Prevention of ice accretion and adhesion on surfaces is relevant to many applications, leading to improved operation safety, increased energy efficiency, and cost reduction. Development of passive nonicing coatings is highly desirable, since current antiicing strategies are energy and cost intensive. Superhydrophobicity has been proposed as a lead passive nonicing strategy, yet the exact mechanism of delayed icing on these surfaces is not clearly understood. In this work, we present an in-depth analysis of ice formation dynamics upon water droplet impact on surfaces with different wettabilities. We experimentally demonstrate that ice nucleation under low-humidity conditions can be delayed through control of surface chemistry and texture. Combining infrared (IR) thermometry and high-speed photography, we observe that the reduction of water-surface contact area on superhydrophobic surfaces plays a dual role in delaying nucleation: first by reducing heat transfer and second by reducing the probability of heterogeneous nucleation at the water-substrate interface. This work also includes an analysis (based on classical nucleation theory) to estimate various homogeneous and heterogeneous nucleation rates in icing situations. The key finding is that ice nucleation delay on superhydrophobic surfaces is more prominent at moderate degrees of supercooling, while closer to the homogeneous nucleation temperature, bulk and air-water interface nucleation effects become equally important. The study presented here offers a comprehensive perspective on the efficacy of textured surfaces for nonicing applications.

BackgroundMetabolic syndrome (MS) comprises a set of conditions that are risk factors for cardiovascular diseases and diabetes. Numerous epidemiological studies on MS have been conducted, but there has not been a systematic analysis of the prevalence of MS in the Chinese population. Therefore, the aim of this study was to estimate the pooled prevalence of MS among subjects in Mainland China.MethodsWe performed a systematic review by searching both English and Chinese literature databases. Random or fixed effects models were used to summarize the prevalence of MS according to statistical tests for heterogeneity. Subgroup, sensitivity, and meta-regression analyses were performed to address heterogeneity. Publication bias was evaluated using Egger’s test.ResultsThirty-five papers were included in the meta-analysis, with a total population of 226,653 Chinese subjects. Among subjects aged 15 years and older, the pooled prevalence was 24.5 % (95 % CI: 22.0–26.9 %). By sex, the prevalences were 19.2 % (95 % CI: 16.9–21.6 %) in males and 27.0 % (95 % CI: 23.5–30.5 %) in females. The pooled prevalence of MS increased with age (15–39 years: 13.9 %; 40–59 years: 26.4 %; and ≥60 years: 32.4 %). Individuals living in urban areas (24.9 %, 95 % CI: 18.5–31.3 %) were more likely to suffer from MS than those living in rural areas (19.2 %, 95 % CI: 14.8–23.7 %). Hypertension was the most prevalent component of MS in males (52.8 %), while the most prevalent component of MS for females was central obesity (46.1 %).ConclusionsOur systematic review suggested a high prevalence of MS among subjects in Mainland China, indicating that MS is a serious public health problem. Therefore, more attention should be paid to the prevention and control of MS.Electronic supplementary materialThe online version of this article (doi:10.1186/s12889-016-2870-y) contains supplementary material, which is available to authorized users.

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Tumor cells metabolize more glucose to lactate in aerobic or hypoxic conditions than non-tumor cells. Pyruvate kinase isoenzyme type M2 (PKM2) is crucial for tumor cell aerobic glycolysis. We established a role for let-7a/c-Myc/hnRNPA1/PKM2 signaling in glioma cell glucose metabolism. PKM2 depletion via siRNA inhibits cell proliferation and aerobic glycolysis in glioma cells. C-Myc promotes up-regulation of hnRNPA1 expression, hnRNPA1 binding to PKM pre-mRNA, and the subsequent formation of PKM2. This pathway is downregulated by the microRNA let-7a, which functionally targets c-Myc, whereas hnRNPA1 blocks the biogenesis of let-7a to counteract its ability to downregulate the c-Myc/hnRNPA1/PKM2 signaling pathway. The down-regulation of c-Myc/hnRNPA1/PKM2 by let-7a is verified using a glioma xenograft model. These results suggest that let-7a, c-Myc and hnRNPA1 from a feedback loop, thereby regulating PKM2 expression to modulate glucose metabolism of glioma cells. These findings elucidate a new pathway mediating aerobic glycolysis in gliomas and provide an attractive potential target for therapeutic intervention.