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Background Chronic active Epstein–Barr virus infection (CAEBV) is defined as Epstein–Barr virus (EBV)-positive T/NK cell-related neoplasia, and its major clinical symptom is systemic inflammation presenting as infectious mononucleocytosis, whereas enteritis and diarrhea are minor clinical symptoms. The complex mixture of tumorigenic processes of EBV-positive cells and physical symptoms of systemic inflammatory disease constitutes the varied phenotypes of CAEBV. Herein, we describe a case of CAEBV that was initially diagnosed as Crohn’s disease (CD) based on ileal ulcers and clinical symptoms of enteritis. Case presentation A 19-year-old woman complained of abdominal pain and fever. Blood examination showed normal blood cell counts without atypical lymphocyte but detected modest inflammation, hypoalbuminemia, slight liver dysfunction, and evidence of past EBV infection. The esophagogastroduodenoscopic findings were normal. However, colonoscopy revealed a few small ulcers in the terminal ileum. The jejunum and ileum also exhibited various forms of ulcers, exhibiting a cobblestone appearance, on capsule endoscopy. Based on these clinical findings, she was strongly suspected with CD. In the course of treatment by steroid and biologics for refractory enteritis, skin ulcers appeared about 50 months after her initial hospital visit. Immunohistology of her skin biopsy revealed proliferation of EBV-encoded small RNA (EBER)-positive atypical lymphocytes. We retrospectively assessed her previous ileal ulcer biopsy before treatment and found many EBER-positive lymphocytes. Blood EBV DNA was also positive. Therefore, she was diagnosed with extranodal NK/T-cell lymphoma with CAEBV-related enteritis rather than CD. She was treated with cyclosporine and prednisolone combination therapy for CAEBV-related systemic inflammation and chemotherapy for malignant lymphoma. Unfortunately, her disease continued to progress, leading to multiple organ failure and death at the age of 23 years. Conclusion Clinicians need to remember the possibility of CAEBV as a differential diagnosis of refractory enteritis. Enteritis with intestinal ulcer is a rare symptom of CAEBV, and it is impossible to acquire a definitive diagnosis by ulcer morphology only. In cases where the possibility of CAEBV remains, tissue EBVR expression should be checked by in situ hybridization and blood EBV DNA.

Additional file 2: Supplementary Table S2. Clinical features of the reported CAEBV cases.

Additional file 1: Supplementary Table S1. Results of her blood test on the first admission.

Ancylostoma (A.) ceylanicum, one of the most common species of hookworms infecting dogs and cats, also causes patent infections in humans and is now considered to be the second most common hookworm species infecting populations in southeast Asia. A Japanese patient who returned from a visit to Thailand and Lao People's Democratic Republic (PDR) was presented with intermittent watery diarrhea with eosinophilia. Hookworm eggs were found in feces samples, and adult worms were confirmed to be present in the jejunum with capsule endoscopy and double balloon enteroscopy. A diagnosis of A. ceylanicum infection was made based on the morphology of the adult worms along with findings of a PCR-based molecular study using larvae obtained from a fecal sample culture. The infection was considered likely to have been obtained during a 1-month stay in a Laotian village, where the patient had eaten local food, worn sandals on bare feet, and lived as a local native villager, though he had stayed in modern hotels during the visit to Thailand.

Table S1. List of gene-specific primers used for PCR. (PDF 60Â kb)

Non-alcoholic fatty liver disease (NAFLD) represents one of the most common causes of chronic liver disease worldwide and is characterized by chronic liver inflammation and fibrosis leading to cirrhosis and increased risk of liver cancer in a proportion of patients. Effective anti-fibrotic agents have yet to be approved for the treatment of NAFLD. The present study aimed to evaluate the efficacy of dipeptidyl peptidase 4 inhibitors (DPP4-I) in the prevention of NAFLD progression in NAFLD patients with type 2 diabetes. The study was a single arm, multi-centre, non-randomised study of NAFLD patients with type 2 diabetes. NAFLD was diagnosed according to ultrasonographic findings. All the patients received 25 mg/day of alogliptin for 12 months. The efficacy of alogliptin in preventing NAFLD progression was assessed using overall NAFIC scores [non-alcoholic steatohepatitis (NASH), ferritin, insulin and type IV collagen 7S] and individual component scores according to baseline haemoglobin A1c (HbA1c) levels. Of the 39 patients enrolled in the study, 16 patients (40.3%) had NAFIC scores >2 points, indicating the presence of NASH. NAFIC scores markedly decreased following 12 months of alogliptin administration, but remained >2 points in 10 patients, indicating that NASH may have persisted in these patients. The relative risks for persistent NASH were 4.92 (95% confidence interval, 0.61–40.0) in the highest HbA1c tertile group compared with those in the lowest group. However, no statistically significant linear trend was observed across all HbA1c categories (P=0.145). DPP4-I may have efficacy against NAFLD progression in patients with type 2 diabetes with relatively lower HbA1c levels. DPP4-I may represent a potential new therapeutic strategy for the prevention of disease progression in NAFLD patients with type 2 diabetes.

Background: Occlusion due to tumor ingrowth is a major drawback in self-expandable metallic stents. Covering the stent is a probable solution to prevent tumor ingrowth. A manufactured covered self-expandable metallic stent, Covered Wallstent, has become commercially available. We evaluated the Covered Wallstent in a prospective uncontrolled multicenter setting. Methods: Between October 2001 and October 2003, 97 patients with common bile duct strictures deemed unfit for surgical resection underwent placement of a single Covered Wallstent, and were followed prospectively until April 2004. Results: Placement of the stent was successful in all the patients attempted. As a procedure-related complication, acute pancreatitis developed in four patients, in one of whom obstruction of the pancreatic duct orifice with the stent body seemed to be a major cause. The 30-day mortality was 9.3% (nine patients). Stent occlusion occurred in 22 patients as a late (greater than 30 days) complication, due to either tumor overgrowth (14 patients) or encrustation (eight patients). Distal migration of the stent was demonstrated in two other patients. No stent occlusions due to tumor ingrowth were observed. Patency rates of the stent for 3-, 6-, and 12-month periods were, respectively, 90.7, 82.5, and 45.9%. Conclusions: The present results in a large series suggest that placement of the Covered Wallstent is feasible and effective in the palliation of patients with malignant common bile duct strictures. The Covered Wallstent seems to be reliable in eliminating tumor ingrowth. The role of stent covering in promoting stent function should be examined in a prospective comparative study between covered- and uncovered Wallstents.

Cysteinyl leukotrienes (LTs) are potent proinflammatory mediators. They are predominantly excreted from blood by hepatobiliary elimination. To explore the clinical significance of biliary cysteinyl LTs, we determined their concentration changes in bile during treatment in patients with obstructive jaundice. Methods: Bile samples were obtained during endoscopic or transhepatic biliary drainage. Leukotrienes C4, D4, and E4 were quantified by two-step reversed-phase high-performance liquid chromatography and subsequent radioimmunoassay. Results: The increased excretion of cysteinyl LTs (LTC4 + LTD4 + LTE4) decreased between day 1 and 14 after drainage (means, 171 pmol/h to 79 pmol/h; P < 0.02). During drainage, the excretion was higher when there was additional cholangitis (mean, 225 and 86 pmol/h, with and without cholangitis, respectively; P < 0.001). The concentrations of LTD4 and LTE4 were also higher with additional cholangitis than without (LTD4, mean 6.0 vs 2.0 nM; P < 0.05; LTE4, 6.8 vs 2.4 nM; P < 0.02, respectively). Biliary LTC4 was detected only in patients with cholangitis. The biliary excretion of cysteinyl LTs was positively correlated with leukocyte concentration (r = 0.68; P < 0.005) and C-reactive protein (r = 0.73; P < 0.005) in blood. Furthermore, only in the absence of cholangitis, the excretion was positively correlated with serum γ-glutamyl transferase (r = 0.76; P < 0.02) and alanine aminotransferase (r = 0.72; P < 0.02). Conclusions: The excretion of biliary cysteinyl LTs increases with the severity of cholestasis and hepatic inflammation in patients with obstructive jaundice. An additional increase of cysteinyl LTs was observed during bacterial cholangitis. The increased biliary excretion of biologically active cysteinyl LTs may contribute to the aggravation of cholestasis and inflammatory reaction in obstructive jaundice.

Therapeutic efficacy of radiofrequency ablation (RFA) for colorectal liver metastases (CRLM) was compared with hepatic resection (HR), focusing on local disease control rate as well as risk factors of recurrence and patients survival.From April 2002 to March 2012, 32 patients underwent RFA and 60 patients underwent HR for CRLM. The rate of local recurrence along the ablated or resected margin was evaluated in these patients.The local recurrence was seen in 8 patients (13.3%) after HR, and 15 (46.9%) after RFA. Multivariate analysis of all patients revealed that RFA as an initial therapy (P0.001), venous invasion liver metastases (P = 0.049) were independent risk factors for local recurrence. Subgroup analysis showed that local recurrence rate after RFA was significantly higher than that after HR in patients with tumors 20 mm or larger (P0.001), while there was no significant difference in local recurrence rate between RFA and HR in patients with tumors less than 20 mm (P = 0.676).RFA showed a high risk of local recurrence in comparison to HR especially in patients with tumors larger than 20 mm. Indication of RFA should be restricted drastically considering the limitation of efficacy.

Background/aims Little is known about endotoxin clearance and secretion of cytokines from macrophages in liver cirrhosis. The aims of this study were to investigate the relationship of endotoxin clearance and release of tumor necrosis factor alpha by various macrophages to hepatic and renal disturbances in liver cirrhosis. Methods Male Sprague-Dawley rats were given 0.04% thioacetamide orally for 6 or 12 months. The organ distribution of infused [3H]-endotoxin (10 microg/kg b.w.) was analyzed at 30 min or at 24 h. Uptake of [3H]-endotoxin and secretion of tumor necrosis factor alpha by Kupffer cells, splenic macrophages and peripheral blood monocytes (1 x 10(4) cells/ml) from cirrhotic and control rats were determined. Results In cirrhotic rats, more endotoxin was left in the body and more endotoxin accumulated in the spleen and kidney, and thus was related to elevation of serum total bilirubin, aspartate aminotransferase, alanine aminotransferase, blood urea nitrogen, creatinine and tumor necrosis factor alpha. Endotoxin uptake and tumor necrosis factor alpha release by the Kupffer cells were decreased and those by the splenic macrophages and peripheral blood monocytes were increased in cirrhotic rats. Conclusions In liver cirrhosis, impaired clearance of endotoxin together with increased secretion of tumor necrosis factor alpha by extrahepatic macrophages may play an important role in the progression of hepatic and renal disturbances.

Background: Endotoxin plays an important role in the initiation and aggravation of alcoholic liver disease. In this study, we evaluated plasma endotoxin levels and serum concentrations of cytokines and lipopolysaccharide binding protein (LBP) during the acute and recovery phase of patients with alcoholic hepatitis; we also explored the prognostic factors associated with a fatal outcome. Methods: Fourteen patients, consisting of eight patients with alcoholic hepatitis (AH), five cirrhotics with superimposed AH (LC+AH), and one patient with severe alcoholic hepatitis (SAH), were studied. Among these, two with LC+AH died of hepatic failure. Results: Plasma endotoxin levels in the acute phase were higher in patients with AH (184.4 ± 159.4 pg/ml) and LC+AH (206.9 ± 174.9 pg/ml) than in healthy subjects (10.4 ± 5.5 pg/ml, p < 0.001). In particular, in one patient with SAH and one of two nonsurvivors, plasma cndotoxin levels were markedly high relative to the other cases. In most survivors, plasma endotoxin levels decreased in the recovery phase, whereas they further increased at the terminal stage in one of two nonsurvivors. Serum interleukin (IL)-6 and IL-8 levels in the acute phase were significantly higher in patients with AH and LC+AH as compared with healthy subjects. These levels were especially high in nonsurvivors and in one patient with SAH. IL-10 increased in two nonsurvivors, one patient with SAH, and one with LC+AH. In the recovery phase, these cytokine levels in survivors tended to decrease, but in nonsurvivors, IL-6 remained high, and IL-8 and IL-10 further increased. Tumor necrosis factor-a levels were below the detection limit throughout the course in all patients. Serum lipopolysaccharide binding protein (LBP) generally was elevated in the acute phase and decreased in the recovery phase in all survivors, but in one of the nonsurvivors, LBP was elevated markedly at the terminal stage. In the acute phase, plasma endotoxin levels were correlated positively with white blood cell counts, neutrophil counts, and serum IL-8. IL-8 was correlated positively with neutrophil counts and negatively with serum cholinesterase, hepaplastin test, and serum albumin levels. IL-6 was correlated positively with white blood cell and neutrophil counts, C-reactive protein, and serum total bilirubin and negatively with hepaplastin test and serum total protein levels. Serum LBP was correlated positively with white blood cell and neutrophil counts. Conclusions: Endotoxemia and related elevation of IL-8 may play an important role in the activation and migration of neutrophils in patients with alcoholic hepatitis. Marked elevation of inflammatory cytokines, IL-6 and IL-8, are related to severity and poor prognosis of alcoholic hepatitis. Serum LBP may serve as an index of inflammatory reaction in alcoholics.

Decreased effective circulating blood volume is an important factor in ascites formation in liver cirrhosis. We designed a "body compression" apparatus as a means to restore effective blood volume and investigated its effectiveness in reducing ascites formation in cirrhotics in terms of its effect on parameters of ascites formation noted below. The subjects, eight cirrhotics with ascites and eight cirrhotics without ascites were given spironolactone (50-75 mg/day) and furosemide (40-80 mg/day) while they received a diet containing 85 mEq of sodium per day. All four limbs and the lower abdomen were compressed with constant pressure [height (cm) divided by 13.6 mmHg] once, for 3h, using stroke rehabilitation splints, while patients lay supine. In cirrhotics both with and without ascites, urine volume, urinary sodium excretion, and creatinine clearance during the body compression were greater than values during control (non-compression) periods (urine volume, means 285 vs 169 ml/3h; P < 0.001, urinary sodium excretion 15.8 vs 9.5 mEq/3h; p < 0.001, creatinine clearance 74 vs 59 ml/min, P < 0.001, respectively). The increased basal plasma renin activity, angiotensin II, aldosterone, and norepinephrine levels in all cirrhotics were significantly decreased by the body compression. In another group of six cirrhotics who received no diuretics or albumin, repeat body compression alleviated ascites in three with well preserved renal function, but was ineffective in three with markedly impaired renal function. These results suggest that the improvement in renal function brought about by the body compression is attributable to an increase in effective circulating blood volume. This maneuver may be a useful complementary therapy in patients with cirrhotic ascites with well preserved renal function.

The pathogenesis of impaired water excretion in liver cirrhosis has not been fully elucidated.We induced an intravenous water overload of 20 ml/kg body weight in 10 cirrhotics without ascites (CLC), 11 cirrhotics with ascites (DLC), and 10 normal subjects (N) and investigated the relationship of plasma levels of substance P (SP), norepinephrine (NE), and antidiuretic hormone (ADH) to impaired water excretion.Free water clearance (CH2O) was lower in DLC (mean, 2.7 ml/min) than in N (8.3 ml/min; P0.001) and CLC (6.9 ml/min; P0.001). In DLC the creatinine clearance (CCr), maximal urine flow rate/CCr, (CH2O + CNa)/CCr, and mean arterial pressure (MAP) were significantly lower than in N and CLC. There was a progressive increase in basal SP, from lowest in N to CLC, to highest in DLC. Basal NE increased in CLC and DLC. Basal ADH did not differ among N, CLC, and DLC. In cirrhotics CH2O was correlated positively with serum albumin and cholinesterase and negatively with the retention rate of indocyanine green at 15 min. Basal SP was negatively correlated with CH2O (r= -0.71: P0.001) and MAP (r= -0.56; P0.005). Basal NE was correlated positively with basal SP (r= 0.67, P0.01 ).Decreased CH2O is closely related to the severity of the liver disturbance. Decreased CCr and reduced delivery of filtrate to the ascending limb of the loop of Henle secondary to an increased sodium reabsorption in the proximal tubule may play an important role in the impairment of water excretion. The increase in SP, which has a potent vasodilatory action, and the associated enhanced activity of the sympathetic nervous system may be responsible for the mild or moderate impairment of water excretion in the absence of nonosmotic hypersecretion of ADH in cirrhotics with ascites.

Using newly-designed primers for semi-nested reverse transcriptase-polymerase chain reaction to detect 5′-untranslated region of HGV GB-C hepatitis virus RNA, we screened 45 patients and found three HGV GB-C positive patients (with fulminant hepatitis and liver cirrhosis, and on hemodialysis). Restriction fragment length polymorphism and single-strand conformation polymorphism analysis revealed a similar pattern in all positive specimens. The sequence amplified by our primers might be a highly conserved sequence. We believe our primers are useful for screening of HGV GB-C virus RNA.

A 22-year-old man complaining of persisting high fever and right hypochondralgia was admitted to our hospital for infectious mononucleosis with splenic infarction detected by computed tomography. The splenic infarction deteriorated with a marked elevation of inflammatory parameters. This necessitated the commencement of methylprednisolone pulse therapy, resulting in prompt amelioration of inflammation and a reduction in cytokine levels. Including our case, only 9 cases of mononucleosis with splenic infarction have been reported to date; however, splenic infarction should be considered because it is a significant complication of infectious mononucleosis.

Background: Prostaglandin (PG) is reported to be involved in hepatic regeneration. However, little is known about the detailed relation in PG-induced stimulation of the proliferation. The present study was attempted to elucidate the relation. Methods: The serial change of PGE 2 level released from the regenerating rat liver and the effect of PGE 2 on the proliferation of rat hepatocytes were studied, with special reference to PGE 2 binding and cyclic AMP (cAMP). Results: The PGE 2 level increased 3 hours and 10 hours after partial hepatectomy. Timings of these increases seemed to coincide with those of the first and second increase of cAMP in the liver before the initiation of DNA synthesis. DNA synthesis of hepatocytes in primary culture between 24 and 36 hours, 36 and 48 hours, and 48 and 60 hours of culture were significantly enhanced by addition of PGE 2 between 4 and 24 hours of culture at concentrations of 2 nmol/L to 1 μmol/L, 2 nmol/L to 200 nmol/L, and 5 μmol/L to 10 μmol/L, and 2 nmol/L and 10 μmol/L, respectively. Enhancement of DNA synthesis with PGE 2 at concentrations less than 1 μmol/L seemed to be associated with the high-affinity binding and that at high concentrations with the lowaffinity binding. Intracellular cAMP level in the hepatocytes increased during culture, and its increase was enhanced by PGE 2 addition. Conclusions: It is suggested that PGE 2 production in the liver increases biphasically during hepatic regeneration and that PGE 2 enhances the proliferation of hepatocytes by a specific receptor-mediated process, which is largely associated with cAMP-dependent process.

Uptake of endotoxin and production of tumor necrosis factor (TNF) by Kupffer cells and splenic macrophages were measured in chronically alcohol-fed rats. Twenty male Sprague—Dawley rats, weighing 200–250 g, were pair-fed by isocaloric control and ethanol-containing Lieber—DeCarli liquid diets for 6 weeks. Endotoxin uptake and TNF production of Kupffer cells and splenic macrophages in the chronic ethanol load-group were significantly ( P < 0.001) greater than those in the control group. The increase in endotoxin uptake was more prominent in Kupffer cells and the increase in TNF production was more marked in splenic macrophages in the chronic ethanol group. When these cells were precultured in the medium containing 10–100 mM ethanol, the endotoxin uptake and TNF production of Kupffer cells isolated from control and chronic ethanol-fed rats were decreased in proportion to the concentration of ethanol in the culture medium. However, the addition of ethanol to the culture medium did not affect the endotoxin uptake and TNF production of splenic macrophages. These results support the hypothesis that the splenic macrophages are important for endotoxin uptake, and excessive production of TNF in rats given large amounts of alcohol.

To investigate the metabolic fate of endotoxin in alcoholics and its possible relationship to cytokines and liver injury, we administered a low-dose radiolabelled endotoxin to rats given alcohol in various conditions and studied the organ distribution of endotoxin and measured plasma levels of tumour necrosis factor (TNF). In the chronic alcohol-fed rats (Lieber-DeCarli liquid diets for 6 weeks) 3H-endotoxin was rapidly cleared by the liver and excreted into faeces. However, the endotoxin clearance was decreased after an acute ethanol load to rats (5 mg/g body wt ethanol i.p.) or in the chronic ethanol-fed rats with an additional 5 mg/g body wt ethanol load. Plasma TNF was not elevated in the control or in the acute ethanol load rats, slightly elevated in the chronic ethanol-fed rats and markedly elevated in the chronic ethanol-fed rats with an additional high-dose ethanol load. Serum GPT was elevated only in the chronic ethanol-fed rats with an additional high-dose ethanol. In conclusion, an additional administration of a high dose ethanol to chronic alcohol-fed rats led to decrease of endotoxin clearance and elevation of plasma TNF, which may play an important role in the pathogenesis of alcoholic hepatitis.

The effects of acetate on antibody production and cell-mediated immunity in mice were investigated. Polyclonal antibody responses could be enhanced in vivo by single intraperitoneal administration of acetate (5 mg/mouse) in C57BL/6 mice but not in DBA/2 mice. No enhancement of antibody production by acetate was also induced in athymic C57BL/6 nude mice and carrageenan-pretreated, macrophage-depleted mice. The inoculation of acetate-nonresponder BDF1 mice with T-cells and peritoneal adherent cells derived from acetate-treated C57BL/6 mice resulted in an enhanced antibody response. These results suggest that acetate increases polyclonal antibody responses in vivo by activating indirectly T-cells and macrophages. Acetate administration increased delayed hypersensitivity to pircryl chloride in C57BL/6 mice but not in DBA/2 mice. Allogeneic mixed lymphocyte reaction (MLR) of T-lymphocytes derived from the spleen of acetate-treated C57BL/6 mice was also enhanced. The natural killer (NK) activity and antibody-dependent cell-mediated cytotoxicity (ADCC) were also increased in C57BL/6 mice that were administered acetate. The possible mechanism of the immunopotentiating effect of this chemical is discussed.

Nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori infection are major causes of gastric mucosal lesions. In Japan, histamine-2 receptor antagonists are frequently prescribed, but the literature regarding their efficacy is limited. In this study, we compare the effects of famotidine and rebamipide on NSAID-associated gastric mucosal lesions using upper gastrointestinal endoscopy.This study examined 112 patients taking NSAIDs for either gastric hemorrhage or erosion. Before treatment, the patients were assessed by endoscopy. Using blind randomization, patients were divided into two groups: group F (famotidine, 20 mg/day) and group R (rebamipide, 300 mg/day). Efficacy was examined 4 weeks later using endoscopy.After treatment, the Lanza score decreased significantly in group F (P0.001) but not in group R (P = 0.478). The change in the Lanza score in group F was significantly greater (P = 0.002) than that in group R.Famotidine was superior to rebamipide in treating NSAID-associated mucosal lesions.

A 64-year-old man, who came to us with diarrhea, presented with ectodermal changes such as hyperpigmentation, alopecia, and onychatrophy, and was affected by polyposis in the colorectum and stomach. The polyps were histologically consistent with those in Cronkhite-Canada syndrome (CCS). Interestingly, the patient also had colon cancer, as well as portal thrombosis and a high concentration of antinuclear antibody. Treatment with prednisolone ameliorated the symptoms and the gastrointestinal polyposis, while the cancer was successfully treated with a hemicolectomy. Six months after the surgery, the patient developed nephropathy, with nephrotic-range proteinuria, without recurrence of the cancer. The biopsied renal specimen showed membranous glomerulonephritis. This is a rare case of CCS associated with various complications such as colon cancer, portal vein thrombosis, a high titer of antinuclear antibodies, and membranous glomerulonephritis. Although the pathogenesis of CCS is essentially unknown, these complications might have been indicative of an underlying immunological abnormality.

A 29-year-old woman with idiopathic portal hypertension was referred to our department for the surgical management of repetitive bleeding from esophageal and gastric varices. At the age of 16 years she had undergone a splenectomy with esophageal transection followed by endoscopic sclerotherapy which had been performed a total of 24 times. Although vericeal hemorrhage was prevented for several months, bleeding from gastric varices and portal hypertensive gastropathy was not able to be controlled readily by endoscopic sclerotherapy from when she was 26 years old. On admission, angiographic studies showed a complete obstruction of the portal vein; however, a portosystemic shunt operation was not able to be performed due to her previous splenectomy. To control her repetitive bleeding, we decided to perform a total gastrectomy and distal esophagectomy with reconstruction by a Roux-en-Y esophagojejunostomy. Her postoperative course was uneventful, and no episodes of recurrent bleeding or other complications have developed, indicating that her quality of life has dramatically improved. Thus, we conclude that distal esophagectomy and total gastrectomy constitute an effective surgical treatment for unshuntable extrahepatic portal hypertension.

To elucidate the cAMP′s bi-directional dual effect on hepatic regeneration with a special reference to RB protein, we studied the serial change of RB protein in the proliferating primary rat hepatocytes and the effect of dibutyryl cAMP (DBcAMP) on it. RB protein in the hepatocytes was down-regulated during the G 1 phase, and the highly phosphorylated / the underphosphorylated ratio of RB protein increased at the S phase. DBcAMP (1mM) addition, inhibitory on the DNA synthesis, enhanced this down-regulation, but did not increase the phosphorylated form of RB protein at the S phase. High dose of cAMP at the late G 1 -G 1 /S phase could block some essential events for G 1 /S transition including phosphorylation of RB protein.

The immunopharmacologic effects of Ringer's acetate on healthy persons and cancer patients were investigated. Enhancement of in vivo polyclonal antibody production in peripheral blood lymphocytes from healthy subjects and cancer patients was elicited after the intravenous administration of 500 ml Ringer's acetate solution. Allogeneic mixed lymphocyte reaction (MLR) and natural killer (NK) activity were also increased in the majority of healthy individuals and cancer patients when administered Ringer's acetate solution but not Ringer's lactate solution.

Specific bindings of [3H]prostaglandin E1 ([3H]PGE1), 125I-glucagon and [3H]norepinephrine to D-galactosamine (GalN)-treated rat hepatocytes in primary culture were investigated. After a two hour-treatment with GalN (1 and 10mg/ml), hepatocytes showed an enhanced specific binding to [3H]PGE1, whereas 125I-glucagon binding was little affected and [3H]norepinephrine binding was strongly diminished. Scatchard plot analysis indicated an increase of binding sites of [3H]PGE1. This unusual manner of [3H]PGE1 binding is suggested to indicate a special property of PGE1 receptor and may be associated with the cytoprotective effect of prostaglandins.

A plasma-derived HBV vaccine was administered to 86 healthy men ranging in age from 40–56 years. A relatively high rate of nonresponders was found among the men who received the HBV vaccine alone. There was a significantly higher HBs antibody response rate among the vaccinees who received an oral adjuvant (taurine) compared to those not receiving the adjuvant. In the vaccinees who received the oral adjuvant, an in vitro polyclonal antibody response to taurine was detected in 17 (58.6%) of the 29 HBs responders, but in none of the HBs nonresponders. The development of oral adjuvants other than aluminum may be a valuable approach to the study of HBV vaccination.