WordNet
- write by means of a keyboard with types; "type the acceptance letter, please" (同)typewrite
- a small metal block bearing a raised character on one end; produces a printed character when inked and pressed on paper; "he dropped a case of type, so they made him pick them up"
- (biology) the taxonomic group whose characteristics are used to define the next higher taxon
- a subdivision of a particular kind of thing; "what type of sculpture do you prefer?"
- all of the tokens of the same symbol; "the word `element contains five different types of character"
- printed characters; "small type is hard to read"
- identify as belonging to a certain type; "Such people can practically be typed" (同)typecast
- a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
- any of several vasoconstrictor substances (trade name Hypertensin) that cause narrowing of blood vessels (同)angiotonin, Hypertensin
- writing done with a typewriter (同)typewriting
PrepTutorEJDIC
- 〈C〉(…の)『型』,タイプ,類型,種類(kind)《+of+名》 / 〈C〉(その種類の特質を最もよく表している)『典型』,手本,模範《+of+名》 / 〈U〉《集合的に》活字;〈C〉(1個の)活字 / 〈U〉(印刷された)字体,活字 / 〈C〉(貨幣・メダルなどの)模様,図柄 / 〈C〉血液型(blood group) / …‘を'タイプに打つ / (…として)…‘を'分類する《+名+as+名(doing)》 / …‘の'型を決める / タイプライターを打つ
- =sense organ / 受信装置
UpToDate Contents
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- 1. 低アルドステロン症（4型RTA）の病因、診断、および治療 etiology diagnosis and treatment of hypoaldosteronism type 4 rta
- 2. 成人の非糖尿病性慢性腎臓病患者に対する降圧療法と病状の進展 antihypertensive therapy and progression of nondiabetic chronic kidney disease in adults
- 3. 高血圧治療におけるレニン・アンギオテンシン系阻害 renin angiotensin system inhibition in the treatment of hypertension
- 4. アンギオテンシン変換酵素阻害剤とアンギオテンシン受容体拮抗剤との相違 differences between angiotensin converting enzyme inhibitors and receptor blockers
- 5. 1型糖尿病における尿中アルブミンの中等度の上昇（微量アルブミン尿） moderately increased albuminuria microalbuminuria in type 1 diabetes mellitus
English Journal
- Angiotensin-(1-7) and angiotensin-(1-9): function in cardiac and vascular remodelling.
- McKinney CA1, Fattah C1, Loughrey CM1, Milligan G2, Nicklin SA1.Author information 1*Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, U.K.2†Institute of Molecular Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, U.K.AbstractThe RAS (renin-angiotensin system) is integral to cardiovascular physiology; however, dysregulation of this system largely contributes to the pathophysiology of CVD (cardiovascular disease). It is well established that AngII (angiotensin II), the main effector of the RAS, engages the AT1R (angiotensin type 1 receptor) and promotes cell growth, proliferation, migration and oxidative stress, all processes which contribute to remodelling of the heart and vasculature, ultimately leading to the development and progression of various CVDs, including heart failure and atherosclerosis. The counter-regulatory axis of the RAS, which is centred on the actions of ACE2 (angiotensin-converting enzyme 2) and the resultant production of Ang-(1-7) [angiotensin-(1-7)] from AngII, antagonizes the actions of AngII via the receptor Mas, thereby providing a protective role in CVD. More recently, another ACE2 metabolite, Ang-(1-9) [angiotensin-(1-9)], has been reported to be a biologically active peptide within the counter-regulatory axis of the RAS. The present review will discuss the role of the counter-regulatory RAS peptides Ang-(1-7) and Ang-(1-9) in the cardiovascular system, with a focus on their effects in remodelling of the heart and vasculature.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jun;126(12):815-27. doi: 10.1042/CS20130436.
- The RAS (renin-angiotensin system) is integral to cardiovascular physiology; however, dysregulation of this system largely contributes to the pathophysiology of CVD (cardiovascular disease). It is well established that AngII (angiotensin II), the main effector of the RAS, engages the AT1R (angiotens
- PMID 24593683
- Modulation of the action of insulin by angiotensin-(1-7).
- Dominici FP1, Burghi V1, Muñoz MC1, Giani JF2.Author information 1*IQUIFIB, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.2†Department of Biomedical Sciences and Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, U.S.A.AbstractThe prevalence of Type 2 diabetes mellitus is predicted to increase dramatically over the coming years and the clinical implications and healthcare costs from this disease are overwhelming. In many cases, this pathological condition is linked to a cluster of metabolic disorders, such as obesity, systemic hypertension and dyslipidaemia, defined as the metabolic syndrome. Insulin resistance has been proposed as the key mediator of all of these features and contributes to the associated high cardiovascular morbidity and mortality. Although the molecular mechanisms behind insulin resistance are not completely understood, a negative cross-talk between AngII (angiotensin II) and the insulin signalling pathway has been the focus of great interest in the last decade. Indeed, substantial evidence has shown that anti-hypertensive drugs that block the RAS (renin-angiotensin system) may also act to prevent diabetes. Despite its long history, new components within the RAS continue to be discovered. Among them, Ang-(1-7) [angiotensin-(1-7)] has gained special attention as a counter-regulatory hormone opposing many of the AngII-related deleterious effects. Specifically, we and others have demonstrated that Ang-(1-7) improves the action of insulin and opposes the negative effect that AngII exerts at this level. In the present review, we provide evidence showing that insulin and Ang-(1-7) share a common intracellular signalling pathway. We also address the molecular mechanisms behind the beneficial effects of Ang-(1-7) on AngII-mediated insulin resistance. Finally, we discuss potential therapeutic approaches leading to modulation of the ACE2 (angiotensin-converting enzyme 2)/Ang-(1-7)/Mas receptor axis as a very attractive strategy in the therapy of the metabolic syndrome and diabetes-associated diseases.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 May;126(9):613-30. doi: 10.1042/CS20130333.
- The prevalence of Type 2 diabetes mellitus is predicted to increase dramatically over the coming years and the clinical implications and healthcare costs from this disease are overwhelming. In many cases, this pathological condition is linked to a cluster of metabolic disorders, such as obesity, sy
- PMID 24450744
- Type 1 angiotensin receptors on macrophages ameliorate IL-1 receptor-mediated kidney fibrosis.
- Zhang JD, Patel MB, Griffiths R, Dolber PC, Ruiz P, Sparks MA, Stegbauer J, Jin H, Gomez JA, Buckley AF, Lefler WS, Chen D, Crowley SD.AbstractIn a wide array of kidney diseases, type 1 angiotensin (AT1) receptors are present on the immune cells that infiltrate the renal interstitium. Here, we examined the actions of AT1 receptors on macrophages in progressive renal fibrosis and found that macrophage-specific AT1 receptor deficiency exacerbates kidney fibrosis induced by unilateral ureteral obstruction (UUO). Macrophages isolated from obstructed kidneys of mice lacking AT1 receptors solely on macrophages had heightened expression of proinflammatory M1 cytokines, including IL-1. Evaluation of isolated AT1 receptor-deficient macrophages confirmed the propensity of these cells to produce exaggerated levels of M1 cytokines, which led to more severe renal epithelial cell damage via IL-1 receptor activation in coculture compared with WT macrophages. A murine kidney crosstransplantation concomitant with UUO model revealed that augmentation of renal fibrosis instigated by AT1 receptor-deficient macrophages is mediated by IL-1 receptor stimulation in the kidney. This study indicates that a key role of AT1 receptors on macrophages is to protect the kidney from fibrosis by limiting activation of IL-1 receptors in the kidney.
- The Journal of clinical investigation.J Clin Invest.2014 Apr 17. pii: 61368. doi: 10.1172/JCI61368. [Epub ahead of print]
- In a wide array of kidney diseases, type 1 angiotensin (AT1) receptors are present on the immune cells that infiltrate the renal interstitium. Here, we examined the actions of AT1 receptors on macrophages in progressive renal fibrosis and found that macrophage-specific AT1 receptor deficiency exacer
- PMID 24743144
Japanese Journal
- 小西賞受賞者 高血圧併用療法とCOPE Trial
- 山口医学 = Yamaguchi medical journal 64(1), 17-23, 2015-02
- NAID 120005601212
- Addition of a Nitric Oxide Donor to an Angiotensin II Type 1 Receptor Blocker May Cancel Its Blood Pressure-Lowering Effects
- International Heart Journal 56(6), 656-660, 2015
- NAID 130005113051
- Mechanisms of Cardiovascular Homeostasis and Pathophysiology – From Gene Expression, Signal Transduction to Cellular Communication –
- Circulation Journal 79(12), 2529-2536, 2015
- NAID 130005110902
Related Links
- ^ a b "Entrez Gene: AGTR2 angiotensin II receptor, type 2". ^ Ewert S, Laesser M, Johansson B, Holm M, Aneman A, Fandriks L (March 2003). "The angiotensin II receptor type 2 agonist CGP 42112A stimulates NO production in ...
- Receptor, angiotensin, type 1; Angiotensin II Type 1 Receptor; Angiotensin Type 1 Receptor; Angiotensin Type 1a Receptor; Angiotensin Type 1b Receptor; Receptor, Angiotensin, Type 1a; Receptor, Angiotensin, Type 1b. On-line ...
Related Pictures
★リンクテーブル★
| リンク元 | 「angiotensin II type 1 receptor」「angiotensin type 1 receptor」「1型アンジオテンシン受容体」 |
| 関連記事 | 「type」「typed」「typing」「angiotensin」 |
「angiotensin II type 1 receptor」
「angiotensin type 1 receptor」
「1型アンジオテンシン受容体」
「type」
- n.
- (windows)ファイル内容表示(linux -> cat])
- ex. type report_20111118.jp.htm | php a.php > report_20111118.jp.jp.jp.html
「typed」
- adj.
- 型の
「typing」
- n.
- タイプで打つこと、タイピング。分類
「angiotensin」