Applicants have discovered a novel induction method for inducing digital dermatitis lesions consistent with the natural disease process. Applicants have prepared a consortium including a macerated tissue culture that may be used in the method as well as a novel inoculation procedure. The consortia of microbes includes isolates of Treponema phagedenis, Porphorymonas, and Bacteroides and the invention includes use of these novel isolates in preventing and treating digital dermatitis. The invention can be used to screen, test or compare the relative efficacy of various drugs and biologics for use in treatment or control of digital dermatitis.

The present invention provides a transgenic mouse which comprises a deficiency for murine T lymphocytes, B lymphocytes and NK cells, a deficiency for murine MHC class I and MHC class II molecules, and a functional xenogenic SIRP transgene. This mouse is useful for in vivo screening of various compounds, including immuno-therapeutic agents and vaccines. The said mouse is also useful for testing the in vivo metabolism of xenobiotic compounds.

This disclosure provides a novel strategy to cope with chronic virus infection by introducing a dominant negative viral structural protein to disturb effective virion production. The dominant negative structural protein mimics antiviral drugs through structural and biochemical interactions during virus assembly. An effective gene therapy model for chronic viral infected diseases is proposed in this disclosure, as represented by HBV Cpdominant1 to clear viral infection.

The present invention provides a mouse with liver damage, having a high degree of damage against the mouse's original hepatocytes while having a uPA gene in a heterozygous form, and a method for efficiently preparing the mouse. Specifically, the method for preparing a mouse with liver damage having the uPA gene in a heterozygous form comprises the following steps of: (i) transforming mouse ES cells with a DNA fragment containing a liver-specific promoter/enhancer and cDNA that encodes a urokinase-type plasminogen activator operably linked under the control thereof; (ii) injecting the transformed mouse ES cells obtained in step (i) into a host embryo; (iii) transplanting the host embryo obtained in step (ii) via the injection of the ES cells into the uterus of a surrogate mother mouse, so as to obtain a chimeric mouse; and (iv) crossing the chimeric mice obtained in step (iii), so as to obtain a transgenic mouse in which the DNA fragment is introduced in a heterozygous form.

A kit for breeding a pig breed with resistance to the porcine transmissible gastroenteritis virus infection and application thereof. The systems includes a genetically edited protein, pAPN-sgRNA-1, pAPN-sgRNA-2, and a donor DNA. Effectively enzymatic cleavage can be made in two target sites of a pAPN gene by the gene editing protein. By replacing the fragment to be site-directed modified located between two target sites with donor DNA, a codon encoding tryptophan at position 737 in pAPN protein can be mutated to a codon encoding alanine, thereby achieving precise mutation of tryptophan to alanine at position 737 in a pAPN protein. The systems can avoid disruption or alteration of the normal expression of other amino acids in pAPN protein, therefore, the present invention maximally retains the physiological activity function of pAPN protein on the basis of resisting TGEV infection.

Provided is a method for building an eye disease model, comprising infecting microorganisms onto a model carrier. Also provided is an eye model carrier infected with microorganisms prepared using said method. The eye model carrier can be used for eye disease research and eye disease drug screening. The eye disease refers to retinal degeneration and the microorganisms refer to intestinal bacteria or bacteria identical to the intestinal bacteria.

A method for preparing pluripotent stem cell-derived hematopoietic stem cells and a method of constructing a humanized mouse model with the prepared hematopoietic stem cells. The method of preparing the hematopoietic stem cells identified an optimal differentiation condition according to a combination of low-molecular-weight compounds and protein growth factors without gene insertion, and thus may differentiate hematopoietic stem cells from pluripotent stem cells at high yield.

The invention provides recombinant adenoviral vectors which are capable of eliciting immunity against the pre-erythrocytic stage of the life cycle of the malaria parasite. In particular, the invention provides a recombinant, replication deficient simian adenoviral vector which encodes an antigen comprising the thrombospondin-related adhesion protein (TRAP), and also immunogenic compositions (e.g. vaccines) comprising the vector and methods of using such compositions.

The present invention provides a transgenic mouse which comprises a deficiency for murine T lymphocytes, B lymphocytes and NK cells, a deficiency for murine MHC class I and MHC class II molecules, and a functional xenogenic SIRP transgene. This mouse is useful for in vivo screening of various compounds, including immuno-therapeutic agents and vaccines. The said mouse is also useful for testing the in vivo metabolism of xenobiotic compounds.

A genetically modified non-human animal comprising a genome containing an endogenous non-human ACE2 locus genetically modified to encode a complete human ACE2 gene. According to a further embodiment the genome is genetically modified to encode a second, a third, and a fourth complete human ACE2 gene, the human ACE2 gene is at least 85 percent identical to SEQ ID No: 1, the animal of is a mouse, the human ACE2 gene encodes six protein variants, an endogenous Tmprss2 gene is unmodified, a LoxP gene flanks each of a 5 and a 3 end of a nucleic acid sequence of the human ACE2 gene, and the human ACE2 gene is expressed in a lung, kidney, spleen, stomach, liver, intestine, heart, and skeletal muscle of the animal, and a cortex, striatum, middle brain, hippocampus, olfactory bulb, and cerebellum of a brain of the animal.