Kelvin-Helmholtz turbulence associated with collisionless shocks in laser produced plasmas.

We report the experimental results of a turbulent electric field driven by Kelvin-Helmholtz instability associated with laser produced collisionless shock waves. By irradiating an aluminum double plane target with a high-power laser, counterstreaming plasma flows are generated. As the consequence of the two plasma interactions, two shock waves and the contact surface are excited. The shock electric field and transverse modulation of the contact surface are observed by proton radiography. Performing hydrodynamic simulations, we reproduce the time evolutions of the reverse shocks and the transverse modulation driven by Kelvin-Helmholtz instability.

Nitric oxide is a mediator of tachykinin NK3 receptor-induced relaxation in rat mesenteric artery.

1. The mechanism of vasodilatation induced by tachykinin peptides was studied in isolated mesenteric arteries of rats. 2. Senktide, a selective NK3 agonist, elicited potent endothelium-dependent relaxation of arteries precontracted with phenylephrine (10(-5) M), but an NK1 agonist did not. 3. A non-peptide NK3 antagonist, SR 142801, inhibited senktide-induced relaxation. However, a non-peptide NK1 antagonist, CP-96,345, and a peptide-based NK2 antagonist, L-659,877, had no effect on senktide-induced relaxation. 4. N omega-nitro-L-arginine (L-NOARG), a nitric oxide synthesis inhibitor, markedly attenuated the relaxant response to senktide. 5. These results suggest that the endothelium of rat mesenteric arteries possesses tachykinin NK3 receptors, and that NK3 agonist-induced vasodilatation is mediated by release of nitric oxide (NO) from the endothelium.

Hepatocellular carcinoma with obstructive jaundice successfully treated with a self-expandable metallic stent.

We report on a 71-year old man with hepatocellular carcinoma (HCC) whose obstructive jaundice was successfully treated with external irradiation and a self-expandable metallic stent (EMS); Wallstent; Schneider (Europe) AG, Bülach, Switzerland. He was admitted to our hospital because of jaundice. HCC was found in S8; the tumor had invaded the bile duct with growth in the common hepatic duct. Endoscopic nasobiliary drainage was performed with difficulty. Radiation therapy to the stenosis enabled us to place a Wallstent endoscopically. He survived without icterus for 1 year.

Effects of internal biliary bypass on the regulation of hepatic cholesterol 7alpha-hydroxylase activity in rats.

In order to re-evaluate the importance of the enterohepatic circulation of bile acid in the regulation of the activities of hepatic cholesterol 7alpha-hydroxylase, bile acid metabolism was examined in internal biliary bypass models of rats. A polyethylene tube was inserted into the common bile duct and another side of the tube was placed in the duodenum (DD), lower jejunum (JD), cecum (CeD), or transverse colon (CoD) as internal biliary bypass models and in the urinary bladder as an external biliary drainage (ED). After bile diversion for 7 days in each group, hepatic cholesterol 7alpha-hydroxylase activities, bile acid concentrations in bile, serum, and portal vein, biliary bile acid compositions, and intestinal absorption rates of infused labeled taurocholic acid were analyzed. Hepatic cholesterol 7alpha-hydroxylase activity was similar in the JD group compared with the DD group, however, it was significantly up-regulated in the CeD (227% of the DD group), CoD (312%), and ED groups (316%). Biliary, serum, and portal bile acid concentrations were not significantly changed in the DD, JD, and CeD groups but those were significantly lower in the CoD and ED groups compared with the DD group. The proportion of the secondary bile acids was significantly increased in the CeD group and was decreased in the CoD and ED groups. The absorption rate of taurocholic acid was almost 100%, 56%, and 23% in the JD, CeD, and the CoD group, respectively. As the cholesterol 7alpha-hydroxylase activity was not significantly changed in the JD group and the predominance of secondary bile acids did not suppress the enzyme activity in the CeD group, the luminal factor, which is absorbed in the presence of bile acids, and the bile acid metabolites are not likely the regulatory factor. The cholesterol 7alpha-hydroxylase activity seems to be primarily regulated by the intestinal absorption of bile acids and partly by the intestinal mucosal factor which is linked to the intestinal bile acid absorption.

Serum 7alpha-hydroxycholesterol levels during liver regeneration after hepatectomy in humans.

BACKGROUND/AIMS: Changes in bile acid synthesis during liver regeneration after hepatectomy is little known in humans. Since it has been reported that the serum 7 alpha-hydroxycholesterol levels reflect the hepatic bile acid synthesis and that the determination of bile acid synthesis is useful to assess the liver regeneration rate, we determined the serum 7 alpha-hydroxycholesterol level during liver regeneration after hepatectomy in clinical patients. METHODOLOGY: The serum 7 alpha-hydroxycholesterol levels were determined by gas-liquid chromatography-mass spectrometry-selected ion monitoring method before and on days 1, 3, 5, 7, 14 and 21 after hepatectomy in twenty consecutive patients. RESULTS: The 7 alpha-hydroxycholesterol levels became lower between days 1 and 7, were increased on day 14, and then decreased on day 21 after hepatectomy. The patients with preoperative external biliary drainage showed a higher serum 7 alpha-hydroxycholesterol level than those without biliary drainage before hepatectomy. The former showed lower serum 7 alpha-hydroxycholesterol levels than the latter throughout the 21 days after hepatectomy. In patients whose liver resection rate was more than 50%, the serum 7 alpha-hydroxycholesterol levels were kept lower until 21 days after hepatectomy compared with those whose liver was excised less than 50%. CONCLUSIONS: It is concluded that the patients who had preoperative biliary drainage or major hepatic resection seem to have less hepatic reserve capacity for bile acid synthesis after hepatectomy.

Differences in biliary lipid excretion after major hepatectomy in obstructive jaundiced rats with preoperative internal, external, or no biliary drainage.

Necessity of preoperative biliary drainage for patients with obstructive jaundice is still controversial. We recently reported that liver regeneration after major hepatectomy was better restored in a rat model of obstructive jaundice with preoperative internal biliary drainage than that without biliary drainage or with external biliary drainage. The aim of this study was to investigate the differences in biliary lipid excretion after hepatectomy in obstructive jaundiced rats with or without preoperative internal or external biliary drainage. After bile duct ligation for 7 days, rats were randomly divided into the three groups; obstructive jaundice-hepatectomy (OJ-Hx), internal biliary drainage-hepatectomy (ID-Hx), and external biliary drainage-hepatectomy (ED-Hx) groups. 70% hepatectomy and internal biliary drainage were carried out 7 days after biliary decompression in the latter two groups and without biliary decompression in the OJ-Hx group. On the day of and on days 1, 2, 3 and 7 after hepatectomy, the liver weight, DNA synthesis rate, biliary lipids excretion rates, and bile acid composition were determined. In the ID-Hx group, the DNA synthesis rate and relative liver weight were significantly higher than those of the OJ-Hx and ED-Hx groups. The excretion rates of biliary lipids were disturbed in the ED-Hx group compared with those in the ID-Hx group and the values in the OJ-Hx group were in-between the ID-Hx and ED-Hx group. The liver regeneration rate was significantly correlated with bile flow and excretion rates of biliary lipids. The maintenance of enterohepatic circulation of biliary lipids before hepatectomy may be important for the liver regeneration.

Suppression and enhancement of the Freund's incomplete adjuvant-induced writhing reaction by sodium ascorbate in mice.

We noticed that an intraperitoneal injection of Freund's incomplete adjuvant (FIA) into mice could stimulate the induction of a writhing reaction. The FIA emulsion-induced writhing reaction was found to be remarkably inhibited by preadministration of oral indomethacin, a non-steroidal anti-inflammatory and analgesic drug. The induction of the writhing reaction was also inhibited by intravenous preadministration of sodium ascorbate (SAs) in saline. In the experiments where SAs was added to FIA, it was demonstrated that SAs had dual activity of suppression and enhancement. At lower concentrations SAs functioned as a suppressor of the writhing reaction, while at concentrations higher than about 1 mg/50 microl/mouse it acted as an enhancer of the reaction. Furthermore, this writhing reaction induced by FIA+SAs emulsion was also inhibited by preadministraion of SAs itself as well as indomethacin. These results suggested that the mechanism of the writhing reaction induced by FIA was concerned with the production of prostaglandins (PGs), and SAs might be involved in regulation of the writhing reaction. In this paper, we propose a mouse writhing model induced by FIA or FIA+SAs emulsion as a novel pain model useful for assessment of analgesic and anti-inflammatory agents.

Detection of anaphylactic reaction in the percutaneously sensitized mouse using the AW method.

Anaphylactic reactions of mice sensitized percutaneously with 2,4-dinitrofluorobenzene (DNFB) were investigated by the AW method assay, which is a mouse anaphylactic model using the abdominal wall as the site for induction with either 2,4-dinitrophenyl (DNP)-human serum albumin or anti-mouse IgE antibody and then estimation of the response. DNP-specific and IgE-dependent anaphylactic reaction after contact sensitization with DNFB could be induced and detected by the abdominal wall (AW) method assay in both groups with and without previous ear challenge with DNFB. Thus, the anaphylactic reaction in the group of twice-contact with 0.5% DNFB was observed on the 9th day from the sensitization (5th day from the ear challenge), and the reaction in the group of a single contact with 0.5% DNFB was observed 10 d after sensitization. The DNP-specific anaphylactic reaction was observed earlier than the 10th day with higher doses of DNFB. As for the mice of the former twice-contact group, the first and second characteristic ear swelling responses appeared within 1-6 h and 2 d of the ear challenge, respectively, and small swelling was observed 7 d after the challenge. It is suggested that Th1 and Th2 cells are activated at the almost same time, in other words, the preparation for both cell-mediated and humoral immunity could be accomplished to function, in vivo by a single percutaneous sensitization with DNFB.