Major hemorrhage and subsequent cardiac tamponade during mediastinoscopy.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Yu-Chung Wu.
Explore the source record for details and available documents.
BACKGROUND: Microsomal prostaglandin E synthase-1 (mPGES-1) has recently been found to overexpress in human cancers, including non-small-cell lung cancer (NSCLC). However, the clinical value is largely unknown. The aim of this study was to investigate the associations between mPGES-1 expression in NSCLC and the clinical characteristics and survival outcome. METHODS: Between 2001 and 2003, paired fresh tumorous and nontumorous samples were prospectively procured from patients undergoing surgery for NSCLC. The expression of mPGES-1 was assessed by using Western blot in 93 subjects and reverse transcriptase-polymerase chain reaction in 35. Overexpression of mPGES-1 was defined as a more than 2-fold expression in the tumorous sample compared with the corresponding nontumorous one. Immunohistochemistry was used to confirm its localization to the tumor cells. In a subset of 30 cases, cyclooxygenase-2 (COX-2) was also analyzed to assess its association with mPGES-1. RESULTS: The protein and messenger RNA of mPGES-1 were both expressed at higher levels in the tumor samples (P < .001 and P = .006, respectively). The expressions of mPGES-1 and COX-2 were unrelated (P = .715). Overexpression of mPGES-1 protein was observed in 61 (65.6%) of 93 patients, but it was not significantly associated with the clinicopathologic characteristics or overall and disease-free survivals. However, mPGES-1 overexpression seemed to be associated with the likelihood of subsequent pulmonary metastases and a lower tendency for developing bony metastases (P = .001 and P = .006, respectively). CONCLUSIONS: Our results demonstrated that mPGES-1 was overexpressed in NSCLC, unassociated with COX-2. Overexpression of mPGES-1 per se was not a prognostic indicator, but it might be implicated in the organ preference of metastasis.
BACKGROUND: Primary chest wall tumor is rare but it encompasses tumors of various origins. We analyzed our experience with primary chest wall tumors with emphasis on its demographic presentation and management. METHODS: From 1991 to 2004, 62 patients with the diagnosis of primary chest wall tumors were enrolled. Lipoma, chest wall metastasis, direct invasion from nearby malignancy, infection, and inflammation of chest wall were excluded. The clinical features, management, and the outcome of these patients were retrospectively reviewed. RESULTS: There were 37 males and 25 females. Malignant and benign tumors were equally distributed. Chondrosarcoma and lymphoma were the 2 most common types of malignant chest wall tumors. The most common clinical symptoms were palpable mass (54.8%) and pain (40.3%). Nine of 31 patients (29.0%) with benign chest wall tumors were free of symptoms whereas patients with malignant chest wall tumors were all symptomatic (p = 0.002). A definite diagnosis was obtained in 21 of 26 patients (80.7%) who received nonexcision biopsy. All patients with primary chest wall tumors, except 6 who had medical treatment only, underwent surgical resection. Patients with malignant chest wall tumors were older than those with benign tumors (p < 0.001). The mean largest diameter of tumors was also larger in malignant tumors than in benign tumors (p = 0.04). CONCLUSION: Patients with primary malignant chest wall neoplasm were older than those with benign tumors. The mean size of malignant tumors was larger than that of benign tumors. Adequate surgical resection remains the treatment of choice for patients with primary chest wall tumors. Nonexcision biopsy should be reserved for patients with a past history of malignancy, suspicion of hematologic disease, and with high operative risk. For patients with isolated chest wall lymphoma, surgical resection followed by chemotherapy can be considered to obtain a better outcome.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cysteinyl leukotrienes (CysLTs) play an important role in the pathogenesis of airway remodeling. We investigated the interaction between epithelium and CysLTC4, and the contribution of this interaction to airway fibrosis. Human airway epithelial cells were grown on air-liquid interface culture inserts. CysLTC4 was employed to stimulate the cells. Conditioned medium following CysLTC4 stimulation was coincubated with human lung fibroblasts. Our results have demonstrated that CysLTC4 stimulates airway epithelial cells, through a p38 mitogen-activated protein kinase (MAPK) activation mechanism, to produce transforming growth factor beta1 (TGF-beta1), which results in fibroblast proliferation. The selective p38 MAPK inhibitor S203580 successfully inhibits p38 MAPK phosphorylation and subsequent TGF-beta1 production. CysLT1 receptor antagonist montelukast and corticosteroid inhibit TGF-beta1 production at the mRNA and protein levels. When treated with LTC4, the conditioned medium from epithelial cells enhances fibroblast proliferation, this mitogenic effect being attributed to TGF-beta1 and LTC4 remaining in the culture medium. In addition, LTC4 itself acts as a potential growth factor for lung fibroblasts. These data indicate that interactions between LTC4 and airway epithelial cells may contribute to the pathogenesis of airway remodeling. Early intervention to stop these processes may be useful in preventing airway fibrosis in chronic allergic inflammation.
AIM: By using comparative genomic hybridization, gain of 3q was found in 45-86% cases of esophageal squamous cell carcinoma (EC-SCC). Chromosome 3q25.3-qter is the minimal common region with several oncogenes found within this region. However, amplification patterns of these genes in EC-SCC have never been reported. The possible association of copy number changes of these genes with pathologic characteristics is still not clear. METHODS: Real-time quantitative PCR (Q-PCR) was performed to analyze the copy number changes of 13 candidate genes within this region in 60 primary tumors of EC-SCC, and possible association of copy number changes with pathologic characteristics was analyzed by statistics. Immunohistochemistry (IHC) study was also performed on another set of 111 primary tumors of EC-SCC to verify the association between TP63 expression change and lymph node metastasis status. RESULTS: The average copy numbers (+/-SE) per haploid genome of individual genes in 60 samples were (from centromere to telomere): SSR3: 4.19 (+/-0.69); CCNL1: 5.24 (+/-0.67); SMC4L1: 2.01 (+/-0.16); EVI1: 2.02 (+/-0.12); hTERC: 5.28 (+/-0.54); SKIL: 2.71 (+/-0.14); EIF5A2: 1.95 (+/-0.12); ECT2: 9.18 (+/-1.68); PIK3CA: 8.13 (+/-1.17); EIF4G1: 1.07 (+/-0.05); SST: 3.07 (+/-0.25); TP63: 2.51 (+/-0.22); TFRC: 2.42 (+/-0.19). Four clusters of amplification were found: SSR3 and CCLN1 at 3q25.31; hTERC and SKIL at 3q26.2; ECT2 and PIK3CA at 3q26.31-q26.32; and SST, TP63 and TFRC at 3q27.3-q29. Patients with lymph node metastasis had significantly lower copy number of TP63 in the primary tumor than those without lymph node metastasis. IHC study on tissue arrays also showed that patients with lymph node metastasis have significantly lower TP63 staining score in the primary tumor than those without lymph node metastasis. CONCLUSION: This study showed that different amplification patterns were seen among different genes within 3q25.3-qter in EC-SCC, and several novel candidate oncogenes (SSR3, SMC4L1, ECT2, and SST) were identified. TP63 is amplified in early stage of EC-SCC carcinogenesis but down-regulated in advanced stage of disease.
Lipomas of the gastrointestinal tract are rare, and those of the esophagus are extremely rare. Indeed, fewer than 20 resected cases of esophageal lipoma have been reported in the literature. In the current case, a 71-year-old man presented with a 4-month history of a slight swallowing disturbance in the upper chest. Upper gastrointestinal endoscopy revealed a submucosal space-occupying mass, with normal mucosa, in the upper third of the thoracic esophagus; the mass was yellowish in color, soft in consistency, and about 3.5 x 3.0 cm in diameter. The patient underwent video-assisted thoracoscopic enucleation of the submucosal esophageal tumor, which pathologically, was proved to be a lipoma.
We investigated the significances of the expressions of dihydrodiol dehydrogenase (DDH) and glutathione-S-transferase (GST) in patients with esophageal squamous cell carcinoma (ESCC). By using immunohistochemistry, we measured expressions of DDH, GST, COX-2, nm23-H1, HER-2/neu and mdr-1 in 145 patients with ESCC. Expression of DDH was confirmed by immunoblotting and reverse transcription-polymerase chain reaction. Relation between DDH expression and clinicopathological parameters was analyzed by statistical analysis. Difference of survivals between different groups was compared by a log rank test. DDH overexpression was detected in 66.9% of pathological sections (97/145) and in 41.6% of metastatic lymph nodes (37/89). The nucleotide sequencing of DNA fragments from 16 tumorous specimens showed that the major isoform was DDH2 for ESCC. GST expression, however, was only detected weakly in 24 patients (16.6%). For patients with ESCC, DDH overexpression was positively correlated with smoking habit, tumor stage, number of metastatic lymph nodes, lymphovascular invasion and COX-2 expression, and inversely correlated with GST and nm23-H1 expressions, but not related to mdr-1 or HER-2/neu expressions. As compared to DDH overexpressed group, patients with low DDH expression had significantly lower incidence of tumor recurrences and better survival (p = 0.026). Using univariate analysis, prognostic factors included tumor stage, number of metastatic lymph nodes, cell differentiation, lymphovascular invasion and expressions of DDH and nm23-H1. Multivariate analysis showed significant correlation of tumor stage, number of metastatic lymph nodes and nm23-H1 expression with patient's survival. In conclusion, inverse expressions of DDH and GST may be associated with carcinogenesis and disease progression for ESCC patients, but their biological function and pathophysiological regulation in tumors require additional studies.
Among patients with adenocarcinoma of the gastric cardia, we noted that patients with higher preoperative serum albumin levels appeared to survive longer than patients with lower levels. Thus, we evaluated serum albumin as a prognostic factor for patient survival. From 1987 to 1997, 314 patients with adenocarcinoma of the gastric cardia underwent curative resection. Patient serum albumin levels were evaluated on the second day after admission, before any nutritional support. Patients were divided into two groups: those with normal serum albumin levels (>3.5 g/dl) and those with abnormal serum albumin levels. The perioperative mortality and morbidity were 5.7% (18 of 314) and 22.3% (70 of 314), respectively. The surgical resectability rate was significantly better among patients with normal serum albumin levels (P < 0.001). The 5-year overall survival rate of patients with normal serum albumin levels was also better than those with abnormally low serum albumin levels (38.4% versus 19.1%, P=0.0003). In each cancer stage, the 5-year survival rate of patients with normal serum albumin levels was better than that among those with hypoalbuminemia. By multivariate analysis, serum albumin level and the pathologic T, N statuses were independent factors correlated with prognosis. Preoperative serum albumin level correlated highly with resectability and survival. Patients with abnormal serum albumin levels had worse survival than did those with normal serum albumin levels. We recommend that postoperative adjuvant therapy be given to all patients with hypoalbuminemia preoperatively.
BACKGROUND: Pulmonary hamartoma is the most common type of benign lung tumors. We retrospectively reviewed the clinicopathological features of 61 patients with pulmonary hamartomas undergoing surgical resection in our institution. METHODS: From 1971 to 2002, 61 patients with 62 pulmonary hamartomas underwent surgical resection in the Division of Thoracic Surgery, Taipei Veterans General Hospital. 45 were men and 16 were women (approximately in 3:1 ratio). Their mean age was 56.9 years (range 20 to 77 years). The medical records of these patients were reviewed. The information collected using a standardized data-collection form consisted of the age at presentation, gender, initial manifestations or symptoms, history of tobacco consumption, location of hamartoma, size of the lesions, state of calcification in the hamartoma, the results of preoperative bronchoscopic examination, operative procedures and pathological report of intra-operative frozen section. All available histological slides were reviewed by the same pathologist to reconfirm the diagnosis of pulmonary hamartoma. RESULTS: Of the 61 patients with pulmonary hamartoma, 41 patients were clinically asymptomatic, 16 patients had new onset of respiratory symptoms and 4 patients had chronic cough. One patient had synchronous 2 separate lesions. The hamartomas were equally distributed in the pulmonary lobes with the mean transverse diameter of 1.8 cm measured in operation (range 0.2 to 5.0). No tumor recurrence developed after resection in our series. The mean follow-up was 8.9 years. CONCLUSIONS: The vast majority of pulmonary hamartomas represent as solitary pulmonary nodule. Definite diagnosis and the treatment can be achieved by surgical resection with minimal morbidity. No tumor recurrence was encountered in the follow-up period.
BACKGROUND: Surgery is the treatment of choice for thymic epithelial tumors (TET), but the resectability is about 60-70%. For those with locally advanced unresectable TETs (LAU-TETs), some controversies about the prognostic factors and treatment modalities existed. The aims of this study are to elucidate the roles of various therapeutic options and to determine the survival and prognostic factors of LAU-TETs. METHODS: Twenty-seven patients diagnosed with LAU-TETs underwent treatment in Taipei Veterans General Hospital between 1979 and 1997. Multiple treatment modalities, including surgical intervention, irradiation and chemotherapy, were advocated for these patients. The clinicopathological factors and the effects of the treatment modalities were evaluated retrospectively. RESULTS: Twenty seven cases of LAU-TETs, included 18 thymomas (12 at stage III and 6 at stage IVa) and 9 thymic carcinomas (4 at stage III and 5 at stage IVa), were enrolled for study. The overall 5-year and 10-year survival rates were 54.6% and 35.1%, respectively. Patients receiving debulking surgery and those with irradiation dosage higher than 4400 cGy had significantly better survivals (P = 0.021 and P = 0.016, respectively). CONCLUSIONS: Aggressive debulking surgery and sufficient irradiation dosage provide better survivals for patients with LAU-TETs, especially for those with thymoma.
BACKGROUND: Postoperative pneumonia is a major cause of mortality and morbidity after lung surgery. The effectiveness of prophylactic antibiotics for preventing postoperative pneumonia and the recovery course after pulmonary lobectomy is still not clarified yet. We conducted this study to evaluate the effectiveness of prophylactic antibiotics on the post-operative recovery course after pulmonary lobectomies. METHODS: Forty-five cases undergoing pulmonary lobectomies between June 2002 and January 2003 were enrolled in this prospective study. Each patient received prophylactic antibiotics of cefuroxime and sisomicin. Sputum culture upon admission and swab culture from the bronchus cut-end during operation were obtained. The clinical vital signs including heart rates, respiratory rates and core body temperature in the postoperative recovery courses were analyzed. RESULTS: Four (8.9%) patients developed pneumonia after lobectomies, and pneumonia occurred only in patients who had positive culture results from bronchial cut-end. The organisms cultured from the sputum seemed to be controlled by prophylactic antibiotics. All the organisms cultured in the bronchus cut-end differed from those in the sputum; it denoted these pathogens were inoculated during anesthesia for surgical operation. The postoperative vital signs including tachycardia and fever improved gradually in the initial 3 days. Patients with pneumonia sustained significant higher fever than the non-pneumonic patients during postoperative course. CONCLUSIONS: The short-term combination of cefuroxime and sisomicin offers sufficient effectiveness in prophylaxis of pneumonia after pulmonary surgery. Positive bronchial cut-end cultures were related to the post-lobectomy pneumonia significantly. Body temperature was the most useful presenting vital sign for early detection of the postoperative pneumonia.
BACKGROUND: Due to its anatomical location, carcinoma of the upper thoracic esophagus (i.e. below the thoracic inlet and above the carina) often results in early invasion of adjacent structures and precludes radical resection. The prognosis of carcinoma of the upper thoracic esophagus was considered worse than that of distal esophagus. There are few studies specifically addressing the prognostic factors in the surgical treatment for carcinoma in this location. Herein we report a retrospective study conducted to analyze the result of surgical treatment for carcinoma of the upper thoracic esophagus. METHODS: From January 1983 to December 2002, 298 cases were diagnosed with upper thoracic esophageal carcinoma in our institute. Among them, 78 cases underwent operation with curative intent and were enrolled for study. RESULTS: The tumors were stage I in 7.7%, stage II in 42.3%, stage III in 33.3% and stage IV in 12.8%. The postoperative morbidity and mortality rates were 59.0% and 6.8%, respectively. Pulmonary complication was the most common morbidity and also the leading cause of postoperative death. The overall median survival time after surgery was 13.1 months. The 1-, 3- and 5-year survival rates were 53.9%, 28.7% and 21.4%, respectively. There was an improvement in surgical result over time. The 5-year survival rate improved from 13.6% in the earlier 10-year period to 37.6% in the latter 10-year period (p = 0.0493). Univariate analysis revealed 5 positive prognostic factors: tumor length (p = 0.0012), pT status (p = 0.0274), pN status (p = 0.001), pathologic stage (p = 0.0322) and R category (p = 0.0009). Multivariate analysis identified pN status, R category and tumor length as independent prognostic indicators. In patients receiving neoadjuvant therapy, the 5-year survival rate after surgery was 23.4%, which was similar to those undergoing surgery alone (p = 0.5174). For patients with advanced tumor stages (ie. pT > 3, pN > 0, pM > 0) or with residual tumors (R1/2 resection), the 5-year survival rates were significantly different in patients with and without postoperative adjuvant chemoradiation therapy (16.0% vs. 0%, p = 0.0045). CONCLUSIONS; For carcinomas in the upper thoracic esophagus, the prognosis was dismal. Surgical resection remains the treatment of choice. In addition to lower resectability, the postoperative morbidity and mortality rates were relatively high. The length of tumor extension, status of lymph node involvement and radicality of surgery were independent prognostic factors.
BACKGROUND: Hepatocellular carcinoma (HCC) is seldom resectable due to advanced status. Even though hepatectomy is feasible, a large proportional of patients may still develops extrahepatic recurrence. Pulmonary metastasis is the most common site of extrahepatic spread. Few articles have discussed the benefit of resection for lung metastasis after curative hepatectomy. We evaluated the general information and the result of lung resection for patients having lung metastasis after curative resection of HCC. METHODS: Six patients who underwent pulmonary metastasectomy for HCC at Taipei Veterans General Hospital between August 1995 and May 2004 were enrolled in the study. All of them had received the hepatectomy for primary HCC. The demographic information of patients, the site and number of extrahepatic recurrence, the method of surgical intervention and the outcome after surgery were retrospectively reviewed. RESULTS: There were 4 men and 2 women with the mean age of 47.3 years. All of them were HBV carriers. Five patients had multiple pulmonary metastases removed by wedge resection. Two patients had bilateral lung metastases upon diagnosis of extrahepatic recurrence. The mean duration of follow-up after hepatic resection was 75.0 +/- 25.1 months (32 to 104 months). The mean survival after pulmonary resection was 47.2 +/- 34.3months (1 to 94 months). Four patients are still alive and free of the disease. One patient is alive but with the disease. One patient who refused further aggressive treatment after resection of lung metastasis died of the disease 40 months after lung resection, 77 months after hepatic resection. CONCLUSIONS: Lung resection for the pulmonary metastasis of HCC can result in a favorable long-term survival when there is no other intrahepatic or extraphepatic recurrence of HCC. For patients with multiple lung metastases in different lobes or different lungs, aggressive surgical resection is recommended if complete resection can be achieved.
The responses of airway epithelium following exposure to neutrophil elastase (NE) were investigated. Human bronchial epithelial cells were explanted on insert surfaces of a modified air-liquid interface culture system to which NE was added to stimulate epithelial cells. PGE2 release significantly increased within 10 min of incubation with NE and peaked 3 h after NE (20 microg/ml) stimulation. This action required proteolytic activity as alpha1-antitrypsin blocked NE-induced PGE2 release. The production of PGE2 was also inhibited by indomethacin; a selective cyclooxygenase (COX)-2 inhibitor, celecoxib; and dexamethasone. Moreover, the mRNA expression for COX-2 relative to that for a housekeeping gene was approximately eightfold that of the unstimulated cells. Dexamethasone inhibited COX-2 gene transcription. We further observed that NE-induced PGE2 release involved activation of p44/42, but not p38, MAP kinases. Such p44/42 MAP kinases were rapidly phosphorylated, with the concentration of phosphorylated p44/42 MAP kinases peaking at 10 min after stimulation and declining in culture at 90 min. The specific p44/42 MAP kinase inhibitor UO126 completely blocked p44/42 phosphorylation and, subsequently, PGE2 production. The airway epithelium may play important bronchoprotective and immunomodulatory roles in chronic neutrophilic inflammation.
BACKGROUND: Esophageal cancer is one of the most aggressive malignancies in the world, and whether multiple therapeutic modalities could improve long-term survival remains controversial. Recent studies have shown an increase of cyclooxygenase-2 (COX-2) expression in various malignancies, but its clinicopathologic role in esophageal squamous cell carcinoma (ESCC) remains unclear. METHODS: From 1993 to 1997, tissue samples from 96 patients with ESCC who underwent esophagectomy at our institution were collected for analysis. Cyclooxygenase-2 expression was examined by immunohistochemical staining, and further confirmed by Western blot analysis on six frozen tissues. Clinicopathologic data were analyzed to verify the significance. RESULTS: Cyclooxygenase-2 immunoreactivity was detected in 59 of 96 ESCC specimens (61%), and COX-2 overexpression (COX-2 high) was observed in 49% (47 of 96) of ESCCs. Statistical differences between COX-2 high and COX-2 low were found with respect to the status of distant metastasis (M factor) (p = 0.035) and tumor stage (p = 0.04). The survival was not significantly different between patients with and without COX-2 overexpression (p = 0.43). Using the Cox regression analysis, only the N factor (p = 0.0034) and M factor (p = 0.0325) were independent prognostic factors. CONCLUSIONS: Our results showed that in patients with ESCC, COX-2 overexpression was significantly correlated with fewer metastases and less advanced stage, but had no impact on survival. The status of local or distant lymph node metastasis was the most important prognostic factor. The biological role and pathophysiologic regulation of COX-2 overexpression in ESCC deserve further investigation.
OBJECTIVES: There is no consensus for the best postoperative follow-up in patients after complete resection of non-small cell lung cancer. Low-dose computed tomography of chest proves valuable in screening primary lung cancer and may be a useful tool in postoperative surveillance. METHODS: In part 1, 30 patients who underwent surgical resection of non-small cell lung cancer and were at the first (n = 14), second (n = 9), or fifth (n = 7) annual postoperative surveillance were selected chronologically and subjected to chest radiography, low-dose computed tomography, and standard-dose computed tomography to verify the diagnostic accuracy of low-dose computed tomography. In part 2, 43 patients were prospectively enrolled and followed up regularly after complete resection of non-small cell lung cancer. The follow-up protocol included physical examination, sputum cytology, serum carcinoembryonic antigen, chest radiography, and low-dose computed tomography every 3 months in the first 2 years postoperatively until tumor recurrence. RESULTS: In part 1, tumor recurrence was detected by standard-dose computed tomography in 7 cases. Low-dose computed tomography and chest radiography missed 1 and 5 of 7 cases, respectively. In part 2, tumor recurrence was found in 14 cases with 19 metastatic sites. Thirteen of the 14 (92.9%) cases were detected by scheduled visiting and 11 (78.6%) detected by low-dose computed tomography including the 7 without symptoms. Of the 19 recurrent sites found in 14 patients, 11 ones (57.9%) were detected by low-dose computed tomography. CONCLUSIONS: Low-dose computed tomography may be of considerable value in early detection of tumor recurrence in postoperative non-small cell lung cancer patients. Further large prospective studies are needed to verify this issue.