The results show that CD-DST is capable of selecting the responders and the respective optimal regimens, and also delineating the patients less likely benefit from treatment.
Tissue sealants can prevent the occurrence of pulmonary air leakage, although few studies have evaluated the seal-breaking pressure properties of the various methods. We developed a new method for repairing visceral pleural defects which combines fibrin glue with a sheet material. We used an animal model to compare its efficacy with that of three current techniques up to 24 h after application. Under thoracotomy, 5 x 20 mm visceral pleural defects with a depth of 3 mm were made in beagles. The defects in the normal lungs were repaired using 1 of 4 methods: Method A, fibrin-glue double layer (fibrinogen solution was dripped, followed by thrombin solution); Method B, pack method (fibrin glue combined with polyglycolic acid sheet); Method C, rubbing and spray (fibrinogen was rubbed, followed by spraying of both fibrinogen and thrombin solutions); Method D, fibrin-glue-coated collagen fleece. The defects were repaired also in an emphysematous lung model using Method A, B or C. In the normal lungs, Method B showed significantly higher pressure resistance compared with the other methods at 5 min, 1 and 3 h post-application. Pressure resistance increased with time for all methods. In the emphysematous lungs, Method B showed significantly higher seal-breaking pressure than Methods A and C. Compared with existing tissue sealant methods, the pack method reliably controlled pulmonary air leakage immediately after application.
Abstract. Expression of copper-transporting P-type adenosine triphosphatase A (ATP7A) is reportedly associated with platinum drug resistance in various types of solid tumors. However, the impact of ATP7A expression on platinum drug resistance in non-small cell lung cancer (NSCLC) has yet to be adequately elucidated. In vitro cisplatin (CDDP) sensitivity was investigated using the collagen gel-droplet embedded culture drug sensitivity test, and the ATP7A mRNA expression levels were assessed by real-time polymerase chain reaction in surgically resected specimens of NSCLC. The relationship between the ATP7A expression levels and the in vitro CDDP sensitivity was then evaluated. The ATP7A mRNA expression levels in the CDDP-resistant tumors were significantly higher than those in the CDDP-sensitive tumors (p=0.0167, Mann-Whitney U test). In conclusion, the results suggest that evaluation of ATP7A expression is useful as a marker for cisplatin chemoresistance.
IntroductionCisplatin (CDDP), an anticancer drug containing platinum, is widely used in the treatment of solid tumors, such as testicular, ovarian, cervical, bladder, head and neck, and non-small cell lung cancers (NSCLC) (1). CDDP has been used as a key drug for chemotherapy against NSCLC for more than 20 years.However, the overall response rate to cisplatin used as a single agent is reported to be no more than 20% in patients with NSCLC (2). Furthermore, development of resistance to CDDP is common during treatment of NSCLC and is therefore a significant factor to be considered by clinical oncologists. Subsequently, exploration of a chemoresistance marker is crucial. The mechanisms underlying the development of CDDP resistance include decreased drug accumulation, enhanced detoxification and increased DNA repair efficiency. However, previous studies have been limited mainly to the in vitro or in vivo level. Additionally, no study has shown factors that have been validated as common contributors to clinical CDDP resistance and prognosis in NSCLC patients (1).Copper-transporting P-type adenosine triphosphatase A (ATP7A) plays a significant role in copper distribution within cells. ATP7A is expressed in the intestinal epithelium as well as in most other tissues apart from the liver (3-7). Binding of Cu to ATP7A triggers highly regulated subcellular relocalization that involves movement from the basal position in the trans-Golgi network to the plasma membrane (3,8). Defective function of ATP7A causes Menkes disease, and the pathology of Menkes disease reflects the inadequate mobilization of Cu from a number of tissues. Previous studies suggested that the copper export system also functions as an efflux transporter for platinum drugs. These studies also showed an association between ATP7A expression and resistance to platinum drugs in malignancies (9-11). However, the ATP7A expression level and its impact on CDDP resistance in NSCLC has yet to be adequately elucidated.The present study aimed to investigate the predictive value of ATP7A gene expression for the in vitr...
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