Surgical treatment in patients with SSP had favourable results. Treatment in which the base of the bulla cannot be definitely shut off with staplers is associated with increased morbidity. Significant emphysematous change on preoperative computed tomography image and pulmonary fibrosis are predictors of recurrence. Patients with these findings should be investigated in terms of the indications of surgery and additional treatment, not only bullectomy.

Endothelin (ET)-1 is an endogenous vasoconstrictor which modulates norepinephrine (NE) release in myocardial ischemia reperfusion. Recent studies have demonstrated the pro- or anti-arrhythmic effects in reperfusion. The present studies were undertaken to test the hypothesis that ET receptors located in sympathetic nerve terminals modulate NE release associated with reperfusion arrhythmias (ventricular fibrillation; VF). Immunohistochemical studies showed that both ETA and ETB receptors exist in the sympathetic nerve varicosities, which were stained positive for tyrosine hydroxylase (TH) in the left ventricular wall in guinea pigs. Isolated guinea pig hearts were subjected to 20 min of normothermic global ischemia followed by 30 min reperfusion. Exogenously applied ET-1 (0.1 and 1 nM) dose-dependently increased NE release and the duration of VF, but these responses were significantly suppressed with the Na(+)/H(+) exchanger inhibitor, 5-(N-ethyl-N-isopropyl)-amiloride (10 microM). The ETA receptor antagonist (BQ123, 1 microM) and nonselective ET receptor antagonist (PD142893, 1 microM) significantly attenuated NE release and VF, whereas the ETB receptor antagonist (BQ788,300 nM) markedly elevated NE release but did not affect VF. These studies provide the first evidence that both ETA and ETB receptors, located in the sympathetic nerve varicosities, modulate NE release, at least in part, in association with reperfusion arrhythmias.

BACKGROUND: Integration of mutational profiling to identify driver genetic alterations in a clinical setting is necessary to facilitate personalized lung cancer medicine. A tumor genotyping panel was developed and the Shizuoka Lung Cancer Mutation Study was initiated as a prospective tumor genotyping study. This study reports the frequency of driver genetic alterations in Japanese lung adenocarcinoma patients, and clinicopathologic correlations with each genotype. METHODS: Between July 2011 and January 2013, 411 lung adenocarcinoma patients admitted to the Shizuoka Cancer Center were included in this study with their written informed consent. Surgically resected tissues, tumor biopsies, and/or body cavity fluids were collected and tested for 23 hotspot sites of driver mutations in 9 genes (EGFR, KRAS, BRAF, PIK3CA, NRAS, MEK1, AKT1, PTEN, and HER2), gene amplifications in 5 genes (EGFR, MET, PIK3CA, FGFR1, and FGFR2), and ALK, ROS1, and RET fusions. RESULTS: Genetic alterations were detected in 54.3% (223 of 411) of all patients. The most common genetic alterations detected in this study were EGFR mutations (35.0%) followed by KRAS mutations (8.5%) and ALK fusions (5.0%). Concurrent genetic alterations were detected in 22 patients (5.4%), and EGFR mutations were observed in 16 patients as the most common partner for concurrent genetic alteration. Significantly more concurrent genetic alterations were observed in older patients. CONCLUSIONS: This is one of the largest reports of a prospective tumor genotyping study on Japanese patients with adenocarcinoma. These data suggest that mutational profiling data using a multimutational testing platform would be valuable for expanding the range of molecular-targeted therapeutics in lung cancer.

The recurrence of mediastinal node cancer in patients undergoing L-SND was significantly greater than that in those undergoing SND.