Sanitation of seawater effluent from seaweed processing plants using a photo-catalytic TiO2 oxidation.

A fine porcelain open-cell photo-catalytic filter with titanium dioxide (TiO(2)) was evaluated for sterilization and sanitation of bio-polluted industrial water. In simulated seawater industrial effluent samples, the populations of Escherichia coli and Vibrio parahaemolyticus quickly decreased and reached non-detectable level within 10min. In seawater effluents from a seaweed processing plant, the bacterial populations in two samples quickly decreased by more than 10(3). In another two samples the decreases were slow and lowered by less than 10(2). Using fluorescence microscopy, it was indicated that the bacterial cells treated with photo-catalytic TiO(2) were damaged. In addition, the protein concentration in simulated seawater effluent slowly decreased using the photo-catalytic TiO(2) reaction; and reached similar concentrations as seawater near cultured seaweed beds. These results indicate that using a reactor with a TiO(2) photo-catalyst filter was effective for the sanitation of seawater effluents.

The rat pink-eyed dilution (p) mutation: an identical intragenic deletion in pink-eye dilute-coat strains and several Wistar-derived albino strains.

We identified the rat pink-eyed dilution (p) and pink eye Mishima (p(m)) mutations. The p(m) mutation, which was isolated from a wild rat caught in Mishima Japan in 1961 and is carried in the NIG-III strain, is a splice donor site mutation in intron 5. The p mutation, which was first described in 1914 and is carried in several p/p rats including the RCS and BDV strains, is an intragenic deletion including exons 17 and 18. In addition to RCS and BDV strains, several albino strains, KHR, KMI and WNA, all descendants of albino stock of the Wistar Institute, are homozygous for the p allele. Analyses revealed that the colored p strains and the Wistar-derived albino p strains had the same marker haplotype spanning approximately 4 Mb around the P locus. This indicates that these p strains share a common ancestor and the p allele did not arise independently via recurrent mutations. The historical relationship among the p strains suggests that the p deletion had been maintained in stock heterogeneous for the C and P loci and then was inherited independently by the ancestor of the Wistar albino stock and the ancestor of the pink-eyed agouti rats in Europe.

Study of portal vein thrombosis in patients with idiopathic portal hypertension in Japan.

BACKGROUND/AIMS: The aim of this study was to elucidate the incidence and clinical manifestations of portal vein thrombosis (PVT) in patients with idiopathic portal hypertension (IPH) in Japan during long-term follow-up. PATIENTS AND METHODS: Twenty-two patients with IPH were examined for PVT by sonography during a follow-up of 12+/-6 years. Clinical manifestations and patient outcome related to PVT were studied. Seventy patients with liver cirrhosis were examined by sonography as an incidence control of thrombosis. RESULTS: Nine IPH patients had portal thrombosis (9/22, 41%), a higher incidence than in liver cirrhosis patients (7/70, 10%). Those with thrombosis showed ascites, marked hypersplenism, and low serum albumin. Four patients with thrombosis died. Patients without thrombosis showed less clinical problems after long-term follow-up. Plasma antithrombin III and protein C activity decreased in almost half of the patients. However, there were no differences in these parameters between patients with and without thrombosis. CONCLUSIONS: In Japan, IPH patients had a high incidence of portal thrombosis, a significant factor for poor prognosis. Whether the management of PVT contributes to an improvement of a clinical course of IPH or not should be clarified in further study.

Sub-zero temperature inactivation of carboxypeptidase Y under high hydrostatic pressure.

High hydrostatic pressure induced cold inactivation of carboxypeptidase Y. Carboxypeptidase Y was fully active when exposed to subzero temperature at 0.1 MPa; however, the enzyme became inactive when high hydrostatic pressure and subzero temperature were both applied. When the enzyme was treated at pressures higher than 300 MPa and temperatures lower than -5 degrees C, it underwent an irreversible inactivation in which nearly 50% of the alpha-helical structure was lost as judged by circular dichroism spectral analysis. When the applied pressure was limited to below 200 MPa, the cold inactivation process appeared to be reversible. In the presence of reducing agent, this reversible phenomenon, observed at below 200 MPa, diminished to give an inactive enzyme; the agent reduces some of disulfide bridge(s) in an area of the structure that is newly exposed area because of the cold inactivation. Such an area is unavailable if carboxypeptidase Y is in its native conformation. Because all the disulfide bridges in carboxypeptidase Y locate near the active site cleft, it is suggested that the structural destruction, if any, occurs preferentially in this disulfide rich area. A possible mechanism of pressure-dependent cold inactivation of CPY is to destroy the alpha-helix rich region, which creates an hydrophobic environment. This destruction is probably a result of the reallocation of water molecules. Experiments carried out in the presence of denaturing agents (SDS, urea, GdnHCl), salts, glycerol, and sucrose led to a conclusion consistent with the idea of water reallocation.

Effect of cholecystokinin1 receptor antagonist loxiglumide (CR1505) on basal pancreatic exocrine secretion in conscious rats.

INTRODUCTION AND AIM: To examine the involvement of cholecystokinin (CCK) in the basal pancreatic exocrine, we investigated the effect of loxiglumide (CR1505), a CCK1 receptor antagonist, on basal pancreatic exocrine secretion in conscious rats. METHODOLOGY: After the basal collection of pancreatic juice for 1 hour, loxiglumide (10 mg/kg/h) or saline was infused via the femoral vein continuously for 2 hours. RESULTS: Loxiglumide significantly suppressed the basal pancreatic protein and amylase outputs. However, loxiglumide did not alter the basal pancreatic juice volume. CONCLUSIONS: These results demonstrate that loxiglumide suppresses basal pancreatic exocrine secretion in normal rats. They also suggest that CCK is involved in basal pancreatic exocrine in conscious rats and that loxiglumide may be useful as a therapeutic agent for pancreatitis, even during fasting, by attenuating the basal pancreatic exocrine burden on the pancreas.