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Article ; Online: Expression, purification and preliminary crystallographic analysis of bacterial transmembrane protein EfeU for iron import.

Okumura, Kenji / Mikami, Bunzo / Oiki, Sayoko / Ogura, Kohei / Hashimoto, Wataru

2024 Volume 219, Page(s) 106487

Abstract: The bacterial Efe system functions as an importer of free ... ...

Abstract	The bacterial Efe system functions as an importer of free Fe
MeSH term(s)	Escherichia coli/genetics ; Escherichia coli/metabolism ; Crystallography, X-Ray ; Escherichia coli Proteins/genetics ; Escherichia coli Proteins/chemistry ; Escherichia coli Proteins/metabolism ; Escherichia coli Proteins/isolation & purification ; Iron/metabolism ; Iron/chemistry ; Gene Expression ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/metabolism ; Recombinant Proteins/biosynthesis ; Iron-Binding Proteins/chemistry ; Iron-Binding Proteins/genetics ; Iron-Binding Proteins/isolation & purification ; Iron-Binding Proteins/metabolism
Chemical Substances	Escherichia coli Proteins ; Iron (E1UOL152H7) ; Recombinant Proteins ; Iron-Binding Proteins
Language	English
Publishing date	2024-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1055455-5
ISSN	1096-0279 ; 1046-5928
ISSN (online)	1096-0279
ISSN	1046-5928
DOI	10.1016/j.pep.2024.106487
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Zs.A 3084: Show issues

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Article: Ethylene polymerization using

Kimura, Nanako / Takeuchi, Daisuke / Ogura, Sayoko / Takazawa, Ayaka / Kakiage, Masaki / Yamanobe, Takeshi / Uehara, Hiroki

Designed monomers and polymers

2023 Volume 26, Issue 1, Page(s) 182–189

Abstract: Various transition metal catalysts have been utilized for ethylene polymerization. Silver catalysts have attracted less attention as the catalysts, but are potential for production of high molecular weight polyethylene. Herein, we report that silver ... ...

Abstract	Various transition metal catalysts have been utilized for ethylene polymerization. Silver catalysts have attracted less attention as the catalysts, but are potential for production of high molecular weight polyethylene. Herein, we report that silver complexes with various
Language	English
Publishing date	2023-07-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2045059-X
ISSN	1568-5551 ; 1385-772X
ISSN (online)	1568-5551
ISSN	1385-772X
DOI	10.1080/15685551.2023.2229641
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Article ; Online: Antihypertensive drug therapy for women with non-severe hypertensive disorders of pregnancy: a systematic review and meta-analysis.

Ogura, Sayoko / Suzuki, Jun / Suzuki, Hiromichi

Hypertension research : official journal of the Japanese Society of Hypertension

2019 Volume 42, Issue 5, Page(s) 699–707

Abstract: Hypertensive disorders of pregnancy (HDP) represent a frequent disorder among pregnancies. Women with severe hypertension in pregnancy are at increased risk of maternal complications and require antihypertensive drug therapy. This study aimed to ... ...

Abstract	Hypertensive disorders of pregnancy (HDP) represent a frequent disorder among pregnancies. Women with severe hypertension in pregnancy are at increased risk of maternal complications and require antihypertensive drug therapy. This study aimed to systematically review randomized control trials of antihypertensive drug(s) treating non-severe hypertension during pregnancy to estimate the effectiveness and safety of this intervention. On May 8, 2018, we searched PubMed, Cochrane Library, and Ichu-Shi with no restriction on publication year. We selected randomized control trials that involved women with HDP being treated with antihypertensive drug(s) as intervention. Fourteen trials (1804 women) were identified for meta-analysis. There were no significant differences in the risk of maternal death (373 women; risk ratio (RR) 0.70; 95% confidence interval (CI) 0.04 to 11.45), proteinuria (1214 women; RR 1.00; 95% CI 0.67 to 1.49), side effects (360 women; RR 2.69; 95% CI 0.32 to 22.64), cesarean section (1239 women; RR 0.97; 95% CI 0.82 to 1.15), neonatal and birth death (1548 women; RR 0.80; 95% CI 0.43 to 1.49), preterm birth (904 women; RR 0.86; 95% CI 0.53 to 1.39), or small for gestational age infants (1082 women; RR 1.04; 95% CI 0.66 to 1.63) with antihypertensive drug therapy versus placebo or no treatment. The current review suggests that antihypertensive drug therapy does not reduce or increase the risk of maternal or perinatal outcomes. Further studies are needed to build reliable estimates of the effectiveness and safety of antihypertensive drug therapy for women with HDP.
MeSH term(s)	Antihypertensive Agents/therapeutic use ; Female ; Humans ; Hypertension, Pregnancy-Induced/drug therapy ; Pregnancy ; Pregnancy Outcome ; Randomized Controlled Trials as Topic ; Treatment Outcome
Chemical Substances	Antihypertensive Agents
Language	English
Publishing date	2019-01-09
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Systematic Review
ZDB-ID	1175297-x
ISSN	1348-4214 ; 0916-9636
ISSN (online)	1348-4214
ISSN	0916-9636
DOI	10.1038/s41440-018-0188-0
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Zs.A 3898: Show issues

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Article ; Online: Oxidative stress and organ damages.

Ogura, Sayoko / Shimosawa, Tatsuo

Current hypertension reports

2014 Volume 16, Issue 8, Page(s) 452

Abstract: Oxidative stress plays a pivotal role in various pathological conditions, including hypertension, pulmonary hypertension, diabetes, and chronic kidney disease, with high levels of oxidative stress in target organs such as the heart, pancreas, kidney, and ...

Abstract	Oxidative stress plays a pivotal role in various pathological conditions, including hypertension, pulmonary hypertension, diabetes, and chronic kidney disease, with high levels of oxidative stress in target organs such as the heart, pancreas, kidney, and lung. Oxidative stress is known to activate multiple intracellular signaling, which induces apoptosis or cell overgrowth, leading to organ dysfunction. As such, targeting oxidative stress is thought to be effective in protecting against organ damage, and measuring oxidative stress status may serve as a biomarker in diverse disease states. Several new intrinsic anti-oxidative or pro-oxidative factors have recently been reported, and are potential new targets. In the present review, we focus on diabetes, pulmonary hypertension, and renal dysfunction, and their relation with new targets - adrenomedullin, oxidized LDL, and mineralocorticoid receptor.
MeSH term(s)	Animals ; Apoptosis/physiology ; Diabetes Mellitus/metabolism ; Humans ; Hypertension/metabolism ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism ; Renal Insufficiency, Chronic/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2014-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2057367-4
ISSN	1534-3111 ; 1522-6417
ISSN (online)	1534-3111
ISSN	1522-6417
DOI	10.1007/s11906-014-0452-x
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Zs.A 5522: Show issues

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Article ; Online: Corrigendum to "Novel round cells in urine sediment and their clinical implications" [Clin. Chim. Acta 457 (2016) 142-149].

Shukuya, Kenichi / Ogura, Sayoko / Tokuhara, Yasunori / Okubo, Shigeo / Yatomi, Yutaka / Tozuka, Minoru / Shimosawa, Tatsuo

Clinica chimica acta; international journal of clinical chemistry

2017 Volume 472, Page(s) 104

Language	English
Publishing date	2017-09
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	80228-1
ISSN	1873-3492 ; 0009-8981
ISSN (online)	1873-3492
ISSN	0009-8981
DOI	10.1016/j.cca.2017.07.026
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Ud II Zs.173: Show issues

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Article ; Online: Targeting LOX-1 in atherosclerosis and vasculopathy: current knowledge and future perspectives.

Tian, Kunming / Ogura, Sayoko / Little, Peter J / Xu, Suo-Wen / Sawamura, Tatsuya

Annals of the New York Academy of Sciences

2018 Volume 1443, Issue 1, Page(s) 34–53

Abstract: LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1; also known as OLR1) is the dominant receptor that recognizes and internalizes oxidized low-density lipoproteins (ox-LDLs) in endothelial cells. Several genetic variants of LOX-1 are ... ...

Abstract	LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1; also known as OLR1) is the dominant receptor that recognizes and internalizes oxidized low-density lipoproteins (ox-LDLs) in endothelial cells. Several genetic variants of LOX-1 are associated with the risk and severity of coronary artery disease. The LOX-1-ox-LDL interaction induces endothelial dysfunction, leukocyte adhesion, macrophage-derived foam cell formation, smooth muscle cell proliferation and migration, and platelet activation. LOX-1 activation eventually leads to the rupture of atherosclerotic plaques and acute cardiovascular events. In addition, LOX-1 can be cleaved to generate soluble LOX-1 (sLOX-1), which is a useful diagnostic and prognostic marker for atherosclerosis-related diseases in human patients. Of therapeutic relevance, several natural products and clinically used drugs have emerged as LOX-1 inhibitors that have antiatherosclerotic actions. We hereby provide an updated overview of role of LOX-1 in atherosclerosis and associated vascular diseases, with an aim to highlighting the potential of LOX-1 as a novel theranostic tool for cardiovascular disease prevention and treatment.
MeSH term(s)	Atherosclerosis/drug therapy ; Biomarkers/metabolism ; Coronary Artery Disease/drug therapy ; Humans ; Risk Factors ; Scavenger Receptors, Class E/drug effects ; Scavenger Receptors, Class E/genetics ; Scavenger Receptors, Class E/metabolism
Chemical Substances	Biomarkers ; Scavenger Receptors, Class E
Language	English
Publishing date	2018-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/nyas.13984
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Article ; Online: Novel round cells in urine sediment and their clinical implications.

Shukuya, Kenichi / Ogura, Sayoko / Tokuhara, Yasunori / Okubo, Shigeo / Yatomi, Yutaka / Tozuka, Minoru / Shimosawa, Tatsuo

Clinica chimica acta; international journal of clinical chemistry

2016 Volume 457, Page(s) 142–149

Abstract: Background: Voided urine contains a variety of cells from the kidney and urinary tract and urinalysis provides us various information by investigating cellular components. We investigated urine sediment from renal impaired patients.: Results: We ... ...

Abstract	Background: Voided urine contains a variety of cells from the kidney and urinary tract and urinalysis provides us various information by investigating cellular components. We investigated urine sediment from renal impaired patients. Results: We found 'round cell' to be distinct from known cells in sediment and is close to proximal convoluted tubule-derived cells based on morphology and molecular marker expression (GGT1 but not podocalyxin). Also it was positive for undifferentiated cell markers, including PAX2, WT1, OSR1, and SIX2. They were observed in end-stage renal failure patients and the number of cells was correlated with the severity of chronic kidney disease. A prospective analysis revealed that patients who had more round cells were more likely to require hemodialysis within a year. Conclusion: Round cells are a novel marker that can be used to predict the need for hemodialysis.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Male ; Middle Aged ; Urinalysis ; Urine/cytology
Language	English
Publishing date	2016-06-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80228-1
ISSN	1873-3492 ; 0009-8981
ISSN (online)	1873-3492
ISSN	0009-8981
DOI	10.1016/j.cca.2016.04.017
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Article ; Online: Low-dose L-NAME induces salt sensitivity associated with sustained increased blood volume and sodium-chloride cotransporter activity in rodents.

Wang, Conghui / Kawakami-Mori, Fumiko / Kang, Lei / Ayuzawa, Nobuhiro / Ogura, Sayoko / Koid, Suang Suang / Reheman, Latapati / Yeerbolati, Alimila / Liu, Beibei / Yatomi, Yutaka / Chen, Xiangmei / Fujita, Toshiro / Shimosawa, Tatsuo

Kidney international

2020 Volume 98, Issue 5, Page(s) 1242–1252

Abstract: To investigate the cause of salt sensitivity in a normotensive animal model, we treated rats with a low-dose of the nitric oxide synthase inhibitor, L-NAME, that does not elevate blood pressure per se or induce kidney fibrosis. A high salt diet increased ...

Abstract	To investigate the cause of salt sensitivity in a normotensive animal model, we treated rats with a low-dose of the nitric oxide synthase inhibitor, L-NAME, that does not elevate blood pressure per se or induce kidney fibrosis. A high salt diet increased the circulating blood volume both in L-NAME-treated and nontreated animals for the first 24 hours. Thereafter, the blood volume increase persisted only in the L-NAME-treated rats. Blood pressure was higher in the L-NAME-treated group from the start of high salt diet exposure. Within the first 24 hours of salt loading, the L-NAME treated animals failed to show vasodilation and maintained high systemic vascular resistance in response to blood volume expansion. After four weeks on the high salt diet, the slope of the pressure-natriuresis curve was blunted in the L-NAME-treated group. An increase in natriuresis was observed after treatment with hydrochlorothiazide, but not amiloride, a change observed in parallel with increased phosphorylated sodium-chloride cotransporter (NCC). In contrast, a change in blood pressure was not observed in L-NAME-treated NCC-deficient mice fed a high salt diet. Moreover, direct L-NAME-induced NCC activation was demonstrated in cells of the mouse distal convoluted tubule. The vasodilatator, sodium nitroprusside, downregulated phosphorylated NCC expression. The effect of L-NAME on phosphorylated NCC was blocked by both the SPAK inhibitor STOCK2S-26016 and the superoxide dismutase mimetic TEMPO which also attenuated salt-induced hypertension. These results suggest that the initiation of salt sensitivity in normotensive rodents could be due to hyporeactivity of the vasculature and that maintaining blood pressure could result in a high circulating volume due to inappropriate NCC activity in the low-dose L-NAME model. Thus, even slightly impaired nitric oxide production may be important in salt sensitivity regulation in healthy rodents.
MeSH term(s)	Animals ; Blood Pressure ; Blood Volume ; Hypertension/chemically induced ; Mice ; NG-Nitroarginine Methyl Ester ; Rats ; Rodentia ; Sodium Chloride Symporters
Chemical Substances	Sodium Chloride Symporters ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2020-06-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2020.05.050
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Zs.A 797: Show issues

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Article ; Online: Pulmonary arterial hypertension in rats due to age-related arginase activation in intermittent hypoxia.

Nara, Akina / Nagai, Hisashi / Shintani-Ishida, Kaori / Ogura, Sayoko / Shimosawa, Tatsuo / Kuwahira, Ichiro / Shirai, Mikiyasu / Yoshida, Ken-ichi

American journal of respiratory cell and molecular biology

2015 Volume 53, Issue 2, Page(s) 184–192

Abstract: Pulmonary arterial hypertension (PAH) is prevalent in patients with obstructive sleep apnea syndrome (OSAS). Aging induces arginase activation and reduces nitric oxide (NO) production in the arteries. Intermittent hypoxia (IH), conferred by cycles of ... ...

Abstract	Pulmonary arterial hypertension (PAH) is prevalent in patients with obstructive sleep apnea syndrome (OSAS). Aging induces arginase activation and reduces nitric oxide (NO) production in the arteries. Intermittent hypoxia (IH), conferred by cycles of brief hypoxia and normoxia, contributes to OSAS pathogenesis. Here, we studied the role of arginase and aging in the pathogenesis of PAH in adult (9-mo-old) and young (2-mo-old) male Sprague-Dawley rats subjected to IH or normoxia for 4 weeks and analyzed them with a pressure-volume catheter inserted into the right ventricle (RV) and by pulsed Doppler echocardiography. Western blot analysis was conducted on arginase, NO synthase isoforms, and nitrotyrosine. IH induced PAH, as shown by increased RV systolic pressure and RV hypertrophy, in adult rats but not in young rats. IH increased expression levels of arginase I and II proteins in the adult rats. IH also increased arginase I expression in the pulmonary artery endothelium and arginase II in the pulmonary artery adventitia. Furthermore, IH reduced pulmonary levels of nitrate and nitrite but increased nitrotyrosine levels in adult rats. An arginase inhibitor (N(ω)-hydroxy-nor-1-arginine) prevented IH-induced PAH and normalized nitrite and nitrate levels in adult rats. IH induced arginase up-regulation and PAH in adult rats, but not in young rats, through reduced NO production. Our findings suggest that arginase inhibition prevents or reverses PAH.
MeSH term(s)	Aging ; Animals ; Arginase/metabolism ; Cell Hypoxia ; Enzyme Activation ; Hypertension/enzymology ; Lung/enzymology ; Male ; Nitrates/metabolism ; Nitric Oxide Synthase Type I/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Nitrites/metabolism ; Pulmonary Artery/enzymology ; Pulmonary Artery/physiopathology ; Rats, Sprague-Dawley ; Tyrosine/analogs & derivatives ; Tyrosine/metabolism
Chemical Substances	Nitrates ; Nitrites ; 3-nitrotyrosine (3604-79-3) ; Tyrosine (42HK56048U) ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, rat (EC 1.14.13.39) ; Arginase (EC 3.5.3.1)
Language	English
Publishing date	2015-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2014-0163OC
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Zs.A 2851: Show issues

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Article ; Online: LOX-1 in atherosclerosis: biological functions and pharmacological modifiers.

Xu, Suowen / Ogura, Sayoko / Chen, Jiawei / Little, Peter J / Moss, Joel / Liu, Peiqing

Cellular and molecular life sciences : CMLS

2012 Volume 70, Issue 16, Page(s) 2859–2872

Abstract: Lectin-like oxidized LDL (oxLDL) receptor-1 (LOX-1, also known as OLR-1), is a class E scavenger receptor that mediates the uptake of oxLDL by vascular cells. LOX-1 is involved in endothelial dysfunction, monocyte adhesion, the proliferation, migration, ... ...

Abstract	Lectin-like oxidized LDL (oxLDL) receptor-1 (LOX-1, also known as OLR-1), is a class E scavenger receptor that mediates the uptake of oxLDL by vascular cells. LOX-1 is involved in endothelial dysfunction, monocyte adhesion, the proliferation, migration, and apoptosis of smooth muscle cells, foam cell formation, platelet activation, as well as plaque instability; all of these events are critical in the pathogenesis of atherosclerosis. These LOX-1-dependent biological processes contribute to plaque instability and the ultimate clinical sequelae of plaque rupture and life-threatening tissue ischemia. Administration of anti-LOX-1 antibodies inhibits atherosclerosis by decreasing these cellular events. Over the past decade, multiple drugs including naturally occurring antioxidants, statins, antiinflammatory agents, antihypertensive and antihyperglycemic drugs have been demonstrated to inhibit vascular LOX-1 expression and activity. Therefore, LOX-1 represents an attractive therapeutic target for the treatment of human atherosclerotic diseases. This review aims to integrate the current understanding of LOX-1 signaling, regulation of LOX-1 by vasculoprotective drugs, and the importance of LOX-1 in the pathogenesis of atherosclerosis.
MeSH term(s)	Animals ; Atherosclerosis/drug therapy ; Atherosclerosis/metabolism ; Humans ; Lipoproteins, LDL/metabolism ; Scavenger Receptors, Class E/antagonists & inhibitors ; Scavenger Receptors, Class E/metabolism
Chemical Substances	Lipoproteins, LDL ; Scavenger Receptors, Class E ; oxidized low density lipoprotein
Language	English
Publishing date	2012-11-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-012-1194-z
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