RESUMEN
There are many commercially available artificial nerve conduits, used mostly to repair short gaps in sensory nerves. The stages of nerve regeneration in a nerve conduit are fibrin matrix formation between the nerve stumps joined to the conduit, capillary extension and Schwann cell migration from both nerve stumps, and, finally, axon extension from the proximal nerve stump. Artificial nerves connecting transected nerve stumps with a long interstump gap should be biodegradable, soft and pliable; have the ability to maintain an intrachamber fibrin matrix structure that allows capillary invasion of the tubular lumen, inhibition of scar tissue invasion and leakage of intratubular neurochemical factors from the chamber; and be able to accommodate cells that produce neurochemical factors that promote nerve regeneration. Here, we describe current progress in the development of artificial nerve conduits and the future studies needed to create nerve conduits, the nerve regeneration of which is compatible with that of an autologous nerve graft transplanted over a long nerve gap.
RESUMEN
Introduction and importance: Iliopsoas and iliacus abscesses are caused by hematogenous and lymphatic infections and the spread of inflammation in neighboring organs. A small number of cases have been reported in which inflammation spread not only within the iliopsoas muscle but also to the thigh. Here we report a case of retroperitoneal infiltration and perforation of cecal cancer that caused extensive abscess formation from the iliacus muscle to the thigh. Case presentation: An 80-year-old man who had undergone chemotherapy for cecal cancer had abdominal pain and right thigh pain without any particular attraction. CT images showed extensive abscess formation from the iliacus muscle to the subcutaneous part of the thigh due to retroperitoneal infiltration and perforation of cecal cancer. Ileocecal resection, colostomy, and retroperitoneal abscess drainage were performed for perforation of cecal cancer and pelvic abscess. Although the thigh was initially drained by a small incision, the infection did not heal. Extensive debridement and drainage were required for all of the contaminated areas, and after all the infection was completely cured. Clinical discussion: The optimal treatment for an abscess that has spread from the inguinal region to the thigh is unclear. In this case, active debridement and drainage of the infected area were effective and should have been done early. Conclusion: We believed that debridement and drainage should have been performed from the time of the first surgery not only by the small incision drainage but also for all of the contaminated areas when the infection had been widespread.
RESUMEN
Herein, we report the in situ transmission electron microscopy observation of the deformation and fracture processes of an epoxy resin thin film containing silica nanoparticles under tensile strain. Under tensile strain, the dispersed silica nanoparticles in the composite arrest the progress of the crack tip and prevent crack propagation. Concomitantly, the generation and growth of nanovoids at the epoxy matrix/nanoparticle interfaces were clearly observed, particularly in the region near the crack tip. These nanovoids contribute to the dissipation of fracture energy, thereby enhancing the fracture toughness. We also analyzed the local distributions of the true strain and strain rate in the nanocomposite film during tensile testing using the digital image correlation method. In the region around the crack tip, the strain rate increased by 3 to 10 times compared to the average of the entire test specimen. However, the presence of large filler particles in the growing crack suppressed the generation of strain, potentially contributing to hindering crack growth.
RESUMEN
The main reasons for failure of cancer chemotherapy are intrinsic and acquired drug resistance. The Hippo pathway effector Yes-associated protein (YAP) is associated with resistance to both cytotoxic and molecular targeted drugs. Several lines of evidence indicate that YAP activates transcriptional programmes to promote cell cycle progression and DNA damage responses. Therefore, we hypothesised that YAP is involved in the sensitivity of cancer cells to small-molecule agents targeting cell cycle-related proteins. Here, we report that the inactivation of YAP sensitises the OVCAR-8 ovarian cancer cell line to AZD1775, a small-molecule WEE1 kinase inhibitor. The accumulation of DNA damage and mitotic failures induced by AZD1775-based therapy were further enhanced by YAP depletion. YAP depletion reduced the expression of the Fanconi anaemia (FA) pathway components required for DNA repair and their transcriptional regulator E2F1. These results suggest that YAP activates the DNA damage response pathway, exemplified by the FA pathway and E2F1. Furthermore, we aimed to apply this finding to combination chemotherapy against ovarian cancers. The regimen containing dasatinib, which inhibits the nuclear localisation of YAP, improved the response to AZD1775-based therapy in the OVCAR-8 ovarian cancer cell line. We propose that dasatinib acts as a chemosensitiser for a subset of molecular targeted drugs, including AZD1775, by targeting YAP.
