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Thoracic impalement injury is an uncommon form of trauma. In the present report, we describe the case of a 78-year-old man who was injured by 2 metal rods. We decided to remove the rod on the right side by performing video-assisted thoracic surgery. However, during this procedure, total pleural adhesion was identified. Therefore, a mini-thoracotomy was performed and the rod was removed safely; the patient's postoperative course was uneventful. The rod on the left side did not pass through the thoracic cavity. There are only a few reports of thoracic impalement injury in literature, and cases with total pleural adhesion are very rare. Careful preoperative planning and a multidisciplinary approach are essential for managing this type of injury.

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We encountered 5 cases of delayed massive hemothorax due to diaphragmatic injury. Delayed hemothorax presented 2∼11 days after injury, with lower rib fractures seen all cases. We performed emergent video-assisted thoracic surgery with mini-thoracotomy for all patients. Lacerations could be clearly visualized in the diaphragm after evacuation of blood clots, which were then sutured. In four cases, the sharp edges of the broken ribs were thought to have caused the diaphragmatic lacerations. The mean blood loss volume was 2,905 ml, and all patients required blood transfusions. However, homeostasis was achieved after surgery, and all patients had an uneventful postoperative course. Although, delayed hemothorax is relatively uncommon, it needs to be considered a lethal condition.

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A 61 year-old male with rectal cancer underwent anterior resection with D2 lymph node dissection in August 2007. Carcinoembryonic antigen (CEA) level was 5.6 before the operation. Pathological findings were Rs, tub2¼>tub1, type 3, pSE, ly1, v2, pN1 (1/23), H0, P0, M0 , pStage IIIA. Adjuvant chemotherapy with tegafur-uracil (UFT) 600 mg/Leucovorin (LV) 75 mg was administered for 1 year. A recurrence at a site of anastomosis developed and lower anterior resection was required in September 2010. CEA level was 5.4 before the operation. After 7 courses of capecitabine plus oxaliplatin (XELOX) treatment, the right #283 lymph node increased to 8 mm in October 2011 and the patient was diagnosed with a re-recurrence of the original tumor (CEA level, 4.6). Carbon ion radiotherapy (73.6 Gy/16 Fr/4 weeks) was performed between November 28 and December 22, 2011. Although the right #283 lymph node had shrunk by January 2012, a single node in the S3 domain of the right lung was observed and became progressively larger, indicating a lung metastasis (CEA level, 5.4). The patient received carbon ion radiotherapy (60.0 Gy/4 Fr) for the lung metastasis between July 30 and August 2, 2012. No additional recurrences have been seen through February 2014.

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A 66-year-old man underwent abdominoperineal resection for rectal cancer in 2003, followed by liver resection for a solitary liver metastasis in 2005. In 2006, the patient underwent abdominal para-aortic lymph node dissection, which was performed concurrently with partial resections of 3 metastases in the right lung. New metastatic lesions were subsequently diagnosed in S8 of the right lung and S1+2 of the left lung. The patient underwent stereotactic body radiotherapy (SBRT) for both lesions. However, the lesions relapsed and salvage surgeries were subsequently performed. These included a partial resection in 2009 for the lesion in the right lung and an upper division segmentectomy in 2010 for the lesion in the left lung. Currently, 11 years after resection of the primary rectal cancer, the patient is asymptomatic, without any signs of recurrence. In this report, we describe the use of SBRT for the treatment of colorectal cancer pulmonary metastases, and the use of salvage surgery for relapsed lesions.

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An 80-year-old man with no complaint was referred to our department because of high serum CEA level. He was diagnosed as non-small cell lung cancer(adenocarcinoma)of the left lower lobe(c-T2aN0M0, stage I B), and therefore the left lower lobectomy with lymph node dissection was performed. Pathological staging was p-T2aN1(#10)M0, stage II A, and EGFR mutation was negative. Adjuvant chemotherapy with UFT was started, but multiple hilar and mediastinal lymph nodes metastases soon appeared. Carboplatin(CBDCA)+paclitaxel(PTX), erlotinib, and docetaxel(DOC)were attempted after that, but the lymph nodes increased in size and the CEA level was up to 159.8 ng/mL. At about the same time, brain and pulmonary metastases were recognized. After radiation for the chest lymph nodes and stereotactic radiosurgery(SRS)for the brain metastasis, oral S-1 monotherapy was introduced. Soon after, the lymph nodes shrinked and the CEA level decreased. Also, the pulmonary metastasis disappeared. Although a right supraclavicular lymph node metastasis was resected during the clinical course, the S-1 monotherapy has been continued with no serious adverse event. He is well(PS 0)without recurrent lesion, and his serum CEA level is within the normal limit.

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The prognosis of granulocyte colony-stimulating factor( G-CSF) -producing lung cancer is very poor. We present a case of G-CSF-producing locally advanced non-small cell lung cancer successfully treated with chemoradiotherapy. A 65-year-old man presented with a slight fever, general fatigue, and cough. A mass was detected in the right upper lobe of his lung, and it was diagnosed as squamous cell carcinoma by computed tomography (CT) -guided needle biopsy. Laboratory data indicated marked leukocytosis and elevated serum G-CSF levels, and therefore, the tumor was strongly suspected to be G-CSF-producing lung cancer. After systemic evaluation, the patient was treated with concurrent chemoradiotherapy for cT3N2M0, stage IIIA non-small cell lung cancer. Complete response (CR) was achieved, and he remained well with no recurrence of the cancer for over 3 years after treatment. Although immunohistochemical staining results for G- CSF were negative, clinically, the tumor was diagnosed as G-CSF-producing lung cancer.

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BACKGROUND: Rheumatoid pleurisy rarely occurs before a diagnosis of rheumatoid arthritis (RA). It is the second leading cause of pseudochylothorax, but there are few reports of RA-associated pseudochylothorax. CASE: A 50-year-old man presented to our hospital with an undiagnosed exudative pleural effusion. In order to obtain a definitive diagnosis, we performed medical thoracoscopy under local anesthesia. The pleural effusion was turbid and was identified as a pseudochylothorax. The parietal pleura was white and slightly thickened with numerous scattered small granules and the pleural biopsy showed an infiltration of inflammatory cells including lymphocytes and plasma cells with a lack of normal mesothelial cells, findings that were highly consistent with rheumatoid pleurisy. Additional laboratory data revealed elevated levels of CCP antibody and rheumatoid factor. During an outpatient visit about 30 days after discharge, the patient complained of polyarthralgia and was diagnosed with RA, resulting in a definitive diagnosis of the pleural effusion as rheumatoid pleurisy. CONCLUSION: We encountered a rare case of a rheumatoid pleural effusion without other symptoms of arthritis, which was identified as a pseudochylothorax by medical thoracoscopy.

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This case concerns a 78-year-old man, who was diagnosed with lung cancer at the age of 73. He underwent right lobectomy and lymph node dissection, and pathological analysis revealed a poorly differentiated adenocarcinoma, pT1N0M0 pStage IA. 15 months after surgery, computed tomography showed recurrence of lung cancer at the apex of thoracic cavity. He underwent radiation to the recurrence site, and 33 months after surgery, fluorodeoxyglucose uptake was observed at the axillary and infraclavicular lymph nodes in positron emission tomography examination. Treatment with pemetrexed was started because carcinomatous pericarditis was also found. Although pericardial effusion disappeared, the patient complained of the enlarged size of the axillary and infraclavicular lymph nodes and severe numbness in an arm. Beyond lymph node involvement, no other metastatic sites were found. An operation was performed to relieve the pain and the pathological analysis of lymph nodes showed metastases of lung cancer. The operation successfully reduced the pain experienced by the patient. There has been no further recurrence in the 9 months following surgery. Axillary lymph node metastasis is thought to be a distant metastasis; however, this is a case where local control was needed and was effective.

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Thoracic impalement injury is uncommon mechanism of injury. We describe a case treated successfully by non-surgical management. An 87-year-old male got impalement injury in his room by a part of stepladder on right anterior chest wall. He was found to be alert and hemodynamically stable, so computed tomography (CT) scan was performed. Chest CT showed right-sided hemopneumothorax and pulmonary contusion, but no cardiac and great vessels injury. We discussed about performing video-assisted thoracic surgery (VATS), but selected non-surgical treatment including chest drainage at that time, because of low possibilities of massive bleeding and apprehension of postoperative complication resulting from patient's high age. He had uneventful recovery and was discharged on foot 13 days after admission.

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We encountered a case of primary racemose hemangioma treatment with successful bronchial artery embolism for massive hemoptysis. A 56-year-old woman with massive hemoptysis was transported to our hospital. The source of the massive hemoptysis was observed to be from around a non-pulsatile polyp covered by normal mucosa occluding the truncus intermedius by fiberoptic bronchoscopy. We stopped the bleeding temporarily using differential lung ventilation, and then bronchial artery angiography was performed. The main right bronchial artery was enlarged, and enlarged and convoluted right peripheral bronchial vessels were also observed. We diagnosed the massive bleeding to be due to racemose hemangioma. A successful bronchial artery embolization (BAE) was performed with gelforms and metallic coils for the treatment of racemose hemangioma. There has been no recurrence of hemoptysis for one year after BAE. There have been many reports on massive hemoptysis as in this patient who were treated by lobectomy, nevertheless we would like to state BAE should be considered as a suitable treatments for primary racemose hemangioma with hemoptysis if there is no recognizable shunt artery.

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Cdc7 kinase, conserved from yeasts to human, plays important roles in DNA replication. However, the mechanisms by which it stimulates initiation of DNA replication remain largely unclear. We have analyzed phosphorylation of MCM subunits during cell cycle by examining mobility shift on SDS-PAGE. MCM4 on the chromatin undergoes specific phosphorylation during S phase. Cdc7 phosphorylates MCM4 in the MCM complexes as well as the MCM4 N-terminal polypeptide. Experiments with phospho-amino acid-specific antibodies indicate that the S phase-specific mobility shift is due to the phosphorylation at specific N-terminal (S/T)(S/T)P residues of the MCM4 protein. These specific phosphorylation events are not observed in mouse ES cells deficient in Cdc7 or are reduced in the cells treated with siRNA specific to Cdc7, suggesting that they are mediated by Cdc7 kinase. The N-terminal phosphorylation of MCM4 stimulates association of Cdc45 with the chromatin, suggesting that it may be an important phosphorylation event by Cdc7 for activation of replication origins. Deletion of the N-terminal non-conserved 150 amino acids of MCM4 results in growth inhibition, and addition of amino acids carrying putative Cdc7 target sequences partially restores the growth. Furthermore, combination of MCM4 N-terminal deletion with alanine substitution and deletion of the N-terminal segments of MCM2 and MCM6, respectively, which contain clusters of serine/threonine and are also likely targets of Cdc7, led to an apparent nonviable phenotype. These results are consistent with the notion that the N-terminal phosphorylation of MCM2, MCM4, and MCM6 may play functionally redundant but essential roles in initiation of DNA replication.

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Human Lats2, a novel serine/threonine kinase, is a member of the Lats kinase family that includes the Drosophila tumour suppressor lats/warts. Lats1, a counterpart of Lats2, is phosphorylated in mitosis and localized to the mitotic apparatus. However, the regulation, function and intracellular distribution of Lats2 remain unclear. Here, we show that Lats2 is a novel phosphorylation target of Aurora-A kinase. We first showed that the phosphorylated residue of Lats2 is S83 in vitro. Antibody that recognizes this phosphorylated S83 indicated that the phosphorylation also occurs in vivo. We found that Lats2 transiently interacts with Aurora-A, and that Lats2 and Aurora-A co-localize at the centrosomes during the cell cycle. Furthermore, we showed that the inhibition of Aurora-A-induced phosphorylation of S83 on Lats2 partially perturbed its centrosomal localization. On the basis of these observations, we conclude that S83 of Lats2 is a phosphorylation target of Aurora-A and this phosphorylation plays a role of the centrosomal localization of Lats2.

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DNA double-strand breaks represent the most potentially serious damage to a genome; hence, many repair proteins are recruited to nuclear damage sites by as yet poorly characterized sensor mechanisms. Here, we show that NBS1, the gene product defective in Nijmegen breakage syndrome (NBS), physically interacts with histone, rather than damaged DNA, by direct binding to gamma-H2AX. We also demonstrate that NBS1 binding can occur in the absence of interaction with hMRE11 or BRCA1. Furthermore, this NBS1 physical interaction was reduced when anti-gamma-H2AX antibody was introduced into normal cells and was also delayed in AT cells, which lack the kinase activity for phosphorylation of H2AX. NBS1 has no DNA binding region but carries a combination of the fork-head associated (FHA) and the BRCA1 C-terminal domains (BRCT). We show that the FHA/BRCT domain of NBS1 is essential for this physical interaction, since NBS1 lacking this domain failed to bind to gamma-H2AX in cells, and a recombinant FHA/BRCT domain alone can bind to recombinant gamma-H2AX. Consequently, the FHA/BRCT domain is likely to have a crucial role for both binding to histone and for relocalization of hMRE11/hRAD50 nuclease complex to the vicinity of DNA damage.

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BACKGROUND: DNA polymerase lambda (Pol lambda) was recently identified as a new member of the family X of DNA polymerases in eukaryotic cells. Pol lambda contains a nuclear localization signal (NLS), a BRCA1-C terminal (BRCT) domain, a proline-rich region, helix-hairpin-helix (HhH) and pol X motifs. Since the amino acid sequence for Pol lambda shares a high degree of homology to Pol beta, Pol lambda is considered to have a similar enzymatic nature to Pol beta. RESULTS: Recombinant human Pol lambda was shown to possess template-directed DNA polymerase activity in its monomeric form. Pol lambda required either Mn2+ or Mg2+ as a metal co-factor to catalyse this activity, and optimal activity was detected at pH 8.5-9.0. Pol lambda was insensitive to aphidicolin, but was sensitive to dideoxynucleoside triphosphates or N-ethylmaleimide. By constructing the truncated Pol lambda, the proline rich region was shown to act in a suppression of its polymerization activity. A chimeric enzyme comprised of the Pol lambda N-terminal region and Pol beta also showed a reduced Pol beta activity. Proliferating cell nuclear antigen (PCNA) directly interacts with Pol lambda through its Pol beta like region in vitro. CONCLUSIONS: Pol lambda possesses similar enzymatic nature to Pol beta; requirements of cations and optimal conditions for pH and NaCl concentration, aside from sensitivity to N-ethylmaleimide and template preference. The proline rich region of Pol lambda functions as a suppressor domain for its polymerization activity (SDPA). Pol lambda interacts directly with PCNA through its Pol beta like region. The functional consequence of this interaction is the negative regulation of Pol lambda activity.

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