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Abstract Background and Aims The last decade has witnessed unprecedented growth in mobile phone use. It links millions of previously unconnected people. The ubiquity of mobile phones, which allows for use of the short message service (SMS), offers new and innovative opportunities for disease prevention and health education. SMS usage appears to be a feasible, popular, and effective way of improving health literacy. This study measured the effect of SMS health education on the improvement of health management in Shenzhen, China. Methods This was a community‐based randomized controlled study. A total of 32 communities were randomly chosen out of 320, then about 200 participants were randomly sampled from each selected community. The subjects were equally divided into two groups at random. About half of the participants received health intervention messages via Internet‐based SMS for almost a year. The data were analyzed by descriptive and inferential statistical methods. Results The proportion of participants involved in self‐health management increased from 30.92% to 38.68% over the year (χ2 = 42.49, p 0.05). No statistical difference in the prevalence of chronic disease (15.16% and 13.89%, p > 0.05) was found before and after the intervention in the intervention group. The prevalence in the intervention group was lower after the intervention than it was in the control group (17.33%, χ2 = 14.45, p

In most acute promyelocytic leukemia (APL) cells, promyelocytic leukemia (PML) fuses to retinoic acid receptor α (RAR α ) due to chromosomal translocation, thus generating PML/RAR α oncoprotein, which is a relatively stable oncoprotein for degradation in APL. Elucidating the mechanism regulating the stability of PML/RAR α may help to degrade PML/RAR α and eradicate APL cells. Here, we describe a deubiquitinase (DUB)-involved regulatory mechanism for the maintenance of PML/RAR α stability and develop a novel pharmacological approach to degrading PML/RAR α by inhibiting DUB. We utilized a DUB siRNA library to identify the ovarian tumor protease (OTU) family member deubiquitinase YOD1 as a critical DUB of PML/RAR α . Suppression of YOD1 promoted the degradation of PML/RAR α , thus inhibiting APL cells and prolonging the survival time of APL cell-bearing mice. Subsequent phenotypic screening of small molecules allowed us to identify ubiquitin isopeptidase inhibitor I (G5) as the first YOD1 pharmacological inhibitor. As expected, G5 notably degraded PML/RAR α protein and eradicated APL, particularly drug-resistant APL cells. Importantly, G5 also showed a strong killing effect on primary patient-derived APL blasts. Overall, our study not only reveals the DUB-involved regulatory mechanism on PML/RAR α stability and validates YOD1 as a potential therapeutic target for APL, but also identifies G5 as a YOD1 inhibitor and a promising candidate for APL, particularly drug-resistant APL treatment., (© 2022 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.)