全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
- 1. 異型鎌状赤血球症候群 variant sickle cell syndromes
- 2. 異常ヘモグロビン症におけるマラリアに対する防御 protection against malaria in the hemoglobinopathies
- 3. 鎌状赤血球症における発熱のマネージメント management of fever in sickle cell disease
- 4. 鎌状赤血球症における赤血球輸血 red blood cell transfusion in sickle cell disease
- 5. 鎌状赤血球症における肝臓の症状 hepatic manifestations of sickle cell disease
- Low-dose chronic lead exposure increases systolic arterial pressure and vascular reactivity of rat aortas.
- Silveira EA1, Siman FD2, de Oliveira Faria T2, Vescovi MV3, Furieri LB2, Lizardo JH4, Stefanon I2, Padilha AS2, Vassallo DV2.Author information 1Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES CEP 29040-091, Brazil. Electronic address: firstname.lastname@example.orgDepartment of Physiological Sciences, Federal University of Espírito Santo, Vitória, ES CEP 29040-091, Brazil.3Center for Exact Sciences, Chemistry Department, Federal University of Espírito Santo, Vitória, ES CEP 29040-091, Brazil.4Department of Morphology, Federal University of Espírito Santo, Vitória, ES CEP 29040-091, Brazil.AbstractChronic lead exposure induces hypertension affecting endothelial function. We investigated whether low-concentration lead exposure alters blood pressure and vascular reactivity, focusing on the roles of NO, oxidative stress, cyclooxygenase-derived vasoconstrictor prostanoids, and the local angiotensin-renin system. Aortic rings from 3-month-old Wistar rats were treated daily with lead acetate (first dose 4mg/100g, subsequent doses 0.05mg/100g, im) or vehicle for 30 days. Treatment increased lead blood levels (12μg/dl), blood pressure, and aortic ring contractile response to phenylephrine (1nM-100mM). Contractile response after L-NAME administration increased in both groups but was higher after lead treatment. Lead effects on Rmax decreased more after apocynin and superoxide dismutase administration compared to control. Indomethacin reduced phenylephrine response more after lead treatment than in controls. The selective COX-2 inhibitor NS398, thromboxane A2/prostaglandin H2 receptor antagonist SQ 29,548, TXA2 synthase inhibitor furegrelate, EP1 receptor antagonist SC 19220, and ACE inhibitor and AT1 receptor antagonist losartan reduced phenylephrine responses only in vessels from lead-treated rats. Basal and stimulated NO release was reduced and local O2- liberation increased in the lead-treated group compared to controls. eNOS, iNOS, and AT1 receptor protein expression increased with lead exposure, but COX-2 protein expression decreased. This is the first demonstration that blood Pb2+ (12µg/dl) concentrations below the WHO-established values increased systolic blood pressure and vascular phenylephrine reactivity. This effect was associated with reduced NO bioavailability, increased reactive oxygen species production, increased participation of COX-derived contractile prostanoids, and increased renin-angiotensin system activity.
- Free radical biology & medicine.Free Radic Biol Med.2013 Dec 2. pii: S0891-5849(13)01526-8. doi: 10.1016/j.freeradbiomed.2013.11.021. [Epub ahead of print]
- Chronic lead exposure induces hypertension affecting endothelial function. We investigated whether low-concentration lead exposure alters blood pressure and vascular reactivity, focusing on the roles of NO, oxidative stress, cyclooxygenase-derived vasoconstrictor prostanoids, and the local angiotens
- PMID 24308934
- Cyclooxygenase-2 inhibition partially protects against 60% O2 -mediated lung injury in neonatal rats.
- Masood A, Yi M, Lau M, Belcastro R, Li J, Kantores C, Pace-Asciak CR, Jankov RP, Tanswell AK.Author information Lung Biology Programme, Physiology and Experimental Medicine, Hospital for Sick Children Research Institute, Toronto, Ontario, Canada; Department of Physiology, University of Toronto, Toronto, Ontario, Canada.AbstractRATIONALE: Use of the anti-inflammatory agent dexamethasone in premature infants with bronchopulmonary dysplasia has been curtailed, and no alternative anti-inflammatory agents are approved for this use. Our objective was to use a neonatal rat model of bronchopulmonary dysplasia to determine if an highly selective cyclooxygenase-2 inhibitor, 5,5-dimethyl-3-(3-fluorophenyl)4-(4-methylsulfonyl)phenyl-2(5H)-furanone (DFU; 10 µg/g body weight), could prevent inflammatory cell influx and protect against lung injury.
- Pediatric pulmonology.Pediatr Pulmonol.2013 Nov 23. doi: 10.1002/ppul.22921. [Epub ahead of print]
- RATIONALE: Use of the anti-inflammatory agent dexamethasone in premature infants with bronchopulmonary dysplasia has been curtailed, and no alternative anti-inflammatory agents are approved for this use. Our objective was to use a neonatal rat model of bronchopulmonary dysplasia to determine if an h
- PMID 24273102
- Prostaglandin E₂ receptor EP1-mediated phosphorylation of focal adhesion kinase enhances cell adhesion and migration in hepatocellular carcinoma cells.
- Bai X, Wang J, Zhang L, Ma J, Zhang H, Xia S, Zhang M, Ma X, Guo Y, Rong R, Cheng S, Shu W, Wang Y, Leng J.Author information Cancer Center, Department of Pathology, Nanjing Medical University, Nanjing 210029, PR China.AbstractThe prostaglandin E₂ (PGE₂) EP1 receptor has been implicated in hepatocellular carcinoma (HCC) cell invasion. However, little is known about the mechanisms of EP1 receptor-mediated cell adhesion and migration. We previously showed that PGE₂ promotes cell adhesion and migration by activating focal adhesion kinase (FAK). The present study was designed to elucidate the association between the EP1 receptor and FAK activation in HCC cells and to investigate the related signaling pathways. The effects of PGE₂, EP1 agonist 17-phenyl trinor-PGE₂ (17-PT-PGE₂), PKC and EGFR inhibitors on FAK activation were investigated by treatment of Huh-7 cells. Phosphorylation of FAK Y397 and c-Src Y416 was investigated by western blotting. Cell adhesion and migration were analyzed by WST and transwell assays, respectively. Protein kinase C (PKC) activity was measured with a PKC assay kit. The results showed that 17-PT-PGE₂ (3 µM) increased FAK Y397 phosphorylation by more than 2-fold and promoted cell adhesion and migration in Huh-7 cells. In transfected 293 cells, expression of the EP1 receptor was confirmed to upregulate FAK phosphorylation, while the EP1 receptor antagonist sc-19220 decreased PGE₂-mediated FAK activation. PKC activity and c-Src Y416 phosphorylation were enhanced after 17-PT-PGE₂ treatment. Both PKC and c-Src inhibitor suppressed the 17-PT-PGE₂-upregulated FAK phosphorylation, as well as 17-PT-PGE₂-induced cell adhesion and migration. In addition, exogenous epidermal growth factor (EGF) treatment increased FAK phosphorylation. The EGF receptor (EGFR) inhibitor also suppressed 17-PT-PGE₂-upregulated FAK phosphorylation. Our study suggests that the PGE₂ EP1 receptor regulates FAK phosphorylation by activating the PKC/c-Src and EGFR signal pathways, which may coordinately regulate adhesion and migration in HCC.
- International journal of oncology.Int J Oncol.2013 May;42(5):1833-41. doi: 10.3892/ijo.2013.1859. Epub 2013 Mar 20.
- The prostaglandin E₂ (PGE₂) EP1 receptor has been implicated in hepatocellular carcinoma (HCC) cell invasion. However, little is known about the mechanisms of EP1 receptor-mediated cell adhesion and migration. We previously showed that PGE₂ promotes cell adhesion and migration by activating fo
- PMID 23525457
- Effects of Imatinib Mesylate in Interstitial Cells of Cajal from Murine Small Intestine
- Kim Byung Joo,Chae Han,Kwon Young Kyu [他],Choi Seok,Jun Jae Yeol,Jeon Ju-Hong,So Insuk,Kim Seon Jeong
- Biological and Pharmaceutical Bulletin 33(6), 993-997, 2010
- … However, SC 19220 (an EP1 receptor antagonist) has no effects. …
- NAID 130000247967
- SC-19220, antagonist of prostaglandin E2 receptor EP1, inhibits osteoclastogenesis by RANKL
- 辻澤 利行
- 九州齒科學會雜誌 : Kyushu-Shika-Gakkai-zasshi 59(1), 付2-付3, 2005-03-25
- NAID 110006420762
- 1. プロスタグランジンE_2受容体EP1のアンタゴニスト,SC-19220は,RANKLによって誘導される破骨細胞形成を阻害する(9月例会講演抄録)
- 辻澤 利行
- 九州齒科學會雜誌 : Kyushu-Shika-Gakkai-zasshi 59(1), 40-41, 2005-03-25
- NAID 110006420758
- A selective of prostaglandin E2 (PGE2) at the EP1 receptor antagonist. 1 mg · 5 mg · 10 mg · 25 mg.
|リンク元||「8-chloro-dibenz(b,f)(1,4)oxazepine-10(11H)-carboxylic acid 2-acetylhydrazide」|