Correction of secondary deformity after Nuss procedure for pectus excavatum by means of cultured autologous cartilage cell injection

Introduction: For some cases of pectus excavatum, ideal chest shape cannot be achieved solely by performing the Nuss procedure. This manuscript presents a case where the residual deformity following Nuss was corrected using injection-transplantation of cultured autologous chondrocytes. Presentation of case: The treatment was performed for an 18-year-old male, who sought improvement of his chest shape after previously undergoing the Nuss procedure. A 1 cm2 auricular cartilage piece was harvested from his ear. Chondrocytes were isolated from the cartilage piece and were cultured. The cultured chondrocytes were processed into gel form and were injection-transplanted to the deformed region of the patient's chest. The grafted chondrocytes consolidated in one month, presenting elasticity equivalent to ordinary costal cartilage. The patient's chest remains in an optimal shape after a one-year postoperative follow up. Discussion: Secondary correction of the chest deformity after previous operation for pectus excavatum is often tricky, because of the possible adhesion of the lungs or pericardium with the thoracic wall. Transplantation of cultured autologous chondrocytes does not require intra-thoracic maneuvers, and so is less invasive than other surgical interventions. Hence, priority can be placed, in some cases, on the chondrocyte transplantation rather than the re-correction of the thorax with the Nuss procedure or Ravitch procedure. Conclusion: Transplantation of cultured autologous chondrocytes is recommended as a useful option for secondary correction of chest deformity after the Nuss procedure

Biomechanical analysis of likelihood of optic canal damage in peri-orbital fracture

Purpose: Detection of optic canal fractures is often difficult because of the subtleness of the fracture. If we could clarify impact on which region around the orbit is likely to accompany the fracture of the optic canal, the knowledge should be useful to make early diagnosis of optic canal fractures. The present study was conducted to elucidate this issue. Methods: Ten finite element models were produced simulating the skulls of ten humans (8 males and 2 females; 43.8 ± 10.2 y/o). The peri-orbital area of each of the ten models was divided into eight regions in a clockwise fashion per 45 degrees. These regions were defined as Superior-Medial (0–45 degrees), Medial-Superior (45–90 degrees), Medial-Inferior (90 to 135 degrees), Inferior-Medial (135 to 180 degrees), Inferior-Lateral (180–225 degrees), Lateral-Inferior (225 to 270 degrees), Lateral-Superior (270–315 degrees), and Superior-Lateral regions (315–360 degrees), respectively. Dynamic simulation of applying traumatic energy on each of these regions was conducted. Resultant fracture patterns were evaluated using finite element analyses. Thereafter, frequencies of fracture involvement of the optic canal were evaluated for each of the eight regions. Results: The involvement of the optic canal was most frequent for the Superior-Medial region (7/10), followed by the Medial-Superior region (5/10). Conclusion: Optic canal fracture is likely to occur when the area between the supra-orbital notch and the medial canthus are strongly impacted. When evident fracture or serious damage of soft tissue is observed in this area, occurrence of optic canal fracture should be suspected

Characterization and treatment of gemcitabine‐ and cisplatin‐resistant bladder cancer cells with a pan‐RAS inhibitor

Combination chemotherapy with gemcitabine and cisplatin (GC) is recommended as the primary treatment for advanced bladder cancer (BC). However, the benefits of this approach are limited owing to the acquisition of drug resistance. Here, we found that gemcitabine‐resistant and cisplatin‐resistant BCs do not exhibit cross‐resistance, and that these BCs exhibit different mRNA patterns, as revealed using RNA sequence analysis. To overcome drug resistance, we used the newly developed pan‐RAS inhibitor Compound 3144. Compound 3144 inhibited cell viability through suppression of RAS‐dependent signaling in gemcitabine‐ and cisplatin‐resistant BCs. RNA sequencing revealed that several genes and pathways, particularly those related to the cell cycle, were significantly downregulated in Compound 3144‐treated BCs. These findings provide insights into potential therapeutic strategies for treating BC