Precise Measurement of Differential Cross Sections of the Σ

The differential cross sections of the Σ^{-}p→Λn reaction were measured accurately for the Σ^{-} momentum (p_{Σ}) ranging from 470 to 650 MeV/c at the J-PARC Hadron Experimental Facility. Precise angular information about the Σ^{-}p→Λn reaction was obtained for the first time by detecting approximately 100 reaction events at each angular step of Δcosθ=0.1. The obtained differential cross sections show a slightly forward-peaking structure in the measured momentum regions. The cross sections integrated for -0.7≤cosθ≤1.0 were obtained as 22.5±0.68 [statistical error(stat.)] ±0.65 [systematic error(syst.)] mb and 15.8±0.83(stat)±0.52(syst) mb for 470

Novel thin bronchoscope with a 1.7-mm working channel for peripheral pulmonary lesions.

In the present study, the authors evaluated the diagnostic utility of a novel thin bronchoscope with a 1.7-mm working channel for peripheral pulmonary lesions. A total of 118 patients were included in this prospective study. Bronchoscopic examination was performed using a 5.9-mm standard bronchoscope. If no visible endobronchial lesion was found, transbronchial biopsies were performed with 1.5-mm biopsy forceps under fluoroscopic guidance and the bronchus were washed with 10-20 mL of saline solution, using a prototype 3.5-mm thin bronchoscope with a 1.7-mm working channel. Endobronchial lesion was visualised with the standard bronchoscope in 16 patients, and the other 102 patients underwent biopsies with the thin bronchoscope. The mean bronchus levels reached with the standard bronchoscope and the thin bronchoscope were 2.3 and 4.3 generations, respectively. Endobronchial abnormality was revealed with the thin bronchoscope in a further 14 patients. Diagnostic material was obtained in 50 of 68 (74%) patients with malignant disease and 18 of 30 (60%) patients with benign disease. Four patients did not return to follow-up. The diagnostic yield was 57%, even in lesions <20 mm. There were no major complications. In conclusion, bronchoscopy using a 3.5-mm thin bronchoscope with a 1.7-mm working channel is useful and safe for the diagnosis of peripheral pulmonary lesions.

Possible involvement of DNA methylation in 5-azacytidine-induced neuronal cell apoptosis.

Eight chemicals that are cytidine analogues or nucleosides (5-azacytidine (5AzC), 5-azadeoxycytidine, 6-azacytidine, 5-azacytosin, cytidine, 3-deazaadenine, 3-deazauridine and 6-azauridine) were examined for the ability to induce neuronal apoptosis. 5AzC and 5-azadeoxycytidine induced apoptosis in the brain and spinal cord of the fetuses at 24 hr after the injection to dams, while the other chemicals tested failed to induce apoptosis. In the system of PC12 cells, only 5AzC induced apoptosis, and other chemicals failed to provoke morphological and biochemical changes characteristic of apoptosis. 5AzC, 5-azadeoxycytidine and 6-azacytidine failed to induce apoptosis in C6 cells. Gel electrophoresis after MspI or HapII digestions revealed no apparent evidence of DNA demethylation after 5AzC-treatment in either fetal brains or PC12 cells. These results indicate that DNA demethylation is possibly involved in 5AzC-induced neuronal apoptosis although no direct evidence of DNA demethylation was obtained.

Expression of ribosomal protein L4 (rpL4) during neurogenesis and 5-azacytidine (5AzC)-induced apoptotic process in the rat.

5-Azacytidine (5AzC) induces neuronal apoptosis in rat and mouse fetuses. 5AzC also induces apoptosis in undifferentiated PC12 cells, and ribosomal protein L4 (rpL4) mRNA expression increases prior to apoptosis. To clarify the roles of rpL4 during neurogenesis, we first examined the distribution of rpL4 mRNA in the developing rat brain by in situ hybridization and RT-PCR, and compared the results to the distribution of TUNEL- or PCNA-positive cells. rpL4 mRNA expression was strong in the ventricular zone (VZ), subventricular zone (SVZ), cortical plate (CP), cerebral cortex, granule cell layer (GCL), pyramidal cell layer (Py) and external granular layer (EGL) during embryonic and early postnatal days, and it was remarkably weakened thereafter. A lot of PCNA-positive cells were observed in VZ, SVZ, and EGL during embryonic and early postnatal days, and such distribution of PCNA-positive cells was almost identical to rpL4 mRNA distribution. Only few TUNEL-positive cells were observed in VZ, SVZ, cerebral cortex, EGL, and hippocampus during embryonic and early postnatal days, and the regions with TUNEL-positive cells were not identical to rpL4 mRNA distribution. Next, the changes of rpL4 mRNA expression in the brain of 5AzC-treated rat fetuses were examined by in situ hybridization and RT-PCR. Apoptotic cells appeared at 9 to 24 hours after treatment (HAT). However, the rpL4 mRNA expression was unchanged during the apoptotic process. From the results, it is suggested that rpL4 would have certain roles in cell proliferation and differentiation during neurogenesis, but have no roles in 5AzC-induced apoptosis in the fetal brain.

Protective effect of the thromboxane A2 receptor antagonist ONO 3708 on ischemia-reperfusion injury in the dog liver.

BACKGROUND: Prostaglandins are widely known to have cytoprotective effects in a variety of conditions. Thromboxane A2 has the opposite effect of prostaglandins. In this study the effects of the thromboxane A2 receptor antagonist ONO 3708 on ischemia and subsequent reperfusion in the dog liver was evaluated. METHODS: Mongrel dogs weighing from 10 to 15 kg were divided into three groups: a control group, a group with induced liver ischemia and subsequent reperfusion, and a group that received ONO 3708 and then underwent induced liver ischemia and subsequent reperfusion. Liver ischemia was induced by the Pringle procedure for 60 minutes. The concentrations of total free amino acids, aromatic amino acids, and branched-chain amino acids in blood taken from the portal and hepatic veins were examined before and after the Pringle procedure in the latter two groups and at the corresponding points in the control group. RESULTS: Disturbances in amino acid metabolism in the liver occurred 5 minutes after the declamping in the ischemic group, and prostaglandin I2 and thromboxane A2 levels and lipid peroxide production, were increased. In contrast, hepatic amino acid metabolism was unchanged, and prostaglandin I2 and thromboxane A2, and lipid peroxide production, were normalized in the group that was treated with ONO 3708. CONCLUSIONS: ONO 3708 appears to protects hepatic tissue from ischemia-reperfusion injury through free-radical scavenging, by increasing prostaglandin I2 levels, and by decreasing thromboxane A2 production.

Protection against preterm delivery in mice by urinary trypsin inhibitor.

OBJECTIVE: To investigate the precise mechanism by which urinary trypsin inhibitor suppresses cytokine production in the prevention of preterm delivery. METHODS: In vivo and in vitro studies were performed using ascites and peritoneal macrophages obtained on day 15 of pregnancy from female C3H/HeN mice that had been impregnated by B6D2F1 male mice. Lipopolysaccharide receptor, the intracellular signal transduction system, and nuclear factor-kappaB level were examined. RESULTS: In the in vivo study, we found that urinary trypsin inhibitor ameliorated the deterioration of intraperitoneal conditions induced by lipopolysaccharide (ie, increases in ascitic volume, peritoneal cell count, and tumor necrosis factor-alpha level) and caused a decrease in the binding of lipopolysaccharide to mouse macrophages. In the in vitro studies, urinary trypsin inhibitor decreased the binding capacity of lipopolysaccharide for its receptor, blocked the intracellular signal transduction induced by lipopolysaccharide, and decreased the nuclear factor-kappaB level. Increases were induced in the binding capacity of the macrophages for urinary trypsin inhibitor and its incorporation into them in the presence of lipopolysaccharide. CONCLUSION: We postulate that urinary trypsin inhibitor may suppress the production of inflammatory cytokines induced by lipopolysaccharide in mouse peritoneal macrophages through suppression of the lipopolysaccharide receptor, inhibition of the intracellular signal transduction system, and decrease in the nuclear factor-kappaB level.

Metabolism of insulin and glucagon in liver and pancreas in dogs with obstructive jaundice.

Insulin and glucagon metabolism in the pancreas with obstructive jaundice caused by complete ligation of the common bile duct and in the cholestatic liver caused by hepatic duct ligation was evaluated experimentally using dogs. The isolated perfused pancreas in obstructive jaundiced dogs, which showed a low insulin response in the peripheral blood after intravenous glucose administration, revealed depression of insulin production and no change of glucagon production in response to cholecystokinin octapeptide. The extraction of insulin in the cholestatic lobe of the liver was decreased compared with that in the noncholestatic lobe. The extraction of glucagon, on the other hand, in the cholestatic lobe and in the noncholestatic lobe showed no significant difference. So the imbalance of glucose metabolism in obstructive jaundice does not depend on the enhanced extraction of insulin in the liver, but on the depression of insulin production in the pancreas.

Effects of parathyroid hormone on pancreatic exocrine secretion.

The role of parathyroid hormone (PTH) and calcium on pancreatic exocrine secretion were observed using sham-operated and parathyroidectomized dogs. First, exocrine secretion of the pancreas stimulated with secretin and cholecystokinin octapeptide (CCK-8) was examined in vivo 3 weeks after parathyroidectomy. Secondly, perfusion experiments of isolated pancreas in the sham-operated and parathyroidectomized dogs were examined. In one experiment, volume of pancreatic juice and bicarbonate output, but not amylase output, was decreased in the parathyroidectomized dogs compared with those in the sham-operated dogs; no participation of calcium in exocrine secretion was revealed. In another experiment, high doses of PTH evoked increases of pancreatic juice and bicarbonate output without changing amylase output; as before, no participation of calcium in the exocrine secretion was observed. We conclude that (a) PTH increases volume of pancreatic juice and bicarbonate output, and (b) pancreatic exocrine secretion is modified by direct effect of PTH, and the pancreatic ductular cells, not the acinar cells, are the target for PTH.

Involvement of endogenous prostaglandins in pancreatic endocrine and exocrine secretion in dog pancreas.

The involvement of endogenous prostaglandins (PGs) in pancreatic endocrine and exocrine secretion was investigated, using the isolated and perfused dog pancreas. Spontaneous production of both PGE2 and 6-keto-PGF1 alpha was recorded in venous effluent. Prostaglandin production increased following stimulation with both 10 x 10(-11) and 20 x 10(-11) mol of CCK-8, but was not affected by a 5 x 10(-11) mol infusion. Insulin, glucagon, and amylase release was stimulated by 10 x 10(-11) mol of CCK-8. Indomethacin pretreatment with 10 mg/kg totally abolished endogenous PG production, but failed to suppress an insulin and glucagon response. On the other hand, an amylase response was accelerated by indomethacin pretreatment. Although low dose CCK-8 failed to stimulate endogenous prostaglandin production, a brisk exocrine secretion was not suppressed by indomethacin pretreatment. From the above results, we conclude that endogenous PGs do not appear to play an important role in pancreatic endocrine and exocrine secretion, but might have a cytoprotective effect on the pancreatic acinar cells damaged by CCK-8.

Evaluation of imaging examination for hepatic invasion of carcinoma of the gallbladder and postoperative patient outcome.

BACKGROUND: Hepatic invasion is an important factor in the selection of an operative procedure for patients with carcinoma of the gallbladder. Imaging modalities to detect the hepatic invasion were evaluated for accuracy, and postoperative patient outcome was analyzed. STUDY DESIGN: Thirty-six patients who were treated for carcinoma of the gallbladder at our institution between 1984 and 1993 were studied. The imaging results of ultrasonography (US), computed tomography, and angiography were compared with histologic findings regarding intrahepatic invasion of the carcinoma. RESULTS: Histologic examination of the operative specimens removed from 21 patients revealed that the detection of hepatic invasion with preoperative US was superior to that with the other two modalities. The preoperative US showed a diagnostic value that was almost the same as that of the intraoperative US. The postoperative patient outcome was not satisfactory, although extended radical operation was performed using image guidance in the 21 patients. The patients died as a result of nodal recurrence rather than hepatic recurrence. CONCLUSIONS: Preoperative US should be performed initially for detecting hepatic invasion from carcinoma of the gallbladder and can be substituted for intraoperative US. Considering the operative treatment for patients with carcinoma of the gallbladder, lymph node dissection is as important as the extent of hepatectomy.

Hepatic resection for hepatocellular carcinoma in the elderly.

BACKGROUND: Although the number of elderly people undergoing surgery for hepatocellular carcinoma (HCC) has increased because of the prolonged life expectancy rate, potential benefits of hepatectomy for elderly patients with HCC have not been fully delineated. STUDY DESIGN: Using medical records, surgical outcomes of HCC in 103 patients 70 years of age or older undergoing hepatic resection (older group) were clarified and compared with those of 283 patients younger than 70 years of age (younger group) in this retrospective study. Postresection prognostic factors were evaluated by multivariate analysis using Cox's proportional hazards model. RESULTS: There were no significant differences in postoperative complication, operative mortality, and overall hospital death rates between the two groups. Overall 3- and 5-year survival rates for the older group and the younger group were 51.0% versus 55.2%, and 42.2% versus 40.0%, respectively (p = 0.95). Disease-free 3- and 5-year survival rates for the older group and the younger group were 35.2% versus 37.6%, and 16.6% versus 24.2%, respectively (p = 0.66). Multivariate analysis revealed that the presence of liver cirrhosis and vascular invasion were independently significant factors of poor overall survival. CONCLUSIONS: Selected elderly patients with HCC benefited from resection as much as young patients, and age by itself may not be a contraindication to surgery. Postresection longterm prognosis in the elderly was determined by the presence of liver cirrhosis and vascular invasion.

Survival and recurrence after hepatic resection of 386 consecutive patients with hepatocellular carcinoma.

BACKGROUND: Although hepatic resection is one of the most effective treatments for hepatocellular carcinoma (HCC), the longterm results of hepatic resection of this malignancy are far from satisfactory. The potential benefits of hepatectomy for patients with HCC have not been fully delineated. This study aimed to identify surgical outcomes of 386 consecutive patients with HCC undergoing hepatic resection. STUDY DESIGN: The retrospective study looked at records of 293 men and 93 women. The mean age was 63.2 years. Preoperative transarterial chemoembolizaton and portal vein embolization were performed in 138 patients (35.8%) and 8 patients (2.1%), respectively. Sixty-two patients (16.1 %) had major hepatectomy and the other 324 (83.9%) had minor hepatectomy. Thirty-seven of 386 patients (9.6%) had a noncurative operation. RESULTS: The 30-day (operative) mortality rate was 4.1%, and there were 11 additional late deaths (2.9%). Two hundred fourteen of 327 patients (65.4%) had recurrence after curative resection. Unfavorable factors for survival and recurrence were resection between 1983 and 1990, Child class B or C, cirrhosis, a high value of indocyanine green retention-15, a large amount of intraoperative blood loss, stage IV disease, positive surgical margin, vascular invasion, and postoperative complications. Preoperative transarterial chemoembolization increased the recurrence rate and showed no contribution to prognosis. Currently, 106 patients (27.5%) are alive: 7 (1.8%) after more than 10 years and 43 (11.1%) after more than 5 years. Mean and median overall survivals after operation were 38 months and 29 months, respectively. The 5-year and 10-year overall or disease-free survival rates after hepatic resection were 34.4% and 10.5% or 23.3% and 7.8%, respectively. CONCLUSIONS: The longterm survival rate after operation remains unsatisfactory mainly because of the high recurrence rate. Preoperative transarterial chemoembolization should be avoided because of a high risk of postoperative recurrence. Treatment strategies for recurrent HCC may play an important role in achieving better prognosis after operation, especially in patients with more than Child class B, cirrhosis, high values of indocyanine green retention-15, massive intraoperative blood loss, stage IV disease, positive surgical margin, vascular invasion, and postoperative complications.

Four resections for hepatic metastasis from gastric cancer: histochemical analysis of cell proliferation, apoptosis, and angiogenesis.

In a patient with gastric cancer (GC) associated with one synchronous and three metachronous hepatic metastases (HM), who underwent four hepatectomies, we carried out histochemical investigations regarding cell proliferation, apoptosis, and angiogenesis in the GC and HM. Tissue samples were taken from the primary GC and four HM. Ki-67 immunostaining was performed to evaluate cell proliferation and determine the labeling index (Ki-67 LI; ie, the percentage of cancer cells with nuclei stained for Ki-67). Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) was performed to evaluate apoptosis and determine the apoptotic index (ie, the percentage of TUNEL-positive cells), and immunostaining for factor VIII-related antigen was performed to evaluate angiogenesis and measure microvessel density (MVD). The Ki-67 LI was 43.2% in the primary GC and 39.9% in the synchronous HM, and the LI increased with the number of resections of metachronous HM. The apoptotic index was 3.36% in the primary GC, and 5.30% in the synchronous HM, and the index decreased after further resections of the metachronous HM. The MVD was 35 in the primary GC, and 22 in the synchronous HM, and it increased with the number of resections of metachronous HM. The primary GC in this patient may have strongly influenced the growth of HM through effects on cell proliferation, apoptosis, and angiogenesis.

A squamous cell carcinoma of the gastric cardia showing submucosal progression.

We report a case of squamous cell carcinoma (SCC) of the gastric cardia showing submucosal progression with direct invasion of the liver. A 71-year-old man was admitted with dysphagia. Esophagogastroscopy showed a protruding tumor covered with normal gastric mucosa in the anterior wall of the gastric cardia, although no abnormal findings were detected in the esophagus, including the esophagogastric junction. Serum SCC-related antigen level was elevated (6.6 ng/ml; normal level, less than 2.5 ng/ml). Endoscopic biopsy specimens taken from this tumor did not show malignant cells. Based on these findings, the preoperative diagnosis was a submucosal tumor of the stomach. Laparotomy was done; however, the tumor was not resected because it had direct invasion to the left lateral segment of the liver and adjacent tissues. As the tumor showed continuous bleeding from the stomach after surgery, total gastrectomy, combined with transhiatal lower esophagectomy, left lateral segmentectomy of the liver, splenectomy, and distal pancreatectomy was performed. Because histologic findings showed poorly or moderately differentiated SCC with direct invasion of the liver, the final diagnosis was SCC of the gastric cardia showing submucosal progression with hepatic invasion. Such a case of SCC of the gastric cardia showing submucosal progression is rare, and accurate preoperative diagnosis was very difficult. However, it may be important to consider SCC of the gastric cardia in such a situation.

Lipoteichoic acid induces preterm delivery in mice.

The purpose of this study was to determine whether or not lipoteichoic acid (LTA) could induce preterm delivery in mice. On days 15 and 17 of pregnancy, female C3H/HeN mice impregnated by male B6D2F1 mice were given intraperitoneal injections of LTA (12.5-75 mg/kg, single dose or repeated doses at a 3-h interval). We examined the changes in cervix, placental trophoblasts, and plasma and amniotic fluid concentrations of interleukin-1alpha (IL-1alpha), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) after dosing with LTA. In addition, the effect of LTA on the contraction of isolated uterine muscle from pregnant mice was also measured. The incidence of preterm delivery was highest (100%), when the pregnant animals were treated with 75 mg/kg LTA twice on day 15 of pregnancy or with 25 mg/kg LTA twice on day 17 of pregnancy. LTA-accelerated cervical ripening and placental abruption preceding the onset of preterm delivery, as well as increased plasma and amniotic fluid concentrations of IL-1alpha, IL-6, and TNF-alpha. Also, LTA increased contraction of uterine muscle strips. In conclusion, LTA induced preterm delivery in mice in the same manner as lipopolysaccharide (LPS), but the effective dose of LTA was larger than that of LPS.

Hepatic resection for large hepatocellular carcinoma.

BACKGROUND: Long-term survival and prognostic factors after hepatic resection for large hepatocellular carcinoma (HCC) remain to be proved. METHODS: The surgical outcome in 133 consecutive patients with HCC in diameter of > or = 5 cm (large HCC; L group) undergoing hepatic resection was retrospectively clarified and compared with that of 253 patients with HCC in diameter of < 5 cm (small HCC; S group). Postresection prognostic factors were evaluated by univariate and multivariate analysis using Cox's proportional hazards model. RESULTS: The disease-free 3- and 5-year survival rates between L group and S group were 26% versus 42% and 20% versus 25%, respectively (P = 0.0032). The overall 3- and 5-year survival rates between L group and S group were 38% versus 67% and 28% versus 47%, respectively (P < 0.0001). Multivariate analysis revealed that large amount of intraoperative blood transfusion was an independently significant factor of poor disease-free and overall survivals. CONCLUSIONS: Long-term survival in patients with large HCC remains unsatisfactory compared with that in patients with non-large HCC. Restriction of intraoperative blood transfusion may play an important role in the improvement of survival and recurrence in such patients.

Prostaglandin E1 reduces thromboxane A2 in hepatic ischemia-reperfusion.

BACKGROUND/AIMS: Prostaglandin E1 is well documented to exert cytoprotective effects in ischemia-reperfusion injury in the liver. This study was designed to evaluate the changes in prostanoid concentrations and to delineate the mechanism of the cytoprotective effect of prostaglandin E1 in hepatic ischemia-reperfusion injury. METHODOLOGY: Mongrel dogs were divided into 3 groups: a control group, an ischemia-reperfusion group (I-R group), and a group that received prostaglandin E1 and was then subjected to ischemia-reperfusion. Liver ischemia was produced for 60 min using the Pringle maneuver. The concentrations of aspartate aminotransferase, alanine aminotransferase, prostaglandin I2, thromboxane A2, and lipid peroxides in hepatic venous blood were examined before and after the Pringle maneuver in the latter 2 groups, and at the corresponding points in the control group. RESULTS: In the I-R group, aspartate aminotransferase and alanine aminotransferase after ischemia-reperfusion were significantly higher than those in the control group, and these values also rose significantly after ischemia-reperfusion in the prostaglandin E1-treated group. However, prostaglandin E1 administration suppressed significantly the increase compared with the I-R group. In the I-R group, prostaglandin I2, thromboxane A2, and lipid peroxide production in the liver increased 5 min after unclamping. The increases in thromboxane A2 and lipid peroxide production before and after ischemia-reperfusion were decreased, and prostaglandin I2 production was increased before ischemia-reperfusion in the group that was pretreated with prostaglandin E1. CONCLUSIONS: Prostaglandin E1 is involved protecting against warm ischemic liver damage by not only suppressing the increased thromboxane A2 production, but also by increasing prostaglandin I2 production.

Hepatic function immediately after hepatectomy as a significant risk factor for early recurrence in hepatocellular carcinoma.

BACKGROUND/AIMS: The aim of this study was to clarify the significant risk factors as they relate to early recurrence after hepatectomy in cirrhotic patients with hepatocellular carcinoma (HCC). METHODOLOGY: We retrospectively investigated 42 cirrhotic patients undergoing hepatectomy for a single HCC. We compared the clinicopathologic features of 14 patients with early intrahepatic recurrence (recurrence was detected within 1 year after hepatic resection; Group 1) with 28 patients without recurrence or with late intrahepatic recurrence (recurrence was confirmed more than 1 year after hepatic resection; Group 2). RESULTS: There were no significant differences in the pre-operative and intra-operative clinical background data or pathological data between the 2 groups. Regarding recurrence pattern, although not significant, the incidence of intrahepatic metastasis in Group 1 (85.7%) was higher than in Group 2 (50.0%). Maximum values of total bilirubin and albumin within 7 days after hepatectomy for patients in Group 2 were significantly better than those in Group 1. Aspatate aminotransferase (AST) and alanine aminotransferase (ALT) immediately after hepatectomy in Group 1 were also higher than in Group 2, although statistically insignificant. The overall 1-year and 3-year survival rates between Group 1 versus Group 2 were 85.7% versus 100% (p < 0.01) and 57.2% versus 90.0% (p < 0.01), respectively. CONCLUSIONS: Hepatic functional damage immediately after hepatectomy is as significant risk factor for early intrahepatic recurrence in cirrhotic HCC. Careful perioperative management of hepatic function may therefore be important in preventing early recurrence and prolonging survival.

Management of gastric cancer patients with synchronous hepatic metastasis: a retrospective study.

BACKGROUND/AIMS: In order to improve the management of patients of gastric cancer with synchronous hepatic metastasis, their records were retrospectively studied. MATERIALS AND METHODS: From January 1981 to July 1993, 558 gastric cancer patients were admitted in our institute. Twenty-five with synchronous hepatic metastasis were used in this study. Among these 25 patients, six had hepatic metastasis alone and nineteen had some other additional noncurative prognostic factors. For the primary lesion, 12 patients received gastrectomy (total or distal subtotal) and 13 patients did not. For the hepatic metastasis, 12 patients had regional therapy (hepatectomy or hepatic arterial chemotherapy) and 13 had not. Both gastrectomy and regional therapy for hepatic metastasis were carried out in 6 patients who had hepatic metastasis alone. RESULTS: Five year cumulative survival rate was 9%. Survival rate of patients with hepatic metastasis alone was significantly better than the patients with additional noncurative factors (p < 0.05). The two long term survivors in this study had no other noncurative factors except hepatic metastasis. CONCLUSIONS: Neither gastrectomy nor regional therapy for hepatic metastasis had beneficial effects on the patients with additional noncurative factors. Gastrectomy and regional therapy for hepatic metastasis should be performed in patients without additional noncurative factors.

Effects of prostaglandin E1 administration during hepatectomy for cirrhotic hepatocellular carcinoma.

BACKGROUND/AIMS: Prostaglandin E1 has been used in hepatectomy based on a few limited clinical studies suggesting that PGE1 improves liver function. The aim of this study was to evaluate the effects of PGE1 administration during hepatectomy for cirrhotic hepatocellular carcinoma. METHODOLOGY: Forty-three patients undergoing hepatectomy for cirrhotic hepatocellular carcinoma were divided into 2 groups: hepatectomy with Prostaglandin E1 treatment (PG group; n = 19) and without Prostaglandin E1 treatment (control group; n = 24). Prostaglandin E1 (0.02-0.07 microgram/kg/min) was administered intravenously from beginning to end of surgery in the PG group. RESULTS: There were no significant differences between groups with respect to age, gender, preoperative liver and renal function, or intraoperative variables such as blood loss, weight of resected liver and total clamping time by the Pringle maneuver. No patient had severe postoperative complications. Initial postoperative maximum concentrations of serum total bilirubin, creatinine, and blood urea nitrogen in the PG group were significantly lower than those in the control group. CONCLUSIONS: Prostaglandin E1 administration during hepatectomy for cirrhotic heptocellular carcinoma resulted in improved renal and hepatic function.