Towards Reducing Health Information Inequities in the Caribbean: The Eastern Caribbean Health Outcomes Research Network Data Sharing Platform Usability Study.

There is a dearth of health research among Caribbean populations. Underrepresented individuals are affected by structural and data inequities that limit the usefulness, availability, and accessibility to health information systems and research-generated data. To overcome this limitation, a data sharing platform was created for the Eastern Caribbean Health Outcomes Research Network Cohort Study. This study aimed to evaluate the usability of the platform. Usability testing was conducted remotely, via video conferencing, using a cognitive walkthrough and think-aloud protocol. Participants completed a self-administered web-based survey which included an adapted version of the System Usability Scale (SUS). The results showed (N=16) overall average SUS score was 73.1 (SD±21.0), translating to a 'good' usability rating. Most recommendations for improvement focused on navigation and error prevention. Participatory data sharing platforms have the potential to reduce health information inequities in the Caribbean, however, usability testing should be conducted to improve user satisfaction and increase engagement.

Metabolic alterations in lung cancer-associated fibroblasts correlated with increased glycolytic metabolism of the tumor.

Cancer cells undergo a metabolic reprogramming but little is known about metabolic alterations of other cells within tumors. We use mass spectrometry-based profiling and a metabolic pathway-based systems analysis to compare 21 primary human lung cancer-associated fibroblast lines (CAF) to "normal" fibroblast lines (NF) generated from adjacent nonneoplastic lung tissue. CAFs are protumorigenic, although the mechanisms by which CAFs support tumors have not been elucidated. We have identified several pathways whose metabolite abundance globally distinguished CAFs from NFs, suggesting that metabolic alterations are not limited to cancer cells. In addition, we found metabolic differences between CAFs from high and low glycolytic tumors that might reflect distinct roles of CAFs related to the tumor's glycolytic capacity. One such change was an increase of dipeptides in CAFs. Dipeptides primarily arise from the breakdown of proteins. We found in CAFs an increase in basal macroautophagy which likely accounts for the increase in dipeptides. Furthermore, we show a difference between CAFs and NFs in the induction of autophagy promoted by reduced glucose. In sum, our data suggest that increased autophagy may account for metabolic differences between CAFs and NFs and may play additional as yet undetermined roles in lung cancer.

Aging-associated changes in cardiac gene expression.

Cardiovascular diseases (e.g., vascular diseases, strokes, heart failure) reach epidemic proportions in the elderly and are the primary limits to survival in man. Age-associated changes in heart structure and function represent the major risk factors in heart failure (HF) syndromes and are associated with altered patterns of gene expression that can generally be seen as relative changes in the abundance of gene transcripts. An understanding of the molecular mechanisms underlying these changes should be tantamount to defining a genetic basis for aging; however, the analysis of processes as complicated as aging requires an accounting of biological diversity. Until recently, most of the changes in transcript abundance were identified one at a time, but the advent of gene expression arrays has permitted rapid, large-scale expression profiling. This has provided information about the dynamics of total gene expression, which can be used to identify pathways and elucidate regulatory events that may be affected during senescence or in response to disease. Importantly, very large sample sizes or meta-analyses of studies of smaller sample sizes should be sufficient to account for the diversity of altered gene expression that directs alterations in specific molecular pathways, which underlie changes in cardiac structure and function in senescence and disease.