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Background: The progression of liver disorders is frequently associated with inflammatory bowel disease through the gut-liver axis. However, no direct evidence showed the mechanisms of ulcerative colitis (UC) in the development of liver fibrosis per se. Thus, this study aimed to evaluate the effects of UC on liver fibrosis and its potential mechanism in the experimental model. Methods: Male C57BL/6 mice were allocated into five groups (n = 10 per group) to receive either drinking water (control), 2% dextran sulfate sodium (DSS), olive oil, carbon tetrachloride (CCl4) or DSS + CCl4 for 4 cycles. Blood was collected for biochemical analysis. Colons were excised for the evaluation of colon length and morphological score. Liver, colon, and mesenteric lymph nodes (MLNs) were collected for histopathological staining, expression analysis, and bacterial translocation assay to evaluate the inflammation, fibrosis, the activation of hepatic stellate cells (HSCs), and gut barrier function. Results: DSS caused severe colitis in mice treated or treated with CCl4, as evident from the elevation of disease activity index (DAI), histological abnormalities, and increased pro-inflammatory cytokines (TNF-α, IFN-γ, and IL-17A). Histopathological staining revealed that DSS treatment aggravated the CCl4-induced extracellular matrix deposition, liver fibrosis, and inflammation in mice. Additionally, biochemical and expression analysis indicated the DSS treatment caused the increase of hydroxyproline and pro-inflammatory cytokines, as well as the abnormal liver function indexes in CCl4-induced mice. Gut barrier function was impaired in DSS- and DSS + CCl4-treated mice, manifesting as the increase in bacterial translocation and lipopolysaccharide level, and the reduction in tight junction proteins (occluding, claudin-1 and ZO-1) expression. Further, the activations of HSCs and TLR4 signaling pathway were observed after DSS + CCl4 treatment, presenting with the increase in expression of α-SMA, vimentin, TGF-β, collagen type I, collagen type II, TIMP-2, TLR4, TRAF6, and NF-κB p65, and a decrease in GFAP and MMP-2 expression. Conclusion: The present study verified that UC aggravated CCl4-induced liver injury, inflammation, and fibrosis in mice through the gut-liver axis. Gut barrier dysfunction in UC leads to bacterial translocation and elevated lipopolysaccharide, which may promote the activation of TLR4 signaling and HSCs in the liver. [ABSTRACT FROM AUTHOR]

C18H14N6O6Cd, monoclinic, C2/c (no. 15), a = 27.000(3) Å, b = 7.0750(8) Å, c = 10.5576(11) Å, β = 110.080(2)°, Z = 4, V = 1894.2(4) Å3, Rgt(F) = 0.0370, wRref(F2) = 0.0584, T = 296 K. [ABSTRACT FROM AUTHOR]

A new Ho(II) polymer [Ho(ctdc)]n 1 (H3ctdc = 5'-(4-Carboxyphenyl)-[1,1':3',1"-terphenyl]-4,4"-dicarboxylic acid) was synthesized under hydrothermal conditions. The compound crystallizes in the Monoclinic system, space groupP2(1)/c with a = 17.5782(4), b = 28.6807(5), c = 9.5889(2)Å, α = 90, β = 101.956(2), γ = 90°, V = 4729.44(16) ų, Z = 4, Mr = 618.34, Dc = 0.868 Mg/m³, µ = 3.321 mm-1, F(000) = 1208, the final R = 0.0723 and wR = 0.2343 for 5974 observed reflections with I > 2σ(I). The compound presents a three-dimensional (3 D) network extended by both ctdc3- anions in which the ctdc3- anions employ a chelating coordination mode. From the topology point of view, the structure could be described as a 6-connected 3 D network with (46. 64) topology net. Infrared spectroscopy, elemental analyses, thermogravimetric analysis and powder X-ray diffraction properties of 1 are also investigated. [ABSTRACT FROM AUTHOR]

(Fe50Co25B15Si10)80Cu20 ribbons are prepared by using the single-roller melt-spinning method. A dual-layer structure consisting of a (Fe, Co)-rich amorphous phase and a Cu-rich crystalline phase forms due to metastable liquid phase separation before solidification. The magnetic hysteresis loops of the as-quenched and annealed samples are measured at room temperature. It is indicated that the coercivity of the ribbon is almost zero in the as-quenched state. The crystallization leads to the increase of coercivity and decrease of saturation magnetization. [ABSTRACT FROM AUTHOR]

The title complex {[Yb(1,4-BDC)(HO)]·HO} (1) (1,4-BDC = 1,4-benzenedicarboxylate) has been hydrothermally synthesized and structurally characterized by the single crystal X-ray diffraction. Crystals of compound 1 belongs to the triclinic crystal system, space group P-1; a = 7.549(3) Å, b = 10.072(4) Å, c = 10.470(4) Å, α = 87.810(4)°, β = 82.531(4)°, γ = 86.306(4)°, V = 787.3(5) Å, Z = 2. The Yb(III) atoms are linked by the deprotonated 1,4-BDC ligands in two kinds of bridging modes. Four Yb(III) atoms at each corner (nodes) and four 1,4-BDC ligands at each edge (spacers) form a edge-sharing 36-membered rings. The rhombohedral Yb(1,4-BDC) arranged in an alternating fashion to construct a 1D ladder-like chain along the c axis. Two neighboring chains are linked to each other in a parallel fashion to construct 3D supramolecular structure by O-H···O hydrogen bonds and π- π stacking interactions. In addition, the properties of thermogravimetric analysis and magnetic behaviors of the complex have been also discussed. Graphical Abstract: 1,4-Benzenedicarboxylate-bridged Yb(III) coordination polymer {[Yb(1,4-BDC)(HO)]·HO} was hydrothermally synthesized and characterized structurally. Yb(III) center is linked to three Yb(III) ions via the three 1,4-BDC ligands to form a edge-sharing 36-membered rings. The rhombohedral Yb(1,4-BDC) arranged in an alternating fashion construct a 1D ladder-like chain along the c axis. Magnetic behaviors have been also discussed.[Figure not available: see fulltext.] [ABSTRACT FROM AUTHOR]

C36H28N8, triclinic, P1̅, a = 10.5381(10) Å, b = 11.2172(11) Å, c = 14.0925(13) Å, α = 73.912(3)°, β = 68.626(3)°, γ = 62.739(3)°, V = 1366.7(2) Å3, Z = 2, Rgt (F) = 0.0593, wRref (F2 ) = 0.1429, T = 293(2) K. [ABSTRACT FROM AUTHOR]