Potential zoonotic pathogens may be transmitted from wildlife to humans through the illegal wild meat trade,which has become a pressing issue.However,research on the antimicrobial resistance genes(ARGs)of Malayan pang...Potential zoonotic pathogens may be transmitted from wildlife to humans through the illegal wild meat trade,which has become a pressing issue.However,research on the antimicrobial resistance genes(ARGs)of Malayan pangolin(Manis javanica)intestinal bacteria is limited.Here,multidrug-resistant Escherichia coli M172-1(ST354)isolated from Malayan pangolin feces in 2019 was found to be resistant to 13 antibiotics.BGWAS analysis revealed 4 plas-mids,namely,pM172-1.1,pM172-1.2,pM172-1.3,and pM172-1.4,in the isolate.The pM172-1.2,pM172-1.3,and pM172-1.4 plasmids carried ARGs,namely,IncHI2-HI2A,IncX1-X1,and IncX1,respectively.pM172-1.3 and pM172-1.4 contained intact IntI1 integrons(Is26/IntI1/arr2/cmlA5/blaOXA-10/ant(3′′)-IIA/dfrA14/Is26).No-tably,pM172-1.3 resulted from the fusion of 2 pM172-1.4 copies and carried many more ARGs.In addition to pM172-1.3 from the same host,other drug-resistant bacteria(E.coli M159-1(ST48),E.coli S171-1(ST206),and Klebsiella pneumoniae S174-1(ST2354))in the same Malayan pangolin fecal samples also carried 3 plasmids with 100%gene coverage of pM172-1.4 and 99.98%identity.Therefore,ARGs in IncX1 might spread in the intestinalflora of Malayan pangolin and between species via the illegal food chain,posing a potential threat to public health and safety.展开更多
目的研究β2受体对心肌梗死（MI）后2～8周心肌细胞钠钙交换电流（INCX）的调控作用。方法雄性健康Wistar大鼠28只，随机分为：正常对照组；MI后2周、4周、8周组。以结扎心脏左前降支方法制作MI模型。正常对照组进行假手术。采用经典的...目的研究β2受体对心肌梗死（MI）后2～8周心肌细胞钠钙交换电流（INCX）的调控作用。方法雄性健康Wistar大鼠28只，随机分为：正常对照组；MI后2周、4周、8周组。以结扎心脏左前降支方法制作MI模型。正常对照组进行假手术。采用经典的酶分离心肌细胞方法，应用全细胞膜片钳技术记录INCX，观察MI后INCX的变化，予以β2受体激动剂salbutamol、β受体激动剂异丙肾上腺素及不同选择性β受体阻滞剂后INCX的变化。结果MI后8周心肌细胞IM显著增高（1．07±0．21pA／pF vs 0．51±0．12pA／pF，P〈0．05）。MI后B2受体激动显著增加心肌细胞INCX（P〈0．05），对INCX的调节作用较正常心肌细胞强。MI后选择性β2受体阻滞剂ICI118，551对B受体激动引发的心肌细胞INCX升高的抑制程度增高；选择性β2受体阻滞剂阿替洛尔对上述作用的抑制程度下降；非选择性β受体阻滞剂普萘洛尔对β受体激动引发的正常和MI后心肌细胞上述离子通道电流升高均能明显抑制。结论MI后β2受体对心肌细胞INCX的调节作用增强，提示MI后β2受体在恶性心律失常发生机制中的地位可能提高。展开更多
Objectives This study is designed to investigate the regulation effects of β2-adrenergic receptors （AR） on expression of the Na^± - Ca^2 ± exchanger （ INCX） in myocytes from the infarcted rat heart. Met...Objectives This study is designed to investigate the regulation effects of β2-adrenergic receptors （AR） on expression of the Na^± - Ca^2 ± exchanger （ INCX） in myocytes from the infarcted rat heart. Methods Twenty-eight adult Wistar rats were randomly divided into four groups ： the control group, the two weeks, four weeks and eight weeks post-myocardial infarction （post-MI） groups, respectively. The chest of rat was opened and a ligature was placed around the left anterior descending coronary artery. Rats in control group were sham-operated without the coronary artery ligation. After the operation, rats were fed for two, four or eight weeks respectively. Myocytes were enzymatically disassociated by Langendorff perfusion. The whole cell-patch clamp recording technique was used to record INCX in specific pipette solution and superfusion according to the specific holding potential and command potential program. Results The INCX in ventricular myocytes from the border zone of infarcted myocardium increased significantly at eight weeks after MI （0. 51 ± 0. 12 pA/pF vs 1.07± 0. 21 pA/pF, P 〈0.05）. β2-AR agonist increased INcx more strongly in myocytes from post- MI heart than in controls. β2-AR antagonist attenuated the rise of INCX, strongly in myocytes from post-MI heart than in controls, whereas β1-AR onist. Conclusion The regulation effects of β2-AR on INCX in myocytes AR had closer relationship with the genesis of malignant arrhythmia afte展开更多
基金supported by the Introduction of Leading Talents Program of the Guangdong Academy of Sciences(No.2016GDASRC-0205)the Open project of Beijing Key Laboratory of captive wildlife technology in Beijing Zoo(ZDK202105).
文摘Potential zoonotic pathogens may be transmitted from wildlife to humans through the illegal wild meat trade,which has become a pressing issue.However,research on the antimicrobial resistance genes(ARGs)of Malayan pangolin(Manis javanica)intestinal bacteria is limited.Here,multidrug-resistant Escherichia coli M172-1(ST354)isolated from Malayan pangolin feces in 2019 was found to be resistant to 13 antibiotics.BGWAS analysis revealed 4 plas-mids,namely,pM172-1.1,pM172-1.2,pM172-1.3,and pM172-1.4,in the isolate.The pM172-1.2,pM172-1.3,and pM172-1.4 plasmids carried ARGs,namely,IncHI2-HI2A,IncX1-X1,and IncX1,respectively.pM172-1.3 and pM172-1.4 contained intact IntI1 integrons(Is26/IntI1/arr2/cmlA5/blaOXA-10/ant(3′′)-IIA/dfrA14/Is26).No-tably,pM172-1.3 resulted from the fusion of 2 pM172-1.4 copies and carried many more ARGs.In addition to pM172-1.3 from the same host,other drug-resistant bacteria(E.coli M159-1(ST48),E.coli S171-1(ST206),and Klebsiella pneumoniae S174-1(ST2354))in the same Malayan pangolin fecal samples also carried 3 plasmids with 100%gene coverage of pM172-1.4 and 99.98%identity.Therefore,ARGs in IncX1 might spread in the intestinalflora of Malayan pangolin and between species via the illegal food chain,posing a potential threat to public health and safety.
文摘目的研究β2受体对心肌梗死（MI）后2～8周心肌细胞钠钙交换电流（INCX）的调控作用。方法雄性健康Wistar大鼠28只，随机分为：正常对照组；MI后2周、4周、8周组。以结扎心脏左前降支方法制作MI模型。正常对照组进行假手术。采用经典的酶分离心肌细胞方法，应用全细胞膜片钳技术记录INCX，观察MI后INCX的变化，予以β2受体激动剂salbutamol、β受体激动剂异丙肾上腺素及不同选择性β受体阻滞剂后INCX的变化。结果MI后8周心肌细胞IM显著增高（1．07±0．21pA／pF vs 0．51±0．12pA／pF，P〈0．05）。MI后B2受体激动显著增加心肌细胞INCX（P〈0．05），对INCX的调节作用较正常心肌细胞强。MI后选择性β2受体阻滞剂ICI118，551对B受体激动引发的心肌细胞INCX升高的抑制程度增高；选择性β2受体阻滞剂阿替洛尔对上述作用的抑制程度下降；非选择性β受体阻滞剂普萘洛尔对β受体激动引发的正常和MI后心肌细胞上述离子通道电流升高均能明显抑制。结论MI后β2受体对心肌细胞INCX的调节作用增强，提示MI后β2受体在恶性心律失常发生机制中的地位可能提高。
文摘Objectives This study is designed to investigate the regulation effects of β2-adrenergic receptors （AR） on expression of the Na^± - Ca^2 ± exchanger （ INCX） in myocytes from the infarcted rat heart. Methods Twenty-eight adult Wistar rats were randomly divided into four groups ： the control group, the two weeks, four weeks and eight weeks post-myocardial infarction （post-MI） groups, respectively. The chest of rat was opened and a ligature was placed around the left anterior descending coronary artery. Rats in control group were sham-operated without the coronary artery ligation. After the operation, rats were fed for two, four or eight weeks respectively. Myocytes were enzymatically disassociated by Langendorff perfusion. The whole cell-patch clamp recording technique was used to record INCX in specific pipette solution and superfusion according to the specific holding potential and command potential program. Results The INCX in ventricular myocytes from the border zone of infarcted myocardium increased significantly at eight weeks after MI （0. 51 ± 0. 12 pA/pF vs 1.07± 0. 21 pA/pF, P 〈0.05）. β2-AR agonist increased INcx more strongly in myocytes from post- MI heart than in controls. β2-AR antagonist attenuated the rise of INCX, strongly in myocytes from post-MI heart than in controls, whereas β1-AR onist. Conclusion The regulation effects of β2-AR on INCX in myocytes AR had closer relationship with the genesis of malignant arrhythmia afte
