Transition to self-management among emerging adults with type 1 diabetes: a mixed methods study.

Introduction: Emerging adulthood is challenging for young people with type 1 diabetes (T1D). This study evaluated transition to diabetes self-management and perceptions of care transfer using mixed methods. Methods: An online survey queried demographics, management characteristics, diabetes knowledge, self-care readiness, adherence, and diabetes distress. T-tests compared survey scores between those with self-reported target A1c <7.0% versus ≥7.0%. Pearson correlations assessed associations between A1c and diabetes distress, stratified by A1c <7.0% versus ≥7.0%. Qualitative semi-structured interviews elicited perceptions of young adults; transcripts were analyzed using directed qualitative content analysis. Results: Of 141 participants (30% male, 84% non-Hispanic white) completing the survey, 41% self-reported target A1c <7.0%. Diabetes knowledge and self-care readiness scores did not differ between those with A1c <7.0% versus ≥7.0%, while diabetes distress was lower (45 ± 20 vs 52 ± 20, p=0.01) and adherence higher (77 ± 12 vs 71 ± 14, p=0.02) in those with A1c <7.0% versus ≥7.0%. Diabetes distress was significantly associated with glycemic outcomes in those reporting A1c ≥7.0% (R=0.36, p<0.01). Qualitative analysis (24 participants) revealed five themes and two sub-themes, notable for need for more mental health support, support from others with T1D, benefits of technology for care autonomy, and challenges of obtaining diabetes supplies. Discussion: Emerging adults with self-reported target A1c endorsed lower diabetes distress and higher adherence than those with elevated A1c. Mental health access, support from others with T1D, technology use, and guidance for supply acquisition may improve transition to self-management and care transfer for emerging adults with T1D.

Disruption in A-to-I Editing Levels Affects C. elegans Development More Than a Complete Lack of Editing.

A-to-I RNA editing, catalyzed by ADAR proteins, is widespread in eukaryotic transcriptomes. Studies showed that, in C. elegans, ADR-2 can actively deaminate dsRNA, whereas ADR-1 cannot. Therefore, we set out to study the effect of each of the ADAR genes on the RNA editing process. We performed comprehensive phenotypic, transcriptomics, proteomics, and RNA binding screens on worms mutated in a single ADAR gene. We found that ADR-1 mutants exhibit more-severe phenotypes than ADR-2, and some of them are a result of non-editing functions of ADR-1. We also show that ADR-1 significantly binds edited genes and regulates mRNA expression, whereas the effect on protein levels is minor. In addition, ADR-1 primarily promotes editing by ADR-2 at the L4 stage of development. Our results suggest that ADR-1 has a significant role in the RNA editing process and in altering editing levels that affect RNA expression; loss of ADR-1 results in severe phenotypes.

In cancer, A-to-I RNA editing can be the driver, the passenger, or the mechanic.

In recent years, A-to-I RNA modifications performed by the Adenosine Deaminase Acting on RNA (ADAR) protein family were found to be expressed at altered levels in multiple human malignancies. A-to-I RNA editing changes adenosine to inosine on double stranded RNA, thereby changing transcript sequence and structure. Although A-to-I RNA editing have the potential to change essential mRNA transcripts, affecting their corresponding protein structures, most of the human editing sites identified to date reside in non-coding repetitive transcripts such as Alu elements. Therefore, the impact of the hypo- or hyper-editing found in specific cancers remains unknown. Moreover, it is yet unclear whether or not changes in RNA editing and ADAR expression levels facilitate or even drive cancer progression or are just a byproduct of other affected pathways. In both cases, however, the levels of RNA editing and ADAR enzymes can possibly be used as specific biomarkers, as their levels change differently in specific malignancies. More significantly, recent studies suggest that ADAR enzymes can be used to reverse the oncogenic process, suggesting a potential for gene therapies. This review focuses on new findings that suggest that RNA editing by ADARs can affect cancer progression and even formation. We also discuss new possibilities of using ADAR enzymes and RNA editing as cancer biomarkers, indicators of chemotherapeutic drug sensitivity, and even to be themselves potential therapeutic tools.