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The objective of this study is to investigate the role and underlying mechanism of Olfactomedin 2 (Olfm2) in smooth muscle cell (SMC) phenotypic modulation and vascular remodeling.Platelet-derived growth factor-BB induces Olfm2 expression in primary SMCs while modulating SMC phenotype as shown by the downregulation of SMC marker proteins. Knockdown of Olfm2 blocks platelet-derived growth factor-BB-induced SMC phenotypic modulation, proliferation, and migration. Conversely, Olfm2 overexpression inhibits SMC marker expression. Mechanistically, Olfm2 promotes the interaction of serum response factor with the runt-related transcription factor 2 that is induced by platelet-derived growth factor-BB, leading to a decreased interaction between serum response factor and myocardin, causing a repression of SMC marker gene transcription and consequently SMC phenotypic modulation. Animal studies show that Olfm2 is upregulated in balloon-injured rat carotid arteries. Knockdown of Olfm2 effectively inhibits balloon injury-induced neointima formation. Importantly, knockout of Olfm2 in mice profoundly suppresses wire injury-induced neointimal hyperplasia while restoring SMC contractile protein expression, suggesting that Olfm2 plays a critical role in SMC phenotypic modulation in vivo.Olfm2 is a novel factor mediating SMC phenotypic modulation. Thus, Olfm2 may be a potential target for treating injury-induced proliferative vascular diseases.

Two new organic-inorganic hybrid compounds, [Cu(phen)(prz)]2[PMoV1MoVI7VIV2VV4O42]·4H2O (1) and [Ag2(phen)4]2[PMoV1MoVI7VIV2VV4O42] (2) (phen = 1,10-phenanthroline, prz = pyrazine), have been synthesized and characterized by IR, XPS, XRD, UV-Vis, fluorescent spectra analyses, elemental analyses, X-ray diffraction analyses, TG analyses, and cyclic voltammetric measurements. Both compounds are formed by Keggin POM cores and transition metal fragments. Compound 1 exhibits an unprecedented 1-D chain structure constructed from [PMoV1MoVI7VIV2VV4O42]4- and [Cu(phen)(prz)]2+ in the -A-B↑-C-B↓- linking mode. Compound 2 shows a supramolecular structure formed by [PMoV1MoVI7VIV2VV4O42]4- and [Ag2(phen)4]2+.

The LOX-1/p38 mitogen-activated protein kinase (MAPK) pathway has been proved to participate in the endothelial dysfunction in atherosclerosis. Trichosanatineis is an active compound isolated from the peel of Trichosanthes kirilowii. This study aims to determine whether trichosanatine prevents the oxidized low-density lipoprotein (ox-LDL)-induced insult through inhibition of the LOX-1/p38 MAPK pathway in HUVECs. HUVECs were treated with 150 mg/ml ox-LDL for 24 h to establish an ox-LDL-induced endothelial injury model. Cell viability, mitochondrial membrane potential (MMP), apoptosis, reactive oxygen species (ROS) level, LOX-1 and p38 MAPK expression level were measured. The results indicated that HUVECs were pretreated with either 100 mM trichosanatine or LOX-1 shRNA prior to exposure to ox-LDL for 24 h. Exposure of HUVECs to 150 mg/ml ox-LDL for 24 h significantly up-regulated the expression levels of LOX-1. The increased expression levels of LOX-1 were markedly attenuated by pretreatment with 100 mM trichosanatine. In addition, the ox-LDL-induced increase in phosphorylated (p) p38 MAPK expression was ameliorated by pretreatment with LOX-1 shRNA. Pretreatment of HUVECs with either trichosanatine or LOX-1 shRNA before exposure to ox-LDL significantly inhibited the ox-LDL-induced injuries, as evidenced by an increase in cell viability, a decrease in apoptotic cells, a ROS generation and a loss of MMP. In conclusion, we have demonstrated for the first time that the LOX-1/p38 MAPK pathway contributes to the ox-LDL-induced injury in HUVECs. Meanwhile, the trichosanatine protects the HUVECs against ox-LDL-induced injury at least in part by inhibiting the activated of LOX-1/p38 MAPK pathway.

The reaction of CuBr2 with 1,10-phen-H2O (1,10-phen = 1,10-phenanthroline) gave two compounds: CuBr2(C12H8N2) and Cu3Br3(C12H8N2)2. Their structures have been characterized by single-crystal X-ray diffraction analysis, elemental analyses, thermogravimetric analyses (TGA) and measurement of variable temperature magnetic susceptibility. Crystal data for CuBr2(C12-H8N2): monoclinic, space group P21/n, a = 0.9977(3) nm, b = 0.65138(14) nm, c = 1.8207(4) nm, β = 91.624(18)°, V = 1.1828(5) nm3, Z = 2. Crystal data for Cu3Br3(C12H8N2)2: monoclinic, space group C2/c, a = 1.00167(11) nm, b = 1.4523(4) nm, c = 1.6295(3) nm, β = 94.386(14)°, V = 2.3635(8) nm3, Z = 3.

Five metal imidazole dicarboxylate based compounds, {[Zn3(MIDC)2(4,4’-bipy)3](4,4’-bipy)·8H2O}n (1), {[Co3(MIDC)2(4,4’-bipy)3](4,4’-bipy)·6H2O}n (2), {[Co3(MIDC)2(py)2(H2O)2]}n (3), {[Mn6(MIDC)4(py)5(H2O)4]}n (4) and {[Mn3(MIDC)2(Phen)3(H2O)2]}n (5) (H3MIDC = 2-methyl-1H-imidazole-4,5-dicarboxylic acid; 4,4’-bipy = 4,4’-bipyridine; py = pyridine; Phen = 1,10-phenanthroline), have been synthesized under hydrothermal conditions and characterized by elemental analyses, IR spectroscopy, thermogravimetric analysis, and single-crystal X-ray diffraction. We control the coordination modes of H3MIDC via hydrazine and obtained a series of coordination compounds containing honeycomb-like [M3(MIDC)2]n layers. We also investigated the effects of different neutral terminal or bridging ligands on [M3(MIDC)2]n layers. Coplanar [M3(MIDC)2]n layers and 4,4-bipy were used to construct 3-D frameworks of 1 and 2. Puckered [M3(MIDC)2]n layers were found in 3-5; 4 is the first [M3(L)2]n layer structure with two crests and troughs during each period (L = imidazole-4,5-dicarboxylic acid or its analogue). Compound 5 is the first puckered [M3(L)2]n layer structure decorated by chelating neutral ligands. Compound 1 exhibits weak blue photoluminescence in the solid state at room temperature. Variable-temperature magnetic susceptibility measurements of 2-5 indicate strong antiferromagnetic interactions.

Supplemental Digital Content is available in the text, Few studies have analyzed the training of endoscopists in the diagnosis of early gastric cancer (EGC). This study assessed whether specific training of endoscopists improves the detection rate of EGC. The rates of detection of EGC by endoscopists at the Digestive Endoscopy Center of the Affiliated Nanfang Hospital of China Southern Medical University between January 2013 and May 2014 were retrospectively analyzed. Because some endoscopists received training in the diagnosis of EGC, beginning in September 2013, the study was divided into 3 time periods: January to September 2013 (period 1), September 2013 to January 2014 (period 2), and January to May 2014 (period 3). The rates of EGC detection during these 3 periods were analyzed. From January 2013 to May 2014, a total of 25,314 gastroscopy examinations were performed at our center, with 48 of these examinations (0.2%) detecting EGCs, accounting for 12.1% (48/396) of the total number of gastric cancers detected. The EGC detection rates by trained endoscopists during periods 1, 2, and 3 were 0.3%, 0.6%, and 1.5%, respectively, accounting for 22.0%, 39.0%, and 60.0%, respectively, of the gastric cancers detected during these time periods. In comparison, the EGC detection rates by untrained endoscopists during periods 1, 2, and 3 were 0.05%, 0.08%, and 0.10%, respectively, accounting for 3.1%, 6.0%, and 5.7%, respectively, of the gastric cancers detected during these times. After training, the detection rate by some trained endoscopists markedly increased from 0.2% during period 1 to 2.3% during period 3. Further, the use of magnifying endoscopy with narrow-band imaging (M-NBI) (odds ratio = 3.1, 95% confidence interval 2.4–4.1, P