In JoVE (4)
- Pairwise Growth Competition Assay for Determining the Replication Fitness of Human Immunodeficiency Viruses
- Assessment of Cardiac Morphological and Functional Changes in Mouse Model of Transverse Aortic Constriction by Echocardiographic Imaging
- Intravital Imaging of Neutrophil Priming Using IL-1β Promoter-driven DsRed Reporter Mice
- A Rat Model of Orthotopic Liver Transplantation Using a Novel Magnetic Anastomosis Technique for Suprahepatic Vena Cava Reconstruction
Articles by Yi Liu in JoVE
Pairwise Growth Competition Assay for Determining the Replication Fitness of Human Immunodeficiency Viruses Siriphan Manocheewa1, Erinn C. Lanxon-Cookson1, Yi Liu1, J. Victor Swain1, Jan McClure1, Ushnal Rao1, Brandon Maust1, Wenjie Deng1, Justine E. Sunshine1, Moon Kim1, Morgane Rolland3,4, James I. Mullins1,2 1Department of Microbiology, University of Washington, 2Departments of Medicine and Laboratory Medicine, University of Washington, 3U.S Military HIV Research Program, Walter Reed Army Institute of Research, 4Henry M. Jackson Foundation Growth competition between nearly isogenic viruses provides a sensitive measurement for determining relative replication fitness. The protocols described here include the construction of recombinant HIV-1 clones, virus propagation and growth competition and analysis methods optimized to yield sensitive and consistent results.
Assessment of Cardiac Morphological and Functional Changes in Mouse Model of Transverse Aortic Constriction by Echocardiographic Imaging Lei Li*1, Xiaoyun Guo*1, Yi Chen1, Haifeng Yin1, Jing Li1, Jessica Doan1, Qinghang Liu1 1Department of Physiology and Biophysics, University of Washington The goal of this protocol is to noninvasively assess cardiac structural and functional changes in a mouse model of heart disease created by transverse aortic constriction, using B- and M-mode echocardiography and color/pulse wave Doppler imaging.
Intravital Imaging of Neutrophil Priming Using IL-1β Promoter-driven DsRed Reporter Mice Yi Yao1,2, Yun Liu1,3, Akira Takashima1 1Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, 2Department of Internal Medicine, Yale University School of Medicine, 3Department of Pathophysiology, Southern Medical University (China) This current protocol employs fluorescent reporters, in vivo labeling, and intravital imaging techniques to enable monitoring of the dynamic process of neutrophil priming in living animals.
A Rat Model of Orthotopic Liver Transplantation Using a Novel Magnetic Anastomosis Technique for Suprahepatic Vena Cava Reconstruction Lifei Yang*1,2, Jianwen Lu*1,2,3, Yue Wang1,2,3, Mei Zhang1,2,3, Yuan Shi4, Shasha Wei1,2, Peng Liu1,2,3, Zheng Wu3, Yi Lv1,2,3, Rongqian Wu1,2 1 The reconstruction of the suprahepatic vena cava (SHVC) remains a difficult step in rat orthotopic liver transplantation. In this article, we show a step-by-step protocol for SHVC reconstruction in rats using a novel magnetic anastomosis technique.
Other articles by Yi Liu on PubMed
Cystic Fibrosis Transmembrane Conductance Regulator is Vital to Sperm Fertilizing Capacity and Male Fertility Proceedings of the National Academy of Sciences of the United States of America. Jun, 2007 | Pubmed ID: 17519339 Cystic fibrosis transmembrane conductance regulator (CFTR) is an anion channel, mutations of which cause cystic fibrosis, a disease characterized by defective Cl(-) and HCO(3)(-) transport. Although >95% of all CF male patients are infertile because of congenital bilateral absence of the vas deferens (CBAVD), the question whether CFTR mutations are involved in other forms of male infertility is under intense debates. Here we report that CFTR is detected in both human and mouse sperm. CFTR inhibitor or antibody significantly reduces the sperm capacitation, and the associated HCO(3)(-)-dependent events, including increases in intracellular pH, cAMP production and membrane hyperpolarization. The fertilizing capacity of the sperm obtained from heterozygous CFTR mutant mice is also significantly lower compared with that of the wild-type. These results suggest that CFTR in sperm may be involved in the transport of HCO(3)(-) important for sperm capacitation and that CFTR mutations with impaired CFTR function may lead to reduced sperm fertilizing capacity and male infertility other than CBAVD.