Search

A series of diorganotin(IV) and triorganotin(IV) compounds of the type [R2Sn(pca)2ClSnR3]2 (R PhCH2 1, 2-ClC6H4CH2 2, 2-FC6H4CH2 3, 4-FC6H4CH2 4, 4-CNC6H4CH2 5, 4-ClC6H4CH2 6, 2,4-Cl2C6H3CH2 7; Hpca 2-methylpyrazine-5-acid), [(nBu)3Sn(pca)]∞ 8, [(CH3)2Cl2Sn(pca)Sn(CH3)2(pca)]∞ 9, {[(nBu)2Sn(pca)]2O}2 10 and {[Ph2Sn(pca)]3O2[Ph2Sn(OCH3)]} 11 have been obtained by reactions of 2-methylpyrazine-5-acid with triorganotin(IV) chloride, diorganotin(IV) dichloride, and diorganotin(IV) oxide. All compounds were characterized by elemental, IR, and NMR spectra analyses. The crystal structure of compounds 1, 8–11 were determined by X-ray single crystal diffraction, which revealed that compound 1 was tetranuclear macrocyclic structures with seven-coordinate and five-coordinate tin atoms, compounds 8 and 9 were polymeric chain structures with five-coordinate and seven-coordinate tin atoms, compounds 10 and 11 were monomeric structures with six-coordinate and five-coordinate tin atoms.

To observe the efficacy of regular or intermittent inhalation of salmeterol/fluticasone propionate (SM/FP) in the treatment of bronchial asthma and its effects on growth and development in children.A total of 112 children diagnosed with bronchial asthma between September 2012 and October 2013 were assigned to standardized treatment (standard group, n=56) and non-standardized treatment (intermittent group, n=56). Comparisons of clinical symptom scores and main pulmonary function indicators between the two groups were carried out before treatment and at 6 and 12 months after treatment. The growth velocity and changes in body mass index (BMI) were observed in the two groups.At 6 and 12 months after the treatment, the standard group had significantly reduced clinical symptom scores and significantly increased pulmonary function indicators (percentage of predicted peak expiratory flow, PEF%; percentage of forced expiratory volume in 1 second, FEV1%) (P0.05); the intermittent group had significantly reduced clinical symptom scores and significantly increased FEV1% (P0.05), but PEF% was significantly increased only at 6 months after treatment (P0.05). At 12 months after treatment, the standard group had significantly lower clinical symptom scores and significantly higher PEF% and FEV1% when compared with the intermittent group (P0.05). The growth velocity and BMI showed no significant differences between the two groups at 6 and 12 months after treatment (P0.05).Compared with intermittent inhalation, long-term regular inhalation of SM/FP performs better in controlling clinical symptoms and enhancing pulmonary function in children with asthma. Inhalation of SM/FP for one year reveals no apparent effect on the growth and development of these children.

Low-temperature heat capacities of a solid complex Zn(Val)SO4·H2O(s) were measured by a precision automated adiabatic calorimeter over the temperature range between 78 and 373 K. The initial dehydration temperature of the coordination compound was determined to be, TD=327.05 K, by analysis of the heat-capacity curve. The experimental values of molar heat capacities were fitted to a polynomial equation of heat capacities (Cp,m) with the reduced temperatures (x), [x=f (T)], by least square method. The polynomial fitted values of the molar heat capacities and fundamental thermodynamic functions of the complex relative to the standard reference temperature 298.15 K were given with the interval of 5 K. Enthalpies of dissolution of the [ZnSO4·7H2O(s)+Val(s)] (Δsol Hm,l0) and the Zn(Val)SO4·H2O(s) (Δsol Hm,20) in 100.00 mL of 2 mol dm−3 HCl(aq) at T=298.15 K were determined to be, Δsol Hm,l0=(94.588±0.025) kJ mol−1 and Δsol Hm,20=–(46.118±0.055) kJ mol−1, by means of a homemade isoperibol solution–react...

Low-temperature heat capacities of the solid coordination compound Zn(Leu)SO(4)center dot 1/2H(2)O(s) were measured by a precision automated adiabatic calorimeter over the temperature range between T = 78 K and T = 371 K. The initial dehydration temperature of the coordination compound was determined to be T-D = 326.50 K by analysis of the heat-capacity curve. The experimental values of molar heat capacities were fitted to a polynomial equation of heat capacities (C-p,C-m) with the reduced temperatures (x), [x = f (T)] by least-squares method. Enthalpies of dissolution of the [ZnSO(4)center dot 7H(2)O(s) + Leu(s)] ( Delta(sol)H degrees(m,1)) and the Zn(Leu)SO(4)center dot 1/2H(2)O(s) (Delta(sol)H degrees(m,2)) in 100.00 mL of 2 mol center dot dm(-3) HCl(aq) at T = 298.15 K were determined to be Delta solH degrees(m,1) = -(85.80 +/- 0.09) kJ center dot mol(-1) and Delta solH(m,2) = (55.97 +/- 0.06) kJ center dot mol(-1) by means of a homemade isoperibol solution-reaction calorimeter. The standard molar enthalpy of formation of the compound was determined as Delta H degrees(m)(Zn(Leu)SO(4)center dot 1/2H(2)O, s, 298.15 K) = -(1999.0 +/- 0.9) kJ center dot mol(-1) from the enthalpies of dissolution and other auxiliary thermodynamic data through a Hess thermochemical cycle. Furthermore, the reliability of the Hess thermochemical cycle was verified by comparing UV/Vis spectra and the refractive indexes of solution A (from dissolution of the [ZnSO(4)center dot 7H(2)O(s) + Leu(s)] mixture in 2 mol center dot dm(-3) hydrochloric acid) and solution A' (from dissolution of the complex Zn(Leu)SO(4)center dot 1/2H(2)O(S) in 2 mol center dot dm(-3) hydrochloric acid).

The two solid-state coordination reactions (1) CuAc 2 · H 2 O ( s )+2 Ala ( s )→trans- Cu ( Ala ) 2 ( s )+2 HAc ( l )+ H 2 O ( l ) (2) CuAc 2 · H 2 O ( s )+2 Gly ( s )→trans- Cu ( Gly ) 2 · H 2 O ( s )+2 HAc ( l ) have been studied by solution calorimetry. The molar dissolution enthalpies of the reactants and the products in some solvents (such as 2 mol l−1 HCl or its solutions) of these solid–solid coordination reactions have been measured by an isoperibol solution calorimeter. The standard molar formation enthalpies of [trans-Cu(Ala)2(s), 298.15 K] and [trans-Cu(Gly)2(s), 298.15 K] have been determined to be −1015.42 ± 0.06 and 1252.36 ± 0.05 kJ mol−1, respectively, from the results of the molar dissolution enthalpies and other auxiliary thermodynamic data.

The solid-state coordination reactions: 2 HQ ( s )+ Co ( Ac ) 2 ·4 H 2 O ( s )→ Co ( HQ ) 2 ·2 H 2 O ( s )+2 HAc ( l )+2 H 2 O ( l ) 2 HQ ( s )+ Zn ( Ac ) 2 ·2 H 2 O ( s )→ Zn ( HQ ) 2 · H 2 O ( s )+2 HAc ( l )+ H 2 O ( l ) have been studied by solution calorimetry. The molar dissolution enthalpies of the reactants and the products in a certain solvent, 4 mol l −1 HCl, of this solid–solid coordination reaction have been measured using an isoperibol calorimeter. From the results and other auxiliary quantities, the standard molar formation enthalpies of [Co(HQ) 2 ·2H 2 O(s), 298.15 K], [Zn(HQ) 2 ·H 2 O(s), 298.15 K] and have been determined to be Δ f H m Θ (Co(HQ) 2 ·2H 2 O(s), 298.15 K)=−766.9±3.0 kJ mol −1 , Δ f H m Θ (Zn(HQ) 2 ·H 2 O(s), 298.15 K)=−580.7±3.0 kJ mol −1 .

Solubilities of potassium tetraphenylborate in water, methanol, ethanol, 1-propanol, 1-butanol, 1-pentanol, 1-hexanol, and 1-octanol at 15, 25, 35, 45, 55°C have been determined by spectrophotometry. The standard Gibbs energy of transfer of potassium tetraphenylborate form water to straightchain n-alkanols and the medium effect of potassium tetraphenylborate from 15 to 55°C have been calculated. Furthermore, the contribution of microscopic interactions to the standard Gibbs energy of transfer of potassium tetraphenylborate is calculated and discussed.

To investigate the mechanism of loss of human esophageal cancer-related gene 4 (ECRG4) expression in esophageal squamous cell carcinoma (ESCC.)PCR-SSCP and DNA sequencing analysis were used to detect the mutation of ECRG4 exons in esophageal cancer and matched adjacent normal tissues of 80 patients. DNA bisulfite-modifying ssPCR sequencing assay was used to examine the methylation status of ECRG4 promoter in human esophageal squamous cell carcinoma EC9706 cells. The re-expression of ECRG4 mRNA was examined by RT-PCR in EC9706 cells, after treatment with either demethylation drug 5-aza-2'-deoxycytidine or arsenic trioxide.No mutation in the four ECRG4 exons was found in all the ESCC and matched normal adjacent tissues. RT-PCR showed that 11 of 16 CpG islands of ECRG4 promoter were hypermethylated, while ECRG4 mRNA expression level was undetectable in the EC9706 cells. The ECRG4 mRNA was re-expressed after treatment with either demethylation drug 5-aza-2'-deoxycytidine or arsenic trioxide.The epigenetic mechanism of methylation is a reason of loss of ECRG4 gene expression in the ESCC cell line EC9706.

To investigate the tumor-suppressing function of human esophageal cancer related gene 4 (ECRG4) in esophageal squamous cell carcinoma (ESCC).The recombinant plasmid pcDNA3.1-ECRG4 with ECRG4 open reading frame was constructed. The EC9706 cell was transfected with either pcDNA3.1 or pcDNA3.1-ECRG4. And the effects of ECRG4 on tumor cell were examined by in vivo assays of cell proliferation, adhesion, migration, invasion and tumor growth. The expression levels of P53 and P21 proteins were detected in EC9706 cell with transfection of ECRG4 gene by Western blotting.The final tumor volume and weight in ECRG4 transfection group were (264±43) mm3 and (0.39±0.09) g, versus (464±128) mm3 and (0.76±0.13) g in control group (both P0.05). And the capacities of tumor cells adhesion, migration and invasion decreased in ECRG4 transfection group versus that in control group (all P0.05). Furthermore, the expression levels of P53 and P21 proteins were higher in ECRG4 transfection group than those in control group (100.00±3.87, 35.71±2.36 vs 16.6±1.92, 1.09±0.11, both P0.05).As a novel candidate tumor suppressor in ESCC, ECRG4 may induce the up-regulation of p21 protein through p53 pathway to inhibit tumor growth in ESCC.

Microtubule (MT) kinesin motor proteins orchestrate various cellular processes (e.g. mitosis, motility and organelle transportation) and have been implicated in human carcinogenesis. Kif18A, a plus-end directed MT depolymerase kinesin, regulates MT dynamics, chromosome congression and cell division. In this study, we report that Kif18A is overexpressed in human breast cancers and Kif18A overexpression is associated with tumor grade, metastasis and poor survival. Functional analyses reveal that ectopic overexpression of Kif18A results in cell multinucleation, whereas ablation of Kif18A expression significantly inhibits the proliferative capability of breast cancer cells in vitro and in vivo. Inhibition of Kif18A not only affects the critical mitotic function of Kif18A but also decreases cancer cell migration by stabilizing MTs at leading edges and ultimately induces anoikis of cells with inactivation of the phosphatidylinositol 3-kinase-Akt signaling pathway. Together, our results indicate that Kif18A is involved in human breast carcinogenesis and may serve as a potential therapeutic target for human breast cancer.

To investigate the correlation between the lack of estrogen receptor (ER) gene expression and hypermethylation of ER gene, and detect whether re-expressed ER protein is activated.The methylation status of ER gene promoter in the ER-negative breast cancer cells was evaluated by methylation specific PCR (MSP) and genomic sequencing. The expression of ER and progesterone receptor (PR) mRNA as well as the production of ER protein were detected by RT-PCR and Western blot method, respectively. MTI assay was used to examine the function of re-expressed ER protein.The ER gene promoter was highly methylated, while ER mRNA and ER protein were not expressed in the ER-negative breast cell line MDA-MB-231. The ER-negative breast cells treated with demethylating agent 5 -aza-2'-deoxycytidine (5-AZA-2'-deoxyC) restored the expression of ER mRNA and ER protein. Expression of the endogenous ER-responsive PR gene was activated and the methylation of ER gene was simultaneously decreased. After MDA-MB-231 was treated with 5-AZA-2'-deoxyC, the protein of ER was re-expressed and the growth of cells treated with tamoxifen were inhibited significantly (P0.05).inactivation of ER gene has a close relationship with the abnormal methylation of ER gene promoter. 5-AZA-2'-deoxyC may effectively cause demethylation and restore functional expression of ER silenced by aberrant hypermethylation. The result may offer a new measure and theory for breast cancer patients with ER-negative expression to receive endocrine therapies.