Our improved criteria are therefore considered to positively contribute to a safe and definite clinical decision regarding postoperative patient management.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease of unknown cause. IPF has a distinct histopathological pattern of usual interstitial pneumonia in which fibroblastic foci (FF) represent the leading edge of fibrotic destruction of the lung. Currently there are three major hypotheses for how FF are generated: (1) from resident fibroblasts, (2) from bone marrow-derived progenitors of fibroblasts, and (3) from alveolar epithelial cells that have undergone epithelial-mesenchymal transition (EMT). We found that FF dissociated capillary vessels from the alveolar epithelia, the basement membranes of which are fused in normal physiological conditions, and pushed the capillaries and elastic fibers down ~100 μm below the alveolar epithelia. Furthermore, the alveolar epithelial cells covering the FF exhibited a partial EMT phenotype. In addition, normal human alveolar epithelial cells in vitro underwent dynamic EMT in response to transforming growth factor-β signaling within 72 h. Because it seems that resident fibroblasts or bone marrow-derived cells cannot easily infiltrate and form FF between the alveolar epithelia and capillaries in tight contact with each other, FF are more likely to be derived from the epithelial-to-mesenchymal transitioned alveolar epithelia located over them. Moreover, histology and immunohistochemistry suggested that the FF formed in the lung parenchyma disrupt blood flow to the alveolar septa, thus destroying them. Consequently, collapse of the alveolar septa is likely to be the first step toward honeycombing in the lung during late stage IPF. On the basis of these findings, inhibition of transforming growth factor-β signaling, which can suppress EMT of the alveolar epithelial cells in vitro, is a potential strategy for treating IPF.

This study demonstrates that VMPR with SND is a feasible surgical therapy for cN0-pN2 NSCLC without loss of curability. It is unnecessary to convert the VATS approach to thoracotomy in order to do SND even if pN2 disease is revealed during VMPR.

Background Completion lobectomy long after segmentectomy in the same lobe is extremely difficult because of severe adhesions around hilar structures, especially in cases involving video-assisted thoracoscopic surgery (VATS) completion lobectomy. We report and compare the surgical outcomes of patients who underwent VATS or thoracotomy completion lobectomy long after radical segmentectomy for lung cancer. Methods We retrospectively evaluated the surgical outcomes of completion lobectomies performed at our institute long after radical segmentectomies for lung cancer in the same lobe. The efficacy and safety of VATS completion lobectomy was compared to that of thoracotomy completion lobectomy. Results Ten of 228 patients who underwent radical segmentectomy for lung cancer between 2009 and 2018 underwent completion lobectomy at least a month after segmentectomy; five patients underwent VATS completion lobectomy. None of the patients underwent VATS left upper completion lobectomy, and conversion to thoracotomy was required in one patient. There were no significant differences between VATS and thoracotomy completion lobectomies in the median operative times (VATS 295 min, thoracotomy 339 min, p = 0.55), intraoperative blood loss volumes (VATS 350 mL, thoracotomy 500 mL, p = 0.84), intervals between initial segmentectomy and completion lobectomy (VATS 40 months, thoracotomy 48 months, p = 0.55), and number of patients with pulmonary artery injury (VATS 1, thoracotomy 2, p = 0.49). There was no operation-related mortality. Conclusions VATS completion lobectomy long after segmentectomy for lung cancer could be performed without fatal complications unless severe adhesions are observed around each main pulmonary artery.

Adults who have undergone surgical repair of congenital diaphragmatic hernia have a prolonged illness. They usually have severe adhesions around the intrathoracic hernial sac; therefore, the adhesion itself as well as misidentification of the hernial defect can make surgical repair difficult, even in open surgery. Here, we present the successful video-assisted thoracoscopic surgical repairs of Bochdalek and Morgagni hernias in patients with severe adhesions of the hernial sac (peritoneum) to the parietal pleura lying over the thoracic wall and diaphragm. An 18-year-old woman with a Bochdalek hernia and a 28-year-old woman with a Morgagni hernia underwent thoracoscopic division of severe adhesions, proper minithoracotomy, and precise repairs of diaphragmatic defects. Postoperative courses of both patients were uneventful with no signs of recurrence of the hernia. Thus, we recommend the thoracoscopic approach as the first choice over an open or laparoscopic approach in the management of adult patients with Bochdalek or Morgagni hernias and severe adhesion.