Skill Requirements for Entry-Level IS Graduates: A Report from Industry

Determining what skills employers of new IS graduates desire is important in guiding IS educators in designing curriculum and in advising students. This study reports the results of a pilot study which attempts to gain insight into the previously mentioned question. The findings indicate that basic technical skills, such as systems analysis and design, and database concepts, and non-technical skills, such as teamwork and communications skills, are more important than specific technical skills

Angiopoietin-1 Mimetic Peptide Promotes Neuroprotection after Stroke in Type 1 Diabetic Rats

Angiopoietin-1 (Ang1) mediates vascular maturation and immune response. Diabetes decreases Ang1 expression and disrupts Ang1/Tie2 signaling activity. Vasculotide is an Ang1 mimetic peptide, and has anti-inflammatory effects. In this study, we test the hypothesis that vasculotide treatment induces neuroprotection and decreases inflammation after stroke in type 1 diabetic (T1DM) rats. T1DM rats were subjected to embolic middle cerebral artery occlusion (MCAo) and treated with: 1) phosphate buffered saline (PBS); 2) vasculotide (3µg/kg, i.p. injection) administered half an hour prior to MCAo and at 8 and 24 hours after MCAo. Rats were sacrificed at 48 h after MCAo. Neurological function, infarct volume, hemorrhage, blood brain barrier (BBB) permeability and neuroinflammation were measured. Vasculotide treatment of T1DM-MCAo rats significantly improves functional outcome, decreases infarct volume and BBB permeability, but does not decrease brain hemorrhagic transformation compared with PBS-treated T1DM-MCAo rats. In the ischemic brain, Vasculotide treatment significantly decreases apoptosis, number of cleaved-caspase-3 positive cells, the expression of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor (TNF-α). Western blot analysis shows that vasculotide significantly decreases expression of receptor for advanced glycation end products (RAGE), MCP-1 and TNF-α in the ischemic brain compared with T1DM-MCAo rats. Vasculotide treatment in cultured primary cortical neurons (PCN) significantly decreases TLR4 expression compared with control. Decreased neuroinflammation and reduced BBB leakage may contribute, at least in part, to vasculotide-induced neuroprotective effects after stroke in T1DM rats

The effect of targeting Tie2 on hemorrhagic shock-induced renal perfusion disturbances in rats

Background: Hemorrhagic shock is associated with acute kidney injury and increased mortality. Targeting the endothelial angiopoietin/Tie2 system, which regulates endothelial permeability, previously reduced hemorrhagic shock-induced vascular leakage. We hypothesized that as a consequence of vascular leakage, renal perfusion and function is impaired and that activating Tie2 restores renal perfusion and function. Methods: Rats underwent 1 h of hemorrhagic shock and were treated with either vasculotide or PBS as control, followed by fluid resuscitation for 4 h. Microcirculatory perfusion was measured in the renal cortex and cremaster muscle using contrast echography and intravital microscopy, respectively. Changes in the angiopoietin/Tie2 system and renal injury markers were measured in plasma and on protein and mRNA level in renal tissue. Renal edema formation was determined by wet/dry weight ratios and renal structure by histological analysis. Results: Hemorrhagic shock significantly decreased renal perfusion (240 +/- 138 to 51 +/- 40, p 0.9 at all time points) or reduce renal injury (NGAL p = 0.26, KIM-1 p = 0.78, creatinine p > 0.9, renal edema p = 0.08), but temporarily improved cremaster perfusion at 3 h following start of fluid resuscitation compared to untreated rats (resuscitation + 3 h: 11 +/- 3 vs 8 +/- 3 perfused vessels, p < 0.05). Conclusion: Hemorrhagic shock-induced renal impairment cannot be restored by standard fluid resuscitation, nor by activation of Tie2. Future treatment strategies should focus on reducing angiopoietin-2 levels or on activating Tie2 via an alternative strategy

Automated generation of gene summaries at the Alliance of Genome Resources

Short paragraphs that describe gene function, referred to as gene summaries, are valued by users of biological knowledgebases for the ease with which they convey key aspects of gene function. Manual curation of gene summaries, while desirable, is difficult for knowledgebases to sustain. We developed an algorithm that uses curated, structured gene data at the Alliance of Genome Resources (Alliance; www.alliancegenome.org) to automatically generate gene summaries that simulate natural language. The gene data used for this purpose include curated associations (annotations) to ontology terms from the Gene Ontology, Disease Ontology, model organism knowledgebase (MOK)-specific anatomy ontologies and Alliance orthology data. The method uses sentence templates for each data category included in the gene summary in order to build a natural language sentence from the list of terms associated with each gene. To improve readability of the summaries when numerous gene annotations are present, we developed a new algorithm that traverses ontology graphs in order to group terms by their common ancestors. The algorithm optimizes the coverage of the initial set of terms and limits the length of the final summary, using measures of information content of each ontology term as a criterion for inclusion in the summary. The automated gene summaries are generated with each Alliance release, ensuring that they reflect current data at the Alliance. Our method effectively leverages category-specific curation efforts of the Alliance member databases to create modular, structured and standardized gene summaries for seven member species of the Alliance. These automatically generated gene summaries make cross-species gene function comparisons tenable and increase discoverability of potential models of human disease. In addition to being displayed on Alliance gene pages, these summaries are also included on several MOK gene pages

The synthetic Tie2 agonist peptide vasculotide protects against vascular leakage and reduces mortality in murine abdominal sepsis

Introduction: Angiopoietin-1 (Angpt1), the natural agonist ligand for the endothelial Tie2 receptor, is a non-redundant endothelial survival and vascular stabilization factor that reduces endothelial permeability and inhibits leukocyte-endothelium interactions. Here we evaluate the efficacy of a novel polyethylene glycol (PEG)-clustered Tie2 agonist peptide, vasculotide (VT), to protect against vascular leakage and mortality in a murine model of polymicrobial abdominal sepsis. Methods: Polymicrobial abdominal sepsis in C57BL6 mice was induced by cecal-ligation-and-puncture (CLP). Mice were treated with different dosages of VT or equal volume of phosphate-buffered saline (PBS). Sham-operated animals served as time-matched controls. Results: Systemic administration of VT induced long-lasting Tie2 activation in vivo. VT protected against sepsis-induced endothelial barrier dysfunction, as evidenced by attenuation of vascular leakage and leukocyte transmigration into the peritoneal cavity. Histological analysis revealed that VT treatment ameliorated leukocyte infiltration in kidneys of septic mice, probably due to reduced endothelial adhesion molecule expression. VT-driven effects were associated with significantly improved organ function and reduced circulating cytokine levels. The endothelial-specific action of VT was supported by additional in vitro studies showing no effect of VT on either cytokine release from isolated peritoneal macrophages, or migratory capacity of isolated neutrophils. Finally, administration of VT pre-CLP (hazard ratio 0.39 [95% confidence interval 0.19-0.81] P < 0.001) and post-CLP reduced mortality in septic mice (HR 0.22 [95% CI 0.06-0.83] P < 0.05). Conclusions: We provide proof of principle in support of the efficacious use of PEGylated VT, a drug-like Tie2 receptor agonist, to counteract microvascular endothelial barrier dysfunction and reduce mortality in a clinically relevant murine sepsis model. Further studies are needed to pave the road for clinical application of this therapeutic concept

Automated generation of gene summaries at the Alliance of Genome Resources.

Short paragraphs that describe gene function, referred to as gene summaries, are valued by users of biological knowledgebases for the ease with which they convey key aspects of gene function. Manual curation of gene summaries, while desirable, is difficult for knowledgebases to sustain. We developed an algorithm that uses curated, structured gene data at the Alliance of Genome Resources (Alliance; www.alliancegenome.org) to automatically generate gene summaries that simulate natural language. The gene data used for this purpose include curated associations (annotations) to ontology terms from the Gene Ontology, Disease Ontology, model organism knowledgebase (MOK)-specific anatomy ontologies and Alliance orthology data. The method uses sentence templates for each data category included in the gene summary in order to build a natural language sentence from the list of terms associated with each gene. To improve readability of the summaries when numerous gene annotations are present, we developed a new algorithm that traverses ontology graphs in order to group terms by their common ancestors. The algorithm optimizes the coverage of the initial set of terms and limits the length of the final summary, using measures of information content of each ontology term as a criterion for inclusion in the summary. The automated gene summaries are generated with each Alliance release, ensuring that they reflect current data at the Alliance. Our method effectively leverages category-specific curation efforts of the Alliance member databases to create modular, structured and standardized gene summaries for seven member species of the Alliance. These automatically generated gene summaries make cross-species gene function comparisons tenable and increase discoverability of potential models of human disease. In addition to being displayed on Alliance gene pages, these summaries are also included on several MOK gene pages