Acceptability and practicability of self-management for patients with Parkinson's disease based on smartphone applications in China.

BACKGROUND: China has had about 1.2 billion mobile-phone users, and this number continues to grow. However, mobile-health services (mHealth) are currently in the initial stage, and have not yet prevailed in China. Additionally, the prevalence of Parkinson's disease (PD) in China is 1700/100,000 (≥65 years). Indeed, these PD patients would benefit from mHealth to manage their disease. Therefore, we designed a study to determine attitudes toward smartphone applications (apps) for chronic condition self-management, and to discover the practicality of these apps among PD patients in China. METHODS: We selected 204 participants with PD between 52 and 87 years old and surveyed their attitudes concerning the use of smartphone apps for chronic condition management via questionnaires. RESULTS: Among the participants, 65.19% had smartphones. Among these smartphone users, 82.84% expressed a preference for using apps for PD management. This group tended to be younger and more frequent web users with higher education and better medication compliance, and they tended to have a longer PD course and worse conditions (P < 0.001, P = 0.001, P < 0.001, P = 0.041, P < 0.001, P = 0.013). Additionally, the willingness to apply apps for PD self-management was positively related to education (P < 0.001) and negatively related to age and PD course (P = 0.017, P < 0.001). CONCLUSION: In China, patients with PD have a generally positive attitude towards self-management through smartphone apps. Consequently, improving the coverage of smartphones with practical and handy apps is a promising strategy for PD self-management.

Progesterone-induced miR-133a inhibits the proliferation of endometrial epithelial cells.

AIM: This study aimed to understand the role of miR-133a in progesterone actions, explore the regulative mechanism of the progesterone receptor, and investigate the effects of miR-133a on the progesterone-inhibited proliferation of mouse endometrial epithelial cells. METHODS: The expression of miR-133a induced by progesterone was detected by quantitative real-time PCR both in vivo and in vitro. Ishikawa subcell lines stably transfected with progesterone receptor subtypes were used to determine the receptor mechanism of progesterone inducing miR-133a. Specific miR-133a mimics or inhibitors were transfected into mouse uteri and primary cultured endometrial epithelial cells to overexpress or downregulate the miR-133a. The roles of miR-133a in the cell cycle and proliferation of endometrial epithelial cells were analysed by flow cytometry and Edu incorporation analysis. The protein levels of cyclinD2 in uterine tissue sections and primary cultured endometrial epithelial cells were determined by immunohistochemistry and Western blot analysis. RESULTS: Progesterone could induce miR-133a expression in a PRB-dependent manner in endometrial epithelial cells. miR-133a inhibited endometrial epithelial cell proliferation by arresting cell cycle at the G1 -S transition. Moreover, miR-133a acted as an inhibitor in downregulating cyclinD2 in endometrial epithelial cells. CONCLUSION: We showed for the first time that progesterone-induced miR-133a inhibited the proliferation of endometrial epithelial cells by downregulating cyclinD2. Our research indicated an important mechanism for progesterone inhibiting the proliferation of endometrial epithelial cells by inducing special miRNAs to inhibit positive regulatory proteins in the cell cycle.

Progesterone-induced cyclin G1 inhibits the proliferation of endometrial epithelial cell and its possible molecular mechanism.

Under normal conditions, progesterone inhi-bits the estrogen-induced proliferation of endometrial epithelium. Our previous studies have shown that cyclin G1 was progesterone-dependent in mouse endometrial epithelium at peri-implantation, and exogenous cyclin G1 suppressed the proliferation of endometrial cancer cells. The objectives of this study are to determine whether cyclin G1, as a negative regulator of the cell cycle, is involved in the antiproliferative action of progesterone on endometrial epithelial cells, and to explore the possible molecular mechanism of cyclin G1 inhibition. The siRNA-mediated elimination of cyclin G1 attenuated the antiproliferative action of progesterone on endometrial epithelial cells. Immunoprecipitation showed that progesterone-induced cyclin G1 could interact with PP2A to mediate its phosphatase activity. The block of PP2A activity also attenuated the antiproliferative action of progesterone on endometrial epithelial cells and increased the phosphorylated Rb. In conclusion, progesterone-induced cyclin G1 mediates the inhibitory effect of progesterone on endometrial epithelial cell proliferation possibly through the recruitment of PP2A to dephosphorylate Rb.