<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Nichols, Emma Hitt</style></author></authors><secondary-authors><author><style face="normal" font="default" size="100%">Kathiresan, Sekar</style></author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Mendelian Randomization as a Promising Approach to Define Which Biomarkers are Causal for Myocardial Infarction</style></title><secondary-title><style face="normal" font="default" size="100%">MD Conference Express</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013-08-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">6-8</style></pages><abstract><style  face="normal" font="default" size="100%">Biomarkers are important diagnostic tools that help physicians determine a patient's risk for developing a disease and can guide clinical decisions. However, at times, it is critical to understand if a specific biomarker causes disease or is merely reflective of the disease process. This distinction is important mainly if the biomarker is intended to be a therapeutic target (ie, lowering a biomarker with a drug with the hopes of lowering risk for disease). In humans, randomized controlled clinical trials and human genetics are two approaches to understand causal factors. This article discusses a human genetics approach—Mendelian randomization—to distinguish causal from noncausal biomarkers.</style></abstract><number><style face="normal" font="default" size="100%">13</style></number><volume><style face="normal" font="default" size="100%">13</style></volume></record></records></xml>