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1.
Shigeki Takeura Hiizu Aoki Tatsuya Tsurumi Yukihiro Nishiyama Hisashi Fujioka Saiji Yoshii Koichiro Maeno 《Microbiology and immunology》1984,28(4):427-437
Host-dependent restriction of influenza B virus replication in L cells was analysed in comparison with productive infection in MDCK or 1–5C-4 cells. The synthesis and intracellular distribution of virus-specific proteins and the production of cytoplasmic ribonucleoproteins in nonpermissive L cells were similar to those in permissive MDCK cells. However, an electron microscopic study of infected L cells showed neither extracellular virions nor budding virus particles on the cell surface, in contrast to MDCK cells which produced numerous virus particles. PAGE analysis of the plasma membrane isolated from the cells demonstrated no significant difference in the composition of viral polypeptides between permissive 1-5C-4 and nonpermissive L cells. It was noted that the abortiveness of influenza B virus infection in L cells may be due to a defect in host cell function involved in the initiation of virus budding. 相似文献
2.
[3H]Dihydroergocryptine ([3H]DHE) was shown to bind to sites in membranes from neuroblastoma X glioma hybrid cells (NG 108-15) that had the characteristics expected of alpha-adrenergic receptors. The binding was saturable with 0.3 pmol [3H]DHE bound per mg of protein and of high affinity, with an apparent dissociation constant (KD) of 1.8 nM. The specificity of the binding site for various ligands was more similar to that of alpha 2 receptors than to that of alpha 1. No specific binding of [3H]WB-4101 was found in the membranes derived from NG 108 cells. This finding also indicated that the [3H]DHE binding site in the cell is the alpha 2 receptor. GTP lowered the affinity of agonists for the [3H]DHE binding site, although the nucleotide hardly affected the affinity of antagonists including [3H]DHE. 相似文献
3.
Tatsuya Matsunami Toshihiro Suzuki Yasuo Hisa Kuniaki Takata Tetsuro Takamatsu Masahito Oyamada 《Cell communication & adhesion》2006,13(1):93-102
To elucidate the role of the spiral limbus in glucose transport in the cochlea, we analyzed the expression and localization of GLUT1, connexin26, connexin30, and occludin in the spiral limbus of the rat cochlea. GLUT1 and occludin were detected in blood vessels. GLUT1, connexin26, connexin30, and occludin were also expressed in fibrocytes just basal to the supralimbal lining cells. Connexin26 and connexin30 were present among not only these GLUT1-positive fibrocytes but also GLUT1-negative fibrocytes. In vivo glucose imaging using 6-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-6-deoxyglucose (6-NBDG, MW 342) together with Evans Blue Albumin (EBA, MW 68,000) showed that 6-NBDG was rapidly distributed throughout the spiral limbus, whereas EBA was localized only in the vessels. Moreover, the gap junctional uncoupler heptanol inhibited the distribution of 6-NBDG. These findings suggest that gap junctions play an important role in glucose transport in the spiral limbus, i.e., that gap junctions mediate glucose transport from GLUT1-positive fibrocytes to GLUT1-negative fibrocytes in the spiral limbus. 相似文献
4.
Compression wood (CW) contains higher quantities of β-1-4-galactan than does normal wood (NW). However, the physiological
roles and ultrastructural distribution of β-1-4-galactan during CW formation are still not well understood. The present work
investigated deposition of β-1-4-galactan in differentiating tracheids of Cryptomeria japonica during CW formation using an immunological probe (LM5) combined with immunomicroscopy. Our immunolabeling studies clearly
showed that differences in the distribution of β-1-4-galactan between NW (and opposite wood, OW) and CW are initiated during
the formation of the S1 layer. At this stage, CW was strongly labeled in the S1 layer, whereas no label was observed in the S1 layer of NW and OW. Immunogold labeling showed that β-1-4-galactan in the S1 layer of CW tracheids significantly decreased during the formation of the S2 layer. Most β-1-4-galactan labeling was present in the outer S2 region in mature CW tracheids, and was absent in the inner S2 layer that contained helical cavities in the cell wall. In addition, delignified CW tracheids showed significantly more labeling
of β-1-4-galactan in the secondary cell wall, suggesting that lignin is likely to mask β-1-4-galactan epitopes. The study
clearly showed that β-1-4-galactan in CW was mainly deposited in the outer portion of the secondary cell wall, indicating
that its distribution may be spatially consistent with lignin distribution in CW tracheids of Cryptomeria japonica. 相似文献
5.
Madhusoodana P. Nambiar Tatsuya Oda Chaohua Chen Yasuo Kuwazuru Henry C. Wu 《Journal of cellular physiology》1993,154(2):222-228
The intracellular pathway following receptor-mediated endocytosis of cholera toxin was studied using brefeldin A (BFA), which inhibited protein secretion and induced dramatic morphological changes in the Golgi region. In both mouse Y1 adrenal cells and CHO cells, BFA at 1 μg/ml caused a 80–90% inhibition of the cholera toxin (CT)-elevation of intracellular cAMP. The inhibition of the cytotoxicity of CT by BFA was also observed in a rounding assay of Y1 adrenal cells. The inhibition of CT cytotoxicity by BFA was dose dependent, with the ID50 value similar to the LD50 of BFA in Y1 adrenal cells. Binding and internalization of [125I]-cholera toxin in Y1 adrenal cells was not affected by BFA. Unlike the BFA-sensitive cell lines such as Y1 adrenal and CHO cells, BFA at 1 μg/ml did not inhibit the cytotoxicity of CT in PtK1 cells, of which the Golgi structure was BFA-resistant. These results strongly suggest that a BFA-sensitive Golgi is required for the protection of CT cytotoxicity by BFA. In contrast, elevation of the intracellular cAMP by forskolin, which acts directly on the plasma membrane adenylate cyclase, was not affected by BFA. These observations indicate that the intoxication of target cells by CT requires an intact Golgi region for its intracellular trafficking and/or processing. In this respect, CT shares a common intracellular pathway with ricin, Pseudomonas toxin, and modeccin, even though their structures and modes of action are very different. © 1993 Wiley-Liss, Inc. 相似文献
6.
7.
M Kashimura M Okuno S Himeno T Kuroshima H Kawamoto Y Shinomura S Tarui 《Prostaglandins》1988,35(4):583-595
The effect of Prostaglandin D2 (PGD2) on ion transport was investigated in the rat colon in vitro. Ion transport across the intestinal mucosa was estimated by transmucosal potential difference (PD) and short circuit current (Isc) in the Ussing chamber. PGD2 added to the serosal reservoir induced a sustained reduction in PD and Isc at the concentration of higher than 10(-7)M, producing the maximal decrease at 10(-5)M. PGD2 at 10(-5)M completely blocked the increase in PD elicited by prostaglandin E1 (PGE1), theophylline, dibutyryl cAMP or serotonin. Adenylate cyclase activity was determined in the colonic mucosal homogenates after addition of PGD2 and PGE1. Treatment with PGD2 or PGE1 caused a significant increase in the enzyme activity. Combined treatment with both prostaglandins induced no more increase than that elicited by PGE1 alone. These results suggest that PGD2 has an anti-secretory effect on the rat colon and it may regulate the ion transport process through other mechanism than the modification of cyclic AMP concentration in mucosal cells. 相似文献
8.
Kato Yoji; Otsuki Tatsuya; Nakajima Tasuku; Ojima Kunihiko; Matsuda Kazuo 《Plant & cell physiology》1988,29(4):539-547
-Glucans (average mol wt, 1.3 ? 104) extracted with perchloricacid from 8-day-old suspension-cultured nonglutinous (var. Sasanishiki)and glutinous rice (var. Miyakogane) cells were compared. Theresults of hydrolysis by alpha;-, ß- and iso-amylasesand methylation analysis of the -glucans suggested that theirbasic structures are almost the same. These -glucans are highly-branchedpolysaccharides with an average chain length of about 910,with exterior and interior chain lengths of about 67and 23, respectively.
1Current address: Laboratory of Food Science, Faculty of Education,Hirosaki University, Hirosaki, Aomori 036, Japan. (Received April 27, 1987; Accepted March 2, 1988) 相似文献
9.
10.
Mechanism for enterohepatic injury caused by circulatory disturbance of hepatic vessels in the rat 总被引:3,自引:0,他引:3
S Kawamoto S Tashiro Y Miyauchi M Inoue 《Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)》1991,198(1):629-635
We reported previously that a transient occlusion followed by reperfusion of the portal vein and the hepatic artery of the rat significantly decreased the transhepatic transport of a cholephilic compound, and that this decrease was prevented by pretreating animals with poly(styrene co-maleic acid butyl ester)-conjugated superoxide dismutase (SM-SOD). To elucidate the mechanism for oxidative injury of the liver and the site for the generation of superoxide radicals, the effect of a portosystemic bypass on the liver function was examined in the rat whose hepatic vessels were temporarily occluded. A portosystemic bypass inhibited the reperfusion-induced decrease in hepatic transport of bromosulfophthalein as effectively as did SM-SOD. Kinetic analysis using 125I-labeled albumin revealed that the permeability of the small intestine markedly increased after a transient occlusion. The increase in intestinal permeability was also inhibited either by SM-SOD or by the portosystemic bypass. Xanthine oxidase activity in portal plasma markedly increased during occlusion and reperfusion, while it remained within normal ranges in the bypassed group. Thus, superoxide radical, and/or its metabolite(s), might play a critical role in increasing the intestinal permeability and in the pathogenesis of reperfusion-induced liver injury. 相似文献