A defunctioning stoma decreases clinical anastomotic leak rate and reoperation rate. It is recommended after low anterior resection for rectal cancer.

The unique surface and pore structure of ordered mesoporous materials make them promising for applications in adsorption and catalysis. However, siliceous mesoporous materials usually suffer from a lack of active sites necessary for adsorption or catalysis, and thus their functionalization becomes paramount for application in industry. This is achieved by incorporating guest species such as metals or metal oxides by direct synthesis (one-pot method) or post-modification after synthesis. In the latter process, the host template is removed by either calcination or extraction to achieve an openporous structure prior to functionalization, in which the thermal transformation of the precursor into the final oxide guest is critical. In order to save energy and time, it is better to remove the template and to transform the guest precursor in one calcination step in order to modify the as-prepared mesoporous materials. This was attempted recently with guest species replacing surfactants in solution, where surfactant extraction releases some space for the surface modification.[1±3]Here, we report a new solvent-free method for directly inserting guest precursors into the occluded pores of as-prepared ordered mesoporous materials followed by calcination, thus preparing a mesoporous functional composite with unexpectedly high oxide dispersion. This new strategy is not only energy-and time-efficient, but also sheds light on how to exploit the confined space between the templated aggregates and the silica walls.Thermogravimetric analysis (TGA) showed 41 % weight loss in the range of 423±823 K for as-prepared SBA-15 samples, and 45 % and 41 % weight loss for as-prepared MCM-41 samples M1 and M2, respectively, due to decomposition of the template species. (As described in the Experimental section, M1 is prepared under acidic conditions, and M2 is prepared under alkaline conditions.) Although these data are slightly lower than previously reported values [4,5] (e.g., a decomposition weight loss of about 46 % observed for SBA-15 [4] ), this means that most of the templated aggregates still occlude the pores of both these as-prepared samples, and that less than 15 % of the pore volume is available for the dispersion of a guest. However, an unexpectedly high dispersion of metal-oxide species can be realized in the mesoporous support by this new method. When the as-prepared SBA-15 was used as a support, no reflections of the CuO crystalline phase were visible in the wide-angle X-ray diffraction (XRD) patterns, even for the CuO/SBA-15(20) composite (Fig. 1A).(The samples are denoted as MO n /Support(X), where MO n represents the metal-oxide species and X is the weight percentage of MO n in the composites.) That is, about 40 wt.-% of Cu(NO 3 ) 2 has been spontaneously dispersed in the host and transformed to copper oxide. As shown in Figure 1B, low-angle XRD patterns of all the calcined CuO/SBA-15 composites (with weight percentages of 15 wt.-%, 20 wt.-%, and 25 wt.-%) are identical to that of SBA-15, with two-dimensional hexagonal por...

The accumulation of adenosine in the tumor microenvironment is associated with tumor progression in many cancers. However, whether adenosine is involved in gastric cancer (GC) metastasis and progression, and the underlying molecular mechanism, is largely unclear. In this study, we find that GC tissues and cell lines had higher A2aR levels than nontumor gastric tissues and cell lines. A2aR expression correlated positively with TNMstage, and associated with poor outcomes. Adenosine enhanced the expression of the stemness and epithelial–mesenchymal transition-associated genes by binding to A2aR. A2aR expression on GC cells promoted metastasis in vivo. The PI3K-AKT-mTOR signaling pathway was involved in adenosine-stimulated GC cell migration and invasion. Our results indicate that adenosine promotes GC cell invasion and metastasis by interacting with A2aR to enhance PI3K–AKT–mTOR pathway signaling.