BackgroundPrediabetes is a high-risk state for the future development of type 2 diabetes, which may be prevented through physical activity (PA), adherence to a healthy diet, and weight loss. Mobile health (mHealth) technology is a practical and cost-effective method of delivering diabetes prevention programs in a real-world setting. Sweetch (Sweetch Health, Ltd) is a fully automated, personalized mHealth platform designed to promote adherence to PA and weight reduction in people with prediabetes. ObjectiveThe objective of this pilot study was to calibrate the Sweetch app and determine the feasibility, acceptability, safety, and effectiveness of the Sweetch app in combination with a digital body weight scale (DBWS) in adults with prediabetes.MethodsThis was a 3-month prospective, single-arm, observational study of adults with a diagnosis of prediabetes and body mass index (BMI) between 24 kg/m2 and 40 kg/m2. Feasibility was assessed by study retention. Acceptability of the mobile platform and DBWS were evaluated using validated questionnaires. Effectiveness measures included change in PA, weight, BMI, glycated hemoglobin (HbA1c), and fasting blood glucose from baseline to 3-month visit. The significance of changes in outcome measures was evaluated using paired t test or Wilcoxon matched pairs test.ResultsThe study retention rate was 47 out of 55 (86%) participants. There was a high degree of acceptability of the Sweetch app, with a median (interquartile range [IQR]) score of 78% (73%-80%) out of 100% on the validated System Usability Scale. Satisfaction regarding the DBWS was also high, with median (IQR) score of 93% (83%-100%). PA increased by 2.8 metabolic equivalent of task (MET)–hours per week (SD 6.8; P=.02), with mean weight loss of 1.6 kg (SD 2.5; P<.001) from baseline. The median change in A1c was −0.1% (IQR −0.2% to 0.1%; P=.04), with no significant change in fasting blood glucose (−1 mg/dL; P=.59). There were no adverse events reported.ConclusionsThe Sweetch mobile intervention program is a safe and effective method of increasing PA and reducing weight and HbA1c in adults with prediabetes. If sustained over a longer period, this intervention would be expected to reduce diabetes risk in this population.Trial RegistrationClincialTrials.gov NCT02896010; https://clinicaltrials.gov/ct2/show/NCT02896010 (Archived by WebCite at http://www.webcitation.org/6xJYxrgse)
The Src family kinases (SFK) are homologs of retroviral oncogenes, earning them the label of proto-oncogenes. Their functions are influenced by positive and negative regulatory tyrosine phosphorylation events and inhibitory and activating intramolecular and extramolecular interactions. This regulation is disrupted in their viral oncogene counterparts. However, in contrast to most other proto-oncogenes, the genetic alteration of these genes does not seem to occur in human tumors and how and whether their functions are altered in human cancers remain to be determined. To look for proteomic-level alterations, we took a more granular look at the activation states of SFKs based on their two known regulatory tyrosine phosphorylations, but found no significant differences in their activity states when comparing immortalized epithelial cells with cancer cells. SFKs are known to have other less well-studied phosphorylations, particularly within their unstructured N-terminal unique domains (UD), although their role in cancers has not been explored. In comparing panels of epithelial cells with cancer cells, we found a decrease in S17 phosphorylation in the UD of Src in cancer cells. Dephosphorylated S17 favors the dimerization of Src that is mediated through the UD and suggests increased Src dimerization in cancers. These data highlight the important role of the UD of Src and suggest that a deeper understanding of proteomic-level alterations of the unstructured UD of SFKs may provide considerable insights into how SFKs are deregulated in cancers.
Implications:
This work highlights the role of the N-terminal UD of Src kinases in regulating their signaling functions and possibly in their deregulation in human cancers.
P ancreas transplantation is a nonpharmacologic approach to glucose homeostasis in patients with diabetes associated with better self-identified health scores than insulin alone. [1][2][3] Patients with diabetes are more likely to be alive at 20 y following deceased donor simultaneous pancreas-kidney (SPK) transplant, which is a robust solution for diabetes management. [4][5][6][7][8] Pancreas transplantation is associated with higher rates of rejection-related graft loss than kidney transplantation. [9][10][11][12][13] Reports suggest that the rate of rejection within 1 y of pancreas transplantation is up to 21% and is 44% after 10 y. 12,13 As such, pancreas transplant recipients undergo routine testing of blood glucose, serum amylase, and serum lipase, which have poor sensitivity and specificity for rejection. 14 Moreover, it is important to distinguish rejection from surgical complications because treatments are diametrically opposed.
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