SLADE: A smart large-scale task decomposer in crowdsourcing

ISSN:1041-4347ISSN:1558-219

THINK Back: KNowledge-based Interpretation of High Throughput data

Results of high throughput experiments can be challenging to interpret. Current approaches have relied on bulk processing the set of expression levels, in conjunction with easily obtained external evidence, such as co-occurrence. While such techniques can be used to reason probabilistically, they are not designed to shed light on what any individual gene, or a network of genes acting together, may be doing. Our belief is that today we have the information extraction ability and the computational power to perform more sophisticated analyses that consider the individual situation of each gene. The use of such techniques should lead to qualitatively superior results

Simplifying access to a clinical data repository using schema summarization

(CDR) integrates over 25 data sources, and as a result has a schema that is too complex to be directly queried by clinical researchers. Schema summarization uses abstract elements and links to summarize a complex schema and allows users with limited knowledge of the underlying database structure to effectively issue queries to the CDR for clinical and translational research. BACKGROUND Our institution developed a Clinical Data Repository (CDR) in 1998 that now integrates information from over 25 data sources distributed across the Health System. The CDR schema contains over 650 tables and nearly 2200 distinct attributes, and is constantly evolving. Unfortunately, issuing even basic querie

Gene expression profiles of diabetic kidney disease and neuropathy in eNOS knockout mice: Predictors of pathology and RAS blockade effects

Diabetic kidney disease (DKD) and diabetic peripheral neuropathy (DPN) are two common diabetic complications. However, their pathogenesis remains elusive and current therapies are only modestly effective. We evaluated genome‐wide expression to identify pathways involved in DKD and DPN progression in db/db eNOS−/− mice receiving renin‐angiotensin‐aldosterone system (RAS)‐blocking drugs to mimic the current standard of care for DKD patients. Diabetes and eNOS deletion worsened DKD, which improved with RAS treatment. Diabetes also induced DPN, which was not affected by eNOS deletion or RAS blockade. Given the multiple factors affecting DKD and the graded differences in disease severity across mouse groups, an automatic data analysis method, SOM, or self‐organizing map was used to elucidate glomerular transcriptional changes associated with DKD, whereas pairwise bioinformatic analysis was used for DPN. These analyses revealed that enhanced gene expression in several pro‐inflammatory networks and reduced expression of development genes correlated with worsening DKD. Although RAS treatment ameliorated the nephropathy phenotype, it did not alter the more abnormal gene expression changes in kidney. Moreover, RAS exacerbated expression of genes related to inflammation and oxidant generation in peripheral nerves. The graded increase in inflammatory gene expression and decrease in development gene expression with DKD progression underline the potentially important role of these pathways in DKD pathogenesis. Since RAS blockers worsened this gene expression pattern in both DKD and DPN, it may partly explain the inadequate therapeutic efficacy of such blockers.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/167018/1/fsb221467_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/167018/2/fsb221467.pd