Bis(µ-2-phenyl-quinoline-4-carboxyl-ato)bis-[aqua-(1,10-phenanthroline)(2-phenyl-quinoline-4-carboxyl-ato)manganese(II)] dihydrate.

In the centrosymmetric dinuclear title complex, [Mn(2)(C(16)H(10)NO(2))(4)(C(12)H(8)N(2))(2)(H(2)O)(2)]·2H(2)O, the Mn(II) cation is in a distorted octa-hedral coordination geometry defined by two N atoms from a 1,10-phenanthroline ligand, one water O atom and three O atoms from three 2-phenyl-quinoline-4-carboxyl-ate anions. A pair of 2-phenyl-quinoline-4-carboxyl-ate anions bridge two Mn cations, forming the dinuclear mol-ecule. An intra-moleculr O-H⋯O hydrogen bond occurs. Inter-molecular O-H⋯O and O-H⋯N hydrogen bonds are present in the crystal structure.

Bis(1,10-phenanthroline-κN,N')[2-(4-sulfonato-anilino)acetato-κO]copper(II) dihydrate.

In the title compound, [Cu(C(8)H(7)NO(5)S)(C(12)H(8)N(2))(2)]·2H(2)O, the Cu(II) ion is coordinated by four N atoms from two 1,10-phenanthroline (phen) ligands and one O atom from a 2-(4-sulfonato-anilino)acetate (spia) ligand in a distorted square-pyramidal geometry. Inter-molecular N-H⋯O and O-H⋯O hydrogen bonds, as well as π-π inter-actions between phen ligands and between phen and spia ligands [centroid-centroid distances = 3.663 (3), 3.768 (3) and 3.565 (3) Å], result in a three-dimensional supra-molecular structure.

Bis(µ-2-phenyl-quinoline-4-carboxyl-ato)-κO,O':O;κO:O,O'-bis-[(2,2'-bipyridine-κN,N')(2-phenyl-quinoline-4-carboxyl-ato-κO,O')cadmium(II)].

The neutral binuclear title complex, [Cd(2)(C(16)H(10)NO(2))(4)(C(10)H(8)N(2))(2)], is centrosymmetric, with the inversion center generating the central (µ-O)(2)Cd(2) bridge. The Cd(II) ion is in a strongly distorted CdN(2)O(5) penta-gonal-bipyramidal geometry, defined by two N atoms from one 2,2'-bipyridine ligand and five O atoms from three 2-phenyl-quinoline-4-carboxyl-ate ligands, one monodentate, two bidentate. Weak inter-molecular π-π inter-actions [centroid-centroid distance = 3.712 (3) Å] help to establish the packing of the structure.

(µ-4,4'-Bipyridine-κN:N')bis-[bis-(N,N-dimethyl-dithio-carbamato-κS,S')zinc(II)].

The title dinuclear Zn(II) complex, [Zn(2)(C(3)H(6)NS(2))(4)(C(10)H(8)N(2))], is centrosymmetric; the mid-point of the C-C bond linking the two pyridine rings is located on an inversion center. The pyridine N atom coordinates to the Zn(II) cation, which is also chelated by two dimethyl-dithio-carbamate anions, giving a trigonal-bipyramidal ZnNS(4) geometry. Weak inter-molecular C-H⋯S hydrogen bonding is present in the crystal structure.

Adipocytokine expression, platelet-to-lymphocyte ratio and TGF-ß1/Smad signaling activity in diabetic patients complicated with pulmonary infection.

OBJECTIVE: To investigate adipocytokine expression levels, platelet-to-lymphocyte ratio (PLR) and transforming growth factor (TGF)-ß1/Smad signaling activity in diabetic patients with pulmonary infection. METHODS: Eighty-two type 2 diabetic patients with pulmonary infection were included in the observation group and 75 patients with simple type 2 diabetes were recruited into the control group. The fasting blood glucose (FBG), glycated hemoglobin (HbA1c), and PLR in the two groups were compared. Complement-C1q/tumor necrosis factor related protein 3 (CTRP-3), complement-C1q/tumor necrosis factor related protein 9 (CTRP-9), leptin, adiponectin, and TGF-ß1/Smad signaling pathway activity in peripheral blood mononuclear cells (PBMCs) was detected. RESULTS: Compared with patients in the control group, patients in the observation group presented with increased levels of FGB, HbA1c, and leptin, an increase in the PLR, and decreased serum CTRP-3, CTRP-9, and adiponectin levels. TGF-ß1, p-Smad2, and p-Smad3 protein expression levels were up-regulated in PBMCs from patients in the observation group compared with the control group. CONCLUSIONS: These results show that in type 2 diabetic patients with pulmonary infection, adipocytokine expression is altered, PLR is disturbed, and the TGF-ß1/Smad signaling pathways in PBMCs are significantly activated.

Preparation of mouse anti-human rotavirus VP7 monoclonal antibody and its protective effect on rotavirus infection.

The aim of the current study was to prepare and identify mouse anti-human rotavirus (RV) VP7 monoclonal antibodies and explore their protective effects on RV infection. The mouse anti-human RV VP7 monoclonal antibody was produced using the ascites method and identified via western blot analysis. In vitro neutralization of mouse anti-human RV VP7 monoclonal antibodies was detected by performing an MTT assay. The TCID50 value was calculated to obtain antibody neutralization titers. A mouse RV infection model was generated to assess the protective effect of the mouse anti-human RV VP7 monoclonal antibody in experimental animals. Monoclonal antibodies were successfully prepared and their purity reached ≥90%. Western blotting demonstrated that monoclonal antibodies specifically bound to the purified Wa RV strain, with a specific reaction band at ~40 kDa. Monoclonal antibody in vitro neutralization results demonstrated that cell survival rate in the virus + monoclonal antibody group was higher than that in virus + maintenance fluid group (P<0.05). Monoclonal antibody neutralization titer detection revealed that the cytopathic effect did not extend beyond 4 days. In addition, the calculated monoclonal antibody neutralization titer was 1:446. The results revealed that the positive rate of colloidal gold RV in the 100 µl monoclonal antibody group was significantly lower than that in the control group (P<0.05). Furthermore, the protection rate of the 100 µl monoclonal antibody group was 71.4%, whereas the 50 µl monoclonal antibody group was 42.9% and the ribavirin group was 57.1%. In conclusion, the results of the current study demonstrated that mouse anti-human RV VP7 monoclonal antibodies can be successfully prepared using ascites method. These antibodies also effectively neutralize the cytotoxic effects of the human RV Wa strain in vitro and mouse anti-human RV VP7 monoclonal antibodies also exhibited a good protective role in mice. Furthermore, greater protective effects were observed at a higher dose and the protective effects of these high dose treatments were superior to that of ribavirin.

Synthesis of an Fe rich amorphous structure with a catalytic effect to rapidly decolorize Azo dye at room temperature.

In this article, an amorphous Fe rich amorphous structure designed based on a competitive atomic cluster model was synthesized and characterized successfully. The constituent zero-valent iron (ZVI) has excellent activity and efficiency for decolorization of Orange G (OG) solution at room temperature. The decolorization is characterized by UV-vis spectrum and pseudo-first-order kinetics. The X-ray Micro fluorescence spectrometer, Inductively Coupled Plasma Optical Emission Spectrometry, and Scanning Electron Microscope were employed to trace the ZVI. The consumption of ZVI destabilizes the local atomic arrangement and yields the phase separation of Fe at the surface and responds to the high activity and the catalysis for decolorization. This observation is in accordance with the change of k1 0.011 min(-1) to k2 0.047 min(-1), which is supported by the cyclic decolorization test. This work provides a new strategy to design multifunctional metal materials and indicates their brilliant future in practical applications.