The current state of clinical trials underscores a need for timely interventions to reduce the cost and length of the average trial. Newly developed health informatics technologies-including electronic health records, telemedicine systems, and mobile health applications-have recently been employed in a wide range of clinical trials in an effort to improve different aspects of the clinical trial process. The current review will focus on the observed benefits and drawbacks of using such technology to improve various patient-centered aspects of the clinical trial process, namely its potential to improve patient recruitment, patient retention, and data collection. Broad future challenges and opportunities in the field as a whole will also be covered.
Objective: Many current Diabetes treatments cause broad-based immunodeficiency, though future organspecific therapies may be developed by exploiting genotypic differences found in regulatory T cell (Treg) subpopulations. This study goaled to determine genes preferentially expressed in pancreatic Tregs relative to other Treg subpopulations, tissues, and immune cells to serve as targets in Diabetes therapy.Methods: Multi-step microarray analysis using GenePattern Software identified genes specific to pancreatic Tregs relative to Tregs in other tissues and to other immune-cell populations. Functional analysis of identified genes was performed using BioGrid and String Databases. Microarray datasets (n=2236) curated from the NCBI GEO database were processed (via RMA normalization, outlier-array exclusion, and global median transformation) to confirm the specificity of these genes to the pancreas, while further microarray comparisons (in R programming language via Mas-5 normalization, log2 transformation, and "trimmed mean" algorithm) were performed to confirm the link of the identified genes to diabetes pathogenesis. Results:Initial microarray analysis identified genes specific to pancreatic Tregs, with the top three genes (Clps, Pnliprp1, and Pla2g1b) expressed at values 23x, 12x, and 7x higher in pancreatic Tregs than in other Treg subpopulations (p<0.05). Further analysis revealed that the pancreatic gene expression of the identified genes was almost triple that of other tissues (n=29), while comparisons among other immune-cell types indicated that these genes were expressed 32x, 12.8x, and 7.5x higher, respectively, in pancreatic Tregs than in other immune cell-types, eliminating the possibility of augmenting the autoimmune response in future treatments. Diabetic vs. nondiabetic microarray analysis confirmed the link of these genes to Type 1, but not Type 2, Diabetes.Conclusions: Future Diabetes therapies should target these genes to solely regulate pancreatic Treg levels, avoiding the broad-based immunosuppression caused by current therapies. However, gene knockout studies should be performed to further validate the functionality of the identified genes.
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