been hypothesized to contribute to tumorigenesis and maintenance of stem cell states. To explore telomerase regulation, we employed a general genetic screen to identify negative regulators of hTERT. We discovered three tumor suppressor/oncogene pathways involved in hTERT repression. One, the Mad1/c-Myc pathway, had been previously implicated in hTERT regulation. The second, SIP1, a transcriptional target of the TGF-β pathway, mediates the TGF-β regulated repression of hTERT. The third, the tumor suppressor Menin, is a direct repressor of hTERT. Depleting Menin immortalizes primary human fibroblasts and causes a transformation phenotype when coupled with expression of SV40 Large and Small T antigen and oncogenic ras. These studies suggest that multiple tumor suppressor/oncogene pathways coordinately repress hTERT expression and imply that telomerase is reactivated in human tumors through oncogenic mutations

Determination of Molecular Structures of HIV Envelope Glycoproteins using Cryo-Electron Tomography and Automated Sub-tomogram Averaging

Since its discovery nearly 30 years ago, more than 60 million people have been infected with the human immunodeficiency virus (HIV) (www.usaid.gov). The virus infects and destroys CD4+ T-cells thereby crippling the immune system, and causing an acquired immunodeficiency syndrome (AIDS) 2. Infection begins when the HIV Envelope glycoprotein "spike" makes contact with the CD4 receptor on the surface of the CD4+ T-cell. This interaction induces a conformational change in the spike, which promotes interaction with a second cell surface co-receptor 5,9. The significance of these protein interactions in the HIV infection pathway makes them of profound importance in fundamental HIV research, and in the pursuit of an HIV vaccine

Oncogenic Transformation by Inhibitor-Sensitive and -Resistant EGFR Mutants

BACKGROUND: Somatic mutations in the kinase domain of the epidermal growth factor receptor tyrosine kinase gene EGFR are common in lung adenocarcinoma. The presence of mutations correlates with tumor sensitivity to the EGFR inhibitors erlotinib and gefitinib, but the transforming potential of specific mutations and their relationship to drug sensitivity have not been described. METHODS AND FINDINGS: Here, we demonstrate that EGFR active site mutants are oncogenic. Mutant EGFR can transform both fibroblasts and lung epithelial cells in the absence of exogenous epidermal growth factor, as evidenced by anchorage-independent growth, focus formation, and tumor formation in immunocompromised mice. Transformation is associated with constitutive autophosphorylation of EGFR, Shc phosphorylation, and STAT pathway activation. Whereas transformation by most EGFR mutants confers on cells sensitivity to erlotinib and gefitinib, transformation by an exon 20 insertion makes cells resistant to these inhibitors but more sensitive to the irreversible inhibitor CL-387,785. CONCLUSION: Oncogenic transformation of cells by different EGFR mutants causes differential sensitivity to gefitinib and erlotinib. Treatment of lung cancers harboring EGFR exon 20 insertions may therefore require the development of alternative kinase inhibition strategies

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts