No abstract

High preoperative NLR was associated with increased tumor size and high ATA risk of recurrence in patients with differentiated thyroid cancer.

Postseismic displacements of as much as 14 cm were recorded by GPS measurements in the 3 months following the MW 7.6 1999 Chi‐Chi, Taiwan earthquake. Data from 35 continuous and 90 campaign‐surveyed stations, which show continued east over west thrusting, are analyzed to estimate the postseismic slip distribution and fault geometry. Assuming the shallow fault dips 24° E, as determined by numerous studies of the mainshock, we invert for the deeper fault structure. Our results show that the fault dip shallows with depth below the hypocenter, merging into a nearly horizontal decollement at a depth of 8–12 km. The afterslip distribution shows a maximum slip of 25 cm in the hypocentral region at 7–12 km depth as well as significant slip on the lower decollement. Afterslip is notably absent in the region of maximum coseismic slip, consistent with the afterslip being driven by the mainshock stress change.

Local anesthetics are frequently used in fine-needle aspiration of thyroid lesions and locoregional control of persistent or recurrent thyroid cancer. Recent evidence suggests that local anesthetics have a broad spectrum of effects including inhibition of cell proliferation and induction of apoptosis in neuronal and other types of cells. In this study, we demonstrated that treatment with lidocaine and bupivacaine resulted in decreased cell viability and colony formation of both 8505C and K1 cells in a dose-dependent manner. Lidocaine and bupivacaine induced apoptosis, and necrosis in high concentrations, as determined by flow cytometry. Lidocaine and bupivacaine caused disruption of mitochondrial membrane potential and release of cytochrome c, accompanied by activation of caspase 3 and 7, PARP cleavage, and induction of a higher ratio of Bax/Bcl-2. Based on microarray and pathway analysis, apoptosis is the prominent transcriptional change common to lidocaine and bupivacaine treatment. Furthermore, lidocaine and bupivacaine attenuated extracellular signal-regulated kinase 1/2 (ERK1/2) activity and induced activation of p38 mitogen-activated protein kinase (MAPK) and c-jun N-terminal kinase. Pharmacological inhibitors of MAPK/ERK kinase and p38 MAPK suppressed caspase 3 activation and PARP cleavage. Taken together, our results for the first time demonstrate the cytotoxic effects of local anesthetics on thyroid cancer cells and implicate the MAPK pathways as an important mechanism. Our findings have potential clinical relevance in that the use of local anesthetics may confer previously unrecognized benefits in the management of patients with thyroid cancer.