Farzana Kazi

GeneMANIA (http://www.genemania.org) is a flexible, user-friendly web interface for generating hypotheses about gene function, analyzing gene lists and prioritizing genes for functional assays. Given a query list, GeneMANIA extends the list with functionally similar genes that it identifies using available genomics and proteomics data. GeneMANIA also reports weights that indicate the predictive value of each selected data set for the query. Six organisms are currently supported (Arabidopsis thaliana, Caenorhabditis elegans, Drosophila melanogaster, Mus musculus, Homo sapiens and Saccharomyces cerevisiae) and hundreds of data sets have been collected from GEO, BioGRID, Pathway Commons and I2D, as well as organism-specific functional genomics data sets. Users can select arbitrary subsets of the data sets associated with an organism to perform their analyses and can upload their own data sets to analyze. The GeneMANIA algorithm performs as well or better than other gene function prediction methods on yeast and mouse benchmarks. The high accuracy of the GeneMANIA prediction algorithm, an intuitive user interface and large database make GeneMANIA a useful tool for any biologist.

Abstract Summary: Cytoscape Web is a web-based network visualization tool–modeled after Cytoscape–which is open source, interactive, customizable and easily integrated into web sites. Multiple file exchange formats can be used to load data into Cytoscape Web, including GraphML, XGMML and SIF. Availability and Implementation: Cytoscape Web is implemented in Flex/ActionScript with a JavaScript API and is freely available at http://cytoscapeweb.cytoscape.org/ Contact: gary.bader@utoronto.ca Supplementary information: Supplementary data are available at Bioinformatics online.

UNLABELLED: The GeneMANIA Cytoscape plugin brings fast gene function prediction capabilities to the desktop. GeneMANIA identifies the most related genes to a query gene set using a guilt-by-association approach. The plugin uses over 800 networks from six organisms and each related gene is traceable to the source network used to make the prediction. Users may add their own interaction networks and expression profile data to complement or override the default data. AVAILABILITY AND IMPLEMENTATION: The GeneMANIA Cytoscape plugin is implemented in Java and is freely available at http://www.genemania.org/plugin/.

A common end-stage consequence of long-term chronic liver illnesses, liver cirrhosis is characterised by severe distortion of normal liver architecture and widespread hepatic fibrosis, which leads to the development of structurally unusual regenerating nodules. The majority of cirrhosis-related problems are caused by portal hypertension (PH), one of the first and most clinically severe effects of the disease. PH is mostly brought on by an increase in portal and hepatic arterial blood flow, as well as increased intrahepatic vascular resistance brought on by fibrotic remodelling and angio-architectural alterations inside the liver. After this stage, which denotes the change from compensated to decompensated cirrhosis, extra-hepatic variables become increasingly important in the development of portal hypertension. Over the past 20 years, there have been major improvements in the treatment of cirrhosis-related comorbidities, and as a result, HCC has become one of the main causes of death for cirrhosis patients. The reversibility of established cirrhosis is still unknown, despite the fact that fibrosis regression is well documented in pre-cirrhotic phases. As a result, the main goals of antifibrotic treatments should be to lower fibrosis, improve portal hypertension, and stop HCC from developing.

A common end-stage consequence of long-term chronic liver illnesses, liver cirrhosis is characterised by severe distortion of normal liver architecture and widespread hepatic fibrosis, which leads to the development of structurally unusual regenerating nodules. The majority of cirrhosis-related problems are caused by portal hypertension (PH), one of the first and most clinically severe effects of the disease. PH is mostly brought on by an increase in portal and hepatic arterial blood flow, as well as increased intrahepatic vascular resistance brought on by fibrotic remodelling and angio-architectural alterations inside the liver. After this stage, which denotes the change from compensated to decompensated cirrhosis, extra-hepatic variables become increasingly important in the development of portal hypertension. Over the past 20 years, there have been major improvements in the treatment of cirrhosis-related comorbidities, and as a result, HCC has become one of the main causes of death for cirrhosis patients. The reversibility of established cirrhosis is still unknown, despite the fact that fibrosis regression is well documented in pre-cirrhotic phases. As a result, the main goals of antifibrotic treatments should be to lower fibrosis, improve portal hypertension, and stop HCC from developing.