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C61H37NO16Zn4, monoclinic, P21/c (no. 14), a = 12.585(6) Å, b = 19.704(8) Å, c = 23.047(5) Å, β = 108.43(1)°, V = 5422.0 Å3, Z = 4, Rgt(F) = 0.0476, wRref(F2) = 0.1168, T = 296 K.

Two new coordination polymers, {[Cd(bda)(bib)]·H2O}n (1) and {[Co(bda) (bib)]·H2O}n (2) (H2bda = benzophenone-2,4′-dicarboxylic acid, bib = 4,4-bis(1-imidazol-yl) -2,5- dimethyl benzene), have been synthesized and characterized by IR, element analysis and single X-ray diffraction. Complexes 1 and 2 are all two-dimensional structure. Complex 1 shows a three-dimensional supramolecular structure through the hydrogen bonding interactions. In 2, the 2D layers adopt AB packing mode. [ABSTRACT FROM PUBLISHER]

Amphibians occupy a key phylogenetic position in vertebrates and evolution of the immune system. But, the resources of its transcriptome or genome are still little now. Bombina maxima possess strong ability to survival in very harsh environment with a more mature immune system. We obtained a comprehensive transcriptome by RNA-sequencing technology. 14.3% of transcripts were identified to be skin-specific genes, most of which were not isolated from skin secretion in previous works or novel non-coding RNAs. 27.9% of transcripts were mapped into 242 predicted KEGG pathways and 6.16% of transcripts related to human disease and cancer. Of 39 448 transcripts with the coding sequence, at least 1501 transcripts (570 genes) related to the immune system process. The molecules of immune signalling pathway were almost presented, several transcripts with high expression in skin and stomach. Experiments showed that lipopolysaccharide or bacteria challenge stimulated pro-inflammatory cytokine production and activation of pro-inflammatory caspase-1. These frog's data can remarkably expand the existing genome or transcriptome resources of amphibians, especially immunity data. The entity of the data provides a valuable platform for further investigation on more detailed immune response in B. maxima and a comparative study with other amphibians. [ABSTRACT FROM PUBLISHER]

The 3D coordination polymer {[Cd(dpa)(bpe)]·2H2O}n (1)[H2dpa = 2,4′-biphenyl dicarboxylic acid and bpe = 1,2-bis(4-pyridyl)ethane] was prepared by hydrothermal synthesis and characterized by single X-ray diffraction, FTIR spectra and element analysis. The title complex 1 exhibits an unusual three-dimensional framework with (6,6)-connected (32.42.52.68.8) (34.44.54.63) topology. Furthermore, the solid-state photoluminescence property of 1 is investigated at room temperature. [ABSTRACT FROM AUTHOR]

Abstract: Enantioselective reduction of β-keto nitriles to optically active 1,3-amino alcohols has been carried out in one step using an excess of borane–dimethyl sulfide complex as a reductant and a polymer-supported chiral sulfonamide as a catalyst with moderate to high enantioselectivity. The facile and enantioselective method to prepare optically active 1,3-amino alcohols to be converted into 3-aryloxy-3-arylpropylamine-type antidepressant drugs (R)-fluoxetine, and (R)-duloxetine is also reported. [Copyright &y& Elsevier]

C61H37NO16Zn4, monoclinic, P21/ c (no. 14), a = 12.585(6) Å, b = 19.704(8) Å, c = 23.047(5) Å, β = 108.43(1)°, V = 5422.0 Å3, Z = 4, Rgt (F) = 0.0476, wRref (F2 ) = 0.1168, T = 296 K. [ABSTRACT FROM AUTHOR]

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Abstract: An operationally simple and mild protocol for the catalytic enantioselective epoxidation of enones has been established using a series of chiral pyrrolidinylmethanol-based dendritic catalysts and tert-butyl hydroperoxide (TBHP) as an oxidant. The epoxides have been obtained in good yields and ee up to 78%. [Copyright &y& Elsevier]

Objective: To explore the toxic effect of bisphenol A on the liver, as well as the influence effect on lipid metabolism., Methods: The toxic effects of bisphenols on human health were studied by using in vivo experiments of bisphenol A exposure in rats and in vitro experiments of human liver cell line HL-7702. Male SD rats were divided into control group(Ctrl), 1 mg/(kg·d) group(low), 5 mg/(kg·d) group(medium) and 25 mg/(kg·d) group(high) for 14 days subacute exposure of bisphenol A, to evaluate the toxic effect of bisphenol A on the liver in terms of body weight, liver organ index, liver pathological tissue sections, serum biochemical indicators. Then HL-7702 was divided into four groups: control group(Ctrl), low concentration treatment group(0. 16 μmol/L), medium concentration treatment group(4 μmol/L) and high concentration treatment group(100 μmol/L). After 24 hours of exposure to bisphenol A, the contents of triglyceride(TG) and total cholesterol(TC) in cells, reactive oxygen species(ROS) levels were detected, and the transcription levels of genes related to lipid metabolism and oxidative stress were detected by fluorescent quantitative PCR., Results: The 14-day subacute exposure had no significant effect on rat body weight and liver body weight ratio, but liver pathological sections clearly showed that bisphenol A exposure can damage liver tissue structure. Serum biochemical indicator of total bile acid(TBA) was significantly reduced in the high-dose group, which was(4. 75±0. 33)μmol/L, creatinine(Cr) was significantly increased in the medium and high-dose group, which were(18. 00±0. 76)μmol/L and(18. 83±0. 75)μmol/L, respectively. TC, high-density lipoprotein(HDL-C) and low-density lipoprotein(LDL-C) were significantly reduced in the middle-and high-dose groups(P<0. 05), which were(1. 44±0. 10), (1. 14±0. 10)mmol/L;(0. 84±0. 04), (0. 63±0. 07)mmol/L and(0. 21±0. 04), (0. 16±0. 05)mmol/L, respectively. Bisphenol A exposure could significantly reduce the content of TC in hepatocytes(P<0. 05). BPA treatment could significantly increase ROS levels in HL-7702 cells. The transcription level of PPARα was significantly increased in the high concentration group, FABP1 was significantly increased in the high concentration group, SOD1 was significantly decreased in the medium and high concentration group(P<0. 05)., Conclusion: Bisphenol A may cause oxidative stress by inducing excessive ROS production in liver cells, leading to liver damage and disorder of lipid metabolism in the body, thereby showing liver toxicity.

Objective: To investigate the role of peroxisome proliferator-activated receptor alpha(PPARα) in perfluorododecanoic acid(PFDoA)-induced liver oxidative damage in rats by observing lentivirus-mediated shRNA targeting and down-regulating PPARα expression in rat hepatocytes BRL 3 A., Methods: A PPARα lentivirus-compatible shRNA interference vector Lenti-iPα and a negative control vector Lenti-NC were constructed, and co-transfected with lentivirus packaging helper plasmids into 293 FT cells for lentivirus packaging. The lentivirus stock solution was collected, concentrated and the virus titer was determined. The experimental grouping was as follows, NC-group(infected with negative control lentivirus, without PFDoA exposure), NC+ group(infected with negative control lentivirus, 75 μmol/L PFDoA exposure), iPα-group(infected with interference lentivirus, without PFDoA exposure), iPα+ group(infected with interference lentivirus, 75 μmol/L PFDoA exposure). Rat hepatocytes BRL 3 A cells were treated with lentivirus for 96 h, and then exposed with 75 μmol/L PFDoA in the NC+ group and iPα+ group in the last 24 h. The interference of PPARα in BRL 3 A cells and the role of PPARα in reactive oxygen species(ROS) changes caused by PFDoA were observed., Results: Lentivirus-mediated shRNA successfully achieved targeted downregulation of PPARα expression in BRL 3 A cells. Compared with the NC-group, the mean fluorescence intensity of ROS in rat hepatocytes BRL 3 A in the iPα-group was 12043. 42±808. 58, significantly increased(P<0. 05); The transcription levels of acyl-CoA thioesterases(Acot) 1 gene and its protein expression levels were 0. 43±0. 04 and 0. 34±0. 08, respectively, both significantly decreased(P<0. 05). After PFDoA treatment, compared with NC+ group, the mean fluorescence intensity of ROS in iPα+ group was 12386. 25±356. 36, which also increased significantly(P<0. 05). The transcription levels of Acot1 gene and its protein expression levels were 0. 85±0. 10 and 0. 33±0. 04, respectively, which also decreased significantly(P<0. 05)., Conclusion: PPARα and its downstream target protein Acot1 may play a role in scavenging ROS in rat hepatocytes BRL 3 A, keeping hepatocytes from oxidative damage caused by foreign substances to the liver.