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In this paper, we showed an example of acid-directed hydrothermal synthesis of three Cd-based metal–organic frameworks (MOFs) under similar conditions, namely, [Cd(TIDB)(AA)0.5(NO3)]n (1), [Cd3(TIDB)2(AA)2(H2O)2(HCOO)2]n (2), and {[Cd4(TIDB)(AA)4(H2O)5](C2H5OH)2(H2O)2}n (3) (TIDB = 1,3,5-tri(1H-imidazol-1-yl)benzene, H2AA = anthracene-9,10-dicarboxylic acid). Compound 1 was synthesized by the introduction of HNO3 as a structure-directing agent. It has 2D coordination networks with the 3,4-c bey topology. The porous 3D supramolecular framework in compound 1 is stabilized by H-bonds. Compound 2 was formed with the use of a HCOOH agent. It has a 3D coordination network with a new 3,4,5-c underlying net topology, and it is also porous. Compound 3 was obtained using a CH3COOH agent. It has a disordered non-porous 3D coordination network. Because 3 was hard to purify, 1 and 2 were chosen for further property investigation. On the one hand, fluorescence studies showed that 1 and 2 are both blue-emitting MOFs with quantum yields of 2.3% and 0.8%, respectively. On the other hand, CO2 cycloaddition performance was also tested, which revealed that 2 has a superior catalytic conversion of epoxybutane at 60 °C and 1 atm with a high yield of up to 95.6%. [ABSTRACT FROM AUTHOR]

The novel proto-oncogene Golgi phosphoprotein (GOLPH)3 is overexpressed in a variety of tumor tissues and is associated with poor prognosis. The authors previously demonstrated that GOLPH3 gene is overexpressed in colorectal cancer tissues and promotes the proliferation of colonic cancer cells by activating the phosphatidylinositol-3-kinase/protein kinase B/the mammalian target of rapamycin and Wnt/ß-catenin signaling pathways. However, to the best of the authors' knowledge, if and how the GOLPH3 gene is involved in inducing resistance to colonic cancer chemotherapy has not been reported. In the present study, the association between the overexpression of the GOLPH3 gene and resistance of HT29 colonic cancer cells to 5-fluorouracil (5-FU) was investigated. Following confirmation of the effective silencing of the GOLPH3 gene, proliferation and apoptosis of colonic cancer cells were detected by MTT assay, colony formation assay and flow cytometry, and then the mechanism of GOLPH3-induced resistance to 5-FU chemotherapy in colonic cancer cells was investigated by western blotting. The results demonstrated that the expression of phosphorylated (p)-glycoprotein and GOLPH3 was increased in HT29 cells following treatment with 5-FU, which resulted in the development of drug resistance. Silencing GOLPH3 increased the sensitivity of HT29 cells to 5-FU, reduced their tumorigenicity and partly reversed their resistance to 5-FU. The expression of p-extracellular signal-regulated kinase (pERK)1/2 and ß-catenin was decreased, which indicated that its mechanism was associated with the activation of the mitogen-activated protein kinase/ERK and Wnt/ß-catenin signaling pathways. Therefore, GOLPH3 may be a potential, novel target for reversing chemotherapy resistance in colon cancer. [ABSTRACT FROM AUTHOR]

Aim: To investigate the effect of Golgi phosphorylation protein 3 (GOLPH3) expression on cell apoptosis, angiogenesis and prognosis in colorectal cancer (CRC)., Methods: The expression of GOLPH3 in CRC tissues and normal colorectal mucosae was determined by immunohistochemistry in 62 patients. In addition, immunohistochemistry was also carried out to detect the expression of vascular endothelial growth factor (VEGF), CD34 and microvessel density (MVD). Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay was used to determine the apoptotic index (AI). The Kaplan-Meier method was used to analyze the relationship between GOLPH3 expression and survival in another 123 CRC cases., Results: Compared with normal colorectal mucosae, a notably higher level of GOLPH3 protein expression was identified in CRC tissues (53.2% vs 24.2%, P < 0.05). Positive GOLPH3 expression was significantly associated with tumor invasion depth, TNM stage, and lymph node metastasis (P = 0.001; P = 0.020; P = 0.020; P < 0.05, respectively), but not with tumor length, tumor site, and age (P = 0.363; P = 0.819; P = 0.599; P > 0.05, respectively). VEGF expression and MVD in GOLPH3-positive CRC was significantly higher than in GOLPH3-negative CRC (VEGF: 69.7% vs 31.0%; MVD: 21.45 ± 9.39 vs 14.24 ± 8.97; P < 0.05). GOLPH3 expression was negatively correlated with AI in CRC as shown by Spearman correlation analysis (r = -0.320, P < 0.05). The 5-year survival rate in GOLPH3-negative CRC (69.4%) was significantly higher than in GOLPH3-positive CRC (48.6%) (log-rank test, P < 0.05)., Conclusion: High expression of GOLPH3 is found in CRC tissues. GOLPH3 expression may be a novel prognostic marker for CRC patients.

Objective: To study the role of Ca2+ overload and energy metabolism in mitochondria in masticatory muscle dysfunctional induced by occlusal trauma., Methods: Mitochondrial Ca2+ contents were measured with atomic emission spectrophotometer. Mitochondrial ATP and ADP contents were measured with high performance liquid chromatography., Results: (1) Mitochondrial Ca2+ contents of masseter muscle ipsilateral to metal splint in ten and twenty days' experimental groups and that contralateral to metal splint in twenty days' experimental group increased significantly (P < 0.05). (2) Mitochondrial ATP contents of masseter muscle ipsilateral to metal splint in experimental groups were higher than that in control groups and contralateral to metal splint after twenty days. (3) Mitochondrial Ca2+ contents of masseter muscle ipsilateral to metal splint were significantly negatively correlated to the mitochondrial ATP contents (r = -0.780, P < 0.05)., Conclusion: Ca2+ overload in mitochondria depresses ATP production, which results in energy metabolism disorder in masticatory muscle cells. It may play an important role in the mechanism that occlusal trauma results in masticatory muscle dysfunction.