The phenotype of the embryo of the genetic murine model is very valuable when investigating the function of the gene underlying embryonic development and birth defects. Although traditional imaging technology such as ultrasonography is very useful for evaluating the murine embryo phenotype, the use of advanced techniques for desirable phenotypes to get more information from genetic research.
This letter tests the feasibility of optical coherence tomography (October) as a high-throughput phenotyping tool for Murine Embryos. The 3-D oct imaging is carried out for direct and clean mouse embryos in the stage of development late (embryonic day 17.5). By using a dynamic focusing method and an oct angiography (Octa) approach, our October imaging about embryos shows visualization of fast and clean organ structures deeper than 5 mm and microvasculate complex vascular perfusion in the murine embryonic body. This demonstration shows that October imaging can be useful for assessing the anatomy of the embryo and genetically engineered mouse angiography. This article is protected by copyright. All copyrights.
In-depth phenotypes reveal the symptoms of general disease and novel in the model of the Knock-in Hemizygous (mut-ki) of the type of metilikalik type.
Insulated metmikalonic aciduria (MMauria) is mainly due to the deficiency of metilmalonyl-coa mutase (MMUT or MUT). Biochemistry, the deficiency of resulted in the accumulation of metilmalonic acid (MMA), propionyl-carnitin (C3) and other metabolites. Patients often show lethargy, failure of developing decompensation and metabolism that lead to commas or even deaths, with kidney and neurological disorders that are often identified in the long term. Here, we report the Mouse Hemizygous model that combines the Knock-in (KI) Missense Allele Of Mix with an artificial allele (KO) (MAT-KO / KI mouse) which was given 51% -Protein diet from day 12 of life, is a MMauria model Who was bespoke. In this diet, mutant rats develop a spoken metabolic phenotype which is characterized by an increase in the level of MMA and C3 which increases drastically compared to the control of the Litter (mut-ki / wt).
With this bellow mouse model, we do a standard phenotypic screen to assess the entire body disorder associated with this powerful metabolic condition. We found that MAT-KO / KI rats showed general clinical manifestations of MMauria, including clear failure to develop, indication of mild neurological and kidney dysfunction, and degenerative morphological changes in the liver, along with symptoms that are less described properly such as cardiovascular and hematological abnormalities ,
The analysis also revealed the characteristics of diseases so far, including low bone mineral density, behavior related to anxiety and ovarian atrophy. The first phenotypic screening of the MMAURIA mouse model confirmed its relevance with human diseases, revealing new changes related to the mutual deficiency, and suggest a series of quantified readings that can be used to evaluate the potential for treatment strategies.
Strategy for transgenic mouse behavior phenotyping.
Techniques and protocols to modify the mouse genome described in this volume allows researchers to produce genetic models of the extraordinary amount and the breadth of human disease. The generation of mice modified by gene offers a very strong approach to bringing human gene disorders that are known or recognized into the mouse model, but the extent to which mouse mutant produced recapitulates the physiological features and complex behavior of the state of the human disease is a key variable in the main usability of the model organism mouse. Thus, the characterization of mouse behavior with new targeted gene mutations is an important initial step in determining the potential impact of a new mouse model.
This chapter discusses a useful strategy in the initial observation of animals that help direct the choice of secondary tests to assess more detailed aspects of potentially disrupted behavior that may be relevant to the mododed diseases. The comprehensive, comprehensive comprehensive screen that assesses general health, reflexes, and sensorimotor functions is the first step in characterizing the phenotype of behavior, and the results often suggest areas where more complex complex behavioral tests can reveal more detailed normal behavior disorders.
This sequential approach reduces variability between subjects; This chapter also discusses the approach to reducing experimental artifacts due to handling, trial commands, environmental testing facilities, and other sources. A brief review of the phenotypical approach This behavior is intended to provide practical information to streamline the initial characterization of a new mouse model and maximize the use of efforts to use models and human diseases.
The Knockout Mouse Phenotype Program (Komp2) and IMPC: Database to find new roles in physiology and cardiovascular disease.
The collaborative goal of the Mouse Phenotype Program is KO. The purpose of this study was to introduce the Komp2 / IMPC program and the public accessible gene-phenotype database to the research community and specifically illustrate its utility to identify candidates of novel genes in cardiovascular disease (CV). In this report, we focus on the elimination of a single genes found related to the CV phenotype as part of the Fenotyping of Komp2 / IMPC from the broad physiological domain in more than 5,500 single genes.
Among 694 single genes found to produce CV phenotypes, we identify about one third (36%, n = 248) previously not associated with a CV system. We also look for leftovers from more than 5,500 genes that were previously not associated with the CV system. We use the results of gene disease analysis of the Medline sentence with an algorithm called Ensemble Biclustering for Classification (EBC), which reveals the relationship between the biomedical entities.
In addition, we studied their interactions in the network of protein-protein interactions. These genes can present opportunities for new CV research and can provide new targets for therapeutic interventions for various CV diseases.