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The 16-electron complex CpCoS2C2B10H10 (1) is found to react with the alkynes HC≡CC(O)R [R = methyl (Me), phenyl (Ph), styryl (St), ferrocenyl (Fc)] at ambient temperature to give two types of 17-electron cobalt complexes 2a-d and 3a-d containing unique B(3)/B(6)-norbornyl carborane moieties. A formation mechanism via a tandem sequence of metal-induced B-H activation, B-Cp formation, Cp delivery and Diels-Alder addition is proposed on the basis of DFT calculations. The reactivity of these paramagnetic 17-electron complexes has been studied: Exposed to a combination of air, moisture and silica, complexes 2a-d undergo alkyl C-S cleavage to give 16-electron complexes 4a-c containing a boron-norbornadienyl moiety, and simultaneous carboranyl C-S cleavage to afford cobalt-free carborane derivatives 5a-d containing a boron-norbornyl unit. Both 2a-d and 3a-d allow further alkyne insertion into the Co-S bond to generate cobalt-free boron-norbornyl carborane derivatives (Z/E)-7a-d and (Z/E)-8a-d, both containing a vinyl sulfido group. Addition of AlCl3 not only promotes the conversion of 2a-d, but also leads predominantly to (E)-9a-d as retro-Diels-Alder products. Upon heating, the isomerization from E to Z-configuration of the vinyl group and reorganization of the norbornyl moiety of (Z/E)-7a-d occur to lead to (Z)-9a-d as well as the unexpected [1,2]-H shifted products (Z)-10b,c. Thus, the 17-electron complexes 2a-d and 3a-d serve as intermediates for synthesis of variety of boron-functionalized carborane derivatives. In this study, efficient routes have been developed through cobalt-mediated B-H activation to prepare boron-functionalized carborane derivatives that are unavailable by conventional routes.

For amine-based carbon dioxide capture, nitrogen oxides and sulfur oxides were the main pollutants that had a negative effect on the regeneration of solvent. Before carbon dioxide capture, the sulfur oxides in flue gas should be removed by the method of calcium salt, and then washed by alkaline solution to eliminate the residual nitrogen oxides and sulfur oxides. The washing wastewater containing sulfate and nitrate needs to be treated. In this study, a novel anaerobic-anoxic process was built up for the treatment of this washing wastewater. Nitrate was reduced to nitrogen by denitrifying bacteria. Sulfate was firstly reduced to sulfide by sulfate reducing bacteria, and then selectively oxidized to element sulfur by sulfide oxidizing bacteria. The treated liquid could be reused as absorption after the adjustment of pH value. The performances of this bioprocess were investigated under various pH values and S/N ratios. It was found that the optimal pH value of influent was 6.0, the percentages of denitrification and sulfate reducing could reach 90 and 89%, respectively. Seventy-six percent of sulfate was transformed into element sulfur. Nitrate significantly had a negative effect on sulfate reduction above 10 mM. As 20 mM nitrate, the sulfate reducing percentage would drop to 67%. These results showed that the anaerobic-anoxic process was feasible for the treatment of flue gas washing wastewater. It would be prospectively applied to other wastewater with the higher ratio of SO4(2-)/NO3(-).

Eleven mononuclear copper(II), nickel(II), zinc(II) and cobalt(II) complexes of Schiff base ligands derived from 3,5-dibromosalicylaldehyde/3,5-dichlorosalicylaldehyde were synthesized and determined by single crystal X-ray analysis. The crystal structures of complexes 1, 2, 4, 5, 6, 8 and 11 present the square-planar coordination geometry at the metal center and complexes 7, 9 and 10 show the distorted tetrahedral geometry. While one copper center in 3 has a square-planar geometry, the other copper is slightly distorted square-planar. The inhibitory activities of all the obtained complexes were tested in vitro against jack bean urease. It was found that Schiff base copper(II) complexes 1, 3, 5, 8 and 11 showed strong urease inhibitory activities (IC(50) = 1.51-3.52 μM) compared with acetohydroxamic acid (IC(50) = 62.52 μM), which was a positive reference. Their structure-activity relationships were further discussed., (Copyright © 2012 Elsevier Masson SAS. All rights reserved.)

A new class of stable, strongly π-accepting and modular bis(perfluoroalkyl)-phosphine-oxazoline ligands (FOX) as CO mimics was prepared. It was demonstrated that these ligands, when coordinated to palladium catalysts, promote the asymmetric alkylation of monosubstituted allyl substrates with excellent regio- and enantioselectivity. Solid and solution structure analysis of the FOX-ligated Pd-allyl intermediate reveals that the combination of relative steric and strong trans influences presented by the P(CF(3))(2) moiety gave rise to the excellent selectivity.

Five mononuclear copper(II) and nickel(II) complexes of Schiff base ligands derived from 4-hydroxyphenethylamine and 2-phenylethylamine were synthesized and determined by single crystal X-ray analysis. The crystal structures of these complexes presented the square planar coordination geometry at the metal center. The inhibitory activity of all the obtained complexes was tested in vitro against jack bean urease. It was found that Schiff base copper(II) complexes, namely [Cu(C(15)H(13)BrNO(2))(2)]·2(C(6)H(7)N) (1), [Cu(C(15)H(12)Br(2)NO(2))(2)]·2(DMF) (2), Cu(C(19)H(16)NO(2))(2) (3) and Cu(C(19)H(16)NO)(2) (5), showed strong inhibitory activity against jack bean urease (IC(50)=1.45-3.59 μM), while Schiff base nickel(II) complex, [Ni(C(19)H(16)NO(2))(2)]·2(DMF) (4), exhibited weak inhibitory activity (IC(50)>50 μM). Their structure-activity relationships were further discussed., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Six transition metal compounds of Schiff base ligands were evaluated for the inhibitory activity on jack bean urease, of which compounds 2-6 were determined by single crystal X-ray analysis. It was found that copper(II) complexes 1 and 4 showed strong inhibitory activity against jack bean urease (IC(50) = 0.52 and 0.46 microM), compared with acetohydroxamic acid (IC(50) = 42.12 microM) as a positive reference. Cobalt(II), nickel(II) and zinc(II) compounds also exhibited potent inhibitory activity (IC(50) = 3.88-25.20 microM). A docking analysis using the AUTODOCK 4.0 program could explain the inhibitory activities of 1 and 4 against urease., (Copyright (c) 2010 Elsevier Masson SAS. All rights reserved.)

Treatment of ortho-carborane, n-butyl lithium, sulfur, and CpCo(CO)I(2) with differing ratios led to four new compounds [(CpCoS(2)C(2)B(10)H(10))(CpCoSC(2)B(10)H(11))(SC(4)H(9))] (3), [(CpCo)(2)S(2)(S(2)C(2)B(10)H(10)) (SC(2)B(10)H(10))(SC(4)H(9))] (4), [(CpCo)(2)Co(SC(4)H(9))(6)](+)[Co(S(2)C(2)B(10)H(10))(2)](-) (5), and [(CpCo)(2)Co(SC(2)B(10)H(11))(SC(4)H(9))(5)](+)[Co(S(2)C(2)B(10)H(10))(2)](-) (6). Compound 3 contains a rhombic Co(2)(mu(2)-S)(2) core and can be considered as an adduct of the two 16e half-sandwich monomers CpCo(S(2)C(2)B(10)H(10)) (1) and CpCo(SC(4)H(9))(SC(2)B(10)H(11)). Compound 4 is a trinuclear complex containing a cuboidal [Co(3)(mu(3)-S)(2)(mu-S)(2)] core, and one cobalt atom is coordinated by six sulfur atoms in a distorted octahedral geometry. Compound 5 consists of a linear-type trinuclear cobalt(III) monocation bridged by six n-butyl thiolato units and a square-planar cobalt(III) monoanion [Co(S(2)C(2)B(10)H(10))(2)](-). However, in 6, one ortho-carborane monothiolato ligand [SC(2)B(10)H(11)](-) has replaced one n-butyl thiolato ligand in 5. This leads to a nonlinear arrangement of the three cobalt atoms in the cation and the nonplanar [Co(S(2)C(2)B(10)H(10))(2)](-) anion in 6. Interestingly, the treatment of the 16e half-sandwich CpCo(S(2)C(2)B(10)H(10)) (1) by [N(n-Bu)(4)]Br afforded the ionic compound 7, [N(n-Bu)(4)](+)[Co(S(2)C(2)B(10)H(10))(2)](-), containing a square-planar anion.

The reactions of the 16e half-sandwich complex, CpCo(S(2)C(2)B(10)H(10)) (1), with alkynones at ambient temperature lead to complexes CpCo(S(2)C(2)B(10)H(9))(CH=CH-C(O)R) (R = Ph (2), 2-naphthyl (3)). Both 2 and 3 are still 16e half-sandwich complexes containing a B(3)-substituted ortho-carborane-1,2-dithiolate ligand. Treatment of 2 with excess alkynes R(1)C[triple bond]CR(2) (R(1) = H, R(2) = Ph, C(O)Ph, CO(2)Me; R(1) = R(2) = CO(2)Me) affords five complexes, CpCo(S(2)C(2)B(10)H(8))(CH(2)CPh)(CH=CH-C(O)Ph) (4), CpCo(S(2)C(2)B(10)H(8))(CH=CH-C(O)Ph)(2) (5), CpCo(S(2)C(2)B(10)H(8))(CH=CH-CO(2)Me)(CH=CH-C(O)Ph) (6), CpCo(S(2)C(2)B(10)H(9))(MeO(2)C-C=C-CO(2)Me)(CH=CH-C(O)Ph) (7), and CpCo(S(2)C(2)B(10)H(9))(MeO(2)C-C=C-CO(2)Me)(2)(CH=CH-C(O)Ph) (8). Complex 4 is an 18e complex bearing a B-CH(2) unit. Both 5 and 6 retain a 16e half-sandwich structure but contain a B(3,6)-disubstituted ortho-carborane-1,2-dithiolate ligand. However, in 7 and 8 one or two alkynes are inserted into one of the Co-S bonds to generate 18e species, respectively. Heating 7 leads to the 16e complex, CpCo(S(2)C(2)B(10)H(8))(MeO(2)C-C=CH-CO(2)Me)(CH=CH-C(O)Ph) (9), having a B(3,6)-disubstituted ortho-carborane-1,2-dithiolate ligand as in 5 and 6. All complexes were fully characterized by spectroscopic techniques and elemental analysis. The solid-state structures of 2 and 3 and 5-9 were further characterized by X-ray structural analysis.

Gap junctions (GJs), collections of multiple intercellular channels between neighboring cells, are specialized channels facilitating intercellular electrical and chemical communication. GJs are important for synchronizing coupling and coordinated contraction in the heart, and are crucial regulators of heart gene transcription, cardiac development, and protection of ischemic cardiomyocytes through second messenger communication. Identification of proteins that interact with Connexin43 (Cx43), the predominant protein in cardiac GJs, may contribute to the understanding of GJ functional regulation. Using a yeast two-hybrid system, we identified Caveolin-3 (Cav3) as a new Cx43-interacting protein. This interaction was confirmed by co-immunoprecipitation and co-localization experiments. CX43 interacts with Cav3, suggesting that Cav3 may participate in the functional regulation of GJs.

The reaction of the 16e half-sandwich complex CpCo(S(2)C(2)B(10)H(10)) (1) with HC[triple bond]C-C(O)Ph leads to a 17e complex 2 containing a bicyclo[2.2.1]heptene unit at the B3/B6 site of carborane. In the presence of air, water and silica 2 converts to two 16e complexes, 3 and 4, bearing new types of functionalized groups.

Objective: To construct an engineering strain of higher desulfurization activity with Vitreoscilla hemoglobin gene (vgb) for desulfurization of diesel., Methods: We constructed the vgb expressing plasmid, pPR-Pdsz-vgb and transformed by electroporation to Pseudomonas delafieldii R-8, then obtained a genetic engineering strain R-8-2., Results: The results of CO-difference spectrum analysis indicated that R-8-2 expressed Vitreoscilla hemoglobin (VHb) having biological activity expressed in strain R-8-2. Compared with the wild-type R-8, the density of strain R-8-2 increased by 20%, and its desulfurization activity is also higher in the lower deliquescence oxygen environment. In the end, about 69.9% of total sulfur in diesel oil was removed by strain R-8-2, whereas only 57.2% of sulfur was removed by strain R-8., Conclusion: The activity of strain R-8-2 was enhanced and furthermore, the work is helpful for further development in biodesulfurization.

We first cloned the dsz operon of Pseudomonas delafieldii R-8 into the expressing plasmid (pPR9TT) to construct the recombinant plasmid pPR-dsz, and then reintroduced it into strain R-8 to obtain a muti-copy dsz operon engineering strain R-8-1. Compared with the wild-type, strain R-8-1 showed a higher desulfurization activity for dibenzothiophene (DBT). Initial rates of DBT removal by strain R-8-1 were 6.25 micromol/g dry cell/h, about 2-fold higher than that for wild-type strain. The recombinant cells were also applied in the desulfurization of diesel. It resulted in a 68% reduction of total sulfur from 310.8 mg/L to 100.1 mg/L, whereas only 53% of sulfur was removed by strain R-8. The stability of pPR-dsz in strain R-8-1 was studied. The results revealed the first obtain a muti-copy dsz operon engineering strain are helpful for further development in biodesulfurization.

Urotensin II (UII) is a potent vasoconstrictive peptide; however, its significance in vascular adventitia has not been clearly elucidated. In this study, rat aortic adventitia showed mRNA expression and immunoreactivity of UII and its receptor (UT). Moreover, radioligand-binding assay showed that maximum binding capacity (Bmax) of [(125)I]-UII was higher in adventitia than in media (28.60+/-1.94 vs. 20.21+/-1.11 fmol/mg, P<0.01), with no difference in binding affinity (dissociation constant [Kd] 4.27+/-0.49 vs. 4.60+/-0.40 nM, P>0.05). Furthermore, in cultured adventitial fibroblasts, UII stimulated DNA synthesis, collagen synthesis and secretion in a concentration-dependent manner. These effects were inhibited by the UII receptor antagonist urantide (10(-6) mol/l), Ca(2+) channel blocker nicardipine (10(-5) mol/l), protein kinase C inhibitor H7 (10(-6) mol/l), and mitogen-activated protein kinase inhibitor PD98059 (10(-6) mol/l) but not the phosphatidyl inositol-3 kinase inhibitor wortmannin (10(-7) mol/l). UII may act as an autocrine/paracrine factor through its receptor and the Ca(2+) channel, protein kinase C, and mitogen-activated protein kinase signal transduction pathways, in the pathogenesis of vascular remodeling by activating vascular adventitia.

Treatment of 1a and 1b with phenylacetylene, 1,4-diethynylbenzene, and ethynylferrocene affords addition complexes, (p-cymene)Ru(mu-E2)Ru(S2C2B10H10)2(R1C=CR2), (R1 = Ph (H), R2 = H (Ph), 2a, 2b, 3a, 3b; R1 = -Ph-C[triple bond]CH (H), R2 = H (-Ph-C[triple bond]CH), 4a, 4b, 5a, 5b; R1 = Fc (H), R2 = H (Fc), 6a, 6b, 7a, 7b). Alkyne addition occurs at sulfur atoms of two different chelating 1,2-dicarba-closo-dodecaborane-1,2-dithiolate ligands that leads to a change of 16e Ru(IV) in 1a and 1b to 18e Ru(II) in 2a-7a and 2b-7b, respectively. Moreover, the reaction of 1a with ethynylferrocene produces an unprecedented tetranuclear mixed-valent Ru(IV)Ru(II)3S12 cluster (8a) consisting of two 1a and one ethynylferrocene through the cleavage and generation of Ru-S, S-S, and C-S bonds. The complexes were characterized by IR, MS, and NMR spectroscopy and microanalysis. X-ray structural analyses were performed on 1b, 2a, 3b, 5a, 5b, 7b, and 8a.

The objective of this study is to investigate the effects of preconditioning on the restoration and distribution of connexin 43 (Cx43) in ischemic myocardium in dogs. In this study, 40 dogs were randomly divided into 5 groups of 8 as follows: control, 0hI-R (ischemia followed by 0 h reperfusion), 6hI-R (ischemia followed by 6 h reperfusion), 24hI-R (ischemia followed by 24 h reperfusion), and 48hI-R (ischemia followed by 48 h reperfusion). Four dogs in each group were preconditioned with brief episodes of ischemia prior to the respective treatments and were referred as the PC groups, while the other 4 were not preconditioned and were referred as the nonPC groups. The myocardial ischemia was induced by ligation of the left anterior descending coronary artery. The expression and distribution of Cx43 within the ischemic myocardium were measured by Western blot analysis and studied using laser confocal microscopy using a double-label immunohistochemistry technique. Compared with the control group, there was a significant reduction in Cx43 content within ischemic myocardium of all test groups both with and without PC (P < 0.01, P < 0.05). Within the 0hI-R, 6hI-R, and 24hI-R groups, an insignificant difference was found in the expression and distribution of Cx43 within the ischemic region between the PC and the nonPC groups. However, in the 48hI-R group, the area and intensity of Cx43 staining within the ischemic region of the PC dogs were significantly larger and more intense than those of the nonPC dogs (P < 0.01), and the ratio of Cx43 pixel density in intercalated disk areas to that in side-to-side junction areas in the PC dogs was significantly greater than that in nonPC dogs (P < 0.01). Our results suggest that preconditioning has a significant effect on the restoration and distribution of Cx43 in the ischemic myocardium in dogs after 48 h. Hence, preconditioning may be a plausible cause for the observed reductions in cardiac arrhythmias.

The vgb gene, encoding Vitreoscilla hemoglobin (VHb), was introduced into a specific desulfurization bacterium, Rhodococcus erythropolis LSSE8-1. The VHb-specific spectrum was observed for the recombinant. Compared to the wild type, the strain bearing vgb showed a higher biomass yield and desulfurizing activity.

Background: The ubiquitin-proteasome system (UPS) is thought to be functionally active in atherosclerosis (AS) lesions. Aspirin was found to be a potent inhibitor of the UPS in some tumour studies; however, its effect on AS remains to be demonstrated in vivo., Methods: New Zealand rabbits were placed on a normal diet (N) or on a normal diet with aspirin (NI) or on an atherogenic diet without (H) or with aspirin (HI) for 12 weeks. Proteasome activity, concentrations of plasma lipids and levels of peroxidation were determined. Ubiquitin/ubiquitin-conjugates (Ub), IkappaBalpha, phosphorylated IkappaB (pIkappaBalpha) and p65 were investigated by Western blotting or immunochemistry., Results: Concentrations of plasma lipids and peroxidation levels were higher in H or HI vs. N or NI. Histological analysis showed that atheroma was increased in H. Ub and IkappaBalpha were mainly localised in subendothelium and media vascular smooth muscle cells. Western blots revealed that Ub, IkappaBalpha, and pIkappaBalpha were increased, whereas p65 was lower in HI vs. H. The activity of the 20S proteasome was functionally active in H vs. N, NI or HI, while the 26S proteasome was not affected in any of the groups., Conclusions: Aspirin can attenuate the pathogenesis of atheroma formation, the degradation of IkappaBalpha and pIkappaBalpha, and lower the expression of p65, indicating that its therapeutic effects on AS may be via inhibition of the UPS.

Background: To study the effect and safety of tissue specific gene therapy of suicide gene for lung adenocarcinoma., Methods: Retroviral vector of G1CEACDNa contained a carcinoembryonic antigen (CEA) promoter regulated cytosine deaminase expression cassete (CEA/CD). By means of infection of virus, tissue specific expressing vectors and non-specific expressing vectors were transfected into A549 cell, which was CEA-producing lung adenocarcinoma cell line and then xenografted in nude mice, and the anti-tumor effect was evaluated. Then the retrovirus was injected directly into the tumor mass on nude mice, and the sensitivity of the xenograft to G1CEACDNa/5-fluorocytosine (5-FC) and the side effects were observed., Results: (1) After transfected and untransfected A549 cells were implanted into nude mice, there was no difference in tumor formation among all the groups. (2) After 5-FC administration, the tumor transfected with tissue-specific gene displayed a higher sensitivity to the drug than those treated with non-specific in vitro gene-therapy. (3) The tumor-bearing nude mice were randomized in a blind manner based on comparable size to receive the supernatant of recombinant retrovirus G1CEACDNa followed by 5-FC, and significant growth suppression could be observed. (4) Comparing to the group with injection of 5-fluorouracil (5-FU) alone, tissue-specific suicide gene therapy showed lower suppression to bone marrow., Conclusions: The results suggest that tissue-specific suicide gene therapy may play an important role in individual treatment of lung cancer.