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698 results on '"Ma, Chunmei"'

202. Correction: Genomic Polymorphism of the Pandemic A (H1N1) Influenza Viruses Correlates with Viral Replication, Virulence, and Pathogenicity In Vitro and In Vivo

Author

Xu, Lili, primary, Bao, Linlin, additional, Zhou, Jianfang, additional, Wang, Dayan, additional, Deng, Wei, additional, Lv, Qi, additional, Ma, Yila, additional, Li, Fengdi, additional, Sun, Huihui, additional, Zhan, Lingjun, additional, Zhu, Hua, additional, Ma, Chunmei, additional, Shu, Yuelong, additional, and Qin, Chuan, additional

Published
2020
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223. Lycorine reduces mortality of human enterovirus 71-infected mice by inhibiting virus replication

Author

Qin Chuan, Ma Chunmei, Xu Yanfeng, Yang Yajun, Liu Jiangning, and Zhang Lianfeng

Subjects
Human enterovirus 71, Lycorine, Mouse model, Drug, Infectious and parasitic diseases, RC109-216
Abstract

Abstract Human enterovirus 71 (EV71) infection causes hand, foot and mouth disease in children under 6 years old and this infection occasionally induces severe neurological complications. No vaccines or drugs are clinical available to control EV71 epidemics. In present study, we show that treatment with lycorine reduced the viral cytopathic effect (CPE) on rhabdomyosarcoma (RD) cells by inhibiting virus replication. Analysis of this inhibitory effect of lycorine on viral proteins synthesis suggests that lycorine blocks the elongation of the viral polyprotein during translation. Lycorine treatment of mice challenged with a lethal dose of EV71 resulted in reduction of mortality, clinical scores and pathological changes in the muscles of mice, which were achieved through inhibition of viral replication. When mice were infected with a moderate dose of EV71, lycorine treatment was able to protect them from paralysis. Lycorine may be a potential drug candidate for the clinical treatment of EV71-infected patients.

Published
2011
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224. A single-amino-acid substitution in the HA protein changes the replication and pathogenicity of the 2009 pandemic A (H1N1) influenza viruses in vitro and in vivo

Author

Ma Chunmei, Zhu Hua, Zhan Lingjun, Li Fengdi, Ma Yila, Deng Wei, Lv Qi, Bao Linlin, Xu Lili, and Qin Chuan

Subjects
Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background The novel pandemic A (H1N1) virus was first identified in Mexico in April 2009 and since then it spread world wide over a short period of time. Although the virus infection is generally associated with mild disease and a relatively low mortality, it is projected that mutations in specific regions of the viral genome, especially within the receptor binding domain of the hemagglutinin (HA) protein could result in more virulent virus stains, leading to a more severe pandemic. Results Here, we found that a single amino acid substitution of Asp-to-Gly at position 222 in the HA protein of the A (H1N1) virus occurred after two passage propagation in the allantoic cavities of chicken embryonated eggs, and this single residue variation dramatically increased the viral replication ability in MDCK cells and pathogenicity in BALB/c mice. Conclusions A substitution of Asp-to-Gly at position 222 in the HA protein was prone to occur under positive selection pressures, and this single amino acid mutation could dramatically increase the virus replication ability in vitro and pathogenicity in vivo. Our finding offers a better understanding of the transmission and evolution of the 2009 pandemic A (H1N1) virus and brings attention to further potentially severe influenza pandemic that may result from cross-host evolution of the influenza viruses.

Published
2010
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225. The relationship between internode elongation of soybean stems and spectral distribution of light in the canopy under different plant densities.

Author

Xu, Yao, Wang, Chang, Zhang, Rui, Ma, Chunmei, Dong, Shoukun, and Gong, Zhenping

Subjects
PLANT spacing, RADIANT intensity, BLUE light, LIGHT emitting diodes
Abstract

The present study carried out with a field plot experiment and light environment simulation experiment in 2017 to assess the effect of spectral distribution on internode elongation in soybean canopy. Henong 60 and Heinong 48 were used as the experimental materials. The spectral distribution in the soybean canopy was studied under four planting densities 200,000(D20), 300,000(D30), 400,000(D40) and 500,000(D50) plant ha−1. Meanwhile, a pot experiment of light environment simulation with light-emitting diode (LED) was carried out to further analyze the effects of light quantity and quality on the elongation of soybean seedlings. The results showed that the intensity of PAR, blue light, red light and far-red light in soybean canopy decreased by varying degrees with density and canopy depth increasing, and the decrease of PAR and R/FR led to significant elongation of internodes and plant height in high density. The spectral intensity in the middle and base of the canopy was strongly reduced, resulting in the strongest internode elongation in the middle of soybean stem. The increase in soybean plant height was also mainly due to the internode elongation in the middle at high density. In addition, the mono-light of far-red light could promote the internode elongation, while the red light and blue light acted as inhibitors and the inhibitory effect of blue light was even greater. [ABSTRACT FROM AUTHOR]

Published
2021
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226. Gasdermin D in peripheral myeloid cells drives neuroinflammation in experimental autoimmune encephalomyelitis

Author

Li, Sheng, Wu, Yuqing, Yang, Dongxue, Wu, Chunyan, Ma, Chunmei, Liu, Xue, Moynagh, Paul N., Wang, Bingwei, Hu, Gang, Yang, Shuo, Li, Sheng, Wu, Yuqing, Yang, Dongxue, Wu, Chunyan, Ma, Chunmei, Liu, Xue, Moynagh, Paul N., Wang, Bingwei, Hu, Gang, and Yang, Shuo

Abstract

The NLRP3 inflammasome is critical for EAE pathogenesis; however, the role of gasdermin D (GSDMD), a newly identified pyroptosis executioner downstream of NLRP3 inflammasome, in EAE has not been well defined. Here, we observed that the levels of GSDMD protein were greatly enhanced in the CNS of EAE mice, especially near the areas surrounding blood vessels. GSDMD was required for the pathogenesis of EAE, and GSDMD deficiency in peripheral myeloid cells impaired the infiltration of immune cells into the CNS, leading to the suppression of neuroinflammation and demyelination. Furthermore, the loss of GSDMD reduced the activation and differentiation of T cell in the secondary lymphoid organs and prevented T cell infiltration into CNS of EAE. The administration of inflammasome-related cytokines partially rescued the impairment of pathogenesis of EAE in GSDMD KO mice. Collectively, these findings provide the first demonstration of GSDMD in peripheral myeloid cells driving neuroinflammation during EAE pathogenesis.

Published
2019

233. Downregulated NDR1 protein kinase inhibits innate immune response by initiating an miR146a-STAT1 feedback loop

Author

Liu, Zhiyong, primary, Qin, Qiang, additional, Wu, Cheng, additional, Li, Hui, additional, Shou, Jia’nan, additional, Yang, Yuting, additional, Gu, Meidi, additional, Ma, Chunmei, additional, Lin, Wenlong, additional, Zou, Yan, additional, Zhang, Yuanyuan, additional, Ma, Feng, additional, Sun, Jihong, additional, and Wang, Xiaojian, additional

Published
2018
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241. The changes of the cardiac structure and function in cTnTR141W transgenic mice

Author

Dong Wei, Huang Lan, Feng Juan, Qin Chuan, Zhang Lian-feng, Ma Chunmei, Di Ran, and Quan Xiongzhi

Subjects
Cardiomyopathy, Dilated, Genetically modified mouse, medicine.medical_specialty, Pathology, Transgene, Cardiomyopathy, Gene Expression, Mice, Transgenic, Muscle hypertrophy, Transgenic Model, Mice, Troponin complex, Internal medicine, Gene expression, medicine, Animals, Transgenes, Staining and Labeling, Reverse Transcriptase Polymerase Chain Reaction, business.industry, Dilated cardiomyopathy, Blotting, Northern, medicine.disease, Immunohistochemistry, Disease Models, Animal, Endocrinology, Echocardiography, Mutation, Cardiology and Cardiovascular Medicine, business
Abstract

Objective To establish the transgenic mouse of cTnT R141W gene to make an animal model of dilated cardiomyopathy. Methods A transgenic plasmid was constructed by inserting the cTnT R141W gene driven by the α-MHC promoter. The expression level of the gene was determined with Northern blotting. Pathologic changes were observed by light microscopy and transmission electronic microscopy and analyzed with echocardiography. The localization of the mutant human cTnT protein was detected by immunohistochemistry. The hypertrophy markers were analyzed by RT-PCR. Results Transgenic mice carrying the cTnT R141W mutation were established. The cTnT R141W was expressed by 1.5- to 2.0-fold that of the endogenous cTnT gene and was showed to assemble in the sarcomere. The transgenic heart exhibited a thinner ventricular wall and an enlarged ventricular chamber. Interstitial fibrosis and the elongated and lysed myofrils were also observed in the transgenic heart tissue. The function on EF%, FS% and movement of the ventricular wall was significantly decreased. The immature death occurred after 4 months of age and the immature death rate was 11.1% before 8 months of age in the cTnT R141W mice. The increased NPPB, ACTA1 and decreased ATP2A2 were detected in the transgenic heart. Conclusions The expression of mutant cTnT R141W in the mouse heart caused ventricular chamber enlargement, systolic dysfunction, myocardial hypertrophy, and interstitial fibrosis, suggesting that the cTnT R141W gene is a causal factor for DCM and that the cTnT R141W transgenic mouse is a useful animal model for the study of human DCM.

Published
2008
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