WordNet
- a potent substance that acts like a hormone and is found in many bodily tissues (and especially in semen); produced in response to trauma and may affect blood pressure and metabolism and smooth muscle activity
- the 5th letter of the Roman alphabet (同)e
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2018/08/15 05:24:14」(JST)
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- 1. 早産児における動脈管開存症の病態生理、臨床症状、および診断 pathophysiology clinical manifestations and diagnosis of patent ductus arteriosus in premature infants
- 2. Techniques for ripening the unfavorable cervix prior to induction
- 3. 早産児の動脈管開存症のマネージメント management of patent ductus arteriosus in preterm infants
- 4. 帝王切開歴がある女性における頸管熟化および陣痛の誘発 cervical ripening and induction of labor in women with a prior cesarean delivery
- 5. 妊娠中期の中絶：子宮内容除去術 second trimester pregnancy termination dilation and evacuation
English Journal
- Diesel and biodiesel exhaust particle effects on rat alveolar macrophages with in vitro exposure.
- Bhavaraju L1, Shannahan J2, William A3, McCormick R3, McGee J4, Kodavanti U4, Madden M5.Author information 1Currciculum in Toxicology, University of North Carolina, Chapel Hill, NC, United States.2School of Pharmacy, University of Colorado, Denver, CO, United States.3National Renewable Energy Laboratory, Golden, CO, United States.4EPHD, NHEERL, US EPA, Research Triangle Park, NC, United States.5EPHD, NHEERL, US EPA, Research Triangle Park, NC, United States. Electronic address: madden.michael@epa.gov.AbstractCombustion emissions from diesel engines emit particulate matter which deposits within the lungs. Alveolar macrophages (AMs) encounter the particles and attempt to engulf the particles. Emissions particles from diesel combustion engines have been found to contain diverse biologically active components including metals and polyaromatic hydrocarbons which cause adverse health effects. However little is known about AM response to particles from the incorporation of biodiesel. The objective of this study was to examine the toxicity in Wistar Kyoto rat AM of biodiesel blend (B20) and low sulfur petroleum diesel (PDEP) exhaust particles. Particles were independently suspended in media at a range of 1-500μgmL(-1). Results indicated B20 and PDEP initiated a dose dependent increase of inflammatory signals from AM after exposure. After 24h exposure to B20 and PDEP gene expression of cyclooxygenase-2 (COX-2) and macrophage inflammatory protein 2 (MIP-2) increased. B20 exposure resulted in elevated prostaglandin E2 (PGE2) release at lower particle concentrations compared to PDEP. B20 and PDEP demonstrated similar affinity for sequestration of PGE2 at high concentrations, suggesting detection is not impaired. Our data suggests PGE2 release from AM is dependent on the chemical composition of the particles. Particle analysis including measurements of metals and ions indicate B20 contains more of select metals than PDEP. Other particle components generally reduced by 20% with 20% incorporation of biodiesel into original diesel. This study shows AM exposure to B20 results in increased production of PGE2in vitro relative to diesel.
- Chemosphere.Chemosphere.2014 Jun;104:126-33. doi: 10.1016/j.chemosphere.2013.10.080. Epub 2013 Nov 21.
- Combustion emissions from diesel engines emit particulate matter which deposits within the lungs. Alveolar macrophages (AMs) encounter the particles and attempt to engulf the particles. Emissions particles from diesel combustion engines have been found to contain diverse biologically active componen
- PMID 24268344
- Ovarian steroid-dependent tumor necrosis factor-α production and its action on the equine endometrium in vitro.
- Szóstek AZ1, Adamowski M2, Galvão AM3, Ferreira-Dias GM2, Skarzynski DJ4.Author information 1Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Olsztyn, Poland.2C.I.I.S.A., Faculty of Veterinary Medicine, University of Lisbon, Lisbon, Portugal.3Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Olsztyn, Poland; C.I.I.S.A., Faculty of Veterinary Medicine, University of Lisbon, Lisbon, Portugal.4Department of Reproductive Immunology and Pathology, Institute of Animal Reproduction and Food Research, Olsztyn, Poland. Electronic address: d.skarzynski@pan.olsztyn.pl.AbstractTumor necrosis factor-α (TNF) is a cytokine that plays important roles in functions of the endometrium. The aims of this study were to determine whether (i) ovarian steroids modulate TNF production by endometrial cells (Experiment 1); (ii) TNF effects on prostaglandin (PG) production in cultured equine endometrial cells and tissue (Experiment 2). Epithelial and stromal cells were isolated from equine endometrium (Days 2-5 of the estrous cycle; n=20) and treated after passage 1. In Experiment 1, epithelial and stromal cells were exposed to progesterone (P4; 10(-7)M), 17-β estradiol (E2; 10(-9)M) or P4+E2 (10(-7)/10(-9)M) for 24h. Then, TNF mRNA transcription was determined using Real-time PCR. Additionally, TNF protein production was investigated in response to ovarian steroids for 24h using Enzyme-Linked Immunosorbent Spot (EliSpot). In Experiment 2, epithelial and stromal cells and endometrial explants (mid-luteal phase of the estrous cycle; n=5) were exposed in vitro to TNF (10ng/ml) and to oxytocin (OT; positive control; 10(-7)M) for 24h. The concentrations of PGE2 and PGF2α were determined using a direct enzyme immunoassay (EIA) method. The transcription of prostaglandin-endoperoxide synthase-2 (PTGS-2), prostaglandin E2 synthase (PGES) and PGF2α synthase (PGFS) mRNAs in the endometrial explants was determined using Real-time PCR. Results showed that TNF is produced by two types of equine endometrial cells and its production is up-regulated by ovarian steroids (P<0.05) in stromal cells and by P4 (P<0.05) and E2 (P<0.01) in epithelial cells. Epithelial and stromal cells can also produce PG in response to TNF. In endometrial explants, TNF stimulated PGE2 production to a large extent and PGF2α secretion to a lesser extent. These actions are mediated by up-regulation of PG synthases mRNA transcription. The study indicates that TNF production is closely related to ovarian steroid actions and that the interaction between TNF and PG regulates physiologic processes in the equine endometrium.
- Cytokine.Cytokine.2014 Jun;67(2):85-91. doi: 10.1016/j.cyto.2014.02.005. Epub 2014 Mar 15.
- Tumor necrosis factor-α (TNF) is a cytokine that plays important roles in functions of the endometrium. The aims of this study were to determine whether (i) ovarian steroids modulate TNF production by endometrial cells (Experiment 1); (ii) TNF effects on prostaglandin (PG) production in cultured eq
- PMID 24642167
- Intratumoral COX-2 inhibition enhances GM-CSF immunotherapy against established mouse GL261 brain tumors.
- Eberstål S1, Sandén E, Fritzell S, Darabi A, Visse E, Siesjö P.Author information 1Glioma Immunotherapy Group, Division of Neurosurgery, Department of Clinical Sciences, Lund University, Lund, Sweden.AbstractImmunotherapy has shown effectiveness against experimental malignant brain tumors, but the clinical results have been less convincing most likely due to immunosuppression. Prostaglandin E2 (PGE2 ) is the key immunosuppressive product of cyclooxygenase-2 (COX-2) and increased levels of PGE2 and COX-2 have been shown in several tumor types, including brain tumors. In the current study, we report enhanced cure rate of mice with established mouse GL261 brain tumors when immunized with granulocyte macrophage-colony stimulating factor (GM-CSF) secreting tumor cells and simultaneously treated with the selective COX-2 inhibitors parecoxib systemically (5 mg/kg/day; 69% cure rate) or valdecoxib intratumorally (5.3 µg/kg/day; 63% cure rate). Both combined therapies induced a systemic antitumor response of proliferating CD4(+) and CD8(+) T cells, and further analysis revealed T helper 1 (Th 1) cell supremacy. The GL261 tumor cell line produced low levels of PGE2 in vitro, and co-staining at the tumor site demonstrated that a large fraction of the COX-2(+) cells were derived from CD45(+) immune cells and more specifically macrophages (F4/80(+)), indicating that tumor-infiltrating immune cells constitute the primary source of COX-2 and PGE2 in this model. We conclude that intratumoral COX-2 inhibition potentiates GM-CSF immunotherapy against established brain tumors at substantially lower doses than systemic administration. These findings underscore the central role of targeting COX-2 during immunotherapy and implicate intratumoral COX-2 as the primary target.
- International journal of cancer. Journal international du cancer.Int J Cancer.2014 Jun 1;134(11):2748-53. doi: 10.1002/ijc.28607. Epub 2013 Nov 25.
- Immunotherapy has shown effectiveness against experimental malignant brain tumors, but the clinical results have been less convincing most likely due to immunosuppression. Prostaglandin E2 (PGE2 ) is the key immunosuppressive product of cyclooxygenase-2 (COX-2) and increased levels of PGE2 and COX-2
- PMID 24243648
Japanese Journal
- The inflammatory network in the gastrointestinal tumor microenvironment: lessons from mouse models
- Oshima Hiroko,Oshima Masanobu
- Journal of Gastroenterology 47(2), 97-106, 2012-02
- … Subsequently, mouse genetic studies have shown that cyclooxygenase (COX)-2, one of the target molecules of NSAIDs, and its downstream product, prostaglandin E 2 (PGE 2), play an important role in gastrointestinal tumorigenesis. …
- NAID 80022322740
- 〈Review〉Target validation and drug discovery for in flammatory diseases
- Takahashi Hideo Kohka
- Acta Medica Kinki University 36(2), 45-52, 2011-12
- … It is reported that monocyte/macropharge releases histamine, prostaglandin (PG)E2, interleukin (IL)-18 and high mobility group box-1 (HMGB1). …
- NAID 80022302903
Related Pictures
★リンクテーブル★
| リンク元 | 「ガルナー症候群」「dinoprostone」 |
| 拡張検索 | 「16,16-dimethylprostaglandin E2」 |
| 関連記事 | 「prostaglandin」「E2」「E」「prostaglandins」 |
「ガルナー症候群」
- 英
- Gullner syndrome
- 低カリウム血性アルカローシスと腎尿細管障害を呈する症候群。
- Gullner et al. (1980, 1983) studied 3 black sibs (2 girls, 1 boy) with hypokalemia. Their disorder resembled Bartter syndrome in the presence of hyperreninemia, high urinary prostaglandin E2, normal blood pressure, and resistance of BP to the pressor effect of angiotensin II. In contrast to Bartter syndrome, the juxtaglomerular apparatus was histologically normal and changes were observed in the proximal tubules: intense staining of the cells, extreme hypertrophy of the basement membranes, and, by electron microscopy, dense cytoplasm, compact mitochondria, and pyknotic nuclei. Glomerular distal tubular and loop of Henle functions were normal. The 3 affected sibs had identical HLA-A and HLA-B types whereas a single unaffected sib had the complementary haplotype. A lod score of 1.322 (21:1 odds; P less than 0.05) for linkage was calculated.(参考1)
参考
- 1. HYPOKALEMIA, FAMILIAL - OMIM
「dinoprostone」
「16,16-dimethylprostaglandin E2」
16
「prostaglandin」
[★] プロスタグランジン prostaglandins PG
「E2」
「E」