Finite element analysis of soft foundation treatment by thermal drainage consolidation of group well

Thermal drainage consolidation method is a new technology of soft foundation treatment, which involves the coupling of thermo-hydro-mechanical field, and the action mechanism is complex. In this paper, taking the model test of thermal drainage consolidation as the prototype, the finite element model of thermal drainage consolidation is established by using Abaqus software, then, the numerical results are obtained and are compared with the results of model test, and the reliability of the numerical model is verified. The results show that when the applied load is constant, the higher the temperature is, the faster the consolidation speed of soil is, but with the increase of temperature, the consolidation effect of the same temperature difference will gradually weaken. In addition, the thermal drainage consolidation method can achieve the best treatment effect when the temperature of the soil reaches 60 ℃.</jats:p

Finite element analysis of soft foundation treatment by thermal drainage consolidation of group well

Thermal drainage consolidation method is a new technology of soft foundation treatment, which involves the coupling of thermo-hydro-mechanical field, and the action mechanism is complex. In this paper, taking the model test of thermal drainage consolidation as the prototype, the finite element model of thermal drainage consolidation is established by using Abaqus software, then, the numerical results are obtained and are compared with the results of model test, and the reliability of the numerical model is verified. The results show that when the applied load is constant, the higher the temperature is, the faster the consolidation speed of soil is, but with the increase of temperature, the consolidation effect of the same temperature difference will gradually weaken. In addition, the thermal drainage consolidation method can achieve the best treatment effect when the temperature of the soil reaches 60 ℃

Correction: Development of muscular dystrophy in a CRISPR-engineered mutant rabbit model with frame-disrupting ANO5 mutations

An amendment to this paper has been published and can be accessed via a link at the top of the paper.</jats:p

A novel rabbit model of Duchenne muscular dystrophy generated by CRISPR/Cas9

Duchenne muscular dystrophy (DMD) is an X-linked muscle-wasting disorder caused by mutations in the dystrophin gene, with an incidence of 1 in 3500 in new male births. Mdx mice are widely used as an animal model for DMD. However, these mice do not faithfully recapitulate DMD patients in many aspects, rendering the preclinical findings in this model questionable. Although larger animal models of DMD, such as dogs and pigs, have been generated, usage of these animals is expensive and only limited to several facilities in the world. Here, we report the generation of a rabbit model of DMD by co-injection of Cas9 mRNA and sgRNA targeting exon 51 into rabbit zygotes. The DMD knockout (KO) rabbits exhibit the typical phenotypes of DMD, including severely impaired physical activity, elevated serum creatine kinase levels, and progressive muscle necrosis and fibrosis. Moreover, clear pathology was also observed in the diaphragm and heart at 5 months of age, similar to DMD patients. Echocardiography recording showed that the DMD KO rabbits had chamber dilation with decreased ejection fraction and fraction shortening. In conclusion, this novel rabbit DMD model generated with the CRISPR/Cas9 system mimics the histopathological and functional defects in DMD patients, and could be valuable for preclinical studies. This article has an associated First Person interview with the first author of the paper

Correction: Development of muscular dystrophy in a CRISPR-engineered mutant rabbit model with frame-disrupting ANO5 mutations

An amendment to this paper has been published and can be accessed via a link at the top of the paper

DMP1 Ablation in the Rabbit Results in Mineralization Defects and Abnormalities in Haversian Canal/Osteon Microarchitecture

DMP1 (dentin matrix protein 1) is an extracellular matrix protein highly expressed in bones. Studies of Dmp1 knockout (KO) mice led to the discovery of a rare autosomal recessive form of hypophosphatemic rickets (ARHR) caused by DMP1 mutations. However, there are limitations for using this mouse model to study ARHR, including a lack of Haversian canals and osteons (that occurs only in large mammalian bones), high levels of fibroblast growth factor 23 (FGF23), and PTH, in comparison with a moderate elevation of FGF23 and unchanged PTH in human ARHR patients. To better understand this rare disease, we deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR, such as the rachitic rosary (expansion of the anterior rib ends at the costochondral junctions), moderately increased FGF23, and normal PTH levels, as well as severe defects in bone mineralization. Unexpectedly, all DMP1 KO rabbits died by postnatal week 8. They developed a severe bone microarchitecture defect: a major increase in the central canal areas of osteons, concurrent with massive accumulation of osteoid throughout all bone matrix (a defect in mineralization), suggesting a new paradigm, where rickets is caused by a combination of a defect in bone microarchitecture and a failure in mineralization. Furthermore, a study of DMP1 KO bones found accelerated chondrogenesis, whereas ARHR has commonly been thought to be involved in reduced chondrogenesis. Our findings with newly developed DMP1 KO rabbits suggest a revised understanding of the mechanism underlying ARHR. (c) 2019 American Society for Bone and Mineral Research