A material with the formula ZrMgMo_(3)O_(12) having negative thermal expansion is presented and characterized.It is shown that ZrMgMo_(3)O_(12) crystallizes in an orthorhombic symmetry with space group Pnma(62)or Pna2...A material with the formula ZrMgMo_(3)O_(12) having negative thermal expansion is presented and characterized.It is shown that ZrMgMo_(3)O_(12) crystallizes in an orthorhombic symmetry with space group Pnma(62)or Pna21(33)and exhibits negative thermal expansion in a large temperature range(αl=-3.8×10^(-6) K^(-1) from 300 K to 1000 K by x-ray diffraction andαl=-3.73×10^(-6) K^(-1) from 295 K to 775 K by dilatometer).ZrMgMo_(3)O_(12) remains the orthorhombic structure without phase transition or decomposition at least from 123 K to 1200 K and is not hygroscopic.These properties make it an excellent material with negative thermal expansion for a variety of applications.展开更多
Background Increased proliferation of airway smooth muscle cells （ASMCs） are observed in asthmatic patients and smoking can accelerate proliferation of ASMCs in asthma. To elucidate the molecular mechanisms leading ...Background Increased proliferation of airway smooth muscle cells （ASMCs） are observed in asthmatic patients and smoking can accelerate proliferation of ASMCs in asthma. To elucidate the molecular mechanisms leading to these changes, we studied in vitro the effect of cigarette smoke extract （CSE） on the proliferation of ASMCs and the expression of cyclin D1, an important regulatory protein implicated in cell cycle. Methods ASMCs cultured from 8 asthmatic Brown Norway rats were studied. Cells between passage 3 and 6 were used in the study and were divided into control group, pcDNA3.1 group, pcDNA3.1-antisense cyclin D1 （ascyclin D1） group, CSE group, CSE＋pcDNA3.1 group and CSE＋pcDNA3.1-ascyclin D1 group based on the conditions for intervention. The proliferation of ASMCs was examined with cell cycle analysis, MTT colorimetric assay and proliferating cell nuclear antigen （PCNA） immunocytochemical staining. The expression of cyclin D1 was detected by reverse transcriptase-PCR （RT-PCR） and Western blotting. Results （1） The percentage of S＋G2M phase, absorbance value at 490 nm wavelength （A490） and the expression rate of PCNA protein in CSE group were （31.22±1.17）%, 0.782±0.221, （90.2±7.0）% respectively, which were significantly increased compared with those of control group （18.36±1.02）%, 0.521±0.109, and （54.1±3.5）%, respectively） （P 〈0.01）. After the transfection with antisense cyclin D1 plasmid for 30 hours, the percentage of S＋G2M phase, A490 and the expression rate of PCNA protein in ASMCs were much lower than in untreated cells （P 〈0.01）. （2） The ratios of A490 of cyclin D1 mRNA in CSE group was 0.288±0.034, which was significantly increased compared with that of control group （0.158±0.006） （P 〈0.01）. After the transfection with antisense cyclin D1 plasmid for 30 hours, the ratios of A49o of cyclin D1 mRNA in ASMCs was much lower than in untreated cells （P 〈0.01）. （3） The ratios of A490 of cyclin D1 protein expression in CSE group was 0.375±0.008, which was significantly increased compared with that of control group （0.268±0.004） （P 〈0.01）. After the transfection with antisense cyclin D1 plasmid for 30 hours, the ratios of A490 of cyclin D1 protein expression in ASMCs was much lower than in untreated cells （P 〈0.01）. Conclusion CSE may increase the proliferation of ASMCs in asthmatic rats via regulating cyclin D1 expression.展开更多
Background Airway smooth muscle （ASM） is suspected to be a determining factor in the structural change of asthma. However, the role of protein kinase C α （PKCα） and cyclin D1 involved in the dysfunction of ASM l...Background Airway smooth muscle （ASM） is suspected to be a determining factor in the structural change of asthma. However, the role of protein kinase C α （PKCα） and cyclin D1 involved in the dysfunction of ASM leading to asthmatic symptoms is not clear. In this study, the central role of PKCα and cyclin D1 in ASM proliferation in asthmatic rats was explored. Methods Thirty-six pathogen-free male Brown Norway （BN） rats were randomly divided into 2 groups： control groups （group N1, N2 and N3） and asthmatic groups （group A1, A2, and A3）. Groups A1, A2 and A3 were challenged with ovalbumin （OA） for 2 weeks, 4 weeks and 8 weeks respectively. Control animals were exposed to an aerosolized sterile phosphate buffered saline （PBS）. The ASM mass and nucleus numbers were studied to estimate the degree of airway remodeling by the hematoxylin-eosin staining method. PKCα and cyclin D1 expression in the ASM cells was detected by reverse transcription polymerase chain reaction （RT-PCR） and immunohistochemistry. The relation between PKCα and cyclin D1 was assessed by linear regression analysis. PKC agonist phorbol 12-myristate 13-acetate （PMA）, PKC inhibitor Ro31-8220 and an antisense oligonucleotide against cyclin D1 （ASOND） were used to treat ASM cells （ASMCs） obtained from the 2 weeks asthmatic rats. The cyclin D1 protein expression level was detected by Western blotting.Results Compared with the control group, the PKCα and cyclin D1 mRNA levels were increased in the asthmatic group. Similar to RT-PCR results, immunohistochemistry analysis for PKCα and cyclin D1 expression revealed an increased production in ASMCs after allergen treatment for 2, 4 and 8 weeks compared with the respective control groups. No difference in expression of PKCα and cyclin D1 in ASM were found in the 2, 4 or 8 weeks asthmatic rats. There were significant positive correlations between PKCα and cyclin D1 expression, both transcriptionally （r=0.944, P 〈0.01） and translationally （r=0.826, P 〈0.01）, in ASM. The content of cyclin D1 in asthmatic ASMCs increased after being stimulated by PMA, and decreased when induced by Ro31-8220. ASOND targeting for cyclin D1 lowered the expression of cyclin D1 induced by PMA.Conclusions Increased expression of PKCα and cyclin D1 in ASM along with smooth muscle structure changes might implicate PKCα and cyclin D1 participation in the proliferation of ASM and contribute to the pathogenesis of asthma after repeated allergen exposure in rats. The results suggested that cyclin D1 might be downstream of PKC signal transduction pathway.展开更多
基金Supported by the National Science Foundation of China(Nos 10974183,11104252)the Ministry of Education of China(No 20114101110003)+1 种基金the Fund for Science&Technology Innovation Team of Zhengzhou(No 112PCXTD337)the Postdoctoral Research Sponsorship in Henan Province(No 2011002).
文摘A material with the formula ZrMgMo_(3)O_(12) having negative thermal expansion is presented and characterized.It is shown that ZrMgMo_(3)O_(12) crystallizes in an orthorhombic symmetry with space group Pnma(62)or Pna21(33)and exhibits negative thermal expansion in a large temperature range(αl=-3.8×10^(-6) K^(-1) from 300 K to 1000 K by x-ray diffraction andαl=-3.73×10^(-6) K^(-1) from 295 K to 775 K by dilatometer).ZrMgMo_(3)O_(12) remains the orthorhombic structure without phase transition or decomposition at least from 123 K to 1200 K and is not hygroscopic.These properties make it an excellent material with negative thermal expansion for a variety of applications.
基金This work was supported by a grant from the National Natural Science Foundation of China （No. 30670925）.
文摘Background Increased proliferation of airway smooth muscle cells （ASMCs） are observed in asthmatic patients and smoking can accelerate proliferation of ASMCs in asthma. To elucidate the molecular mechanisms leading to these changes, we studied in vitro the effect of cigarette smoke extract （CSE） on the proliferation of ASMCs and the expression of cyclin D1, an important regulatory protein implicated in cell cycle. Methods ASMCs cultured from 8 asthmatic Brown Norway rats were studied. Cells between passage 3 and 6 were used in the study and were divided into control group, pcDNA3.1 group, pcDNA3.1-antisense cyclin D1 （ascyclin D1） group, CSE group, CSE＋pcDNA3.1 group and CSE＋pcDNA3.1-ascyclin D1 group based on the conditions for intervention. The proliferation of ASMCs was examined with cell cycle analysis, MTT colorimetric assay and proliferating cell nuclear antigen （PCNA） immunocytochemical staining. The expression of cyclin D1 was detected by reverse transcriptase-PCR （RT-PCR） and Western blotting. Results （1） The percentage of S＋G2M phase, absorbance value at 490 nm wavelength （A490） and the expression rate of PCNA protein in CSE group were （31.22±1.17）%, 0.782±0.221, （90.2±7.0）% respectively, which were significantly increased compared with those of control group （18.36±1.02）%, 0.521±0.109, and （54.1±3.5）%, respectively） （P 〈0.01）. After the transfection with antisense cyclin D1 plasmid for 30 hours, the percentage of S＋G2M phase, A490 and the expression rate of PCNA protein in ASMCs were much lower than in untreated cells （P 〈0.01）. （2） The ratios of A490 of cyclin D1 mRNA in CSE group was 0.288±0.034, which was significantly increased compared with that of control group （0.158±0.006） （P 〈0.01）. After the transfection with antisense cyclin D1 plasmid for 30 hours, the ratios of A49o of cyclin D1 mRNA in ASMCs was much lower than in untreated cells （P 〈0.01）. （3） The ratios of A490 of cyclin D1 protein expression in CSE group was 0.375±0.008, which was significantly increased compared with that of control group （0.268±0.004） （P 〈0.01）. After the transfection with antisense cyclin D1 plasmid for 30 hours, the ratios of A490 of cyclin D1 protein expression in ASMCs was much lower than in untreated cells （P 〈0.01）. Conclusion CSE may increase the proliferation of ASMCs in asthmatic rats via regulating cyclin D1 expression.
基金This work was supported by a grant from National Natural Science Foundation of China （No. 3067092）.Acknowledgements： The authors are grateful to the staff in Department of Respiratory Medicine for their excellent technical assistance.
文摘Background Airway smooth muscle （ASM） is suspected to be a determining factor in the structural change of asthma. However, the role of protein kinase C α （PKCα） and cyclin D1 involved in the dysfunction of ASM leading to asthmatic symptoms is not clear. In this study, the central role of PKCα and cyclin D1 in ASM proliferation in asthmatic rats was explored. Methods Thirty-six pathogen-free male Brown Norway （BN） rats were randomly divided into 2 groups： control groups （group N1, N2 and N3） and asthmatic groups （group A1, A2, and A3）. Groups A1, A2 and A3 were challenged with ovalbumin （OA） for 2 weeks, 4 weeks and 8 weeks respectively. Control animals were exposed to an aerosolized sterile phosphate buffered saline （PBS）. The ASM mass and nucleus numbers were studied to estimate the degree of airway remodeling by the hematoxylin-eosin staining method. PKCα and cyclin D1 expression in the ASM cells was detected by reverse transcription polymerase chain reaction （RT-PCR） and immunohistochemistry. The relation between PKCα and cyclin D1 was assessed by linear regression analysis. PKC agonist phorbol 12-myristate 13-acetate （PMA）, PKC inhibitor Ro31-8220 and an antisense oligonucleotide against cyclin D1 （ASOND） were used to treat ASM cells （ASMCs） obtained from the 2 weeks asthmatic rats. The cyclin D1 protein expression level was detected by Western blotting.Results Compared with the control group, the PKCα and cyclin D1 mRNA levels were increased in the asthmatic group. Similar to RT-PCR results, immunohistochemistry analysis for PKCα and cyclin D1 expression revealed an increased production in ASMCs after allergen treatment for 2, 4 and 8 weeks compared with the respective control groups. No difference in expression of PKCα and cyclin D1 in ASM were found in the 2, 4 or 8 weeks asthmatic rats. There were significant positive correlations between PKCα and cyclin D1 expression, both transcriptionally （r=0.944, P 〈0.01） and translationally （r=0.826, P 〈0.01）, in ASM. The content of cyclin D1 in asthmatic ASMCs increased after being stimulated by PMA, and decreased when induced by Ro31-8220. ASOND targeting for cyclin D1 lowered the expression of cyclin D1 induced by PMA.Conclusions Increased expression of PKCα and cyclin D1 in ASM along with smooth muscle structure changes might implicate PKCα and cyclin D1 participation in the proliferation of ASM and contribute to the pathogenesis of asthma after repeated allergen exposure in rats. The results suggested that cyclin D1 might be downstream of PKC signal transduction pathway.
