Objective:To investigate the effect of estrogen on the expression and distribution of IL-1 in the remodeling osteoporotic alveolar bone.Methods:Ovariectomy was performed on 30 female SD rats and sham operation on 15(control group).When osteoporosis was developed in the 30 ovary-removed rats,the left maxillary molars of all the rats were extracted.On the following day 15 of them were treated with intramuscular estrogen injection at 20 ?g/kg once every 3 days(treatment group).Another 15 rats with ovary removed received no treatment(osteoporosis group).7,30 and 60 days after teeth extraction 5 rats were killed respectively in each group.IL-1 expression in alveolar bone was examined immunohistochemically,and semiquantitative analysis of cellular-staining intensity was done by microphotometry.Results:The positive IL-1 expression were mainly located in the osteoclasts,vascular endothelial cells and fibroblasts.7 days after teeth extraction the cellular-staining intensity of IL-1 in control group,osteoporosis group and treatment group was 0.11?0.019,0.36?0.038 and 0.18?0.025 respectively(control or treatment group vs osteoporosis group,P

Ion beam enhanced deposition (IBED) has been applied to prepare titanium oxide layer on titanium alloy (Ti6A14V) in order to improve its biocompatibility. The layer on titanium alloy is even, and the elements Al and V in substrate are not detected. The layer is composed of TiO containing nitrogen oriented along (111) plane. The critical load of the layer in scratch test is 16.8 N. Morphological observation reveals the layer ends in a failure caused by plastic deformation.
Biocompatible Materials ; chemistry ; Coated Materials, Biocompatible ; chemistry ; Ions ; chemistry ; Surface Properties ; radiation effects ; Titanium ; chemistry ; X-Ray Diffraction

Objective To isolate enterovirus 71 from a death children,and analyze whether the neurovirulence was related to the variation of nucleotide and amino acid. Methods Enterovirus 71 was isolated from throat swabs which were colleted from Shandong Linyi People's Hospital. The full length genome was sequenced by amplification with RT-PCR and sequencing of 9 overlapped gene fragments covering full length of the genomes. The nucleotide and amino acid sequenced was aligned by BLAST, Bioedit and MEGA 4. Results A strain of enterovirus 71 was isolated and named as SDLY107. The full length was 7405 bp. The results of homology analysis of overall nucleotide sequence showed that strain Fuyang. Anhui. P. R. C/17.08/2 had highest homology (98.6%)with strain SDLY107, and the homology was 80.0% between strain SDLY107 with prototype strain BrCr/70,and 86. 5% between strain SDLY107 with nerve strain MS/87. Phylogenetic analysis showed that the phylogeny was close between SDLY107 with some isolated strains from Chinese Mainland, such as Beijing, Henan, Guangxi, Sbenzhen, Lanzhou, Fuyang, Chongqing and Zhejiang strains, which was clustered for C4 subtype. The results of amino acid sequence analysis showed that there were 2 mutations, E947D and K1873R, for strain SDLY107. Conclusion SDLY107 belonged to C4 subtype, amino acid mutations E947D and K1873R of which may be relevant to the pathogenicity of EV71.

Objective:To study the modulatory effect of hydrogen sulfide (H2S) on oxidative stress in the development of pulmonary hypertension induced by hypoxia. Methods:Twenty male Wistar rats were randomly divided into control group (n=6), hypoxic group (n=6) and hypoxia+NaHS group (n=8). Hypoxic challenge was performed everyday for 21 days. NaHS solution was injected intra-peritoneally everyday before hypoxic challenge for rats in the hypoxia+NaHS group. After 21 days of hypoxia, the mean pulmonary artery pressure(mPAP) was measured by cardiac catheterization. The weight ratio of right ventricle to left ventricle+septum [RV/(LV+SP) ] was also measured. The lung homogenates were assayed for total antioxidant capacity(T-AOC), superoxide dismutase (SOD), oxidized glutathione (GSSG), reduced glutathione (GSH), malondiadehyde(MDA) and hydroxy radical(?OH), and the SOD mRNA levels were assayed by real time polymerse chain reaction. Results: After three weeks of hypoxic disposure, hypoxic hypertension and vascular remodeling developed. Compared with the control group, the mPAP[(23.7?2.2) mm Hg vs. (16.3?3.7) mm Hg,P

OBJECTIVE: To explore the effect of 1,2-dichloroethane(1,2-DCE) induced apoptosis on the expression of related proteins in human neuroblastoma cells(SH-SY5 Y cells). METHODS: SH-SY5 Y cells were cultured in complete medium with 1,2-DCE at final concentrations of 0,10,20,30,40,50,60,70 and 80 mmol/L. After being cultured for24 hours,the apoptosis of SH-SY5 Y cells was tested by flow cytometry using annexin Ⅴ-fluorescein isothiocyanate and propidium iodide. Western blot was used to detect the protein expression of P53,B cell lymphoma/leukmia-2(BCL-2)and BCL-2 associated X protein(BAX). RESULTS: At 1,2-DCE concentrations of 0-80 mmol/L,the total apoptosis rate of SH-SY5 Y cells increased with 1,2-DCE concentrations in a dose-dependent manner(P < 0. 01). At 1,2-DCE concentrations of 30-80 mmol/L,the early apoptosis rate and total apoptosis rate of SH-SY5 Y cells increased significantly than the control group(P < 0. 05). Compared with the other groups,the protein expression of P53 was the lowest when the1,2-DCE concentration was 20 mmol/L(P < 0. 05),and the protein expression of BCL-2 and the BCL-2/BAX ratio were the lowest when the 1,2-DCE concentration was 70 mmol/L(P < 0. 05). There is no dose-response relationship in the1,2-DCE concentrations and the protein expression levels of P53,BCL-2 and BAX,and BCL-2/BAX ratio. Linear multiple regression analysis revealed that the total apoptosis rate of SH-SY5 Y cells treated with 1,2-DCE was associated with the protein expression of P53 and BCL-2,and BCL-2/BAX ratio(P < 0. 05). CONCLUSION: 1,2-DCE could inhibit the apoptosis of SH-SY5 Y cells. The mechanisms may be related to the changes of P53 and BCL-2 protein expression,and BCL-2/BAX relative amount.

ObjectiveTo study the inhibitory effect of polyphyllin Ⅰ （PPI） on the growth of colorectal cancer cells and its molecular mechanism. MethodRKO cells were cultured and divided into a blank group and PPI treatment groups with concentrations of 0.6， 0.8， 1.0 μmol·L^-1， respectively. HRT18 cells were cultured and divided into a blank group and PPI treatment groups with concentrations of 1.2， 1.4， 1.6 μmol·L^-1， respectively. The effects of PPI on the proliferation and morphology of colorectal cancer were detected by cell proliferation toxicity assay， trypan blue exclusion assay， plate clone formation assay， and confocal high-intension cell imaging analysis system. Flow cytometry was used to detect the apoptosis rate of colorectal cancer cells. The pQCXIP-GFP-LC3 plasmid transfection assay was used to detect the formation of autophagosomes in colorectal cancer cells after PPI treatment. Western blot was used to detect the expression of apoptosis-related proteins Caspase-3， Caspase-8， and poly ADP ribose polymerase （PARP）， the expression of autophagy related protein LC3Ⅱ， and the expression and phosphorylation of Hippo signaling pathway proteins LATS1 and YAP. In the plvx-Flag-YAP plasmid transfection assay， YAP was overexpressed and treated with PPI， and the proliferation of colorectal cancer cells was detected by cytotoxicity assay. The expression of LC3Ⅱ and PARP in colorectal cancer cells was detected by Western blot. SwissADME predicted pharmacokinetic parameters of PPI. ResultAs compared with the blank group， the survival rate and clone formation ability of colorectal cancer cells in the PPI group were significantly decreased （P<0.01）， the cell area of colorectal cancer cells in the PPI group was significantly decreased， and the roundness of colorectal cancer cells was significantly increased （P<0.01）. As compared with the blank group， the apoptosis rate of colorectal cancer cells in PPI treatment groupw was significantly increased （P<0.01）， the expression of apoptotic proteins Caspase-3 and Caspase-8 protein precursor in PPI treatment groups was decreased， and the cleavage of PARP was increased （P<0.01）. As compared with the blank group， the expression level of autophagy-related protein LC3Ⅱ in colorectal cancer cells in PPI treatment groups was significantly increased， and the formation of autophagosomes was promoted （P<0.01）. As compared with the blank group， the expression of YAP protein in colorectal cancer cells in PPI treatment groups was significantly decreased， and the expressions of phosphorylated LATS1 and YAP were significantly increased （P<0.01）. As compared with the blank group， overexpression of YAP could significantly antagonize the effect of PPI on apoptosis， autophagy activation， and proliferation inhibition of colorectal cancer cells. SwissADME simulation results showed that PPI had good drug like activity. ConclusionPPI can induce apoptosis and autophagy of colorectal cancer cells through targeted activation of Hippo signaling pathway， thereby inhibiting their proliferation.