Background: Modified tension band wiring is one of the most preferred surgical methods for transverse patellar fractures. However, the optimal depth or sagittal position of a Kirschner wire (K-wire) in modified tension band wiring has yet to be determined.The purpose of this study was to evaluate whether the depth of a K-wire affects the biomechanical characteristics of modified tension band wiring using the finite-element method. Methods: A patella model was designed with a cuboid shape (length, 34.3 mm; width, 44.8 mm; and thickness, 22.4 mm) and divided into the cortical and cancellous bone parts. A transverse fracture line was formed on the midline of the cuboid shape model.The cuboidal model was applied to modified tension band wiring. The depth or sagittal position of the K-wire was divided into superficial, center, and deep. With the Abaqus v2017 program (Dassault System Inc.), the distal part of the model was fixed, and a tensile load of 850 N was applied to the proximal part of the model at an angle of 45°. The maximum pressures of the cortical and cancellous bones at the fracture plane were measured. The largest von Mises values of the K-wire and stainless steel wire were also measured. The fracture gap on the distracted or anterior side was measured. Results: In deep K-wire placement, the highest peak von Mises values of the cortical and cancellous bones were observed. The Kwire and stainless steel wire showed the highest von Mises values in deep K-wire placement. The fracture gap was also largest in deep K-wire placement. Conclusions The depth of the K-wire affects the biomechanical characteristics of modified tension band wiring. Deep placement of the K-wire will be more favorable for bone union than the empirically known 5-mm anterior or center placement of the K-wire.

Background: Modified tension band wiring is one of the most preferred surgical methods for transverse patellar fractures. However, the optimal depth or sagittal position of a Kirschner wire (K-wire) in modified tension band wiring has yet to be determined.The purpose of this study was to evaluate whether the depth of a K-wire affects the biomechanical characteristics of modified tension band wiring using the finite-element method. Methods: A patella model was designed with a cuboid shape (length, 34.3 mm; width, 44.8 mm; and thickness, 22.4 mm) and divided into the cortical and cancellous bone parts. A transverse fracture line was formed on the midline of the cuboid shape model.The cuboidal model was applied to modified tension band wiring. The depth or sagittal position of the K-wire was divided into superficial, center, and deep. With the Abaqus v2017 program (Dassault System Inc.), the distal part of the model was fixed, and a tensile load of 850 N was applied to the proximal part of the model at an angle of 45°. The maximum pressures of the cortical and cancellous bones at the fracture plane were measured. The largest von Mises values of the K-wire and stainless steel wire were also measured. The fracture gap on the distracted or anterior side was measured. Results: In deep K-wire placement, the highest peak von Mises values of the cortical and cancellous bones were observed. The Kwire and stainless steel wire showed the highest von Mises values in deep K-wire placement. The fracture gap was also largest in deep K-wire placement. Conclusions The depth of the K-wire affects the biomechanical characteristics of modified tension band wiring. Deep placement of the K-wire will be more favorable for bone union than the empirically known 5-mm anterior or center placement of the K-wire.

Cancer immunotherapy, in the form of vaccination, adoptive cellular transfer, or immune checkpoint inhibitors, has emerged as a promising practice within the field of oncology. However, despite the developing field's potential to revolutionize cancer treatment, the presence of immunotherapeutic-resistant tumor cells in many patients present a challenge and limitation to these immunotherapies. These cells not only indicate immunotherapeutic resistance, but also show multi-modal resistance to conventional therapies, abnormal metabolism, stemness, and metastasis. How can immunotherapeutic-resistant tumor cells render multi-malignant phenotypes? We reasoned that the immune-refractory phenotype could be associated with multi-malignant phenotypes and that these phenotypes are linked together by a factor that acts as the master regulator. In this review, we discussed the role of the embryonic transcription factor NANOG as a crucial master regulator we named “common factor” in multi-malignant phenotypes and presented strategies to overcome multi-malignancy in immunotherapeutic-resistant cancer by restraining the NANOG-mediated multi-malignant signaling axis. Strategies that blunt the NANOG axis could improve the clinical management of therapy-refractory cancer.
Humans ; Immunotherapy ; Metabolism ; Neoplasm Metastasis ; Phenotype ; Transcription Factors ; Vaccination

Cancer immunotherapy, in the form of vaccination, adoptive cellular transfer, or immune checkpoint inhibitors, has emerged as a promising practice within the field of oncology. However, despite the developing field's potential to revolutionize cancer treatment, the presence of immunotherapeutic-resistant tumor cells in many patients present a challenge and limitation to these immunotherapies. These cells not only indicate immunotherapeutic resistance, but also show multi-modal resistance to conventional therapies, abnormal metabolism, stemness, and metastasis. How can immunotherapeutic-resistant tumor cells render multi-malignant phenotypes? We reasoned that the immune-refractory phenotype could be associated with multi-malignant phenotypes and that these phenotypes are linked together by a factor that acts as the master regulator. In this review, we discussed the role of the embryonic transcription factor NANOG as a crucial master regulator we named “common factor” in multi-malignant phenotypes and presented strategies to overcome multi-malignancy in immunotherapeutic-resistant cancer by restraining the NANOG-mediated multi-malignant signaling axis. Strategies that blunt the NANOG axis could improve the clinical management of therapy-refractory cancer.