Background: The H5 avian influenza viruses (AIVs) of clade 2.3.4.4 circulate in wild and domestic birds worldwide. In 2017, nine strains of H5N6 AIVs were isolated from aquatic poultry in Xinjiang, Northwest China. Objectives: This study aimed to analyze the origin, reassortment, and mutations of the AIV isolates. Methods: AIVs were isolated from oropharyngeal and cloacal swabs of poultry. Identification was accomplished by inoculating isolates into embryonated chicken eggs and performing hemagglutination tests and reverse transcription polymerase chain reaction (RT-PCR). The viral genomes were amplified with RT-PCR and then sequenced. The sequence alignment, phylogenetic, and molecular characteristic analyses were performed by using bioinformatic software. Results: Nine isolates originated from the same ancestor. The viral HA gene belonged to clade 2.3.4.4B, while the NA gene had a close phylogenetic relationship with the 2.3.4.4C H5N6 highly pathogenic avian influenza viruses (HPAIVs) isolated from shoveler ducks in Ningxia in 2015. The NP gene was grouped into an independent subcluster within the 2.3.4.4B H5N8 AIVs, and the remaining six genes all had close phylogenetic relationships with the 2.3.4.4B H5N8 HPAIVs isolated from the wild birds in China, Egypt, Uganda, Cameroon, and India in 2016–2017, Multiple basic amino acid residues associated with HPAIVs were located adjacent to the cleavage site of the HA protein. The nine isolates comprised reassortant 2.3.4.4B HPAIVs originating from 2.3.4.4B H5N8 and 2.3.4.4C H5N6 viruses in wild birds. Conclusions These results suggest that the Northern Tianshan Mountain wetlands in Xinjiang may have a key role in AIVs disseminating from Central China to the Eurasian continent and East African.

Background: The H5 avian influenza viruses (AIVs) of clade 2.3.4.4 circulate in wild and domestic birds worldwide. In 2017, nine strains of H5N6 AIVs were isolated from aquatic poultry in Xinjiang, Northwest China. Objectives: This study aimed to analyze the origin, reassortment, and mutations of the AIV isolates. Methods: AIVs were isolated from oropharyngeal and cloacal swabs of poultry. Identification was accomplished by inoculating isolates into embryonated chicken eggs and performing hemagglutination tests and reverse transcription polymerase chain reaction (RT-PCR). The viral genomes were amplified with RT-PCR and then sequenced. The sequence alignment, phylogenetic, and molecular characteristic analyses were performed by using bioinformatic software. Results: Nine isolates originated from the same ancestor. The viral HA gene belonged to clade 2.3.4.4B, while the NA gene had a close phylogenetic relationship with the 2.3.4.4C H5N6 highly pathogenic avian influenza viruses (HPAIVs) isolated from shoveler ducks in Ningxia in 2015. The NP gene was grouped into an independent subcluster within the 2.3.4.4B H5N8 AIVs, and the remaining six genes all had close phylogenetic relationships with the 2.3.4.4B H5N8 HPAIVs isolated from the wild birds in China, Egypt, Uganda, Cameroon, and India in 2016–2017, Multiple basic amino acid residues associated with HPAIVs were located adjacent to the cleavage site of the HA protein. The nine isolates comprised reassortant 2.3.4.4B HPAIVs originating from 2.3.4.4B H5N8 and 2.3.4.4C H5N6 viruses in wild birds. Conclusions These results suggest that the Northern Tianshan Mountain wetlands in Xinjiang may have a key role in AIVs disseminating from Central China to the Eurasian continent and East African.

OBJECTIVE：To in vestigate the effects of quercetin （Que）on the expressio n of angiotensin Ⅱ（AngⅡ）-induced myocardial contractile proteins of primary rats through angiotensin-converting enzyme 2-angiotensin-（1-7）-Mas （ACE2-Ang- （1-7）-Mas）axis. METHODS ：Cardiac tissue of rats aged 1-2 d were collected ，and primary cardiomyocytes were isolated and cultured. The gene silencing model of cardiomyocytes ACE2 was constructed. Experiments were divided into 12 groups. Among them，AngⅡ group，AngⅡ+ small interference RNA （siRNA）group，and Ang Ⅱ+ A 779 group were the model groups ；AngⅡ+ losartan group was positive control group ；AngⅡ+Que40 group，AngⅡ+Que80 group，AngⅡ+siRNA+Que40 group，AngⅡ+ siRNA+Que80 group，AngⅡ+A779+Que40 group and Ang Ⅱ+A779+Que80 group were the experimental groups ；blank group and siRNA group were set up. Ang Ⅱ concentration was 1×10－6 mol/L；siRNA final concentration was 50 nmol/L；Que concentration was 40 and 80 μmol/L；A779（Mas receptor inhibitor ）concentration was 1 μmol/L；losartan concentration was 1×10－4 mol/L. mRNA and protein expression of ACE 2，Ang-（1-7） and Mas in primary cardiomyocytes were detected ；the expressions of myocardial contractile proteins were also determined ，such as Na +/Ca2+ exchange channel （NCX），calcium pump （SERCA2a）， phosphoprotein （PLB）. RESULTS ：Compared with Ang Ⅱ group，mRNA expression of Mas was increased significantly in Ang Ⅱ + Que 80 group （P＜0.05）；mRNA expression of ACE2 and Mas were increased significantly in Ang Ⅱ + CZ0210-01） losartan group （P＜0.05）. Compared with Ang Ⅱ group，the 851136165@qq.com protein expression of ACE 2 and Ang- （1-7） were increased significantly in Ang Ⅱ+ Que 40 group（P＜0.05）；compared with Ang Ⅱ + siRNA group ，the protein expression of Ang-（1-7）were increased significantly in Ang Ⅱ+ siRNA+Que 40 group（P＜0.05）；compared with Ang Ⅱ+A779 group，the protein expression of Ang- （1-7）were increased significantly in Ang Ⅱ+A779+ Que 40 group（P＜0.05）. Compared with Ang Ⅱ group，the protein expression of NCX was decreased in Ang Ⅱ+Que40 group（P＜0.05），protein expression of NCX was reduced in Ang Ⅱ+ losartan group （P＜0.05）；compared with Ang Ⅱ+A779 group，the protein expression of NCX was decreased in Ang Ⅱ+A779+ Que80 group （P＜0.05）. CONCLUSIONS ：Que improves the expression of Ang Ⅱ -induced ACE 2-Ang-（1-7）-Mas axis in cardiomyocyte model to some extent ，so as to regulate myocardial contractile protein.

OBJECTIVE To explore the mechanism of Tingli dazao xiefei decoction on ventricular remodeling in model rats with heart failure after myocardial infarction. METHODS The rat model of heart failure after myocardial infarction was established by ligation of anterior descending branch of left coronary artery， which was divided into 8 groups： sham operation group， model group， A779 group （1 mg/kg）， A779 （1 mg/kg）+Tingli dazao xiefei decoction equivalent-dose group （0.8 g/kg）， A779 （1 mg/kg） +Tingli dazao xiefei decoction high-dose group （1.6 g/kg）， Tingli dazao xiefei decoction equivalent-dose group （0.8 g/kg）， Tingli dazao xiefei decoction high-dose group （1.6 g/kg） and losartan potassium group （10 mg/kg）. Each group was given equal volume of distilled water or corresponding drugs intragastrically for 4 weeks. Masson staining was used to determine the distribution of collagen fibers in rat myocardium. The content of hydroxyproline （Hyp） in myocardium was determined by alkaline hydrolyzation. The expressions of type Ⅰ and Ⅲ collagen （COLⅠ， COLⅢ）in myocardium were detected by immunohisto-chemistry. Myocardial fibrosis-related indexes such as matrix metalloproteinase-2 （MMP-2）， MMP-9， tissue inhibitor of metalloproteinase-1 （TIMP-1） and soluble suppression of tumorigenicity-2 （sST-2） were detected by ELISA. The protein expressions of angiotensin converting enzyme 2-angiotensin-（1-7）-Mas [ACE2-Ang-（1-7）-Mas] axis were detected by Western blot. RESULTS Compared with sham operation group， myocardial cells in model group and A779 group were disordered， collagen fiber deposition was significantly increased and myocardial fibrosis was obvious； the Hyp content and MMP-2， MMP-9， sST-2 levels were increased， and COL Ⅰ and COL Ⅲ positive expressions were significantly enhanced； TIMP-1 level， protein expressions of ACE2， Ang-（1-7） and Mas were significantly decreased （P＜0.05）. Compared with model group， above indexes of Tingli dazao xiefei decoction equivalent-dose and high-dose groups were improved to different extents. Compared with A779 group， A779+Tingli dazao xiefei decoction equivalent-dose and A779+high-dose groups could improve myocardial arrangement and collagen distribution， reduce the Hyp content and MMP-2， MMP-9 levels， reduce positive expressions of COL Ⅰ and COL Ⅲ （P＜0.05）， but couldn’t improve Ang-（1-7） and Mas protein expression. CONCLUSIONS Tingli dazao xiefei decoction can improve ventricular remodeling in myocardial failure model rats after myocardial infarction by improving the expression of ACE2- Ang（- 1-7）-Mas axis proteins.