Three-Dimensional Interpenetrating Frameworks Based on {P4Mo6} Tetrameric Clusters and Filled with In Situ Generated Alkyl Viologens.

Four novel three-dimensional interpenetrating frameworks based on {P4Mo6} units, H[C12H14N2]4[TM4(PO4)(H2O)4Na6][TM2(Mo6O12(HPO4)3(PO4)(OH)3)4]·8H2O (1, 2) and H[C14H18N2]4[TM4(PO4)(H2O)4Na6][TM2(Mo6O12(HPO4)3(PO4)(OH)3)4]·8H2O (3, 4) (TM = Co2+ (1, 3), Mn2+ (2, 4)) were synthesized and characterized using infrared spectroscopy, elemental analyses, thermogravimetric analysis, and single-crystal X-ray diffraction. In situ generated methyl viologen (compounds 1 and 2) or ethyl viologen (compounds 3 and 4) cations function as templates to induce the generation of 2-fold interpenetrating structures in which the {P4Mo6} tetrameric clusters with [TM4(PO4)Na6] (TM = Co2+ (1, 3) and Mn2+ (2, 4)) as the core were bridged by transition metal ions. Compounds 1-4 possess high thermal stabilities and the decomposition temperature of the inorganic frameworks were all >500 °C. It is worth noting that the four compounds all exhibited the bifunctional catalytic performance that they not only had an excellent photocatalytic activity for the reduction of hexavalent chromium (Cr(VI)) under visible light irradiation but also showed a good electrocatalytic activity for the reduction reaction of hydrogen peroxide.

Preliminary study of retinal pathological features in preterm birth pups exposed to an animal model of oxygen-induced retinopathy in mice.

BACKGROUND: The main risk factors of retinopathy of prematurity (ROP) are low gestational age and low birth weight, which are mainly caused by preterm birth. Currently, the animal model of oxygen-induced retinopathy (OIR) in mice is the most widely used model in ROP-associated studies. However, the experimental mice are normal-term pups, and may not mimic the pathogenic status of human ROP patients. In this study, we investigated the retinal pathological features in preterm birth pups exposed to an animal model of oxygen-induced retinopathy in mice. METHODS: Preterm-birth mice were obtained from pregnant C57BL/6J mice that were induced by an intraperitoneal injection of lipopolysaccharide (LPS). The preterm and control mice were treated with high oxygen (75%) from postnatal day 7 (P7) to P12. The mice were perfused with high-molecular-weight FITC-dextran on P12, P15 and P17, and the retinas were whole-mounted and imaged. Vascular endothelial growth factor (VEGF) mRNA was also detected. Cross-sections of the retina were stained with hematoxylin and eosin (H&E) to identify preretinal neovascular tufts. For general observation, whole retinal images were also obtained using a microscope. RESULTS: Leakage of the retinal blood vessels was aggravated in the preterm mice, particularly on P12 and P15. The non-perfused areas of the retina (pixel value, 183,673 ± 28,148 vs 132,110 ± 23,732, P = 0.009) and the number of preretinal endothelial cell nuclei were smaller (30.17 ± 8.33 vs 22.17 ± 6.74, P < 0.0001) on P17. The VEGF mRNA levels in the retinas were higher on P12 and P15 but lower on P17, compared with the control mice. Retinal hemorrhage was observed in the preterm mouse group (five out of six examined eyes). CONCLUSIONS: Preterm-birth mice that were subject to OIR exhibited several pathological features, such as retinal hemorrhage, severe retinal leakage and moderate retinal neovascularization, which were similar to the clinical manifestations in ROP patients.

[Possible mechanism of endothelial progenitor cells in the development of rat choroidal neovascularization].

OBJECTIVE: To investigate the role and possible mechanism of endothelial progenitor cell (EPC) in the development of choroidal neovascularization (CNV). METHODS: Experimental study. Twenty-four BN rats were divided into 3 groups.One eye of each animal was induced by laser photocoagulation with 532 nm laser and the contralateral eye was taken as control. Three, seven and fourteen days after photocoagulation the formation of CNV was observed by histopathological study and the recruitment of EPC and the possible pro-angiogenic growth factors released by EPC during the development of CNV were examined by multi-labeled immunofluorescence staining. The difference among the 3 groups was analyzed by ANOVA and the comparison between any 2 groups was further checked by LSD-t test. RESULTS: Both the histopathological study and the immunofluorescence staining indicated that within the laser lesions proliferated and migrated cells grew into the subretinal space through the broken Bruch membrane 3 days after photocoagulation, 7 days after photocoagulation lumen-like structures were observed and CNV became stable until 14 days after photocoagulation. No EPC was observed in the normal retina whereas EPC were recruited into the laser lesions 3 days after photocoagulation, comprising (79.29 ± 11.27)% of the total endothelial cell population within CNV. At 7-day EPC constituted new vessels within CNV area and the proportion decreased to (47.13 ± 5.78)%. Then its number decreased dramatically 14 days after photocoagulation contributing to (10.83 ± 2.79)% of the endothelial cells in CNV. The differences either among the 3 groups (F = 104.623, P < 0.05) or between any 2 groups (P < 0.05) were statistically significant. Moreover, triple labelled immunofluorescence staining showed that the EPC within CNV area could also secret pro-angiogenic factors such as vascular endothelial growth factor, IL-10, bFGF and MMP9. CONCLUSION: EPC involves in the development of CNV not only through participating in the formation of new vessels within the CNV area but also through secreting pro-angiogenic factors.

Treat-to-Target urate-lowering therapy in primary gout patients: A real-world retrospective study at a dedicated gout clinic in China.

BACKGROUND: Gout is the most common inflammatory arthritis affecting 1.1% of the population in mainland China with a higher prevalence in coastal areas. OBJECTIVE: The purpose of the study was to investigate the clinical outcomes following urate-lowering therapy (ULT) in a real-world group study of primary gout patients in China. METHODS: Electronic medical records of all the gout patients (n= 1588) that visited the Clinical Medical Center of Gout of the Affiliated Hospital of Qingdao University from September 2016 to February 2018 were analyzed in this study. The patients were treated with a standard treat-to-target (T2T) ULT strategy according to the 2016 EULAR Guidelines. Clinical data were collected in the first visit and one-month (defined as the baseline of ULT), 7-month, and 13-month follow-ups were completed. RESULTS: Amongst the patients in the study, 92.70% accepted ULT and 82.93% completed ULT for 3 months, 63.54% for 6 months, and 40.49% (n= 643) for 12 months. Further analysis of the 643 patients included the following data: the sUA level reduced at month 7 and reduced further at month 13. The gout flares, patient global pain visual analogue score, and health assessment questionnaire score improved at month 7 but did not improve further at month 13, and the index tophus size did not.

Integrin-Linked Kinase Controls Choroidal Neovascularization by Recruitment of Endothelial Progenitor Cells.

Purpose: Vasculogenesis has been shown to contribute to the formation of choroidal neovascularization (CNV). However, the mechanism behind the recruitment of endothelial progenitor cells (EPC) to CNV is not well understood. Therefore, we were interested to know whether integrin-linked kinase (ILK) plays a role in recruiting EPC to CNV, and its possible mechanism. Methods: We investigated the effect of hypoxia on retinal pigment epithelium (RPE) cells expressing ILK, hypoxia-inducible factor 1α (HIF-1α), stromal-derived factor-1 (SDF-1), and vascular endothelial growth factor (VEGF), and we further examined the effect of ILK small interfering RNA (siRNA) on their expression. The function of ILK expressed by RPE on EPC in vitro with regard to angiogenic effect was also studied. In vivo, we determined the expression levels of the above factors in CNV. We also examined the role of ILK on their expression, on EPC recruiting, and on the growth of CNV. Results: We found that hypoxia strongly induced the expression of ILK, HIF-1α, SDF-1, and VEGF. Moreover, the silencing of ILK attenuated their expression. It also decreased the phosphorylation of protein kinase B (PKB/AKT) and extracellular regulated protein kinases (ERK) and nearly abolished the proliferation, migration, and adhesion of EPC to RPE cells. In vivo, we showed that these factors were upregulated in CNV. Inhibiting the expression of ILK prohibited the "homing" of EPC to CNV lesions and attenuated the growth of CNV. Conclusions: We demonstrate that ILK controls the development of CNV by regulating the recruitment of EPC to CNV lesions, possibly through ILK-dependent expression of SDF-1 and VEGF in RPE.