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From a material viewpoint, modern concrete's frequent propensity to plastic shrinkage cracking can be attributable to a combination of low water-binder ratio use and ever-changing properties of binding materials. To obtain a better understanding of this phenomenon, this paper explores the effects of cement fineness and alkali content on the plastic shrinkage cracking of concrete manufactured with two water-binder ratios. Results indicate that within the range 275-385m 2 /kg, cement specific surface area is approximately directly and inversely proportional to hydration rate and evaporation rate respectively; a trend generally leading to higher plastic shrinkage and resulting areas of plastic cracking. Similar effects were observed for alkali contents which resulted in increased levels of plastic shrinkage. Furthermore, while decreasing crack tendency was noted as alkali content increased from 0.4 to 0.8% by mass of cement, further increases in alkali content caused significant decreases of compressive strength and slump; thereby lowering overall concrete performance. It is also found that plastic shrinkage cracking is closely related to the kinetics of plastic shrinkage. In summary, the experimental programme confirmed that cement with relatively low surface area (less than 340 m 2 /kg) and low alkali content (less than 0.8%) is preferred for modern concretes with minimal plastic cracking problems.

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BackgroundThis study aims to investigate the molecular mechanism of Adenovirus type 36 (Ad36) in adipocyte differentiation and glucolipid metabolism.MethodsRat obesity model was established by Ad36 infection and high-fat diet, respectively. Comparison of the body weight, clinical biochemical indicators, insulin sensitivity and lipid heterotopic deposition between these two models was performed. Ad36-induced adipocyte in vitro model was also established. The binding rate of FoxO1, PPARγ and its target gene promoter was detected using ChIP. The mRNA and protein expression levels of PPARγ and downstream target genes were detected by RT-PCR and Western blot, respectively. Oil red O staining was used to measure differentiation into adipocyte. Wortmannin (WM), inhibitor of PI3K, was used to act on Ad36-induced hADSCs.ResultsAd36-induced obese rats did not exhibit disorders in blood glucose and blood TG, insulin resistance and lipid ectopic deposition. The expression of Adipoq, Lpin1 and Glut4 in the adipose tissue increased. Oil red O staining showed that Ad36 induced the differentiation of hAMSCs into human adipocytes in vitro. During this process, the binding rate of FoxO1 and PPARγ promoter regions was weakened. However, the binding rate of the transcription factor PPARγ to its target genes Acc, Adipoq, Lpin1 and Glut4 was enhanced, and thus increased the protein expression of P-FoxO1, PPARγ2, ACC, LPIN1, GLUT4 and ADIPOQ. The PI3K inhibitor Wortmannin reduced the expression of P-Akt, P-FoxO1 and PPARγ2, thereby inhibiting adipogenesis of hADSC.ConclusionAd36 may promote fatty acid and triglyceride synthesis, and improve insulin sensitivity by affecting the PI3K/Akt/FoxO1/PPARγ signaling pathway.

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