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Protective effects of phillyrin against influenza A virus in vivo
Xin-yan Qu,Qing-jun Li,Hui-min Zhang,Xiao-juan Zhang,Peng-hui Shi,Xiu-juan Zhang,Jing Yang,Zhe Zhou,Sheng-qi Wang 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.7
Influenza A virus infection represents a great threat to public health. However, owing to side effects and the emergence of resistant virus strains, the use of currently available anti-influenza drugs may be limited. In order to identify novel anti-influenza drugs, we investigated the antiviral effects of phillyrin against influenza A virus infection in vivo. The mean survival time, lung index, viral titers, influenza hemagglutinin (HA) protein and serum cytokines levels, and histopathological changes in lung tissue were examined. Administration of phillyrin at a dose of 20 mg/kg/day for 3 days significantly prolonged the mean survival time, reduced the lung index, decreased the virus titers and interleukin-6 levels, reduced the expression of HA, and attenuated lung tissue damage in mice infected with influenza A virus. Taken together, these data showed that phillyrin had potential protective effects against infection caused by influenza A virus.
Zhu, Hong-Lin,Wei, Xing,Qu, Shun-Lin,Zhang, Chi,Zuo, Xiao-Xia,Feng, Yan-Sheng,Luo, Qi,Chen, Guang-Wen,Liu, Mei-Dong,Jiang, Lei,Xiao, Xian-Zhong,Wang, Kang-Kai Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.8
Cardiomyocytes can resist ischemia/reperfusion(I/R) injury through ischemic postconditioning (IPoC) which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40 family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models, an $in$ $vivo$ open chest rat coronary artery occlusion model and an $in$ $vitro$ model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration) followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion, MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the $in$ $vitro$ model. These effects were blunted by transfection with MIP2 siRNA in the H9c2 cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.
PROGRAMMABLE INDUCTANCE AND CAPACITANCE GENERATOR
Hua, Shang Qing,Hua, Wu Li,Sheng, Qu Yan,Jian, Ma Huai 대한전자공학회 1992 HICEC:Harbin International Conference on Electroni Vol.1 No.1
This paper introduces an impedance converter principle of simulated pure inductance and capacitance by using operational amplifiers, in addition, it provides the circuitry configurations according to this principle. The generator can produce equivalent inductance from 0.1H to 6553500H or equivalent capacitance from 10^(-10) F to 65535 × 10^(-7) by programming control. Its circuit is very simple, this generator can be programmed control conveniently and integrated easily. It especially has certain advantages in simulating large inductance or capacitance and programming control.
Hong-Lin Zhu,Kang-Kai Wang,Xing Wei,Shun-Lin Qu,Chi Zhang,Xiao-Xia Zuo,Yan-Sheng Feng,Qi Luo,Guang-Wen Chen,Mei-Dong Liu,Lei Jiang,Xian-Zhong Xiao 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.8
Cardiomyocytes can resist ischemia/reperfusion (I/R)injury through ischemic postconditioning (IPoC)which is repetitive ischemia induced during the onset of reperfusion. Myocardial ischemic preconditioning up-regulated protein 2 (MIP2) is a member of the WD-40family proteins, we previously showed that MIP2 was up-regulated during ischemic preconditioning (IPC). As IPC and IPoC engaged similar molecular mechanisms in cardioprotection, this study aimed to elucidate whether MIP2 was up-regulated during IPoC and contributed to IPoC-mediated protection against I/R injury. The experiment was conducted on two models,an in vivo open chest rat coronary artery occlusion model and an in vitro model with H9c2 myogenic cells. In both models, 3 groups were constituted and randomly designated as the sham, I/R and IPoC/hypoxia postconditioning (HPoC) groups. In the IPoC group, after 45 min of ischemia, hearts were allowed three cycles of reperfusion/ischemia phases (each of 30 s duration)followed by reperfusion. In the HPoC group, after 6 h of hypoxia, H9c2 cells were subjected to three cycles of 10 minute reoxygenation and 10 minute hypoxia followed by reoxygenation. IPoC significantly reduced the infarct size, plasma level of Lactate dehydrogenase and creatine kinase MB in rats. 12 h after the reperfusion,MIP2 mRNA levels in the IPoC group were 10 folds that of the sham group and 1.4 folds that of the I/R group. Increased expression of MIP2 mRNA and attenuation of apoptosis were similarly observed in the HPoC group in the in vitro model. These effects were blunted by transfection with MIP2 siRNA in the H9c2cells. This study demonstrated that IPoC induced protection was associated with increased expression of MIP2. Both MIP2 overexpression and MIP2 suppression can influence the IPoC induced protection.
( Wen Qian Wei ),( Fang Qi Liu ),( Lei Liu ),( Zuo Feng Li ),( Xiao Yan Zhang ),( Fan Jiang ),( Qu Shi ),( Xiao Yan Zhou ),( Wei Qi Sheng ),( San Jun Cai ),( Xuan Li ),( Ye Xu ),( Peng Nan ) 생화학분자생물학회(구 한국생화학분자생물학회) 2011 BMB Reports Vol.44 No.5
Hereditary non-polyposis Colorectal Cancer (HNPCC) is an autosomal dominant inheritance syndrome. HNPCC is the most common hereditary variant of colorectal cancer (CRC), which accounts for 2-5% CRCs, mainly due to hMLH1 and hMSH2 mutations that impair DNA repair functions. Our study aimed to identify the patterns of hMSH2 and hMLH1 mutations in Chinese HNPCC patients. Ninety-eight unrelated families from China meeting Amsterdam or Bethesda criteria were included in our study. Germline mutations in MLH1 and MSH2 genes, located in the exons and the splice-site junctions, were screened in the 98 probands by direct sequencing. Eleven mutations were found in ten patients (11%), with six in MLH1 (54.5%) and five in MSH2 (45.5%) genes. One patient had mutations in both MLH1 and MSH2 genes. Three novel mutations in MLH1 gene (c.157_160delGAGG, c.2157dupT and c.-64G>T) were found for the first time, and one suspected hotspot in MSH2 (c.1168C>T) was revealed. [BMB reports 2011; 44(5): 317-322]