Hematite-cuprous oxide (α-Fe2O3/Cu2O) nanocomposites are synthesized based on the design of Z-scheme photocatalyst for CO2 reduction. The band structure for the typical Fe2O3/Cu2O (with 1:1 mole ratio) is characterized by UV-vis reflectance spectroscopy and X-ray/ultraviolet photoelectron spectroscopy, and its heterojunction is determined to be Type II band alignment. The photoreduction CO2 activities of the heterostructures are investigated in the presence of water vapor. The CO yields are changed with Fe/Cu mole ratio, and the maximal CO yield attains 5.0 μmol·g cat(-1) after 3 h of visible-light irradiation. Besides the effect of light wavelength, H2O/CO2 molar ratio and temperature on the products is studied. The selectivity of the prepared catalysts is tunable by modulating the light wavelength. The reaction mechanism is proposed and further confirmed experimentally. The results gained herein may provide some insights into the design of Z-scheme photocatalysts for CO2 reduction.

Lysophosphatidic acid (LPA) is both a potential marker and a therapeutic target for ovarian cancer. It is critical to identify the sources of elevated LPA levels in ascites and blood of patients with ovarian cancer. We show here that human peritoneal mesothelial cells constitutively produce LPA, which accounts for a significant portion of the chemotactic activity of the conditioned medium from peritoneal mesothelial cells to ovarian cancer cells. Both production of LPA by peritoneal mesothelial cells and the chemotactic activity in the conditioned medium can be blocked by HELSS [an inhibitor of the calcium-independent phospholipase A 2 (iPLA 2 )] and AACOCF 3 [an inhibitor of both cytosolic PLA 2 (cPLA 2 ) and iPLA 2 ]. Moreover, cell-based enzymatic activity assays for PLA 2 indicate that peritoneal mesothelial cells have strong constitutive PLA 2 activity. Receptors for LPA, LPA 2 , and LPA 3 are involved in the conditioned medium-induced chemotactic activity. Invasion of ovarian cancer cells into peritoneal mesothelial cells has also been analyzed and shown to require PLA 2 , LPA receptors, and the mitogen-activated protein/ extracellular signal-regulated kinase kinase/extracellular signal-regulated kinase signaling pathway. Thus, we show here, for the first time, that human peritoneal mesothelial cells constitutively produce bioactive lipid signaling molecules, such as LPA, via iPLA 2 and/or cPLA 2 activities. Conditioned medium from peritoneal mesothelial cells stimulate migration, adhesion, and invasion of ovarian cancer cells, and may play similar roles in vivo.

Neoadjuvant chemoradiotherapy has become the standard treatment for locally advanced rectal cancer. Neoadjuvant chemoradiotherapy not only can reduce tumor size and recurrence, but also increase the tumor resection rate and anus retention rate with very slight side effect. Comparing with preoperative chemotherapy, preoperative chemoradiotherapy can further reduce the local recurrence rate and downstage. Middle and low rectal cancers can benefit more from neoadjuvant chemradiotherapy than high rectal cancer. It needs to refine the selection of appropriate patients and irradiation modes for neoadjuvant chemoradiotherapy. Different therapeutic reactions to neoadjuvant chemoradiotherapy affect the type of surgical techniques, hence calling for the need of much attention. Furthermore, many problems such as accurate staging before surgery, selection of suitable neoadjuvant chemoradiotherapy method, and sensitivity prediction to preoperative radiotherapy need to be well settled.

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Cholesterol metabolism disorder in hepatocytes predicts a higher risk of metabolic syndrome (MetS). Long noncoding RNAs (lncRNAs) have emerged as critical players in cellular cholesterol metabolism, but their functions are not systematically clarified. Here, we have identified a novel lncRNA named lnc-HC negatively regulating cholesterol metabolism within hepatocytes through physical interaction with hnRNPA2B1. By further binding to the target messenger RNA of Cyp7a1 or Abca1, the lnc-HC-hnRNPA2B1 complex decreases expressions of the two genes that are implicated in cellular cholesterol excretion. lnc-HC knockdown can strongly recover the cholesterol disorder in vivo. In the upstream pathway, lnc-HC is up-regulated by high cholesterol by the transcription activator, CCAAT/enhancer-binding protein beta. Conclusion: These findings suggest a subtle feed-forward regulation of lnc-HC in cholesterol metabolism and define a novel line of evidence by which lncRNAs modulate the metabolic system at the post-transcriptional level. (HEPATOLOGY 2016;64:58-72) SEE EDITORIAL ON PAGE 16M etabolic syndrome (MetS) refers to a set of metabolic disorders. Liver, as "the metabolic center," is involved in the development of obesity and lipid disorders. (1-3) Higher dietary cholesterol anticipates a higher risk of cirrhosis and nonalcoholic fatty liver disease, inkling strong threats to people health. (4)(5)(6) In hepatocytes, cholesterol homeostasis is maintained by a complex network involving cholesterol uptake, synthesis, intracellular transport, and excretion. (7) 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) is essential for cholesterol synthesis. Cholesterol 7a-hydroxylase (CYP7A1) is critical for the conversion of cholesterol into bile acids and is the first identified liver X receptor alpha (LXRa) target gene. (8) LXRs are ligand-activated nuclear receptors which act as cholesterol sensors (9) . ATP-binding cassette transporter (ABCA1) induces high-density

Catalytic hydrogenation of nitroaromatics is an environment‐benign strategy to produce industrially important aniline intermediates. Herein, we report that Fe(OH)x deposition on Pt nanocrystals to give Fe(OH)x/Pt, enables the selective hydrogenation of nitro groups into amino groups without hydrogenating other functional groups on the aromatic ring. The unique catalytic behavior is identified to be associated with the FeIII‐OH‐Pt interfaces. While H2 activation occurs on exposed Pt atoms to ensure the high activity, the high selectivity towards the production of substituted aniline originates from the FeIII‐OH‐Pt interfaces. In situ IR, X‐ray photoelectron spectroscopy (XPS), and isotope effect studies reveal that the Fe3+/Fe2+ redox couple facilitates the hydrodeoxygenation of the ‐NO2 group during hydrogenation catalysis. Benefitting from FeIII‐OH‐Pt interfaces, the Fe(OH)x/Pt catalysts exhibit high catalytic performance towards a broad range of substituted nitroarenes.

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Tissue-specific stem cells are maintained by both local secreted signals and cell adhesion molecules that position the stem cells in the niche microenvironment. In the Drosophila midgut, multipotent intestinal stem cells (ISCs) are located basally along a thin layer of basement membrane that composed of extracellular matrix (ECM), which separates ISCs from the surrounding visceral musculature: the muscle cells constitute a regulatory niche for ISCs by producing multiple secreted signals that directly regulate ISC maintenance and proliferation. Here we show that integrin-mediated cell adhesion, which connects the ECM and intracellular cytoskeleton, is required for ISC anchorage to the basement membrane. Specifically, the α-integrin subunits including αPS1 encoded by mew and αPS3 encoded by scb, and the β-integrin subunit encoded by mys are richly expressed in ISCs and are required for the maintenance, rather than their survival or multiple lineage differentiation. Furthermore, ISC maintenance also requires the intercellular and intracellular integrin signaling components including Talin, Integrin-linked kinase (Ilk), and the ligand, Laminin A. Notably, integrin mutant ISCs are also less proliferative, and genetic interaction studies suggest that proper integrin signaling is a pre-requisite for ISC proliferation in response to various proliferative signals and for the initiation of intestinal hyperplasia after loss of adenomatous polyposis coli (Apc). Our studies suggest that integrin not only functions to anchor ISCs to the basement membrane, but also serves as an essential element for ISC proliferation during normal homeostasis and in response to oncogenic mutations.