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To study the diabetic mellitus (DM) patient's reaction to sepsis, we investigated the survival rate, the bacteremia, plasma endotoxin and plasma endothelin-1 levels in E. coli septic peritonitis rats with or without streptozotocin-induced DM. No significant difference could be detected between the DM and nondiabetic rats in the survival rate, the bacteremia level or the plasma endotoxin level. The DM rat manifested a significant increase compared to the nondiabetic rat in the plasma endothelin-1 level four hours after the outbreak of peritonitis. Endothelin-1 may thus play some role in the E. coli septic peritonitis rat with DM.

Esophageal cancer is one of the most difficult malignancies to cure. The prognosis remains unsatisfactory despite significant advances in surgical techniques and perioperative management. The optimal treatment strategy for localized esophageal cancer has not yet been established. Surgical resection remains the mainstay of treatment for esophageal cancer, and curative resection is the most important surgery. Extended esophagectomy with three-field lymphadenectomy provides the highest quality of tumor clearance and prolongation of patient survival. There has been intense effort in developing novel strategies to treat patients with resectable esophageal cancer. Various combined-modality approaches have been attempted to improve treatment outcomes. Definitive chemoradiotherapy has an impact on long-term survival in patients with resectable esophageal cancer. Accordingly, there are three main combined-modality approaches: esophagectomy with adjuvant chemotherapy or chemoradiotherapy; primary definitive chemoradiotherapy with or without salvage esophagectomy, and preoperative chemoradiotherapy followed by planned esophagectomy. Recently, owing to the remarkable advances in optical technology, minimally invasive esophagectomy using endoscopic instruments has been introduced into esophageal cancer surgery. This article reviews recent changes in the treatment of esophageal cancer surgery, and considers the role of esophagectomy.

Background Laparoscopic repair of large paraesophageal hernias (LPEH) is technically challenging, and requires advanced laparoscopic skills. We have developed a novel technique for facilitating laparoscopic repair of LPEHs safely and easily, using a Nelaton catheter. Patients and Methods Seven patients with LPEHs were operated on through a laparoscopic approach. During surgery, the left lobe of the liver and right diaphragmatic crus were elevated using a suspended thread covered by a Nelaton catheter. Results All patients were operated on laparoscopically using this technique. No patient required conversion to open method. The median operating time was 205 minutes and the range was from 155 to 295 minutes. No intraoperative or early complications occurred in any patient. Late complications occurred in 2 patients due to a small sliding hernia: a slipped fundoplication in 1 patient, and a gastric ulcer in the other. Conclusions In conclusion, laparoscopic repair of LPEH is a challenging procedure that requires wide experience in laparoscopic gastroesophageal surgery. Further refinement for this operation may be necessary.

Positron emission tomography (PET), a functional imaging modality, has provided the transition between the research environment and the clinical environment over the last 10 years. Its primary use is in the field of oncology, where it is being increasingly used in the management of several tumor types including esophageal cancer. 18F-Fluorodeoxyglucose PET (FDG-PET) scans may also be used to distinguish between benign and malignant tumors, to identify different stages of tumor spread, to assess for tumor recurrence, and monitor the response to therapy of malignant diseases. This review aims to outline the current and future roles of PET scanning in the field of esophageal cancer.

BACKGROUND: Obesity is reported to increase the risk of colorectal cancer. We investigated whether it was associated with mortality or morbidity after colorectal-cancer surgery. METHODS: 70 colorectal-cancer patients who underwent elective surgery were investigated in this study. The intra-abdominal fat (IAF) and subcutaneous fat (SCF) areas were quantified by CT scan preoperatively. We investigated whether body mass index (BMI), IAF, or SCF were associated with postoperative mortality or morbidity. RESULTS: The mortality rate was 0%. 11 (16%) of 70 patients had medical complications (pneumonia, 9; arrhythmia, 2) and 16 (23%) had surgery-related complications (wound infection, 12; anastomotic leakage, 5) postoperatively. There was no significant difference in the postoperative medical or surgery-related morbidity rate between the IAF+ (males, ≥160 cm2; females, ≥120 cm2) and IAF– groups. The surgery-related morbidity rate was significantly higher in the SCF+ group (male, ≥180 cm2; female, ≥250 cm2) than in the SCF– group and multilogistic regression analysis confirmed that diabetes mellitus and SCF were significant for surgery-related morbidity. CONCLUSIONS: Subcutaneous fat accumulation is significantly associated with postoperative surgery-related morbidity after colorectal-cancer surgery.

Tissue inhibitor of metalloproteinase-3 (TIMP-3) inhibits the activity of matrix metalloproteinase, which may play an important role in carcinoma invasion and metastasis. We have investigated the relationship between TIMP-3 reduction and clinicopathological factors in oesophageal squamous cell carcinoma (ESCC). We examined tissue specimens that had been removed from 90 patients with thoracic oesophageal cancer who had undergone surgery between 1983 and 2001. Immunohistochemical staining was performed by the standard streptavidin-biotin method. Immunostaining of TIMP-3 was seen in the cytoplasm of cancer cells and normal oesophageal epithelial cells, particularly in cells located in shallow areas of the tumour. TIMP-3 preserved (+), moderate (+/-), and reduced (-) cases accounted for 30, 27, and 33 of the 90 patients, respectively (33, 30, 37%). Significant correlations were observed between TIMP-3 expression and depth of tumour invasion (P=0.001), number of lymph node metastases (P=0.003), infiltrative growth pattern (P=0.003), and disease stage (P=0.005). The survival rates of patients with TIMP-3 (-) cancer were significantly lower than those of patients with TIMP-3 (+) and TIMP-3 (+/-) cancer (P=0.0003). The mean 5-year survival rates of patients with TIMP-3 (+), (+/-), and (-) were 50, 58, and 21%, respectively. In conclusion, decreased expression of TIMP-3 protein correlates with invasive activity and metastasis. This makes the prognosis for patients with cancer that has lost TIMP-3 significantly less favourable than that for patients with cancer that has maintained TIMP-3.

Purpose: Transforming growth factor (TGF)-β regulates cell growth inhibition. When tumor cells lose their sensitivity to TGF-β growth inhibition, the excess TGF-β that results may act on tumor cells to facilitate tumor development. Previously, we have shown that an elevated systemic TGF-β1 level is not related to tumor progression in esophageal cancer (Y. Fukai et al., Int J Cancer 2003;104:161–6). We considered that systemic inflammation or chronic disease, in addition to the tumor, may influence the plasma TGF-β level. Therefore, we examined the hypothesis that the plasma TGF-β level measured from the azygos vein would independently predict tumor progression and prognosis in patients with esophageal cancer. Experimental Design: Fifty-seven plasma samples were obtained intraoperatively from the azygos vein in patients with esophageal cancer. ELISA was used to quantify the plasma TGF-β1 levels, which were correlated with pathological features and patient survival. Results: The mean plasma TGF-β1 level measured from the azygos vein of esophageal cancer patients was 5.09 ± 0.48 ng/ml (mean ± SE). The survival rates of patients with a high TGF-β1 level (defined as a level above the 4.6 ng/ml level of normal controls) in the azygos vein were significantly lower than those of patients with a low TGF-β1 level (P = 0.0317). Moreover, the TGF-β1 level in the azygos vein was an independent prognostic factor for overall survival (P = 0.0474). Conclusions: The level of plasma TGF-β1 measured from the azygos vein is an independent predictor in patients with esophageal cancer and may reflect tumor progression more specifically because the azygos vein is responsible for venous return from the esophagus.

Transforming growth factor-beta (TGF-beta) regulates cell growth inhibition, and inactivation of the TGF-beta signaling pathway contributes to tumor development. In our previous study, altered expression of TGF-beta, TGF-beta-specific receptors and Smad4 was shown to correlate with tumor progression in esophageal squamous cell carcinoma (SCC). These components, however, were maintained normally in some patients with esophageal SCC. In our study, the mechanism by which aggressive esophageal SCC maintains these components was investigated, with particular emphasis on the participation of c-Ski and SnoN as transcriptional co-repressors in TGF-beta signaling. Immunohistochemistry for c-Ski and SnoN was carried out on surgical specimens obtained from 80 patients with esophageal SCC. The expression of c-Ski and SnoN was also studied in 6 established cell lines derived from esophageal SCC and compared to an immortalized human esophageal cell line by Western blotting. High levels of expression of c-Ski, detected immunohistologically, were found to correlate with depth of invasion (p = 0.0080) and pathologic stage (p = 0.0447). There was, however, no significant correlation between expression of SnoN and clinicopathologic characteristics. A significant correlation between c-Ski and TGF-beta expression was observed. Moreover, in patients with TGF-beta negative expression, the survival rates of patients with c-Ski positive expression were significantly lower than those of patients with c-Ski negative expression (p = 0.0486). c-Ski was expressed at a high level in 5 of 6 cell lines derived from esophageal SCC compared to immortalized esophageal keratinocytes. Furthermore, the cyclin-dependent kinase (CDK) inhibitor, p21 that was up-regulated by TGF-beta signaling was expressed at a low level in the 5 cell lines. The expression of c-Ski protein as a transcriptional co-repressor in TGF-beta signaling seems to be correlated with tumor progression of esophageal SCC.

Focal adhesion kinase (p125(FAK); 'FAK') is a tyrosine kinase that is localised to cellular focal adhesions and is associated with a number of other proteins, such as integrin adhesion receptors. We performed an immunohistochemical analysis of FAK protein expression to determine the relationship between FAK overexpression and clinicopathological factors in oesophageal squamous cell carcinoma (ESCC). We examined tissue specimens that had been removed from 91 patients with thoracic oesophageal cancer who had undergone surgery between 1983 and 2001. Immunohistochemical staining was performed by the standard streptavidin-biotin method. Seven human ESCC cell lines-TE-1, TE-2, TE-8, TE-13, TE-15, TT, and TTn-and one immortalized human keratinocyte cell line-HaCaT-were used in Western blot analysis. Immunostaining of FAK was seen in the cytoplasm of cancer cells, particularly in cells located in the invasive fronts of cancer nests. FAK overexpression was detected in 54 of the 91 patients (59.3%). Significant correlations were observed between FAK overexpression and cell differentiation (P=0.0057), depth of tumour invasion (P=0.0023), presence of regional lymph node metastasis (P=0.0097), number of lymph node metastases (P=0.0026), and disease stage (P=0.012). The survival rates of patients with FAK-overexpressing cancer were significantly lower than those of patients without FAK-overexpression cancer (P=0.006). The 5-year survival rate of patients without FAK overexpression was 69%, whereas that of patients with FAK overexpression was 38%. On Western blot analysis, FAK was expressed at a high level in TE-1, TE-8, TE-15, and TT cells, at a moderate level in TE-2 and TTn cells, and at a low level in TE13 and HaCaT cells. FAK phosphorylation at tyrosine 397 was demonstrated in proportion to the intensity of FAK in all cell lines except TE15 and HaCaT. In conclusion, FAK overexpression of ESCC was related to cell differentiation, tumour invasiveness, and lymph node metastasis. Consequently, patients with ESCC who had FAK overexpression had a poor prognosis.

Anastomotic insufficiency is considered to be one of the most serious complications associated with esophageal reconstruction. The purposes of this study were to identify (1) the relationship between anastomotic insufficiency and tissue blood flow (TBF) in the gastric tube in the perioperative period, and (2) the effects of intravenous prostaglandin E1 (PGE1) on TBF in the gastric tube. The study group consisted of 44 patients who were to undergo esophagectomy for esophageal cancer. Intraoperative and postoperative TBF on the serosal side of the gastric tube were measured by laser-Doppler tissue blood flowmetry. The TBF of the Leakage(+) group (n = 5) was poorer than that of the Leakage(?) group (n = 39) during the intraoperative and postoperative periods. There was a significant difference in TBF between the two groups at postoperative day (POD) 3. There was a tendency in the PGE1(+) group (n = 18) to exhibit richer blood flow through the anastomosis than the PGE1(?) group (n = 26), intraoperatively, but the difference was not significant. Two of five Leakage(+) cases were also in the PGE1(+) group. There was no relationship between intraoperative medication with PGE1 and incidence of leakage. The TBF of three-field lymph node dissection and reconstruction of the retrosternal route group (n = 21) was poorer than that of the two-field lymph-node dissection and reconstruction of the posterior mediastinal route group (n = 23). The TBF in the gastric tube after esophagectomy may be a predictor of anastomotic insufficiency. However, PGE1 treatment in the intraoperative period alone is not effective in preventing anastomotic insufficiency.

Triple therapy is accepted as the treatment of choice for Helicobacter pylori eradication, but there is no consensus on how long the therapy should be maintained in haemodialysis (HD(+)) patients. Our aims in this study were to evaluate the safety and efficacy of the 7-day triple therapy in HD(+) patients.Forty-seven HD(+) and 55 HD(-) patients with dyspepsia underwent endoscopy. The prevalence of H. pylori was detected by Giemsa stain, followed by the urea breath test (UBT). H. pylori(+) patients were scheduled to undergo 7-day triple therapy and the success of eradication was investigated by UBT.Forty-five (44%) patients were positive for H. pylori. Forty of them underwent triple therapy and 39 (98%) patients completed the treatment. Eradication was successful in 32 (82%) and unsuccessful in 7 (18%) patients. There was no significant difference between these groups in age, gender, endoscopic findings or HD, and only previous treatment was significant for eradication failure by univariate and multivariate logistic regression analysis. Side effects were observed in 2 (15%) of 13 HD(+) and 3 (11%) of 27 HD(-) patients, and one HD(-) patient had to stop medication because of severe nausea and vomiting. The eradication rate was 93% (28/30) in patients without previous treatment. The triple therapy was unsuccessful in 7 patients, and 4 of them again underwent 7-day triple therapy, but all resulted in failure.Seven-day triple therapy is safe and effective for primary treatment of H. pylori infection in both HD(+) and HD(-) patients, but a new treatment is necessary for patients with previous treatment.

In esophageal squamous cell carcinoma (SCC), we used immunohistochemical analysis to further elucidate the correlation of p53 protein expression with clinicopathological factors, as well as with risk factors, such as tobacco smoking, alcohol consumption and a family history of cancer, using odds ratios (ORs). The expression of p53 protein was demonstrated in 55.1% of 89 esophageal SCC cases examined by immunohistochemistry. The expression of p53 protein did not correlate with gender, age, histological grading, lymph node metastasis, or TNM stage. The prevalence of p53 expression was significantly higher in patients with multiple primary esophageal cancers (P0.05). p53 expression did not correlate with prognosis in univariate survival analysis. The esophageal SCC in either smokers or alcohol users was 4.67-5.83 times more likely to express p53 protein, while the likelihood of p53 expression in patients who use both tobacco and alcohol was more than 14.0 times. However, a significant association was not found between p53 expression and a family history of cancer, this having an OR as low as 1.85. The expression of p53 protein did not correlate with clinicopathological factors and prognosis in univariate and multivariate survival analyses. In contrast, tobacco smoking and alcohol consumption were shown to be strongly associated with p53 mutations in esophageal carcinogenesis.

BACKGROUND KAI1/CD82, a tumor metastasis suppressor gene, is correlated inversely with the progression and invasion of several tumors. It also has been reported that the KAI1 gene is related to the tumor suppressor gene p53. This study was performed to clarify the correlation between KAI1/CD82 expression and clinicopathologic characteristics and p53 expression in patients with esophageal squamous cell carcinoma (ESCC). The authors also investigated mutation of the KAI1 gene coding region to determine whether this may reduce KAI1 expression in ESCC. METHODS Using immunohistochemistry with anti-KAI1 polyclonal antibody and monoclonal antibody against p53, KAI1/CD82 and p53 expression were detected in 55 patients with ESCC who had undergone surgery. The authors examined the KAI1 gene mutation in 22 patients with ESCC by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis and DNA sequencing. RESULTS KAI1/CD82 expression was positive in 36 of 55 patients (65.5%). There was a significant inverse correlation between KAI1/CD82 expression and regional lymph node metastasis (P = 0.0045), distant metastasis (P = 0.0092), the number of lymph node metastases (P = 0.0019), and pathologic stage (P = 0.0046). The survival rates of KAI1/CD82 negative patients were poorer than those of positive patients (P = 0.024). The correlation between KAI1 positive and p53 positive tumors was not statistically significant. None of the 22 patients with ESCC showed mutation of the KAI1 gene by PCR-SSCP. In one patient, there was polymorphism in the SSCP assay and DNA sequencing. CONCLUSIONS The authors demonstrated immunohistochemically that the expression of KAI1 protein appeared to be correlated with lymph node metastasis. Mutation does not seem to be a mechanism for dysregulation of the KAI1 protein in ESCC. Cancer 2000;89:955–62. © 2000 American Cancer Society.

Prostaglandins (PGs), which play a pivotal role in the cytokine network, have been implicated in the pathophysiology of circulatory shock, but the precise role of cyclooxygenase-2 (COX-2) in circulatory shock is still not known. This study investigated whether or not COX-2 affects liver and bowel injury during hemorrhagic shock (HS). Male Sprague-Dawley rats were subjected to decompensated HS followed by resuscitation. Besides the time course of tissue injury and mRNA expression of COX-2 in the liver and bowel during HS, we investigated the effect of N-(2-cyclohexyloxy-4-nitrophenyl)methane sulfonamide (NS398), a specific inhibitor of COX-2, on injury to these organs. The liver injury, evaluated by plasma aminotransferase levels and histology, was evident at the end of the shock period (Shock-0h) and had significantly increased 1 h after the start of resuscitation (Shock-1h) (P < 0.01). The bowel injury, assessed by histological findings in the terminal ileum, was scarcely detectable at Shock-0h but became noticeable at Shock-1h (P < 0.01). COX-2 mRNA expression was up-regulated in the liver during HS whereas it did not change in the bowel. NS398 treatment significantly exacerbated both liver and bowel injury. These lines of evidence suggest that COX-2-derived PGs provide protection against HS-induced liver and bowel injury.

We have examined the expression of nitrotyrosine, a marker of peroxynitrite formation, in 55 esophageal cancers by immunohistochemistry. Nitrotyrosine was detected in 21 of 55 (38.2%) esophageal cancers. Comparison of nitrotyrosine expression and the pathological findings showed that there was a significant association between the expression of nitrotyrosine and each of the depth of tumor invasion (P

Background: It remains unproven whether nitric oxide (NO) exerts a toxic effect on hepatocytes directly or through the formation of a more toxic compound during hemorrhagic shock (HS). NO reacts at a very high rate constant with superoxide to give peroxynitrite, a potentially toxic molecule. In this study, we investigated whether or not peroxynitrite contributed to tissue injury in the liver during HS. Methods: Male Sprague-Dawley rats were subjected to decompensated HS followed by resuscitation. In addition to the time course of tissue injury and inducible NO synthase (iNOS) messenger RNA (mRNA) expression in the liver during HS, we investigated the effect of N6-(iminoethyl)- L -lysine( LNIL) (a specific inhibitor of iNOS) and also that of uric acid (a natural scavenger of peroxynitrite) on tissue injury and nitrotyrosine formation (a footprint of peroxynitrite) in the liver. Results: The liver injury, evaluated by plasma aminotransferase levels and histology, became evident at the end of the shock period and had significantly increased 1 hour after the start of resuscitation (Shock-1h). There was no iNOS mRNA expression in the liver at baseline, and it had clearly increased by Shock-1h. Treatment with LNIL or uric acid significantly attenuated the tissue injury with a prominent reduction in nitrotyrosine formation in the liver. Conclusions: These lines of evidence suggest that one of the mechanisms by which NO production causes liver injury during HS may be its reaction with superoxide to form peroxynitrite. (Surgery 2000;127:439-46.)

Hemorrhagic shock (HS) initiates an inflammatory cascade that includes the production of cytokines and recruitment of neutrophils (PMN) and may progress to organ failure, inducing acute respiratory distress syndrome (ARDS). To examine the hypothesis that interleukin-6 (IL-6) contributes to PMN infiltration and lung damage in HS, we examined the lungs of rats subjected to unresuscitated and resuscitated HS for the production of IL-6 and activation of Stat3. Using semiquantitative RT-PCR, we found a striking increase in IL-6 mRNA levels only in resuscitated HS, with peak levels observed 1 h after initiation of resuscitation. Increased IL-6 protein expression was localized to bronchial and alveolar cells. Electrophoretic mobility shift assay of protein extracts from shock lungs exhibited an increase in Stat3 activation with kinetics similar to IL-6 mRNA. In situ DNA binding assay determined Stat3 activation predominantly within alveoli. Intratracheal instillation of IL-6 alone into normal rats resulted in PMN infiltration into lung interstitium and alveoli, marked elevation of bronchoalveolar lavage cellularity, and increased wet-to-dry ratio. These findings indicate that IL-6 production and Stat3 activation occur early in HS and may contribute to PMN-mediated lung injury, including ARDS after HS.

Hemorrhagic shock (HS) initiates a series of inflammatory processes that includes the activation of polymorphonuclear granulocytic neutrophils (PMN). We tested the hypothesis that HS induces granulocyte colony-stimulating factor (G-CSF), a cytokine that augments PMN effector functions, in the lungs of rats. Sprague-Dawley rats were subjected to compensated or decompensated HS followed by resuscitation and death at 4 or 8 h. Animals subjected to HS demonstrated acute lung injury with PMN infiltration, edema, and hypoxia. Using semiquantitative reverse transcriptase-polymerase chain reaction, we detected a 1.9- to 7.1-fold increase in G-CSF mRNA levels in the lung of animals subjected to HS compared with sham controls. Levels of G-CSF mRNA increased with increased duration of the ischemic phase of resuscitated shock. In situ hybridization revealed that bronchoepithelial cells were the major cellular site of G-CSF mRNA. Thus production of G-CSF mRNA by bronchoepithelial cells is dramatically increased in a rat model of HS that also demonstrated lung injury. Increased local G-CSF levels may contribute to PMN recruitment and activation and resultant lung injury in HS.

The effects of vasoconstrictors on bile flow and bile acid excretion were examined in single-pass isolated perfused rat livers. Administration of norepinephrine (NE), 4 nmol/min, plus continuous infusion of taurocholate (TC) (1.0 mumol/min) rapidly increased bile flow in 1 min, and from min 5 until the end of NE administration (late period) bile flow remained above the basal level (111.7 +/- 2.2%), as did bile acid output (114.6 +/- 1.8%). Without TC infusion, administration of NE produced no increase in the late period. Administration of NE plus taurochenodeoxycholate (1.0 mumol/min) increased bile flow and bile acid output in the late period to 121.9 +/- 7.0 and 137.1 +/- 6.8%, respectively. With NE plus taurodehydrocholate, the respective values were only 105.4 +/- 1.6 and 104.1 +/- 4.0%. When horseradish peroxidase (HRP) (25 mg) was infused over 1 min with continuous NE, the late peak (20-25 min) of HRP elimination into bile significantly exceeded that of untreated controls (P0.01). These observations suggest that vasoconstrictors enhance biliary excretion of more hydrophobic bile acids, in part by stimulating vesicular transport.

ラット分離肝細胞においてエタノール(EtOH)によるフォスフォリパーゼC(PLC)活性化に対するプロテインフォスファターゼ阻害剤のokadaic acid (OKA)の効果とvasopressinによるPLC活性化に対するEtOHとOKAの相互作用について検討した.EtOH (300mM)刺激によりイノシトールリン脂質(PtdInsP, PtdInsP2)は上昇し,OKA前処置(1μM, 5分間)により,さらに上昇した.EtOH (30-300mM)による細胞内Ca2+([Ca2+]C)の上昇,イノシトール三リン酸(InsP3)の産生はOKA前処置により有意に抑制された.EtOH, OKAはそれぞれvasopressinによるPtdInsP2の分解,InsP3の産生,[Ca2+]C上昇を抑制し,受容体-G蛋白-PLC複合体に作用すると考えられたが,両者併用により相乗・相加効果がみられた.また,この併用効果は飽和濃度のEtOHにおいても認められ,OKAとEtOHは作用部位が異なることが示唆された.

症例は64歳,男性.1989年10月低血糖による異常行動を主訴として入院した.理学的所見では前胸部,後頭部に皮疹がみられ肝脾腫を認めた.画像診断では肝・脾内に腫瘤性病変は見られなかったが,腹腔鏡検査では肝表面に地図状の白斑が認められ,組織学的には門脈域を中心に肉芽腫様病変の形成を特徴とする,異型性を有する小型リンパ球浸潤からなる病変が多発し,免疫染色・電顕所見も併せてT細胞性リンパ腫と診断した.皮疹からの生検組織でも同様の所見がみられ,皮膚T細胞性リンパ腫(small cerebriform cell type)と診断した.血清学的に抗インスリン受容体抗体が陽性を示し,低血糖は,paraneoplastic syndromeと考えられた.本症例は1975年に紅皮症と診断されたが,当時の皮膚生検組織にもlymphoma cellが認められ,15年間subclinicalな状態で経過したものと考えられた.皮膚T細胞性リンパ腫に肝肉芽腫様病変を合併した例は稀であり,さらに肝浸潤により低血糖を招来した例は,本邦では文献的に検索し得た範囲内では第1例目と考えられた.

This paper describes a patient with malignant lymphoma of the small intestine who developed perforated peritonitis in a remission-stage four months after chemotherapy. A 65-year-old male was admitted to the hospital because of abdominal pain and distension. He had received chemotherapy for a malignant lymphoma of the small intestine four months previously and was in remission. Plain chest X-ray revealed free air in the bilateral subphrenic areas. Emergency laparotomy was performed following a diagnosis of perforated peritonitis. Perforation of the jejunum was recognized. Partial jejunal resection and drainage were performed. The resected specimens exhibited a simple ulcer and no lymphoma cells. With recent progression of chemotherapy therapeutic outcomes of malignant lymphomas become better. However, careful attention is still needed, because there are some cases causing perforation even in a remmssion stage after successful chemotherapy like this case.

In this study we investigated the interleukin-8 concentration (IL-8) and granulocyte elastase activity (GE) after elective abdominal surgery. Postoperative interleukin-6 (IL-6), IL-8 concentrations and GE in the peritoneal fluid were examined in 27 patients who underwent various types of elective abdominal surgery. We compared these results with clinical parameters of surgical stress, operating time (OT) and blood loss during the operation (BL). P-IL-6 and P-IL-8 were significantly correlated with OT (P-IL-6; r = 0.67, P < 0.001: P-IL-8; r = 0.59, P < 0.001) and BL (P-IL-6; r = 0.61, P < 0.001: P-IL-8: r = 0.48, P < 0.01). P-IL-8 was significantly correlated with P-IL-6 (r = 0.68, P < 0.001) and there was a positive correlation between GE and P-IL-8 (r = 0.37, P < 0.05). These findings indicate that IL-8 might activate granulocytes in the peritoneal cavity after elective abdominal surgery and that assaying P-IL-6 and P-IL-8 is useful in assessing the host's response to surgical stress.

To determine the risk of death at an early stage of fulminant viral hepatitis, we created severity indexes drawn from clinical data on the day of development of encephalopathy in 128 patients with fulminant hepatitis B and 103 with fulminant hepatitis non-A, non-B. In fulminant hepatitis B, the risk score was 2.75×BL+2.75×BR+2.7×AG+2.3×WB+1.67×CD+1.56×AL−0.098×PR−0.88, where BL is 1 if total bilirubin is higher than 20 mg/dl, BR is 1 if the ratio of total to direct bilirubin exceeds 2.2, AG is 1 if age is above 40 yr, WB is 1 if white blood cell count is less than 4,000 cells/mm3 or more than 18,000 cells/mm3, CD is 1 if a hazardous disease coexists and AL is 1 if ALT is less than 100 times the upper limit of normal (otherwise all are 0), and PR is prothrombin time (percentage of normal value). Using a cutoff score of 0, we found the positive predictive value, negative predictive value and predictive accuracy to be 0.90, 0.86 and 0.89, respectively. Sensitivity and specificity were 0.94 and 0.77, respectively. In fulminant non-A, non-B hepatitis, the risk score was 2.66×BR+2.25×BL+2.24×DI+2.05×AL ± 1.38×AG+0.00021×WB−6.33. BR is 1 if the ratio of total to direct bilirubin is more than 1.5, BL is 1 if total bilirubin is higher than 15 mg/dl, DI is 1 if the duration of illness before encephalopathy is less than 4 days or more than 12 days, AL is 1 if the ALT level exceeds 40 times the upper limit of normal and AG is 1 if age exceeds 50; otherwise all variables are 0. WB is WBC count per cubic millimeter. Positive predictive value, negative predictive value and predictive accuracy were 0.92, 0.80 and 0.89, respectively. Sensitivity and specificity were 0.95 and 0.70, respectively. These prediction equations were validated prospectively on a population of testing samples comprising 52 patients with fulminant hepatitis B and 47 with fulminant non-A, non-B hepatitis. Positive predictive values were 0.92 and 0.92, negative predictive values were 0.71 and 0.78 and predictive accuracies were 0.87 and 0.89 for patients with fulminant hepatitis B and fulminant non-A, non-B hepatitis, respectively. They may be used for selecting candidates for liver transplantation and for evaluating efficacy of a new therapy. (HEPATOLOGY 1994;19:1065–1071.)

ラット分離肝細胞において,エタノール(EtOH), vasopressin刺激によるホスホリパーゼC (PLC)活性化(細胞内Ca2+ ([Ca2+]c)の上昇,イノシトール三リン酸(InsP3)の産生)に対するウルソデオキシコール酸(UDC)の効果について検討した.vasopressinによるPLC活性は持続性であるのに対し,EtOHによるPLC活性は一過性であった.肝細胞をUDC及びタウリン飽合体であるTUDCで前処置すると,EtOHによるInsP3の産生には有意な変化はみられなかったが,[Ca2+]cの上昇は増強された.一方,vasopressinによる[Ca2+]cの上昇,InsP3の産生はUDC, TUDC前処置により有意に抑制され,PLC活性が抑制されることが明らかとなった.また,vasopressinによる[Ca2+]c上昇はEtOH前処置により抑制され,さらにUDC, TUDCと併用することによりこの抑制効果は増強された.このようにUDCはPLC作動性肝細胞内情報伝達機構に影響を及ぼし,種々の細胞機能の発現に関与することが示唆された.

ラット分離肝細胞において,タウロケノデオキシコール酸(TCDCA)による細胞内遊離Ca2+(〔Ca2+〕c)上昇の機序について検討した.浮遊肝細胞においてTCDCA (0.1～1mM)刺激により濃度依存性に〔Ca2+〕cが上昇し,イノシトール三リン酸(InsP3)も濃度依存性,一過性に産生された.単一肝細胞レベルにおける〔Ca2+〕cの変化はホルモン刺激による周期的なCa2+-oscillationとは異なり,TCDCA添加では単一のスパイクを示した.この反応はTCDCAの濃度に影響されず,濃度依存性に反応する細胞数が増加した.透過性肝細胞においてもTCDCA添加によりCa2+の放出がみられ,飽和濃度のTCDCA (1mM)の反応後にIns (1, 4, 5) P3を添加しても反応が得られず,TCDCAによるCa2+放出はInsP3感受性Ca2+貯蔵部位に由来するものと考えられた.肝細胞におけるTCDCAによる〔〔Ca2+〕c上昇の機序はPLC活性化によるものと直接細胞内Ca2+貯蔵部位に作用するものと,少なくとも2つの経路が存在することが明らかとなった.

A 63-year-old woman was admitted with high fever. Laboratory tests showed leukocytosis and elevated C-reactive protein (CRP) levels. Abdominal ultrasonography and computed tomography revealed multiple liver and splenic tumors. We diagnosed phlegmonous gastritis with multiple liver and splenic abscesses based on a discharge of pus from the gastric ulcer on biopsy obtained during esophagogastroduodenoscopy. She showed remission after spontaneous drainage and treatment with antibiotics. A search of the literature yielded no other cases of phlegmonous gastritis with multiple liver and splenic abscesses, and we therefore report this case.

The incidence of HCV positivity and its relation to surgical and disease history was studied in elderly Japanese. The subjects included 230 individuals (97 men and 133 women) aged 60 to 102 years (mean: 79.2 years), and anti-HCV positivity was found in 42 cases (18.3%). More than 10% of the subjects in each age decade were anti-HCV positive, with the highest rate seen in the 60–69-year-old group (31.0%). No age-related differences in anti-HCV titer were observed. Twenty-eight of 32 subjects examined were HCV-RNA positive and analysis of HCV-RNA status revealed that most anti-HCV-positive subjects had a persistent HCV infection. About 60% of the anti-HCV-positive subjects had undergone surgery, supporting the conclusion that horizontal transmission via surgery or blood transfusion was an important route of HCV transmission. Liver dysfunction was noted in 33.3% of the anti-HCV-positive subjects, always in association with the presence of HCV RNA. Liver cirrhosis was diagnosed for two subjects, but no liver cancers were detected. One of two autopsied cases, a 91-year-old female who had undergone surgery 20 years before, showed characteristic features of chronic persistent hepatitis in spite of normal liver function tests before death. Our findings suggest that not only long-term monitoring for liver cirrhosis and liver cancer but also attention to the infection risk of transmission to others is needed in the care of elderly anti-HCV-positive individuals.

Postoperative peritoneal interleukin-6 (P-IL-6), serum beta-2 microglobulin (SBMG) and urinary beta-2 microglobulin (UBMG) concentrations were examined in 33 patients who underwent various types of abdominal surgery. Similar time-dependent changes in SBMG and UBMG were observed in five other patients who underwent abdominal surgery. SBMG decreased the first day after the operation (1POD), then increased and reached the preoperative level by the third day after the operation (3POD). UBMG started to increase 1POD, reached the maximum 3POD, then decreased. The 1POD SBMG concentration was significantly correlated with P-IL-6, and 3POD UBMG was also significantly correlated with P-IL-6. These findings indicate that serum and urinary beta-2 microglobulin concentrations are closely correlated with P-IL-6.

In order to study the mortality rate and bacteremia, plasma endotoxin, and plasma endothelin-1 levels in antibiotic therapy for E. coli peritonitis, blood samples were obtained from rats given intraperitoneal injections of latamoxef or placebo. Intraperitoneal injections of latamoxef improved the prognosis of peritonitis rats. Two h after treatment, bacteremia levels were noticeably higher in rats treated with placebo than in rats treated with latamoxef, but the latamoxef-treated group manifested a significant elevation of plasma endotoxin and endothelin-1 levels compared to the placebo-treated group. The results of this study demonstrate that treating E. coli septic peritonitis with selected antibiotics induces increased plasma endotoxin levels, which are associated with elevation of plasma endothelin-1 levels.

症例は50歳,女性.1987年11月クモ膜下出血にて左右中大脳動脈瘤クリッピング術を施行し,赤血球濃厚液5単位の輸血を受けた.輸血1ヵ月後に肝機能障害が出現.輸血後肝と診断し,安静・輸液などの治療により肝機能は一時改善したが,発症2ヵ月後に再び悪化し,意識障害はなかったが,PT 43.2%と重症化した.G-I療法,FFPなどの投与により肝機能は軽快した.経過中に抗ミトコンドリア抗体(AMA)が高力価陽性を示したが,肝炎の改善とともに力価は陰性化した.しかし発症約3年後,肝機能が正常にもかかわらず,AMAは再び,一過性に陽性となったが,現在はまた陰性が持続している.回復期に施行した腹腔鏡では肝両葉に大きな結節性病変を認め,馬鈴薯肝と診断した.組織学的には再生結節の所見であり,原発性胆汁性肝硬変(PBC)の所見はみられなかった.本例はAMAの産生機序,生理的意義を考える上で興味深いと思われた.

Cell cycle regulators, such as cyclinD1 and p53, play major roles in the tumor response to radiation and chemotherapy in esophageal squamous cell carcinoma (SCC). Pin1-mediated prolyl-isomerization potentiates cell cycle progression and cell proliferation, including the regulation of cyclinD1 and p53. Herein, we investigated the effect of Pin1 in association with cyclinD1 and p53 on the sensitivity of esophageal SCC to chemoradiotherapy (CRT). The expression levels of Pin1, cyclinD1 and p53 were examined immunohistochemically in endoscopic biopsy specimens from 68 advanced esophageal SCC patients before CRT to determine whether their expression levels predicted the clinical effectiveness of CRT in individual cancers. Forty-six of the 68 patients (67.6%) had an effective response to CRT, whereas 22 patients (32.4%) had an ineffective response. There was no significant correlation between clinical responses and expression levels of cyclinD1 or p53. However, the clinical response of the high Pin1 expression group was significantly higher than that of the low expression group (P=0.0200). Moreover, our data indicate that the combined immunohistochemical evaluation of Pin1, cyclinD1 and p53 expression in pretreatment biopsy samples is a useful indicator of sensitivity to CRT in advanced esophageal SCC. Thus, Pin1 may influence cyclinD1 and p53 functions and predict CRT sensitivity.

The purpose of the present study was to assess the contribution of simultaneous functional/anatomical imaging using integrated 18F-fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT), compared with PET alone for the evaluation of initial lymph node staging in esophageal cancer. We studied 167 consecutive patients with thoracic esophageal squamous cell carcinoma (SCC) who had radical esophagectomy performed between January 1999 and April 2007. For individual nodal group evaluation, PET/CT showed 46.0% sensitivity (p

Circulating vascular endothelial growth factor-C (VEGF-C) levels were measured in patients with esophageal cancer to assess the value of VEGF-C as a biomarker for predicting tumor recurrence.Preoperative serum samples were acquired from 80 patients and healthy volunteers who served as normal controls. VEGF-C levels were assessed using enzyme-linked immunosorbent assay (ELISA).The preoperative serum VEGF-C level in patients with esophageal cancer was significantly higher than in healthy volunteers. Furthermore, patients with recurrence had significantly higher preoperative serum VEGF-C levels than patients without recurrence, and a high preoperative serum VEGF-C level was found to be an independent risk factor for recurrence, in addition to lymph node metastasis.Preoperative VEGF-C levels may reflect malignancy, such as lymph node metastasis, and predict recurrence in patients with esophageal cancer. Therefore, the preoperative VEGF-C level may be a useful biomarker for choice of multimodality therapy.

After esophagectomy a swallowing abnormality is the predominant symptom for esophageal cancer. The aims of this study were to examine (i) oropharyngeal swallowing by comparing pre- and postoperative period, and (ii) the relationship between oropharyngeal swallowing and the alimentary reconstruction route after esophagectomy.We studied 27 patients in the upright position using videofluoroscopy in the lateral projection. Each patient was studied during 10 mL barium swallows in the pre- and post-operative period.Of the 27 patients studied, alimentary reconstruction with the retrosternal route (RS group) was performed in 8 patients, that with posterior mediastinal route (PM group) in 8 patients, and the intrathoracic (IT group) esophagogastrostomy inside the posterior mediastinum in 11 patients. With regard to the maximal extent of structural movement, the superior and anterior excursion of the hyoid bone was significantly reduced postoperatively among all groups. The maximal extent of the cricopharyngeal opening was significantly reduced postoperatively in the RS group, but not in the IT group. The changes in the peri-operative structural movement were the lowest in the RS group.A new-onset oropharyngeal swallowing abnormality following retrosternal reconstruction after esophagectomy may have appeared because the change in the peri-operative movement was the lowest. The results of the swallowing evaluation using videofluoroscopy suggest that to avoid oropharyngeal swallowing abnormalities the intrathoracic or cervical anastomosis with posterior mediastinal route should be chosen as reconstruction after esophagectomy if possible.

Three-hundred and eighty-five strains of Pseudomonas aeruginosa were isolated from Gunma University Hospital from 1984 to 1987. Out of these strains, thirty strains (7.8%) were resistant to GM. We investigated antibiograms, serotyping, phage typing, and plasmid profiles of these strains. The following results were obtained. 1) Only one kind of GM-resistant (GMr) plasmid was obtained in 1984. Two kinds of GMr plasmids were found in 1985, and three kinds of GMr plasmids in 1987, respectively. 2) A strain of I-serotype and Hh8-phage type containing the plasmid I (GM-SM-SA-PIPC, Tra-, 22.6Kb or 22.5 Kb) was suspected to cause the nosocomial infection mainly in Departments of Internal Medicine, and a strain of non-serotypable and Hh8-phage type containing the plasmid IV (GM-SM-SA-CP-Hg, Tra+, IncP-2) was suspected to cause the nosocomial infection mainly in Surgical Departments. 3) Plasmid profiles adding to serotyping and phagetyping contribute to the epidemiological analysis of Pseudomonas aeruginosa infection.

Self-expandable metallic stents (SEMS) have been used for many years in the palliation of esophageal cancer symptoms. Stent migration is one of the most recognized complications of SEMS. To prevent SEMS migration, this study reported the use of endoscopic clips, and carefully analyzed the patients who underwent implantation.From January 2000 to December 2002, nine patients consecutively underwent SEMS implantation. After successful placement of the SEMS and to maintain its position, endoscopic clips were used to fix the branch of the upper end of the stent to the esophageal mucosa.Stent implantation was technically successful in all patients, three of whom had strictures and six of whom had digestive-respiratory fistulas. No stent migration was observed in any of the patients, and dysphagia improved significantly after stent placement. Five patients did, however, experience delayed complications, two in the form of obstructions, two with recurrent fistulas, and one with a perforation.In conclusion, this new technique is recommended as endoscopic clipping can diminish the risks of stent migration, in particular those associated with esophago-respiratory fistulas without luminal obstruction.

Esophageal cancer is one of the most difficult malignancies to cure. The prognosis remains unsatisfactory despite significant advances in surgical techniques and perioperative management. The optimal treatment strategy for localized esophageal cancer has not yet been established. Surgical resection remains the mainstay of treatment for esophageal cancer, and curative resection is the most important surgery. Extended esophagectomy with three-field lymphadenectomy provides the highest quality of tumor clearance and prolongation of patient survival. There has been intense effort in developing novel strategies to treat patients with resectable esophageal cancer. Various combined-modality approaches have been attempted to improve treatment outcomes. Definitive chemoradiotherapy has an impact on long-term survival in patients with resectable esophageal cancer. Accordingly, there are three main combined-modality approaches: esophagectomy with adjuvant chemotherapy or chemoradiotherapy; primary definitive chemoradiotherapy with or without salvage esophagectomy, and preoperative chemoradiotherapy followed by planned esophagectomy. Recently, owing to the remarkable advances in optical technology, minimally invasive esophagectomy using endoscopic instruments has been introduced into esophageal cancer surgery. This article reviews recent changes in the treatment of esophageal cancer surgery, and considers the role of esophagectomy.

Postoperative pulmonary complications are often fatal in patients with esophageal cancer. The aim of this study was to clarify the association between cytokines and temporary ventilation during one-lung ventilation.Serum and BALF IL-6, 8 were measured in 39 patients with esophageal cancer, and the relationship between cytokine response and temporary ventilation during one-lung ventilation in esophagectomy was examined.Pulmonary complications did not occur in our patients. Serum IL-6 levels were significantly increased in the high one-lung ventilation ratio and long-term one-lung ventilation groups. Serum IL-6 levels in the one or more times ventilation group during one-lung ventilation were significantly low compared to the no-ventilation group. There were no significant differences in serum IL-8 and BALF IL-6, 8 levels.Our results indicate that it is important to ventilate one or more times during one-lung ventilation in order to reduce postoperative pulmonary complications.

Background Carcinoid tumors rarely arise in the extrahepatic bile duct and can be difficult to distinguish from carcinoma. There are no reports of clear cell carcinoid (CCC) tumors in the distal bile duct (DBD) to the best of our knowledge. Herein, we report a CCC tumor in the DBD and review the literature concerning extrahepatic bile duct carcinoid tumors. Case presentation A 73-old man presented with fever and occult obstructive jaundice. Ultrasonography, computed tomography (CT) and magnetic resonance cholangiopancreaticography (MRCP) demonstrated a nodular tumor projection in the DBD without regional lymph node swelling. Under suspicion of carcinoma, we resected the head of the pancreas along with 2nd portion duodenectomy and a lymph node dissection. The surgical specimen showed a golden yellow polypoid tumor in the DBD (0.8 × 0.6 × 0.5 cm in size). The lesion was composed of clear polygonal cells arranged in nests and a trabecular pattern. The tumor invaded through the wall into the fibromuscular layer. Immunohistochemical stains showed that neoplastic cells were positive for neuron-specific enolase (NSE), chromogranin A, synaptophysin, and pancreatic polypeptide and negative for inhibin, keratin, CD56, serotonin, gastrin and somatostatin. The postoperative course was uneventful and he is living well without relapse 12 months after surgery. Conclusion Given the preoperative difficulty in differentiating carcinoid from carcinoma, the pancreaticoduodenectomy is an appropriate treatment choice for carcinoid tumors located within the intra-pancreatic bile duct.

Neuroleptic malignant syndrome (NMS), a potentially hazardous side effect of antipsychotic agents, usually develops within 10 days after receiving these agents. We describe a 65-year-old male who developed NMS after taking neuroleptics for alcohol dependence syndrome for several years. He was successfully treated by stopping these agents but three months later, an advanced sigmoid colon cancer was detected. He underwent surgery and the clinical course was uneventful. The present case is rare in that he developed NMS after long-term neuroleptic therapy and concurrent alimentary tract malignancy can be a risk factor for the development of NMS.

Esophageal carcinoma is one of the most lethal tumors, and identification of prognostic factors for patients with this disease is important. Propyl isomerase Pin1 is overexpressed in some human cancers and thought to be an important regulator of cyclinD1. However, the relationships between Pin1 expression and clinicopathologic features in patients with esophageal squamous cell carcinoma (SCC) have not been explored. Here, we investigated the role of Pin1 in association with cyclinD1 in esophageal SCC progression and its clinicopathological significance. The expressions of Pin1 and cyclinD1 were examined immunohistochemically in surgical specimens from 119 esophageal SCC patients. The expression levels of Pin1 and cyclinD1 in 6 esophageal SCC-derived cell lines were compared with those in an immortalized human esophageal cell line by western blotting. Pin1 overexpression was correlated with lymph node metastasis (P=0.0384), and its expression was related to cyclinD1 expression. Pin1 expression was correlated with poor prognosis in esophageal SCC patients (P=0.0044), and found to be an independent prognostic factor (P=0.0277). Pin1 was overexpressed in 5 of 6 esophageal SCC-derived cell lines compared with immortalized esophageal keratinocytes. Moreover, the Pin1 level was correlated with the cyclinD1 level in 4 of the 6 cell lines. In conclusion, Pin1 expression is correlated with cyclinD1 expression and may be a useful prognostic factor for esophageal SCC.

Background and Objectives: Transforming growth factor-β (TGF-β) regulates cell growth in various cells, and inactivation of the TGF-β-signaling pathway contributes to tumor progression. In this study, we investigated the expression of Smad2 and Smad3, which are specific intracellular mediators of TGF-β signaling. We also examined the relationship between the expression levels of activated Smad2 by TGF-β and clinicopathologic characteristics of patients with esophageal squamous cell carcinoma (SCC). Methods: Immunohistochemical staining with anti-phosphorylated Smad2 (P-Smad2) polyclonal antibody, anti-Smad2 monoclonal antibody, and anti-Smad3 polyclonal antibody was performed on surgical specimens obtained from 80 patients with esophageal SCC. Results: Our data indicated that a low level of P-Smad2, as detected immunohistologically, correlated with lymph node metastasis (P = 0.0002), distant metastasis (P = 0.0338), pathologic stage (P = 0.0093), and poor survival rate (P = 0.0246). All patients without positive Smad2 immunostaining were included among those without positive P-Smad2 immunostaining. There was no significant correlation between expression of Smad2 or Smad3 and clinicopathologic characteristics. Conclusions: We demonstrated that a lack of Smad2-P appears to be correlated with tumor development and poor prognosis in patients with esophageal SCC. J. Surg. Oncol. 2006;94:51–56. © 2006 Wiley-Liss, Inc.

Positron emission tomography (PET) with 18-F-fluorodeoxyglucose (FDG) has already proved useful in assessing the extension of esophageal carcinomas, detecting tumor recurrence and monitoring responses to therapy. This study aimed to elucidate the potential role of FDG-PET compared with technetium-99m methylene diphosphonate (Tc-99m MDP) bone scintigraphy in the evaluation of bony metastasis in esophageal carcinoma patients.Forty-four patients with thoracic esophageal carcinomas, who underwent FDG-PET together with bone scintigraphy within 1 month between January 2000 and September 2003, were included in this study.Of the 44 patients, 13 had 31 bone metastases and, of these, 6 were diagnosed pretreatment and 7 had recurrence after esophagectomy surgery. Of the 31 metastases, 9 were in the vertebral column, 11 in the thoracic cage (including the ribs, clavicle, sternum and scapula), 9 in the pelvic bones and 2 in the long bones of the extremities. In evaluating the detection of bony metastasis, FDG-PET showed 92% sensitivity, 94% specificity and 93% accuracy, compared with 77%, 84% and 82%o, respectively, for bone scintigraphy. Although the sensitivity, specificity and accuracy of PET were slightly higher than those of bone scintigraphy, these differences were not statistically significant according to the McNemar's test. Three patients with false-negative findings on their bone scans had positive findings with PET; all of these lesions were osteolytic metastases.FDG-PET scans were superior to bone scintigraphy in detecting bony metastases of esophageal carcinomas. Therefore, FDG-PET can be used for the detection and follow-up of bone tumors when Tc-99m MDP bone scintigraphy gives negative findings.

CT has proven useful in diagnosing appendicitis, but it also has some disadvantages. In this study we investigated clinical factors influencing CT findings of acute appendicitis and identified the most appropriate patients for preoperative CT.Enhanced helical CT scans were obtained preoperatively in 95 patients who underwent appendectomy. They were gangrenous in 52 (55%), phlegmonous in 38 (40%) and catarrhal in 5 (5%) and we usually indicated emergent surgery for phlegmonous or gangrenous appendicitis patients. 62 (69%) of 90 phlegmonous or gangrenous cases had both an enlarged appendix (or = 6mm) and periappendiceal fat strand in CT, which strongly suggested the need for emergent operation (Positive group). We compared clinical factors in the positive group with those in the other 28 patients (Equivocal group).There was no significant difference between the positive and equivocal groups in age, gender, or white blood cell count. The depth of subcutaneous fat (SCF) at the umbilicus level in CT and the number of patients with gangrenous appendicitis were significantly increased in the positive group compared with the equivocal group by both univariate and multilogistic regression analysis.These indicated that the degree of inflammation and SCF were significantly associated with CT findings of appendicitis and CT should be routinely done in obese patients.

We have been investigating various molecules correlated with the malignancy of esophageal squamous cell carcinoma and, in the present study, we examined the correlation of four of them (KAI1, FAK, EphA2, Ki-67 labeling index) with the prognosis of affected patients. Furthermore, the use of biopsy samples was studied to evaluate whether the grade of tumor malignancy can be determined before treatment in a clinical setting.Tissue specimens that had been surgically removed from 91 patients with thoracic esophageal cancer and 247 biopsy samples were examined. The malignancy index (MI) was defined in terms of the KAI1, FAK and EphA2 scores and the Ki-67 labeling index, and the reliability and utility of the correlation between MI and prognosis was evaluated.The mean 5-year survival rate of patients with MI=0 was 100%, while that of patients with MI=1, 2 and 3 was 70%, 48% and 10%, respectively. Patients with MI=4 all died, with the exception of one who has been observed for 3 years. The rate of concordance between the biopsy samples and surgical specimens was 79.4% for KAI1, 88.2% for FAK and 73.5% for EphA2, and the rates of concordance for 1, 2, 3, 4, 5, 6, 7 and 8 biopsy samples were 66.7%, 64.1%, 74.5%, 90.7%, 91.7%, 83.3%, 100% and 100%, respectively.It may be feasible to evaluate the malignancy of tumor cells and to predict patient outcome by using multiple marker molecules. It is anticipated that such data will accelerate the development of "tailor-made" therapy.

Background Perioperative steroid therapy is often used in oesophageal cancer surgery and we evaluate the effect of this therapy on the secretory leukocyte protease inhibitor levels in the lungs (a major antiprotease in the conducting airways) and postoperative course in oesophageal cancer patients. Methods Twenty-one patients operated on for oesophageal cancer in 2003–2004 were treated with perioperative steroid therapy (250 mg of methylprednisolone intravenously 1 h before the operation). Fifteen consecutive patients operated on in 2002 served as a control group. Secretory leukocyte protease inhibitor in bronchoalveolar lavage fluid and the postoperative course in the two groups were compared. Results The mortality rate was 0% and there was no significant difference in the morbidity rate between the two groups. Days of intubation and systemic inflammatory response syndrome were significantly shorter for the steroid group. The bronchoalveolar lavage fluid secretory leukocyte protease inhibitor level was significantly higher in the steroid group than in the control group on postoperative days 2 and 3. The secretory leukocyte protease inhibitor level on postoperative day 3 was remarkably lower for the patients intubated for ≥5 days and for those with pulmonary complications. Conclusion Perioperative steroid therapy increased the bronchoalveolar lavage fluid secretory leukocyte protease inhibitor level and reduced the days of intubation and systemic inflammatory response syndrome in patients with oesophagectomy.