Ninety-one patients over 60 year old with type 2 diabetes mellitus(T2DM) were selected from our outpatient department. The patients of experimental group uploaded their blood glucose data detected with glucometers, and obtained integrated management called " Mobile Health(M-health)" management such as medicines,diet,exercise from medical groups. The patients of control group got medical care in a traditional way without receiving other interventions. Regular follow-up was conducted in 2 groups every 3 months. The results showed that 3 months later,postprandial 2h plasma glucose in the experimental group was significantly improved compared with that of control group (P<0.05). Six months later, postprandial 2h plasma glucose and HbA1Clevels in the experimental group showed a decline comparing to the baseline, showing a statistical significance compared with control group(P<0.05). These results suggest that smartphone-based telemedicine is helpful of blood glucose control in elderly T2DM patients.

Objective To investigate the mechanism of rapamycin inhibiting the differentiation and proliferation of newborn porcine pancreatic adult stem cells, and to explore the therapeutic methods that may effectively reduce the side effects of rapamycin. Method Porcine NPCCs were treated with rapamycin alone or in combination with IGF-Ⅱ, and the caspase-3 and [ 3 H ]-thymidine uptake assays were performed to detect apoptosis and proliferation. The expression of insulin, PDX-1, NeuroD/Beta2, and Foxo1, a downstream transcription factor of IGF-Ⅱ, were analyzed by RT-PCR and Western blot to evaluate the differentiation ability of pancreatic adult stem cells. Results The NPCCs treated with rapamycin inhibited the proliferation ofβ-cells, increased apoptosis, reduced insulin secretion, inhibited the expression of PDX-1 and NeuroD/Beta2, and decreased the expression of IGF-Ⅱ. Foxo1 expression and induction of Foxo1 from the cytoplasm to the nucleus of the ectopic. The combined treatment of rapamycin and IGF-Ⅱcan reduce the side effects of rapamycin, inhibit the decrease ofβ-cell number and insulin content, repair the expression of insulin, PDX-1, NeuroD/Beta2, inhibit Foxo1 expression and intracellular ectopic. Conclusion Aberrant expression of IGF-Ⅱ and Foxol genes is the key inducing factor of rapamycin inhibiting the proliferation and differentiation of NPCCs, and IGF-Ⅱtreatment can effectively reduce the side effects of rapamycin on NPCCs differentiation.