OBJECTIVEWe conducted comprehensive assessments of emotional distress to examine relations with diabetes medication adherence over time.RESEARCH DESIGN AND METHODSEthnically and socioeconomically diverse adults treated for type 2 diabetes completed validated self-reports (SRs) for diabetes distress and depression, were administered semistructured depression interviews, and provided blood samples for A1C. Medication adherence among 104 participants was electronically monitored (EM) over the subsequent 3 months; validated SRs of medication adherence were also obtained. Hierarchical linear regression evaluated independent effects of diabetes distress and depression on adherence.RESULTSMean ± SD 3-month medication adherence was 76.1% ± 25.7% for EM and 83.7% ± 21.9% for SR. Higher levels of SR (P < 0.001) and interview-based (P < 0.05) depressive symptom severity (P < 0.05) and diabetes-related distress (P < 0.01) showed a significant bivariate association with EM and SR nonadherence. Regression models showed baseline diabetes distress was a significant independent predictor of EM (β = −0.29; P = 0.001) and SR adherence (β = −0.24; P < 0.02) at follow-up. SR depression was an independent predictor of EM and SR adherence and reduced the effects of diabetes distress to nonsignificance. Subsequent models indicated this effect was driven by somatic rather than cognitive-affective symptoms of depression. Results were consistent but weaker for interview-based depressive symptoms.CONCLUSIONSFindings support diabetes-related distress and depression symptom severity as risk factors for type 2 diabetes medication nonadherence. Somatic symptoms captured by depression measures, but not cognitive-affective symptoms, independently predict nonadherence and should be further investigated as a potential link between emotional distress and nonadherence.
Aims To explore diabetes distress in a sample of adults with type 2 diabetes, treated and not treated with insulin. Methods Six focus groups were conducted with 32 adults with type 2 diabetes, divided by treatment regimen (insulin-treated N=15; 67% female; 60% black; 46% Hispanic; M age 54; M HbA1c 73 mmol/mol (8.8%); non-insulin-treated N=17; 53% female; 65% black; 13% Hispanic; M age 58; M HbA1c 55 mmol/mol (7.2%)). A coding team transcribed and analyzed interviews to describe themes. Themes were then compared between groups and with existing diabetes distress measures. Results Participants in both groups described a range of sources of diabetes distress, including lack of support/understanding from others, difficulties communicating with providers, and distress from the burden of lifestyle changes. Insulin-treated participants described significant emotional distress related to the burden of their insulin regimen. They were more likely to report physical burden related to diabetes; to describe feeling depressed as a result of diabetes; and to express distress related to challenges with glycemic control. Non-insulin-treated participants were more likely to discuss the burden of comorbid medical illnesses. Conclusions Our data generate hypotheses for further study into the emotional burdens of diabetes for insulin-treated adults with type 2 diabetes, and are in line with quantitative research documenting increased diabetes-related distress among insulin-treated individuals. Data describe needs, currently unmet by most models of care, for comprehensive assessment and tailored management of diabetes-related distress.
Nucleolin is an abundant multifunctional nucleolar protein with defined roles in ribosomal RNA processing, RNA polymerase I-catalyzed transcription, and the regulation of apoptosis. Earlier we reported that human nucleolin binds to the p53-antagonist Hdm2 as determined by reciprocal co-immunoprecipitation assays using cell lysates. We also demonstrated that nucleolin antagonizes Hdm2-mediated degradation of p53. Here, we identify specific domains of nucleolin and Hdm2 proteins that support mutual interaction and investigated the implications of complex formation on p53-ubiquitination and protein levels. Our data indicate that the nucleolin N-terminus as well as the central RNA-binding domain (RBD) are predominantly involved in binding to Hdm2. The nucleolin RBD robustly bound to the NLS/NES (nuclear localization and export signals) domain of Hdm2 in vitro, while N-terminus of nucleolin preferentially associated with the Hdm2 RING domain expressed in cells. We further demonstrate that the C-terminal GAR (Glycine-Arginine Rich) domain of nucleolin serves as the predominant binding domain for direct interaction with p53. While over-expression of nucleolin or its various domains had no significant effect on Hdm2 auto-ubiquitination, the nucleolin RBD antagonized the Hdm2 E3 ligase activity against p53, leading to p53 stabilization. Conversely, the adjacent GAR domain of nucleolin interacted with p53 causing a modest stimulatory effect on p53 ubiquitination. These data suggest that changes in nucleolin conformation can alter the availabilities of such domains in vivo to modulate the overall impact of nucleolin on Hdm2 activity and hence on p53 stability.
Aims Diabetes‐related distress is common among adults with Type 2 diabetes and is consistently associated with poorer self‐management and treatment outcomes. However, little is known about the psychological factors that may contribute to or protect against diabetes distress. This study examined illness burden, and positive and negative ways of thinking and relating to oneself in times of stress, as independent correlates of diabetes distress, cross sectionally and longitudinally. Method A total of 120 adults treated for Type 2 diabetes reported their physical symptom complaints, cognitive emotion regulation, self‐compassion and diabetes distress at baseline; 110 completed a 3‐month follow‐up assessment of diabetes distress. Pearson correlations and multivariable linear regression tested baseline and longitudinal relationships. Results Baseline diabetes distress was associated with greater use of negative cognitive emotion regulation strategies (r = 0.43, P < 0.01), greater tendency towards self‐criticism, self‐judgement and over‐identification (r = 0.37, P < 0.01), and greater physical symptom burden (r = 0.50, P < 0.01). Baseline physical symptoms and negative cognitive emotion regulation were independently associated with baseline diabetes distress. Baseline physical symptoms and negative aspects of self‐compassion significantly predicted diabetes distress over 3 months. Positive aspects of cognitive emotion regulation and self‐compassion were not independently associated with diabetes distress cross sectionally or longitudinally. Conclusion Greater symptom burden along with the use of negative cognitive emotion regulation and negative aspects of self‐compassion were independently associated with diabetes distress. If these relations are explained by causal influence, these modifiable factors could be fruitful targets for intervention research.
A high-throughput platform was developed to analyze struvite formation, finding that peptide addition modulates growth in a potentially favorable way.
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