ObjectiveTo assess the prevalence of diabetes and its risk factors.DesignPopulation based, cross sectional study.Setting31 provinces in mainland China with nationally representative cross sectional data from 2015 to 2017.Participants75 880 participants aged 18 and older—a nationally representative sample of the mainland Chinese population.Main outcome measuresPrevalence of diabetes among adults living in China, and the prevalence by sex, regions, and ethnic groups, estimated by the 2018 American Diabetes Association (ADA) and the World Health Organization diagnostic criteria. Demographic characteristics, lifestyle, and history of disease were recorded by participants on a questionnaire. Anthropometric and clinical assessments were made of serum concentrations of fasting plasma glucose (one measurement), two hour plasma glucose, and glycated haemoglobin (HbA1c).ResultsThe weighted prevalence of total diabetes (n=9772), self-reported diabetes (n=4464), newly diagnosed diabetes (n=5308), and prediabetes (n=27 230) diagnosed by the ADA criteria were 12.8% (95% confidence interval 12.0% to 13.6%), 6.0% (5.4% to 6.7%), 6.8% (6.1% to 7.4%), and 35.2% (33.5% to 37.0%), respectively, among adults living in China. The weighted prevalence of total diabetes was higher among adults aged 50 and older and among men. The prevalence of total diabetes in 31 provinces ranged from 6.2% in Guizhou to 19.9% in Inner Mongolia. Han ethnicity had the highest prevalence of diabetes (12.8%) and Hui ethnicity had the lowest (6.3%) among five investigated ethnicities. The weighted prevalence of total diabetes (n=8385) using the WHO criteria was 11.2% (95% confidence interval 10.5% to 11.9%).ConclusionThe prevalence of diabetes has increased slightly from 2007 to 2017 among adults living in China. The findings indicate that diabetes is an important public health problem in China.

Black phosphorene has attracted much attention as a semiconducting two‐dimensional material. Violet phosphorus is another layered semiconducting phosphorus allotrope with unique electronic and optoelectronic properties. However, no confirmed violet crystals or reliable lattice structure of violet phosphorus had been obtained. Now, violet phosphorus single crystals were produced and the lattice structure has been obtained by single‐crystal x‐ray diffraction to be monoclinic with space group of P2/n (13) (a=9.210, b=9.128, c=21.893 Å, β=97.776°). The lattice structure obtained was confirmed to be reliable and stable. The optical band gap of violet phosphorus is around 1.7 eV, which is slightly larger than the calculated value. The thermal decomposition temperature was 52 °C higher than its black phosphorus counterpart, which was assumed to be the most stable form. Violet phosphorene was easily obtained by both mechanical and solution exfoliation under ambient conditions.

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Axonal and dendritic degeneration is a common, early pathological feature of many neurodegenerative disorders and thought to be regulated by mechanisms distinct from that of the soma death. The unique structures of axons and dendrites (collectively neurites) may cause them to be particularly vulnerable to the accumulation of protein aggregates and damaged organelles. Autophagy is a known catabolic mechanism whereby cells clear protein aggregates and damaged organelles. Basal autophagy occurs continuously as a housekeeping function, and can be acutely expanded in response to various stress or injuries. Emerging evidence shows that insufficient or excessive autophagy contributes to neuritic degeneration. Here, we review the recent progress that has begun to reveal the role of autophagy in neuritic functions and degeneration.

Aims: Ero1 flavoproteins catalyze oxidative folding in the endoplasmic reticulum (ER), consuming oxygen and generating hydrogen peroxide (H 2 O 2 ). The ER-localized glutathione peroxidase 7 (GPx7) shows protein disulfide isomerase (PDI)-dependent peroxidase activity in vitro. Our work aims at identifying the physiological role of GPx7 in the Ero1a/PDI oxidative folding pathway and at dissecting the reaction mechanisms of GPx7. Results: Our data show that GPx7 can utilize Ero1a-produced H 2 O 2 to accelerate oxidative folding of substrates both in vitro and in vivo. H 2 O 2 oxidizes Cys57 of GPx7 to sulfenic acid, which can be resolved by Cys86 to form an intramolecular disulfide bond. Both the disulfide form and sulfenic acid form of GPx7 can oxidize PDI for catalyzing oxidative folding. GPx7 prefers to interact with the a domain of PDI, and intramolecular cooperation between the two redox-active sites of PDI increases the activity of the Ero1a/GPx7/PDI triad. Innovation: Our in vitro and in vivo evidence provides mechanistic insights into how cells consume potentially harmful H 2 O 2 while optimizing oxidative protein folding via the Ero1a/GPx7/PDI triad. Cys57 can promote PDI oxidation in two ways, and Cys86 emerges as a novel noncanonical resolving cysteine. Conclusion: GPx7 promotes oxidative protein folding, directly utilizing Ero1a-generated H 2 O 2 in the early secretory compartment. Thus, the Ero1a/ GPx7/PDI triad generates two disulfide bonds and two H 2 O molecules at the expense of a single O 2 molecule. Antioxid. Redox Signal. 20, 545-556.