WordNet
- the 2nd letter of the Roman alphabet (同)b
- the blood group whose red cells carry the B antigen (同)type_B, group B
- 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
PrepTutorEJDIC
- =sense organ / 受信装置
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/09/06 07:14:01」(JST)
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- 1. 自然免疫系の概要 an overview of the innate immune system
- 2. 喘息の治療において5-リポキシゲナーゼ経路に影響する薬剤 agents affecting the 5 lipoxygenase pathway in the treatment of asthma
- 3. 痛風性関節炎の病態生理 pathophysiology of gouty arthritis
- 4. アナフィラキシーの病態生理 pathophysiology of anaphylaxis
- 5. 慢性疼痛の定義および病因 definition and pathogenesis of chronic pain
English Journal
- Monitoring tissue inflammation and responses to drug treatments in early stages of mice bone fracture using 50MHz ultrasound.
- Chen YC, Lin YH, Wang SH, Lin SP, Shung KK, Wu CC.SourceDepartment of Cell Biology & Anatomy, National Cheng Kung University, Tainan 701, Taiwan.
- Ultrasonics.Ultrasonics.2014 Jan;54(1):177-86. doi: 10.1016/j.ultras.2013.06.008. Epub 2013 Jul 11.
- Bone fracture induces moderate inflammatory responses that are regulated by cyclooxygenase-2 (COX-2) or 5-lipoxygenase (5-LO) for initiating tissue repair and bone formation. Only a handful of non-invasive techniques focus on monitoring acute inflammation of injured bone currently exists. In the cur
- PMID 23871514
- Neural processing of itch.
- Akiyama T, Carstens E.SourceUniversity of California, Davis, Department of Neurobiology, Physiology & Behavior, 1 Shields Avenue, Davis, CA 95616, United States.
- Neuroscience.Neuroscience.2013 Oct 10;250:697-714. doi: 10.1016/j.neuroscience.2013.07.035. Epub 2013 Jul 24.
- While considerable effort has been made to investigate the neural mechanisms of pain, much less effort has been devoted to itch, at least until recently. However, itch is now gaining increasing recognition as a widespread and costly medical and socioeconomic issue. This is accompanied by increasing
- PMID 23891755
- Natural resolution of inflammation.
- Freire MO, Van Dyke TE.AbstractInflammation is a protective response essential for maintaining human health and for fighting disease. As an active innate immune reaction to challenge, inflammation gives rise to clinical cardinal signs: rubor, calor, dolor, tumor and functio laesa. Termination of acute inflammation was previously recognized as a passive process; a natural decay of pro-inflammatory signals. We now understand that the natural resolution of inflammation involves well-integrated, active, biochemical programs that return tissues to homeostasis. This review focuses on recent advances in the understanding of the role of endogenous lipid mediators that modulate cellular fate and inflammation. Biosynthesis of eicosanoids and other lipids in exudates coincides with changes in the types of inflammatory cells. Resolution of inflammation is initiated by an active class switch in lipid mediators, such as classic prostaglandins and leukotrienes, to the production of proresolution mediators. Endogenous pro-resolving lipid mediators, including arachidonic acid-derived lipoxins, aspirin-triggered lipoxins, ω3-eicosapentaenoic acid-derived resolvins of the E-series, docosahexaenoic acid-derived resolvins of the D-series, protectins and maresins, are biosynthesized during the resolution phase of acute inflammation. Depending on the type of injury and the type of tissue, the initial cells that respond are polymorphonuclear leukocytes, monocytes/macrophages, epithelial cells or endothelial cells. The selective interaction of specific lipid mediators with G protein-coupled receptors expressed on innate immune cells (e.g. G protein-coupled receptor 32, lipoxin A4 receptor/formyl peptide receptor2, chemokine-like receptor 1, leukotriene B4 receptor type 1 and cabannoid receptor 2) induces cessation of leukocyte infiltration; vascular permeability/edema returns to normal with polymorphonuclear neutrophil death (mostly via apoptosis), the nonphlogistic infiltration of monocyte/macrophages and the removal (by macrophages) of apoptotic polymorphonuclear neutrophils, foreign agents (bacteria) and necrotic debris from the site. While an acute inflammatory response that is resolved in a timely manner prevents tissue injury, inadequate resolution and failure to return tissue to homeostasis results in neutrophil-mediated destruction and chronic inflammation. A better understanding of the complex mechanisms of lipid agonist mediators, cell targets and actions allows us to exploit and develop novel therapeutic strategies to treat human inflammatory diseases, including periodontal diseases.
- Periodontology 2000.Periodontol 2000.2013 Oct;63(1):149-64. doi: 10.1111/prd.12034.
- Inflammation is a protective response essential for maintaining human health and for fighting disease. As an active innate immune reaction to challenge, inflammation gives rise to clinical cardinal signs: rubor, calor, dolor, tumor and functio laesa. Termination of acute inflammation was previously
- PMID 23931059
Japanese Journal
- P2-006 Profiles of Receptors for Specialized Lipid Mediators on Synoviocyte from Osteoarthritis
- MURAKAMI Kosaku,IOAN-FACSINAY Andreea,TOES Rene,KLOPPENBURG Margreet,HUIZINGA Tom
- 日本臨床免疫学会会誌 37(4), 338b-338b, 2014
- … Receptors for SPMs have been found, such as leukotriene B4 receptor (BLT1), formyl peptide receptor 2 (FPR2), and chemokine like receptor 1 (CMKLR1). …
- NAID 130004694244
- Role of leukotriene B4 receptor 1 (BLT1) signaling in liver repair after hepatic ischemia reperfusion injury
- , , , ,
- Microvascular Reviews and Communications 7(1), 29a-29a, 2014
- … Aims: Leukotriene B4 (LTB4) is a potent chemoattractant for macrophages, and recruited macrophages play a critical role in liver repair and recovery from acute liver injury. … The objective of the present study was to examine the role of LTB4 receptor 1 (BLT1) signaling in liver repair after hepatic ischemia/reperfusion (I/R) injury.Methods: BLT1knockout mice (BLT1-/-) and wild-type mice (WT) were subjected to 60 min of partial (70%) hepatic warm ischemia followed by reperfusion. …
- NAID 130004678498
- Potential New Therapeutic Targets for Pathological Pruritus
- Biological and Pharmaceutical Bulletin 36(8), 1228-1234, 2013
- … (histamine H4 receptor, leukotriene B4 receptors, interleukin-31 receptor A, bombesin BB2 receptor, toll-like receptor 3, α-adrenoceptor, and opioid μ- and κ-receptors), channels (transient receptor potential (TRP) V3 and TRPA1 channels), and enzymes (histidine decarboxylase, sphingomyelin glucosylceramide deacylase, 5-lipoxygenase, leukotriene A4 hydrolase, and …
- NAID 130003361502
Related Links
- Leukotriene B4 receptor 2 is a protein that in humans is encoded by the LTB4R2 gene. This is a low-affinity receptor for ... "Cell-Specific Transcriptional Regulation of Human Leukotriene B4 Receptor Gene". J Exp Med 192 (3): 413–20.
Related Pictures
★リンクテーブル★
| リンク元 | 「LTB4 receptor」「ロイコトリエンB4受容体」「ロイコトリエンB4レセプター」 |
| 関連記事 | 「B」「leukotriene」「leukotrienes」 |
「LTB4 receptor」
「ロイコトリエンB4受容体」
「ロイコトリエンB4レセプター」
「B」
- 気管分岐部下緑
- 補体のalternative pathwayに関わる蛋白質
- Mg2+存在下でC3, B, Dが反応してC3bBbとなり、これがC3転換酵素(C3bBb)あるいはC5転換酵素(C3bBb3b)を形成する。これらはP(properdin)と結合して活性化し、それぞれC3、C5を活性化する