WordNet

(physical chemistry) a sample of matter in which substances in different phases are in equilibrium; "in a static system oil cannot be replaced by water on a surface"; "a system generating hydrogen peroxide"
instrumentality that combines interrelated interacting artifacts designed to work as a coherent entity; "he bought a new stereo system"; "the system consists of a motor and a small computer"
a group of independent but interrelated elements comprising a unified whole; "a vast system of production and distribution and consumption keep the country going" (同)scheme
a complex of methods or rules governing behavior; "they have to operate under a system they oppose"; "that language has a complex system for indicating gender" (同)system of rules
a group of physiologically or anatomically related organs or parts; "the body has a system of organs for digestion"
a procedure or process for obtaining an objective; "they had to devise a system that did not depend on cooperation"
the living body considered as made up of interdependent components forming a unified whole; "exercise helped him get the alcohol out of his system"
of or relating to or having vessels that conduct and circulate fluids; "vascular constriction"; "a vascular bundle"
the act of supplying food and nourishment (同)alimentation

PrepTutorEJDIC

〈C〉(関連した部分から成る)『体系』,系統,組織[網],装置 / 〈C〉(教育・政治などの)『制度』,機構;《the~》体制 / 〈C〉(思想・学問などの)『体系』,学説 / 〈C〉(…の)『方法』,方式,やり方《+of doing》 / 〈U〉正しい方針(筋道,順序) / 〈U〉《the~》(身体の)組織,系統 / 〈U〉《the~,one's~》身体,全身
(血液・樹液などを運ぶ)管の,導管の,血管の

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1. 血管新生阻害剤の概要 overview of angiogenesis inhibitors
2. 心不全におけるアンギオテンシン変換酵素阻害剤およびアンギオテンシン受容体拮抗剤：作用機序 angiotensin converting enzyme inhibitors and receptor blockers in heart failure mechanisms of action
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. 肝細胞癌における病期分類および予後因子 staging and prognostic factors in hepatocellular carcinoma
5. 重度の四肢外傷の外科的マネージメント surgical management of severe extremity injury

English Journal

Vascularization and nutrient delivery at root-knot nematode feeding sites in host roots.

Bartlem DG1, Jones MG, Hammes UZ.Author information 1Research Faculty of Agriculture, Hokkaido University, Sapporo 060-8589, Japan.AbstractPlants are constantly challenged by pathogens and pests, which can have a profound impact on the yield and quality of produce in agricultural systems. The vascular system of higher plants is critical for growth and for their ability to counteract changing external conditions, serving as a distribution network for water, nutrients, and photosynthates from the source organs to regions where they are in demand. Unfortunately, these features also make it an attractive target for pathogens and pests that demand access to a reliable supply of host resources. The vascular tissue of plants therefore often plays a central role in pathogen and parasite interactions. One of the more striking rearrangements of the host vascular system occurs during root-knot nematode infestation of plant roots. These sedentary endoparasites induce permanent feeding sites that are comprised of 'giant cells' and are subject to extensive changes in vascularization, resulting in the giant cells being encaged within a network of de novo formed xylem and phloem cells. Despite being considered critical to the function of the feeding site, the mechanisms underlying this vascularization have received surprisingly little attention when compared with the amount of research on giant cell development and function. An overview of the current knowledge on vascularization of root-knot nematode feeding sites is provided here and recent advances in our understanding of the transport mechanisms involved in nutrient delivery to these parasite-induced sinks are described.
Journal of experimental botany.J Exp Bot.2014 Apr;65(7):1789-98. doi: 10.1093/jxb/ert415. Epub 2013 Dec 14.
Plants are constantly challenged by pathogens and pests, which can have a profound impact on the yield and quality of produce in agricultural systems. The vascular system of higher plants is critical for growth and for their ability to counteract changing external conditions, serving as a distributi
PMID 24336493

Dietary Vitamin D Inadequacy Accelerates Calcification and Osteoblast-Like Cell Formation in the Vascular System of LDL Receptor Knockout and Wild-Type Mice.

Schmidt N1, Brandsch C, Schutkowski A, Hirche F, Stangl GI.Author information 1Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle/Saale, Germany.AbstractVitamin D insufficiency is highly associated with cardiovascular morbidity and mortality. We have demonstrated enhanced vascular calcification in LDL receptor knockout (LDLR-/-) mice fed a diet low in vitamin D. This study aimed to investigate the impact of a diet low in vitamin D on vascular calcification in wild-type (WT) mice lacking atherosclerotic plaques and the effects of a persistent and discontinuous vitamin D insufficiency on atherosclerotic plaque composition in LDLR-/- mice. The study was performed with 4-wk-old male WT and LDLR-/- mice that were fed a normal calcium/phosphate Western diet (210 g/kg fat, 1.5 g/kg cholesterol) containing either adequate [1000 IU/kg (+D)] or low [50 IU/kg (-D)] amounts of vitamin D3 for 16 wk. Four groups of LDLR-/- mice received 1 of the 2 diets for additional 16 wk (total 32 wk) and were compared with mice fed the diets for only 16 wk. WT and LDLR-/- mice that were fed the -D diet for 16 wk tended to develop more calcified spots in the aortic valve than mice fed the +D diet (+50% and +56%, respectively; P < 0.10). In LDLR-/- mice, the extent of calcification increased from week 16 to week 32 and was higher in the -D than in the +D group (P < 0.05). The calcification, owing to the -D diet, was accompanied by highly expressed osteoblast differentiation factors, indicating a transdifferentiation of vascular cells to osteoblast-like cells. Feeding the +D diet subsequent to the -D diet reduced the vascular calcification (P < 0.05). LDLR-/- mice fed the -D diet for 32 wk had higher plaque lipid depositions (+48%, P < 0.05) and a higher expression of cluster of differentiation 68 (+31%, P < 0.05) and tumor necrosis factor α (+134%, P < 0.001) than the +D group. Collectively, the findings imply low vitamin D status as a causal factor for vascular calcification and atherosclerosis.
The Journal of nutrition.J Nutr.2014 Mar 19. [Epub ahead of print]
Vitamin D insufficiency is highly associated with cardiovascular morbidity and mortality. We have demonstrated enhanced vascular calcification in LDL receptor knockout (LDLR-/-) mice fed a diet low in vitamin D. This study aimed to investigate the impact of a diet low in vitamin D on vascular calcif
PMID 24647396

Vascular endothelial tight junctions and barrier function are disrupted by 15(S)-hydroxyeicosatetraenoic acid partly via protein kinase C ε-mediated zona occludens-1 phosphorylation at threonine 770/772.

Chattopadhyay R1, Dyukova E, Singh NK, Ohba M, Mobley JA, Rao GN.Author information 1From the Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163.AbstractDisruption of tight junctions (TJs) perturbs endothelial barrier function and promotes inflammation. Previously, we have shown that 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE), the major 15-lipoxygenase 1 (15-LO1) metabolite of arachidonic acid, by stimulating zona occludens (ZO)-2 tyrosine phosphorylation and its dissociation from claudins 1/5, induces endothelial TJ disruption and its barrier dysfunction. Here, we have studied the role of serine/threonine phosphorylation of TJ proteins in 15(S)-HETE-induced endothelial TJ disruption and its barrier dysfunction. We found that 15(S)-HETE enhances ZO-1 phosphorylation at Thr-770/772 residues via PKCε-mediated MEK1-ERK1/2 activation, causing ZO-1 dissociation from occludin, disrupting endothelial TJs and its barrier function, and promoting monocyte transmigration; these effects were reversed by T770A/T772A mutations. In the arteries of WT mice ex vivo, 15(S)-HETE also induced ZO-1 phosphorylation and endothelial TJ disruption in a PKCε and MEK1-ERK1/2-dependent manner. In line with these observations, in WT mice high fat diet feeding induced 12/15-lipoxygenase (12/15-LO) expression in the endothelium and caused disruption of its TJs and barrier function. However, in 12/15-LO(-/-) mice, high fat diet feeding did not cause disruption of endothelial TJs and barrier function. These observations suggest that the 12/15-LO-12/15(S)-HETE axis, in addition to tyrosine phosphorylation of ZO-2, also stimulates threonine phosphorylation of ZO-1 in the mediation of endothelial TJ disruption and its barrier dysfunction.
The Journal of biological chemistry.J Biol Chem.2014 Feb 7;289(6):3148-63. doi: 10.1074/jbc.M113.528190. Epub 2013 Dec 15.
Disruption of tight junctions (TJs) perturbs endothelial barrier function and promotes inflammation. Previously, we have shown that 15(S)-hydroxyeicosatetraenoic acid (15(S)-HETE), the major 15-lipoxygenase 1 (15-LO1) metabolite of arachidonic acid, by stimulating zona occludens (ZO)-2 tyrosine phos
PMID 24338688