Faculty Profiles - akihide Tanimoto

Papers - akihide Tanimoto

Division display 501 - 520 of about 561 ／ All the affair displays >>

自見政一郎, 佛坂正幸, 松本伸二, 藤井圭, 柴田恵介, 谷本昭英, 武田成彰 . 術前に診断しえた瘻孔形成を伴う回腸原発T細胞性悪性リンパ腫の1例 . 日本消化器外科学会雑誌36 ( 4 ) 289 - 293 2003.4

Publisher：(一社)日本消化器外科学会

症例は64歳男性で,便秘・右下腹部痛を主訴に,近医の注腸検査で回盲部腫瘍を指摘され,紹介入院となった.小腸造影透視では回腸末端に潰瘍性病変を認め,回腸末端と上行結腸の間には約6cmの瘻孔がみられた.ガリウムシンチでは右下腹部に集積を認め,大腸内視鏡検査では回腸末端に一部潰瘍形成を伴う全周性腫瘤を認めた.生検にてT細胞性悪性リンパ腫と診断し,右半結腸切除術を施行した.切除標本にて回腸末端に潰瘍性病変を認め,潰瘍性病変と上行結腸の間には瘻孔が確認された.病理組織学的に異型細胞は消化管壁内に限局し,免疫組織染色にてLCAおよびUCHL-I陽性,CD2,CD3,CD4,CD5,CD7陽性を示し,回腸原発T細胞性悪性リンパ腫stage Iと確診した.術後,CHOP療法を4クール行い,術後2年8ヵ月経過した現在,再発はみられない

Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2003&ichushi_jid=J01117&link_issn=&doc_id=20030417120008&doc_link_id=10.5833%2Fjjgs.36.289&url=https%3A%2F%2Fdoi.org%2F10.5833%2Fjjgs.36.289&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

LH Wu, A Tanimoto, Y Murata, T Sasaguri, JL Fan, Y Sasaguri, T Watanabe . Matrix metalloproteinase-12 gene expression in human vascular smooth muscle cells . GENES TO CELLS8 ( 3 ) 225 - 234 2003.3

Publisher：BLACKWELL PUBLISHING LTD

Background: Matrix metalloproteinases (MMPs) play an important role in smooth muscle cell (SMC) migration and proliferation during vascular remodelling. To investigate the expression of MMP-12 by SMCs, we examined the protein secretion and mRNA expression of MMP-12 by cultured medial SMCs and intimal SMCs derived from human aortic atherosclerotic lesions. To further elucidate the molecular mechanism for MMP-12 expression in SMCs, we determined the sequence requirements for MMP-12 gene transcriptional activity.
Results: Cultured medial SMCs and intimal SMCs showed substantial MMP-12 expression at both the protein and mRNA levels. A series of 5'-deletion and site-directed mutants of the human MMP-12 promoter demonstrated that an AP-1 site spanning -81 to -75 bp was critical for the MMP-12 promoter activity in SMCs. An electrophoretic mobility shift assay confirmed the AP-1 binding activity in SMCs and showed that the protein bound to the AP-1 site consisted predominantly of c-Jun, JunD and Fra-1. Two structurally different inhibitors of phosphatidylinositol 3-kinase, wortmannin and LY294002, inhibited MMP-12 transcriptional activity and AP-1 binding.
Conclusion: These results indicated the expression of MMP-12 in vascular SMCs and showed that the MMP-12 gene expression was dependent on the AP-1 binding activity. Phosphatidylinositol 3-kinase signalling may be involved in MMP-12 transcriptional activation through AP-1 binding activity.

Y Matsuki, A Tanimoto, T Hamada, Y Sasaguri . Histidine decarboxylase expression as a new sensitive and specific marker for small cell lung carcinoma . MODERN PATHOLOGY16 ( 1 ) 72 - 78 2003.1Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

Histidine decarboxylase is one of the enzymes of the amine precursor uptake and decarboxylation. system and is known to be distributed in mast cells and enterochromaffin-like cells. With the hypothesis that histidine decarboxylase expression is a marker for neuroendocrine differentiation, we studied the immunoreactivity of histidine decarboxylase in neuroendocrine cells and tumors of the thyroid gland, adrenal medulla, lung, and gastrointestinal tract. Formalin-fixed paraffin sections were subjected to immunohistochemistry using and histidine decarboxylase antibody, and the sensitivity and specificity were compared with those of conventional neuroendocrine markers (CD56, chromogranin A, synaptophysin, and neuron-specific enolase). Enterochromaffin or enterochromaffin-like cells, adrenal chromaffin cells, and thyroid C-cells were positive for histidine decarboxylase, and related tumors (carcinoid tumor, pheochromocytoma, medullary carcinoma) showed a high percentage of positive staining. Furthermore, we used the antibody to distinguish small cell lung carcinoma from non-neuroendocrine lung carcinoma and also to detect neuroendocrine differentiation in large-cell neuroendocrine carcinoma and gastrointestinal small-cell carcinoma. The anti-histidine decarboxylase antibody stained most small cell lung carcinoma (18 of 23, sensitivity 0.78), and was rarely reactive with non-neuroendocrine lung tumors (2 of 44; specificity, 0.95). These values were close to those obtained from CD56 staining (sensitivity/specificity, 0.87/0.98). Histidine decarboxylase was also positive for 6 of 12 large cell neuroendocrine carcinomas and 4 of 7 gastrointestinal small cell carcinomas. In conclusion, we demonstrated that histidine decarboxylase is useful to distinguish between small cell lung carcinoma and non-neuroendocrine carcinoma and to demonstrate neuroendocrine differentiation.

DOI： 10.1097/01.MP.0000044485.14910.3A

Sasaguri Y, Tanimoto A . Multi-functional roles of granulocyte macrophage-colony stimulating factor in atherosclerosis. . Journal of Japanese Colleage of Angiology43 585 - 594 2003Reviewed

R Padmanabhan, A Tanimoto, Y Sasaguri . Transactivation of human cdc2 promoter by adenovirus E1A . ADENOVIRUSES: MODEL AND VECTORS IN VIRUS-HOST INTERACTIONS272 365 - 397 2003Invited Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：SPRINGER-VERLAG BERLIN

Expression of the adenovirus oncoprotein E1A 12S induces the heterotrimeric transcription factor, NF-Y. NF-Y binds to the two CCAAT motifs upstream of the transcriptional start site of the human cdc2 promoter and is required for activation of the promoter by El A 12S in cycling cells. The observations that a number of eukaryotic cell cycle regulatory genes also contain the CCAAT motifs and NF-Y binds to them support the notion that E1A 12S could play an important role in deregulated expression of these genes through activation of NF-Y gene in cycling cells.

笹栗靖之, 谷本昭英 . 【動脈硬化と細胞外マトリックス】動脈硬化における細胞外マトリックスとマトリックスメタロプロテアーゼの役割(Atherosclerosis and Extracellular Matrix Extracellular Matrix and Matrix Metalloproteinases in Atherosclerosis) . Connective Tissue34 ( 4 ) 327 - 336 2002.12Reviewed

T Morishita, M Tsutsui, H Shimokawa, M Horiuchi, A Tanimoto, O Suda, H Tasaki, PL Huang, Y Sasaguri, N Yanagihara, Y Nakashima . Vasculoprotective roles of neuronal nitric oxide synthase . FASEB JOURNAL16 ( 12 ) 1994 - + 2002.10Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：FEDERATION AMER SOC EXP BIOL

Nitric oxide (NO) has multiple important actions that contribute to the maintenance of vascular homeostasis. NO is synthesized by three different isoforms of NO synthase (NOS), all of which have been reported to be expressed in human atherosclerotic vascular lesions. Although the regulatory roles of endothelial NOS (eNOS) and inducible NOS (iNOS) on the development of atherosclerosis have been described, little is known about the role of neuronal NOS (nNOS). Here, we show that nNOS also exerts important vasculoprotective effects in vivo. In a carotid artery ligation model, nNOS gene-deficient (nNOS-KO) mice exhibited accelerated neointimal formation and constrictive vascular remodeling caused by blood flow disruption. In a rat balloon injury model, the selective inhibition of nNOS activity potently enhanced vasoconstrictor responses to a variety of calcium-mobilizing stimuli, suppressed tissue cGMP concentrations, a marker of vascular NO production, and exacerbated neointimal formation. In both models, nNOS was absent before injury and was up-regulated only after the injury, and was predominantly expressed in the neointima and medial smooth muscle cells. These results provide the first direct evidence that nNOS plays important roles in suppressing arteriosclerotic vascular lesion formation in vivo.

DOI： 10.1096/fj.02-0155fje

K Imada, T Sato, K Hashizume, A Tanimoto, Y Sasaguri, A Ito . An antiprogesterone, onapristone, enhances the gene expression of promatrix metalloproteinase 3/prostromelysin-1 in the uterine cervix of pregnant rabbit . BIOLOGICAL & PHARMACEUTICAL BULLETIN25 ( 9 ) 1223 - 1227 2002.9Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：PHARMACEUTICAL SOC JAPAN

Using a progesterone receptor antagonist, onapristone/ZK 98.299, we examined the in-vivo effects of progesterone on the function of uterine cervix during pregnancy. Onapristone was intravenously administered to pregnant rabbits on day 20 post coitum. After 24 h, the antiprogesterone increased the wet weight of the uterine cervix and decreased the DNA concentration in the cervix. In-situ hybridization also indicated that antiprogesterone augmented the expression of matrix metalloproteinase (MMP)-3/stromelysin-1 mRNA in the uterine cervix. These changes are very similar to those observed and reported thus far in ripened and dilated uterine cervix. These results suggest that during pregnancy, progesterone closely participates in the maintenance of the function of uterine cervix by preventing the production of MMPs and thereby destruction of extracellular matrix, and thus add support to the theory that antiprogesterone has the potential to accelerate for the uterine cervical ripening and dilatation.

DOI： 10.1248/bpb.25.1223

O Suda, M Tsutsui, T Morishita, A Tanimoto, M Horiuchi, H Tasaki, PL Huang, Y Sasaguri, N Yanagihara, Y Nakashima . Long-term treatment with N-omega-nitro-L-arginine methyl ester causes arteriosclerotic coronary lesions in endothelial nitric oxide synthase-deficient mice . CIRCULATION106 ( 13 ) 1729 - 1735 2002.9Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

Background-N-omega-nitro-L-arginine methyl ester (L-NAME) is widely used to inhibit endothelial synthesis of NO in vivo. However, it is controversial whether the long-term vascular effects Of L-NAME are mediated primarily by inhibition of endothelial NO synthesis. We addressed this point in mice that are deficient in the endothelial NO synthase gene (eNOS-KO mice).
Methods and Results-Wild-type and eNOS-KO mice received L-NAME in drinking water for 8 weeks. In wild-type mice, long-term treatment with L-NAME caused significant medial thickening and perivascular fibrosis in coronary microvessels but not in large coronary arteries. Importantly, in eNOS-KO mice, treatment with L-NAME also caused an extent of medial thickening and perivascular fibrosis in coronary microvessels that was comparable to that in wild-type mice and that was not prevented by supplementation Of L-arginine. Vascular NO and cGMP levels were not significantly reduced by L-NAME treatment, and no expression of inducible or neuronal NO synthase was noted in microvessels of eNOS-KO mice, suggesting an involvement of NO-independent mechanisms. Treatment with L-NAME caused an upregulation of vascular ACE and an increase in cardiac lucigenin chemiluminescence that were comparable in both strains and that were abolished by simultaneous treatment with temocapril (ACE inhibitor) or CS866 (angiotensin 11 type I receptor antagonist) along with the suppression of vascular lesion formation.
Conclusions-These results provide the first direct evidence that the long-term vascular effects Of L-NAME are not mediated by simple inhibition of endothelial NO synthesis. Direct upregulation of local ACE and increased oxidative stress appear to be involved in the long-term vascular effects Of L-NAME in vivo.

DOI： 10.1161/01.CIR.0000029749.16101.44

A Tanimoto, T Hamada, T Yamamoto, S Kimura, Y Matsuki, Y Sasaguri . MALT lymphoma with extreme plasma cell differentiation of the rectum . AMERICAN JOURNAL OF GASTROENTEROLOGY97 ( 7 ) 1860 - 1862 2002.7Reviewed International journal

R Narita, T Oto, Y Mimura, M Ono, S Abe, A Tabaru, Yoshikawa, I, A Tanimoto, M Otsuki . Biliary obstruction caused by intrabiliary transplantation from hepatocellular carcinoma . JOURNAL OF GASTROENTEROLOGY37 ( 1 ) 55 - 58 2002.1Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：SPRINGER-VERLAG TOKYO

A rare autopsy case of hepatocellular carcinoma (HCC) presenting as extrahepatic bile duct obstruction is reported. A 54-year-old man who had been treated at another hospital for obstructive jaundice was referred to our hospital and admitted on March 1, 1998, because of progressive jaundice. On hospital day 94, he died of bleeding esophageal varices. At autopsy, a bile duct tumor, measuring 3.0 X 3.5 cm and adhering to the wall of the left hepatic duct, occluded the common hepatic duct at the hilus. A tumor measuring 2.0 X 2.0 cm was found in the parenchyma of the left liver lobe. The parenchymal tumor was not continuous with the extrahepatic bile duct tumor. Histologically, the bile duct tumor and the parenchymal tumor of the left lobe were diagnosed as HCC. The bile duct tumor was attached to the mucosa of the bile duct with a thin stalk. No invasive growth into the submucosa was observed. The tumor may have been an intrabiliary transplantation from the HCC in the left lobe via the bile duct.

DOI： 10.1007/s535-002-8134-0

K Yoshimura, A Tanimoto, T Abe, M Ogawa, T Yutsudo, M Kashimura, S Yoshida . Shiga toxin 1 and 2 induce apoptosis in the amniotic cell line WISH . JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION9 ( 1 ) 22 - 26 2002.1Reviewed International journal

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE INC

Objective: The aim of this study was to evaluate the toxicity of Shiga toxin (Stx) 1 and 2 on amniotic cells in vitro.
Methods: WISH cells, which were derived from human amniotic cells, and Vero cells were cultivated with or without Stxs. After 24 hours of culture, cell viability was measured by Cell Counting Kit-8, and extracted DNA was electrophoresed on a 1% agarose gel. The morphologic changes were observed by Papanicolaou staining, and the apoptotic index (percentage of apoptotic nuclei per total nuclei) was calculated. Quantification of apoptotic cells was also measured by an enzyme-linked immunosorbent assay.
Results: The viability of WISH cells decreased in proportion to the concentrations of Stxs. Cellular ladder formation was observed by DNA electrophoresis of Stx-treated WISH cells, and the typical morphologic changes were observed by Papanicolaon staining. The proportion of apoptotic cells increased in response to Stxs.
Conclusions: Stxs injured WISH cells directly and induced apoptosis in vitro. WISH cells were as sensitive as Vero cells to Stxs and cell death occurred by apoptosis. (J Soc Gynecol Investig 2002;9:22-6) Copyright (C) 2002 by the Society for Gynecologic Investigation.

DOI： 10.1016/S1071-5576(01)00143-5

A Tanimoto, Y Murata, M Nomaguchi, S Kimura, N Arima, H Xu, T Hamada, Y Sasaguri . Histamine increases the expression of LOX-1 via H2 receptor in human monocytic THP-1 cells . FEBS LETTERS508 ( 3 ) 345 - 349 2001.11Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE BV

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a member of the scavenger receptor family, and is known to be expressed in monocytes/macrophaaes. We investigated the effect of histamine on the expression of LOX-1 in cells of the human monocytic leukemia cell line THP-1. Histamine as well as forskolin and dibutyryl cyclic AMP (Bt(2)-cAMP) stimulated the THP-1 monocytes to express the LOX-1 gene at the transcription level. This histamine effect on LOX-1 gene expression, via the histamine H2 receptor-mediated cAMP signal transduction pathway, was reduced after differentiation of the cells into macrophages, even though forskolin and Bt(2)-cAMP still enhanced the gene expression. The alteration of the responsiveness of LOX-1 expression to histamine was related to suppressed expression of the H2 receptor in THP-1 macrophages. The switch of the predominant class of histamine receptors between H1 and H2 would modulate the effects of histamine on LOX-1 gene expression in monocytes and macrophages, and therefore, would play a certain role in the inflammatory aspects of atherogenesis. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

DOI： 10.1016/S0014-5793(01)03073-3

S Higuchi, A Tanimoto, N Arima, H Xu, Y Murata, T Hamada, K Makishima, Y Sasaguri . Effects of histamine and interleukin-4 synthesized in arterial intima on phagocytosis by monocytes/macrophages in relation to atherosclerosis . FEBS LETTERS505 ( 2 ) 217 - 222 2001.9Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE BV

We investigated the localization of histidine decarboxylase (HDC), which is the rate-limiting enzyme that generates histamine from histidine, in human aorta/coronary artery. RT-PCR and immunohistochemical staining revealed that the HDC gene was expressed in monocytes/macrophages and T cells in the arterial intima but not in smooth muscle cells in either the arterial intima or the media. A luciferase promoter assay with U937 and Jurkat cells demonstrated that interleukin-4 (IL-4) inhibited the expression of the HDC gene. In contrast, among a scavenger receptor family, IL-4 as well as histamine upregulated U937 cells to express the LOX-1 gene but not the SR-A gene, which genes encode receptors that scavenge oxidized lipids. These findings suggest that histamine synthesized in the arterial wall participates in the initiation and progression of atherosclerosis and that IL-4 can act as an important inhibitory and/or stimulatory factor in the function of monocytes/macrophages modulated by histamine in relation to the process of atherosclerosis. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

DOI： 10.1016/S0014-5793(01)02823-X

LH Wu, A Tanimoto, Y Murata, JL Fan, Y Sasaguri, T Watanabe . Induction of human matrix metalloproteinase-12 gene transcriptional activity by GM-CSF requires the AP-1 binding site in human U937 monocytic cells . BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS285 ( 2 ) 300 - 307 2001.7Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：ACADEMIC PRESS INC

Matrix metalloproteinase-12 (MMP-12) is critical for the migration of monocytes/macrophages into inflammatory sites through the basement membranes. We previously reported that MMP-12 expression was initially induced by granulocyte macrophage colony-stimulating factor (GM-CSF) in human peripheral blood monocytes and U937 monocytic cells. To further elucidate the molecular mechanism for the regulation of MMP-12 expression by GM-CSF in monocytes, we determined the sequence requirements for the MMP-12 gene transcriptional response of U937 monocytic cells to GM-CSF by using luciferase reporter and electrophoretic mobility shift assays. A series of 5 ' -deletion and site-directed mutation of the human MMP-12 promoter demonstrated that an AP-1 site spanning the -81 to -75-bp region is critical for the induction of MMP-12 promoter activity by GM-CSF. The electrophoretic mobility shift assay revealed that AP-1 binding activity was increased by GM-CSF treatment and that the AP-1 complex induced by GM-CSF consisted of multiple Jun and Fos isoforms. These results indicate that MMP-12 expression in U937 monocytes was initially induced by GM-CSF through the AP-1 binding activity. (C) 2001 Academic Press.

DOI： 10.1006/bbrc.2001.5161

A Tanimoto, N Arima, R Hayashi, T Hamada, Y Matsuki, Y Sasaguri . Teratoid carcinosarcoma of the ovary with prominent neuroectodermal differentiation . PATHOLOGY INTERNATIONAL51 ( 10 ) 829 - 832 2001Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL PUBLISHING ASIA

We present what we believe to be only the second report of ovarian teratoid carcinosarcoma. The patient, a 59-year-old woman, was admitted to hospital complaining of a pelvic mass and of abdominal fullness. Advanced ovarian cancer was diagnosed, and a tumorectomy was done. The tumor occupied the pelvis, and metastasis was found in the liver and spleen. The solid tumor was composed of chondrosarcoma, squamous cell carcinoma, adenocarcinoma and malignant neuroectodermal components, which contained ganglioneuroblastoma-like and medulloepithelioma-like areas. Immunohistochemically, the neuroectodermal cells were positive for both neural and epithelial markers. This ovarian tumor consisted of frankly malignant components, with prominent neuroectodermal elements mixed with epithelial and mesenchymal elements in an organoid fashion; a quite rare tumor.

DOI： 10.1046/j.1440-1827.2001.01275.x

N Arima, A Tanimoto, T Hamada, Y Sasaguri, E Sasaki, T Shimokobe . MALT lymphoma arising in giant diverticulum of ascending colon . AMERICAN JOURNAL OF GASTROENTEROLOGY95 ( 12 ) 3673 - 3674 2000.12Reviewed

N Arima, A Tanimoto, R Hayashi, T Hamada, Y Sasaguri . Ovarian yolk sac tumor with virilization during pregnancy: Immunohistochemical demonstration of Leydig cells as functioning stroma . PATHOLOGY INTERNATIONAL50 ( 6 ) 520 - 525 2000.6Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL SCIENCE ASIA

A case is reported of yolk sac tumor occurring in the left ovary and complicated by pregnancy. The 22-year-old patient presented at 28 weeks gestation with virilization and elevated serum levels of testosterone and alpha-fetoprotein. The tumor showed the typical features of yolk sac tumor with a mixture of islands of Leydig cells. The accumulations of Leydig cells were well demarcated from the cellular components of the yolk sac tumor and were distributed throughout the tumor, although with predominant localization at the periphery. By immunohistochemistry the Leydig cells were intensely positive for vimentin and negative for cytokeratins, allowing clear distinction from the cell components of the yolk sac tumor, which were positive for cytokeratins and negative for vimentin. Testosterone was also identified in the cytoplasm of the Leydig cells. After tumor resection the testosterone and alpha-fetoprotein levels declined simultaneously; this, together with the immunohistochemical demonstration of testosterone, indicates that the Leydig cells were responsible for the endocrine manifestations. Furthermore, antibodies against inhibin alpha-subunit and calretinin could be used to detect the Leydig cells. The present case, a combination of yolk sac tumor and Leydig cells acting as a functioning stroma and causing virilization during pregnancy, is very rare.

DOI： 10.1046/j.1440-1827.2000.01073.x

KY Wang, N Arima, S Higuchi, S Shimajiri, A Tanimoto, Y Murata, T Hamada, Y Sasaguri . Switch of histamine receptor expression from H2 to H1 during differentiation of monocytes into macrophages . FEBS LETTERS473 ( 3 ) 345 - 348 2000.5Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE BV

It is known that histamine suppresses gene expression and synthesis of tumor necrosis factor alpha (TNF-alpha) induced by lipopolysaccharide (LPS) in human peripheral blood mononuclear monocytes (HPM) or alveolar macrophages via histamine H2 receptors. We investigated the effect of histamine and differentiation in macrophages an the expression and secretion of TNF-alpha TNF-alpha-converting enzyme (TACE), and histamine H1 and H2 receptors by use of a leukemia cell line, U937, and HPM. Differentiation of U937 and HPM cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced the H1 receptor expression and rather suppressed the H2 receptor, resulting in up-regulation of the histamine-induced expression and secretion of TNF-alpha, modulated via TACE. Therefore, histamine failed to inhibit up-regulated expression of TNF-alpha induced by LPS in macrophages. The switch from H2 to H1 receptors during differentiation in the monocyte/macrophage lineage could participate in the pathogenic processes of atherosclerosis and inflammatory reactions in the arterial wall. (C) 2000 Federation of European Biochemical Societies.

DOI： 10.1016/S0014-5793(00)01560-X

K Yoshimura, J Fujii, A Tanimoto, T Yutsudo, M Kashimura, SI Yoshida . Effects of Shiga toxin 2 on lethality, fetuses, delivery, and puerperal behavior in pregnant mice . INFECTION AND IMMUNITY68 ( 4 ) 2254 - 2258 2000.4Reviewed

Language：English Publishing type：Research paper (scientific journal) Publisher：AMER SOC MICROBIOLOGY

Shiga toxin 2 (Stx2) is produced by enterohemorrhagic Escherichia coli (EHEC) and is known as the major virulence factor of EHEC, The aim of this study was to evaluate the effects of Stx2 on (i) maternal lethality, (ii) fetuses, (iii) delivery period, and (iv) maternal behavior after delivery. Timed pregnant ICR mice were injected intravenously with Stx2 on day 5 of pregnancy (early stage) or on day 15 (late stage). In early-stage experiments, the number of normal fetuses of mice injected with Stx2 was significantly lower than that of control mice. In late-stage experiments, mothers injected with Stx2 delivered normal numbers of neonates, but could not take care of them. The lethal doses of Stx2 were not different for pregnant and nonpregnant female mice at either stage. We conclude that Stx2 is toxic to the fetus in early pregnancy and affects maternal puerperal behavior in late pregnancy.

DOI： 10.1128/IAI.68.4.2254-2258.2000

　 PREV - NEXT 　

1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29