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New fossil remains from the Pliocene Koetoi Formation of northern Japan provide insights into growth rates and the vertebral evolution of porpoises

100%

Murakami M., Shimada C., Hikida Y., Hirano H.

Acta Palaeontologica Polonica

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2015

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tom 60

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nr 1

Extant porpoises (Phocoenidae) are odontocetes characterized by their small size, short and wide rostrum, late (or absent) completion of epiphyseal ankylosis in the vertebral column (= physical maturity), and short life cycles, all of which are thought to have resulted from progenetic evolution. We describe a small fossil phocoenid from the lower Pliocene Koetoi Formation of Hokkaido (northern Japan), preserving a small, narrow rostrum, as well as anteroposteriorly elongate thoracic and lumbar vertebral centra with completely fused epiphyses. Physical maturity in this specimen occurred significantly earlier than in extant phocoenids, as shown by dental data indicating that the specimen died at only four years of age. The difference between the present material and extant porpoises may be attributable to different growth rates during ontogeny. The long centra and caudally inclined neural spines of the specimen from Hokkaido are primitive characters among phocoenids. By contrast, the great height of its neural spines is highly derived, even among extant species, and suggestive of a fast swimmer. In terms of its vertebral morphology, the new specimen falls within a morphological continuum defined by the archaic Numataphocoena yamashitai and the highly derived vertebral morphology of Phocoenoides dalli. Phocoenid vertebral evolution has been complex and frequently convergent, as opposed to stepwise and unidirectional. The different vertebral morphologies of the new specimen and the contemporaneous extinct taxa Numataphocoena and Piscolithax longirostris indicate that they were adapted to different environments.

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Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II

100%

Nakagiri A., Sunamoto M., Takeuchi K., Murakami M.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 2

Reactive oxygen species are known to be derived from NADPH oxidase in several tissues. Angiotensin II was suggested to be involved in the activation of NADPH oxidase; however, its role in the gastric mucosa is unclear. We examined the roles of angiotensin II receptor and NADPH oxidase in ischemia/reperfusion-induced gastric damage in rats. Under urethane anesthesia, male Sprague-Dawley rat stomachs were mounted in an ex-vivo chamber, had 100 mM HCl applied to them, and then a catheter was passed through the femoral vein. Ischemia/reperfusion was accompanied by blood collection and reperfusion through the catheter. Losartan, candesartan, valsartan, which are AT1 receptor blockers (ARB); PD123319, an AT2 receptor blocker; enalapril, an ACE inhibitor; or diphenylene iodonium, a NADPH oxidase inhibitor, was given i.v. 10 mins, and ß-NADPH, a NADPH oxidase substrate, was given i.v. 5 mins before reperfusion. The gastric damage by ischemia/reperfusion was attenuated by treatment with any of ARB or enalapril, but was not affected by PD123319. The increase in gastric H2O2 production and microvascular permeability by ischemia/reperfusion was also suppressed by treatment with any of ARB or enalapril. In rat gastric mucosa, the NADPH oxidase subunit p47phox was detected. Additionally, diphenylene iodonium had similar effects to ARB against ischemia/reperfusion-caused gastric damage, increased H2O2 production, and microvascular permeability. Ischemia/reperfusion activated NADPH oxidase in the gastric mucosa, and the activation was significantly attenuated by treatment with losartan or diphenylene iodonium. These results suggest that ischemia/reperfusion generated reactive oxygen species are derived from NADPH oxidase activation via AT1 receptor in rat stomachs.

3

Effects of indomethacin and rofecoxib on gastric mucosal damage in normal and Helicobacter pylori - infected Mongolian gerbils

100%

Kanatani K., Ebata M., Murakami M., Okabe S.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

This study examined the effects of indomethacin and rofecoxib on normal and Helicobacter pylori (H. pylori)-infected gastric mucosa of Mongolian (M.) gerbils. M. gerbils (6-wk-old) were orally administered H. pylori (ATCC43504, 2×108 CFU/ml) after fasting for 24 hours. Beginning 3 mo after inoculation, indomethacin (2 mg/kg, s.c) or rofecoxib (10 mg/kg, p.o.) was administered once daily for 2 wk to the gerbils. At autopsy, gastric mucosal ulcer area, myeroperoxidase (MPO) activity, prostaglandin (PG) E2 synthesis, and H. pylori viability were determined. Histamine-stimulated gastric acid secretion was measured with the acute gastric fistula method. Histological study was performed with H&E staining. H. pylori infection caused severe mucosal damage and production of lymphoid follicles in the gastric submucosa. In H. pylori-infected gerbils, indomethacin aggravated the gastric mucosal damage induced by H. pylori infection. Furthermore, indomethacin by itself induced gastric ulcers at an incidence of 6/10. In contrast, rofecoxib did not aggravate the H. pylori-induced mucosal damage. Indomethacin and rofeocoxib significantly reduced H. pylori viability. MPO activity was significantly increased in H. pylori-infected gerbils compared with H. pylori-uninfected gerbils. Indomethacin and rofecoxib reduced MPO activity in H. pylori-infected gerbils. PGE2 synthesis was markedly increased in H. pylori-infected gerbils (approximately 3-times) compared with the normal gerbils. Indomethacin significantly inhibited PGE2 synthesis in the gastric mucosa, both in normal and H. pylori-infected gerbils. Rofecoxib did not reduce PGE2 synthesis in normal gerbils, however, PGE2 synthesis was reduced to normal levels in H. pylori-infected gerbils. In H. pylori-infected gerbils, histamine-stimulated gastric acid secretion was reduced compared with normal gerbils. Indomethacin significantly increased histamine-stimulated gastric acid secretion and rofecoxib tended to increase secretion in H. pylori-infected gerbils. It was concluded that indomethacin enhances development of gastric mucosal damage in normal gerbils and aggravates H. pylori-induced gastric damage, resulting in gastric ulcers. Rofecoxib did not induce gastric damage in normal gerbils and did not aggravate damage in H. pylori-infected gerbils, suggesting that rofecoxib is less damaging to the stomach than indomethacin.

4

Glycoconjugates with NeuAc-NeuAc-Gal-Glc are more effective at preventing adhesion of Helicobacter pylori to gastric epithelial cells than glycoconjugates with NeuAc-Gal-Glc

100%

Hata Y., Murakami M., Okabe S.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 3

Helicobacter pylori (H. pylori) adheres to human gastric epithelial cells, eliciting various gastroduodenal diseases. Gangliosides play a critical role in bacterial adhesion to cell surfaces. The present study examined how residues of gangliosides are important for inhibition of adhesion of H. pylori to MKN-45 cells. We measured adhesion or detachment effects of gangliosides on the interaction between MKN-45 cells and H. pylori, as well as interleukin-8 production. Among the gangliosides, O-Ac-GD3, GT1b, GD1a, GD1b, GT1a, and GD3 had potent dose dependent inhibitory effects on adhesion of H. pylori to MKN-45 cells, interleukin-8 production, and vacuole formation induced by H. pylori toxin binding to Vero cells. GD3 also accelerated bacterial detachment of MKN-45 cells with adherent H. pylori in a dose dependent manner. Such results strongly suggest that the mechanism involved in the inhibition of H. pylori adhesion is mediated by the variations of the residues of the NeuAc-NeuAc-Gal-Glc chain of gangliosides. NeuAc-NeuAc-Gal-Glc exhibits a more inhibitory effect on adhesion than the NeuAc-Gal-Glc chain. Such gangioside and oligosaccrharide sequences appear to have therapeutic importance for prevention of H. pylori adhesion, as well as reduction of both inflammation and gastric mucosal injuries.

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Roles of endogenous prostaglandins and cyclooxygenase isozymes in mucosal defense of inflamed rat stomach

88%

Takeeda M., Hayashi Y., Yamato M., Murakami M., Takeuchi K.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

Endogenous prostaglandins (PGs) are involved in adaptive gastric protection against acute injury, and cyclooxygenase (COX)-1 is responsible for the production of PGs in this phenomenon. In the present study, we examined the effect of various COX inhibitors on gastric ulcerogenic and acid secretory responses following daily exposure of the stomach to iodoacetamide (IA) and investigated the role for COX isozyme in gastric protection under subchronic mucosal irritation. Gastric mucosal irritation was induced by addition of 0.1% IA to drinking water, and the gastric mucosa was examined on the 6th day. Indomethacin (5 mg/kg) or SC-560 (selective COX-1 inhibitor, 5 mg/kg) or rofecoxib (selective COX-2 inhibitor, 5 mg/kg) was given p.o. twice 24 hr and 3 hr before the termination of IA treatment. Giving IA in drinking water for 5 days produced minimal damage in the stomach. The damage was significantly worsened by indomethacin, resulting in hemorrhagic lesions. Both SC-560 and rofecoxib also aggravated such lesions, although the effect of rofecoxib was more pronounced. Treatment with IA decreased acid secretion in pylorus-ligated stomachs, and this change was significantly reverted by indomethacin as well as SC-560 and rofecoxib. Mucosal PGE2 content was increased following IA treatment, with apparent expression of COX-2 mRNA in the stomach, and the increased PGE2 production was significantly suppressed by SC-560 and rofecoxib as well as indomethacin. These results suggest that endogenous PGs derived from both COX-1 and COX-2 are involved in the mucosal defense of the inflamed stomach, partly by decreasing acid secretion and contribute to maintaining the mucosal integrity under such conditions.

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The reverse-direction method links mass experimental data to human diseases

64%

Ogura H., Atsumi T., Bando H., Sabharwal L., Yamada M., Jiang J.-J., Nakamura A., Arima Y., Kamimura D., Murakami M.

Archivum Immunologiae et Therapiae Experimentalis

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2014

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tom 62

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nr 1

7

Co-transfection of EYFP-GH and ECFP-rab3B in an experimental pituitary GH3 cell: a role of rab3B in secretion of GH through porosome

52%

Matsuno A., Itoh J., Mizutani A., Takekoshi S., Osmura R. Y., Okinaga H., Ide F., Miyawaki S., Uno T., Asano S., Tanaka J., Nakaguchi H., Sasaki M., Murakami M.

Folia Histochemica et Cytobiologica

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2008

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tom 46

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nr 4

419-421

Ograniczanie wyników

New fossil remains from the Pliocene Koetoi Formation of northern Japan provide insights into growth rates and the vertebral evolution of porpoises

Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II

Effects of indomethacin and rofecoxib on gastric mucosal damage in normal and Helicobacter pylori - infected Mongolian gerbils

Glycoconjugates with NeuAc-NeuAc-Gal-Glc are more effective at preventing adhesion of Helicobacter pylori to gastric epithelial cells than glycoconjugates with NeuAc-Gal-Glc

Roles of endogenous prostaglandins and cyclooxygenase isozymes in mucosal defense of inflamed rat stomach

The reverse-direction method links mass experimental data to human diseases

Co-transfection of EYFP-GH and ECFP-rab3B in an experimental pituitary GH3 cell: a role of rab3B in secretion of GH through porosome