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The angle steel member is the most commonly used component form of the transmission tower structure. Considering its connection characteristics, we must deal with its stability analysis under semi-rigid constraint conditions for the proper study of the overall structure’s mechanical performance. Therefore, in order to establish a simple and high-precision method suitable for the ultimate bearing capacity analysis of the transmission tower, we build the refined finite element models of typical steel tower joints, analyze its moment-rotation curve and utilize simulation technique of spring elements to acquire the calculation method of its single angle stability bearing capacity, which is considering initial imperfection and residual stress. Furthermore, we analyze its bearing capacity under different constraint conditions such as rigid, semi-rigid and articulated connection. The results show that it is necessary to consider joint stiffness in the bearing capacity analyses. Finally, it’s confirmed that the calculation results of this method agree well with the experimental data, which validates its high accuracy. Therefore, the method provides technical support for high efficient component stability simulation in overall stability analyses of the transmission steel tower.

Heterotopic ossification (HO) is pathological bone formation characterized by ossification within muscle, tendons, or other soft tissues. However, the cells of origin and mechanisms involved in the pathogenesis of HO remain elusive. Here we show that deletion of suppressor of fused (Sufu) in cathepsin K-Cre-expressing (Ctsk-Cre-expressing) cells resulted in spontaneous and progressive ligament, tendon, and periarticular ossification. Lineage tracing studies and cell functional analysis demonstrated that Ctsk-Cre could label a subpopulation of tendon-derived progenitor cells (TDPCs) marked by the tendon marker Scleraxis (Scx). [Ctsk.sup.+][Scx.sup.+] TDPCs are enriched for tendon stem cell markers and show the highest self-renewal capacity and differentiation potential. Sufu deficiency caused enhanced chondrogenic and osteogenic differentiation of Ctsk-Cre-expressing tendon-derived cells via upregulation of Hedgehog (Hh) signaling. Furthermore, pharmacological intervention in Hh signaling using JQ1 suppressed the development of HO. Thus, our results show that Ctsk-Cre labels a subpopulation of TDPCs contributing to HO and that their cell-fate changes are driven by activation of Hh signaling., Introduction Heterotopic ossification (HO) is a pathological process in which ectopic bone forms within muscles, tendons, or other soft tissues (1). HO currently develops after trauma induced by deep burns, [...]

Bone osteogenic sarcoma has a poor prognosis, as the exact cell of origin and the signaling pathways underlying tumor formation remain undefined. Here, we report an osteogenic tumor mouse model based on the conditional knockout of liver kinase b1 (Lkb1, also known as Stk11) in Cathepsin K-Cre-expressing (Ctsk-Cre-expressing) cells. Lineage-tracing studies demonstrated that Ctsk-Cre could label a population of periosteal cells. The cells functioned as mesenchymal progenitors with regard to markers and functional properties. LKB1 deficiency increased proliferation and osteoblast differentiation of [Ctsk.sup.+] periosteal cells, while downregulation of mTORC1 activity, using a Raptor genetic mouse model or mTORC1 inhibitor treatment, ameliorated tumor progression of Ctsk-Cre [Lkb1.sup.fllfl] mice. Xenograft mouse models using human osteosarcoma cell lines also demonstrated that LKB1 deficiency promoted tumor formation, while mTOR inhibition suppressed xenograft tumor growth. In summary, we identified periosteum-derived Ctsk-Cre-expressing cells as a cell of origin for osteogenic tumor and suggested the LKB1/mTORC1 pathway as a promising target for treatment of osteogenic tumor., Introduction Osteogenic tumor is the most common primary tumor of the bone tissue, including benign bone-forming neoplasm, osteoma, osteoblastoma, and a malignant neoplasm called osteogenic sarcoma, also referred to as [...]