AIM: This study aims to investigate the medical expenditure of people with type 2 diabetes mellitus in Chongqing, China; to explore factors that contribute to the expenditure; and to examine the financial burden placed on households, particularly poor households.
METHODS: A cross sectional survey was conducted with a sample of people diagnosed with Type 2 diabetes mellitus in 2014. Of the 664 people eligible, 76% were interviewed. Descriptive statistics and log-linear regression were used to examine respondents' age, sex and level education, location of residence, income and type of health insurance associated with out-of-pocket expenditure on accessing diabetes mellitus care.
RESULTS: In a year, average out-of-pocket expenditure on the purchase of drugs from pharmacies and having outpatient care were US $333 and US $310, respectively. The average out-of-pocket expenditure on accessing inpatient care was 3.7 times (US $1159) that of accessing outpatient care. After adjusting for age and sex, out-of-pocket expenditure on diabetes care was significantly higher for people covered by the Urban Employee Basic Medical Insurance programme and those enrolled in the identified priority diseases reimbursement programme, which provided higher reimbursement rates for outpatient and (or) inpatient care. Out-of-pocket expenditures on the purchase of drugs from pharmacies, having outpatient and inpatient care, respectively, were 9.8%, 16.2% and 62.6% of annual household income in low-income group.
CONCLUSION: Even with health insurance coverage, poor people with Type 2 diabetes mellitus suffered from significant financial hardship. This has significant implications for models of care and healthcare financing in China with the growing burden of diabetes.
Study site: Township or community health centres, Chongqing, China
Aurantii Fructus Immaturus total flavonoids (AFIF) is the main effective fraction extracted from AFI, which has a good effect on promoting gastrointestinal motility. This study aimed to investigate AFIF which regulates miR-5100 to improve constipation symptoms in mice by targeting Frizzled-2 (Fzd2) to alleviate interstitial cells of Cajal (ICCs) calcium ion balance and autophagy apoptosis. The constipated mouse model was induced by an antibiotic suspension, and then treated with AFIF. RNA-seq sequencing, luciferase assay, immunofluorescence staining, transmission electron microscopy, ELISA, flow cytometry, quantitative polymerase chain reaction (PCR), and Western blot were applied in this study. The results showed that AFIF improved constipation symptoms in antibiotic-induced constipated mice, and decreased the autophagy-related protein Beclin1 levels and the LC3-II/I ratio in ICCs. miR-5100 and its target gene Fzd2 were screened as key miRNAs and regulator associated with autophagy. Downregulation of miR-5100 caused increased expression of Fzd2, decreased proliferation activity of ICCs, increased apoptotic cells, and enhanced calcium ion release and autophagy signals. After AFIF treatment, miR-5100 expression was upregulated and Fzd2 was downregulated, while autophagy-related protein levels and calcium ion concentration decreased. Furthermore, AFIF increased the levels of SP, 5-HT, and VIP, and increased the expression of PGP9.5, Sy, and Cx43, which alleviated constipation by improving the integrity of the enteric nervous system network. In conclusion, AFIF could attenuate constipation symptoms by upregulating the expression of miR-5100 and targeting inhibition of Fzd2, alleviating calcium overload and autophagic death of ICCs, regulating the content of neurotransmitters, and enhancing the integrity of the enteric nervous system network.
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.