WordNet
- cultivate by growing, often involving improvements by means of agricultural techniques; "The Bordeaux region produces great red wines"; "They produce good ham in Parma"; "We grow wheat here"; "We raise hogs here" (同)raise, farm, produce
- come to have or undergo a change of (physical features and attributes); "He grew a beard"; "The patient developed abdominal pains"; "I got funny spots all over my body"; "Well-developed breasts" (同)develop, produce, get, acquire
- become attached by or as if by the process of growth; "The tree trunks had grown together"
- become larger, greater, or bigger; expand or gain; "The problem grew too large for me"; "Her business grew fast"
- cause to grow or develop; "He grows vegetables in his backyard"
- increase in size by natural process; "Corn doesnt grow here"; "In these forests, mushrooms grow under the trees"; "her hair doesnt grow much anymore"
- (biology) the process of an individual organism growing organically; a purely biological unfolding of events involved in an organism changing gradually from a simple to a more complex level; "he proposed an indicator of osseous development in children" (同)growing, maturation, development, ontogeny, ontogenesis
- (pathology) an abnormal proliferation of tissue (as in a tumor)
- a progression from simpler to more complex forms; "the growth of culture"
- something grown or growing; "a growth of hair"
- vegetation that has grown; "a growth of trees"; "the only growth was some salt grass"
- limit, block, or decrease the action or function of; "inhibit the action of the enzyme"; "inhibit the rate of a chemical reaction"
- control and refrain from showing; of emotions, desires, impulses, or behavior (同)bottle up, suppress
- limit the range or extent of; "Contact between the young was inhibited by strict social customs"
- a substance that retards or stops an activity
PrepTutorEJDIC
- 『成長する』,育つ,〈植物が〉生える,茂る / (類・量・程などにおいて)『増大する』,大きくなる / 『しだいになる』 / …‘を'成長させる,大きくする,育てる / …から生じる(起こる)
- 〈U〉(…の)『成長』,発育;『発達』,発展《+『of』+『名』》 / 〈U〉(数・量,重要性・力などの)『増加』,増大,拡張《+『of』+『名』》 / 〈U〉《修飾語[句]を伴って》栽培,生産,…産 / 〈C〉成育した物,(草,木,髪,ひげなどの)生えたもの / 〈C〉腫瘍(しゅよう)
- 〈感情・欲望・行動・作用など〉‘を'抑制する / (…しないように)〈人〉‘を'抑制する,妨げる《+『名』+『from』+『名』(do『ing』)》
- 抑制する人(物) / 化学反応抑制剤
UpToDate Contents
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- 1. 小児における成長ホルモン欠乏症の治療 treatment of growth hormone deficiency in children
- 2. 血管新生阻害剤の概要 overview of angiogenesis inhibitors
- 3. インスリン様成長因子 Iの生理学 physiology of insulin like growth factor i
- 4. 成長ホルモンの生理学 physiology of growth hormone
- 5. 小児における成長ホルモン欠乏症の診断 diagnosis of growth hormone deficiency in children
English Journal
- Smad7 inhibits AngII-mediated hypertensive nephropathy in a mouse model of hypertension.
- Liu GX1, Li YQ1, Huang XR, Wei LH2, Zhang Y2, Feng M2, Meng XM2, Chen HY2, Shi YJ1, Lan HY.Author information 1*Department of Nephrology, Central Municipal Hospital of Huizhou, Huizhou, Guangdong, China.2‡Department of Medicine & Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.AbstractThe TGFβ (transforming growth factor β)/SMAD and NF-κB (nuclear factor κB) signalling pathways play a key role in hypertensive nephropathy. The present study examined whether targeting these pathways by SMAD7, a downstream inhibitor of both pathways, blocks AngII (angiotensin II)-induced hypertensive kidney disease in mice. A doxycycline-inducible SMAD7-expressing plasmid was delivered into the kidney by a non-invasive ultrasound-microbubble technique before and after AngII infusion. Results showed that pre-treatment with SMAD7 prevented AngII-induced progressive renal injury by inhibiting an increase in proteinuria and serum creatinine while improving the glomerular filtration rate. Similarly, treatment with SMAD7 in the established hypertensive nephropathy at day 14 after AngII infusion halted the progressive renal injury. These preventive and therapeutic effects of SMAD7 on hypertensive kidney injury were associated with inhibition of AngII-induced up-regulation of SMURF2 (SMAD-specific E3 ubiquitin protein ligase 2) and Sp1 (specificity protein 1), blockade of TGFβ/Smad3-mediated renal fibrosis and suppression of NF-κB-driven renal inflammation. Moreover, overexpression of SMAD7 also prevented AngII-induced loss of renal miR-29b, an miRNA with an inhibitory role in both TGFβ/Smad3 and NF-κB pathways. In conclusion, SMAD7 may be a therapeutic agent for AngII-mediated hypertensive nephropathy. Inhibition of the Sp1/SMAD3/NF-κB/miR-29b regulatory network may be a mechanism by which SMAD7 inhibits hypertensive nephropathy.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Aug 1;127(3):195-208. doi: 10.1042/CS20130706.
- The TGFβ (transforming growth factor β)/SMAD and NF-κB (nuclear factor κB) signalling pathways play a key role in hypertensive nephropathy. The present study examined whether targeting these pathways by SMAD7, a downstream inhibitor of both pathways, blocks AngII (angiotensin II)-induced hyperte
- PMID 24511990
- Thrombin induces ICAM-1 expression in human lung epithelial cells via c-Src/PDGFR/PI3K/Akt-dependent NF-κB/p300 activation.
- Cheng SE1, Lee IT2, Lin CC1, Hsiao LD2, Yang CM2.Author information 1*Department of Anesthetics, Chang Gung Memorial Hospital at Lin-Kou and College of Medicine, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan.2†Department of Physiology and Pharmacology and Health Ageing Research Center, College of Medicine, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan.AbstractUp-regulation of ICAM-1 (intercellular adhesion molecule-1) is frequently implicated in lung inflammation and lung diseases, such as IPF (idiopathic pulmonary fibrosis). Thrombin has been shown to play a key role in inflammation via the induction of adhesion molecules, which then causes lung injury. However, the mechanisms underlying thrombin-induced ICAM-1 expression in HPAEpiCs (human pulmonary alveolar epithelial cells) remain unclear. In the present study, we have shown that thrombin induced ICAM-1 expression in HPAEpiCs. Pre-treatment with the inhibitor of thrombin [PPACK (D-Phe-Pro-Arg-chloromethyl ketone)], c-Src (PP1), PDGFR (platelet-derived growth factor receptor) (AG1296), PI3K (phosohinositide 3-kinase) (LY294002), NF-κB (nuclear factor κB) (Bay11-7082) or p300 (GR343) and transfection with siRNAs of c-Src, PDGFR, Akt, p65 and p300 markedly reduced thrombin-induced ICAM-1 expression and monocyte adherence to HPAEpiCs challenged with thrombin. In addition, we established that thrombin stimulated the phosphorylation of c-Src, PDGFR, Akt and p65, which were inhibited by pre-treatment with their respective inhibitors PP1, AG1296, LY294002 or Bay11-7082. In addition, thrombin also enhanced Akt and NF-κB translocation from the cytosol to the nucleus, which was reduced by PP1, AG1296 or LY294002. Thrombin induced NF-κB promoter activity and the formation of the p65-Akt-p300 complex, which were inhibited by AG1296, LY294002 or PP1. Finally, we have shown that thrombin stimulated in vivo binding of p300, Akt and p65 to the ICAM-1 promoter, which was reduced by AG1296, LY294002, SH-5 or PP1. These results show that thrombin induced ICAM-1 expression and monocyte adherence via a c-Src/PDGFR/PI3K/Akt/NF-κB-dependent pathway in HPAEpiCs. Increased understanding of the signalling mechanisms underlying ICAM-1 gene regulation will create opportunities for the development of anti-inflammatory therapeutic strategies.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Aug 1;127(3):171-83. doi: 10.1042/CS20130676.
- Up-regulation of ICAM-1 (intercellular adhesion molecule-1) is frequently implicated in lung inflammation and lung diseases, such as IPF (idiopathic pulmonary fibrosis). Thrombin has been shown to play a key role in inflammation via the induction of adhesion molecules, which then causes lung injury.
- PMID 24506791
- Kisspeptin-10 induces endothelial cellular senescence and impaired endothelial cell growth.
- Usui S, Iso Y, Sasai M, Mizukami T, Mori H1, Watanabe T2, Shioda S3, Suzuki H1.Author information 1*Division of Cardiology, Showa University Fujigaoka Hospital, 1-30 Fujigaoka, Yokohama City, Kanagawa 227-8501, Japan.2§Laboratory of Cardiovascular Medicine, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.3†Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.AbstractThe KPs (kisspeptins) are a family of multifunctional peptides with established roles in cancer metastasis, puberty and vasoconstriction. The effects of KPs on endothelial cells have yet to be determined. The aim of the present study was to investigate the effects of KP-10 on endothelial cell growth and the mechanisms underlying those effects. The administration of recombinant KP-10 into the hindlimbs of rats with ischaemia significantly impaired blood flow recovery, as shown by laser Doppler, and capillary growth, as shown using histology, compared with the controls. HUVECs (human umbilical vein endothelial cells) express the KP receptor and were treated with KP-10 in culture studies. KP-10 inhibited endothelial cell tube formation and proliferation in a significant and dose-dependent manner. The HUVECs treated with KP exhibited the senescent phenotype, as determined using a senescence-associated β-galactosidase assay, cell morphology analysis, and decreased Sirt1 (sirtuin 1) expression and increased p53 expression shown by Western blot analysis. Intriguingly, a pharmacological Rho kinase inhibitor, Y-27632, was found to increase the proliferation of HUVECs and to reduce the number of senescent phenotype cells affected by KP-10. In conclusion, KP-10 suppressed endothelial cells growth both in vivo and in vitro in the present study. The adverse effect of KP on endothelial cells was attributable, at least in part, to the induction of cellular senescence.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jul 1;127(1):47-55. doi: 10.1042/CS20130505.
- The KPs (kisspeptins) are a family of multifunctional peptides with established roles in cancer metastasis, puberty and vasoconstriction. The effects of KPs on endothelial cells have yet to be determined. The aim of the present study was to investigate the effects of KP-10 on endothelial cell growth
- PMID 24405415
Japanese Journal
- 研究室紹介 海洋生物からの新しい医薬シーズの探索
- 小林 資正
- 生産と技術 66(1), 42-45, 2014
- NAID 40019942105
- Discovery of a Novel Nicotinamide Phosphoribosyl Transferase (NAMPT) Inhibitor via in Silico Screening
- Takeuchi Mikio,Niimi Tatsuya,Masumoto Mari,Orita Masaya,Yokota Hiroyuki,Yamamoto Tomoko
- Biological and Pharmaceutical Bulletin 37(1), 31-36, 2014
- … AS1604498 was the most potent inhibitor, with an IC50 of 44 n<span style="font-variant: small-caps;">M</span>, and inhibited THP-1 and K562 cell line growth with the IC50 of 198 n<span style="font-variant: small-caps;">M</span> …
- NAID 130003382094
- Effects of in vitro growth culture duration and prematuration culture on maturational and developmental competences of bovine oocytes derived from early antral follicles
- Huang Weiping,Nagano Masashi,Kang Sung-Sik,Yanagawa Yojiro,Takahashi Yoshiyuki
- Theriogenology 80(7), 793-799, 2013-10-15
- … The effects of in vitro growth (IVG) culture duration (10, 12, and 14 days) on the viability and growth of bovine oocytes derived from early antral follicles (0.5-1 mm diameter) in this study. … In addition, the effect of pre-IVM culture with phosphodiesterase inhibitor (3-isobutyl-1-methylxanthine) on nuclear maturation of IVG oocytes was also evaluated. …
- NAID 120005345325
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★リンクテーブル★
| リンク元 | 「成長抑制物質」 |
| 拡張検索 | 「cell growth inhibitor」 |
| 関連記事 | 「inhibit」「grow」「inhibitor」「growth」 |
「成長抑制物質」
「cell growth inhibitor」
「inhibit」
- v.
- 抑制する、阻害する、阻止する
- 関
- abrogate、block、depress、depression、deter、inhibition、interdict、prevent、prevention、repress、repression、restrain、restraint、suppress、suppression
「grow」
- v.
「inhibitor」
- n.
「growth」
- n.
- 成長