Reversible control of exo- and endo-budding transitions in a photosensitive lipid membrane.

We have developed a method for the photomanipulation of lipid membrane morphology in which the shape of a vesicle can be switched by light through the use of a synthetic photosensitive amphiphile containing an azobenzene unit (KAON12). We prepared cell-sized liposomes from KAON12 and 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) and conducted real-time observations of vesicular transformation in the photosensitive liposome by phase-contrast microscopy. Budding transitions-either budding toward the centre of the liposome (endo-bud) or budding out of the liposome (exo-bud)-could be controlled by light. We discuss the mechanism of this transformation in terms of the change in the effective membrane surface area due to photoisomerization of the constituent molecules.

Dynamic processes in endocytic transformation of a raft-exhibiting giant liposome.

The dynamic response of a raft-exhibiting giant liposome to external stimuli, such as the addition of Triton X-100 or osmotic stress, was studied. We observed that daughter vesicles are generated inside of the liposome through endocytic budding. It was found that the budding to generate daughter vesicles is classified into two different routes, simple budding through the invagination of a whole raft and budding from the boundary of a raft accompanied by waving motion. Smaller rafts show a preference for simple budding, whereas large rafts mainly adopt the other process. We discuss the mechanism of this difference in terms of the kinetic pathway of internalization by considering the line energy and bending energy of the membrane.

[A case report: Severe bone marrow suppression caused by 6-mercaptopurin in Crohn's disease patient].

A 23-year-old man was admitted for treatment of acute exacerbation of ileitis and perianal abscess caused by Crohn's disease. After incision and drainage of the abscess, coupled with antibiotic therapy, 6-mercaptopurine (6-MP) was commenced. His white blood cell (WBC) count on day 12 after initiation of 6-MP was not decreased. However, on day 24 he was re-admitted because of severe myelosuppression (WBC: 300/microl), which was complicated by the recurrence of the perianal abscess. Myelosuppression was prolonged and required the administration of granulocyte colony stimulating factor (G-CSF). G-CSF was continued for 17 days to achieve recovery of his WBC count to a normal level.

Survey of cattle fascioliasis in Tsuyama Abattoir.

OBJECTIVES: The aim of this study was to survey the prevalence of fascioliasis in slaughtered cattle in order to provide breeders with feedback which may prevent cattle fascioliasis, as well as human fascioliasis. METHODS: The results of meat inspection and the information extracted from the Discriminative Data Base on Individual Livestock in Japan were analyzed statistically in 6,224 cattle slaughtered at the Tsuyama Abattoir during the fiscal year 2002. RESULTS: The age-adjusted fascioliasis and cholangitis rates of all cattle were 2.0% and 7.2%, respectively. When analyzed by cattle breed, both rates were significantly higher in Japanese native cattle than in Holstein or Jersey (Chi-square test, p<0.01). The cattle raised in Okayama Prefecture, Tochigi Prefecture and Shimane Prefecture were significantly different from cattle raised in other prefectures in the age-adjusted fascioliasis and cholangitis rates. CONCLUSION: The age-adjusted fascioliasis and cholangitis rates of all cattle can be considered as nationwide rates for slaughtered cattle. The results of the comparisons suggest that cattle fascioliasis is related to feeding with rice straw and that the measures to prevent cattle fascioliasis might differ a mong prefectural governments.

Negative regulation of the protein kinase C activator-induced ICAM-1 expression in the human bronchial epithelial cell line NCI-H292 by p44/42 mitogen-activated protein kinase.

The role of p44/42 mitogen-activated protein kinase (MAPK) in the expression of intercellular adhesion molecule-1 (ICAM-1) in NCI-H292 cells, a human bronchial epithelial cell line, was analyzed. Treatment with the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol 13-acetate (TPA) (16.2 nM) or interferon-gamma (IFN-gamma) (100 U/ml) induced phosphorylation of p44/42 MAPK. The MEK inhibitor U0126 (0.1 to 10 microM) enhanced the TPA-induced ICAM-1 expression but not the IFN-gamma-induced one. U0126 also enhanced the ICAM-1 expression induced by two other PKC activators teleocidin (22.5 nM) and aplysiatoxin (14.9 nM). Furthermore, PD98059 (0.5 to 50 microM), another MEK inhibitor, enhanced the TPA-induced ICAM-1 expression as well. The inhibitor of p38 MAPK SB203580 did not affect the TPA-induced ICAM-1 expression. BAY11-7082, an inhibitor of nuclear factor kappaB (NF-kappaB) activation, and MG132, a 26S proteasome inhibitor, reduced the TPA-induced ICAM-1 expression but not the IFN-gamma-induced one. TPA partially decreased the level of IkappaB-alpha and the reduction was further augmented by U0126 in a concentration-dependent manner. These findings suggested that, in NCI-H292 cells, p44/42 MAPK suppresses PKC activator-induced NF-kappaB activation, thus negatively regulating the PKC activator-induced ICAM-1 expression but not the IFN-gamma-induced one.