Mild traumatic brain injury (mTBI) is a common occurrence, with over 3 million cases reported every year in the United States. While research into the underlying pathophysiology is ongoing, there is an urgent need for better clinical guidelines that allow more consistent diagnosis of mTBI and ensure safe return-to-play timelines for athletes, nonathletes, and military personnel. The development of a suite of biomarkers that indicate the pathogenicity of mTBI could lead to clinically useful tools for establishing both diagnosis and prognosis. Here, we review the current evidence for mTBI biomarkers derived from investigations of the multifactorial pathology of mTBI. While the current literature lacks the scope and size for clarification of these biomarkers’ clinical utility, early studies have identified some promising candidates.

Despite a growing interest in multi-omic research, individual investigators may struggle to collect large-scale omic data, particularly from human subjects. Publicly available datasets can help to address this problem, including those sponsored by the NIH Common Fund, such as the Genotype-Tissue Expression (GTEx) database. This database contains genotype and expression data obtained from 54 non-diseased tissues in human subjects. But these data are often underutilized, because users may find the browsing tools to be counterintuitive or have difficulty navigating the procedures to request controlled data access. Furthermore, there is limited knowledge of these resources among nurse scientists interested in incorporating such information into their programs of research. This article outlines the procedures for using the GTEx database. Next, we provide one exemplar of using this resource to enhance existing research by investigating expression of dopamine receptor type 2 (DRD2) across brain tissues in human subjects.

The aim of this study was to investigate the association of gene expression profiles in subcutaneous adipose tissue with weight change in kidney transplant recipients and to gain insights into the underlying mechanisms of weight gain. A secondary data analysis was done on a subgroup (n = 26) of existing clinical and gene expression data from a larger prospective longitudinal study examining factors contributing to weight gain in transplant recipients. Measurements taken included adipose tissue gene expression profiles at time of transplant, baseline and six-month weight, and demographic data. Using multivariate linear regression analysis controlled for race and gender, expression levels of 1553 genes were significantly (p<0.05) associated with weight change. Functional analysis using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes classifications identified metabolic pathways that were enriched in this dataset. Furthermore, GeneIndexer literature mining analysis identified a subset of genes that are highly associated with obesity in the literature and Ingenuity pathway analysis revealed several significant gene networks associated with metabolism and endocrine function. Polymorphisms in several of these genes have previously been linked to obesity. We have successfully identified a set of molecular pathways that taken together may provide insights into the mechanisms of weight gain in kidney transplant recipients. Future work will be done to determine how these pathways may contribute to weight gain.

Stroke remains the fifth leading cause of mortality in the United States with an annual rate of over 128,000 deaths per year. Differences in incidence, pathogenesis, and clinical outcome have long been noted when comparing ischemic stroke among different ethnicities. The observation that racial disparities exist in clinical outcomes after stroke has resulted in genetic studies focusing on specific polymorphisms. Some studies have focused on matrix metalloproteinases (MMPs). MMPs are a ubiquitous group of proteins with extensive roles that include extracellular matrix remodeling and blood-brain barrier disruption. MMPs play an important role in ischemic stroke pathophysiology and clinical outcome. This review will evaluate the evidence for associations between polymorphisms in MMP-1, 2, 3, 9, and 12 with ischemic stroke incidence, pathophysiology, and clinical outcome. The role of polymorphisms in MMP genes may influence the presentation of ischemic stroke and be influenced by racial and ethnic background. However, contradictory evidence for the role of MMP polymorphisms does exist in the literature, and further studies will be necessary to consolidate our understanding of these multi-faceted proteins.