966 resultados para prostaglandin E1
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利用能量为42MeV和45MeV的9Be束流轰击160Gd自支撑靶,通过160Gd(9Be,4n)165Er熔合蒸发反应研究了165Er核的高自旋态结构。基于实验测量结果,扩展了基于ν5/2−[523]和ν5/2+[642]准粒子组态的转动带,观测到了连接这两条具有不同宇称的转动带的强电偶极跃迁。利用跃迁分支比,提取了带间电偶极跃迁的约化跃迁概率,并讨论了强电偶极跃迁与八极关联之间的关系。提取了ν5/2−[523]和ν5/2+[642]转动带的顺排角动量和能级能量旋称劈裂值,并进行了简单讨论。
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采用盆栽实验研究了小叶白蜡(Fraxinus sogdiana)接种4种外生菌根真菌(E1-毛边滑锈伞(Hebeloma mesophaeusm)、E2-劣味乳菇(Lactarius insulsns)、E3-松塔牛肝菌(Stro-bilomyces floccopus)和E4-丝膜菌(Cortinarius russus)对沈抚灌区土壤石油烃的降解效果。结果表明:在白蜡不同组合双接种及混合接种中,以混合接种对土壤石油烃的降解效果最好,降解率比对照提高23.6%;其次为双接种中的E1E3和E2E4组合,降解率分别比对照提高21.0%和12.7%。接种外生菌根真菌可促进白蜡生长,尤其可明显提高其根生物量,增加侧根数,接种E1E3、E2E4和混合菌使白蜡侧根数分别增加了100%、67%和81%。相关分析表明,石油烃降解率与白蜡的侧根数呈显著相关,可能是其降解率提高的主要原因。
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依据东北西部沙质荒漠化地区植被的分类与排序,分析了不同演替梯度上植被群落多样性指数与DCA排序坐标值的相关关系,利用其探讨群落多样性与沙质荒漠化过程的关系;科尔沁沙地、呼伦贝尔沙地,1)植物群落的生态优势度λ、Renyi的均匀度E1与群落分布的地下水位有显著的相关关系;2)植物群落Hill的多样性指数H0,H1、Hill的均匀度Eh、Hill指数的均匀度E′1与海拔、湿润系数、Thornthwaite指数、降水量、地下水位、放牧干扰等有显著的相关关系;3)植物群落Renyi的多样性指数N0,N1、Heip修正的均匀度Ep、Alatalo修正的均匀度E′h与经度、温暖指数、冷暖指数、Thornthwaite指数、土壤有机质、地下水位、放牧等干扰有显著的相关关系。4)呼伦贝尔沙地的完工-海拉尔沙带,樟子松林、贝加尔针茅羊草草甸草原;科尔沁沙地的油松林、羊草草甸草原、丛生禾草草原具有较高的多样性,各群落类型随着沙质荒漠化过程的逐渐加剧,物种丰富度逐渐降低,其递减趋势分为旱生沙化系列、湿生沙化系列、盐水至水生系列。按各群落类型的物种丰富度递减顺序可分为6个级别,6个级别所含的群落类型分别对应着稳定沙地(A、B),固定沙丘(C),半固定沙丘(D),半流动沙丘(E),流动沙丘(F)。
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对DS9701菌株产生的聚β-羟基丁酸酯(PHB)解聚酶进行了分离、纯化及有关性质的表征.通过SephadexG-100分离出两种PHB解聚酶(E1和E2),经聚丙烯酰胺凝胶电脉检测为一条谱带.E1的最适反应温度为40℃~45℃,稳定性优于E2,最适反应pH=4.0,稳定范围3.6~7.0,Km值为0.182g/L.E2的最适反应温度为40℃,pH=6.0,稳定范围4.0~8.0,Km值为0.65g/L.通过质谱仪测得E1的相对分子质量为4.5×104,E2的相对分子质量为4.4×104.
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We evaluated the effects of high molecular-weight phlorotannins from Sargassum thunbergii (STP) on ADP-induced platelet aggregation and arachidonic acid (AA) metabolism in New Zealand white rabbits and Wistar rats. The inhibition of STP on platelet aggregation was investigated using a turbidimetric method, and the levels of the terminal products of AA metabolism were measured using the corresponding kits for maleic dialdehyde (MDA), thromboxane B-2 (TXB2) and 6-keto-prostaglandin F-1 alpha (6-keto-PGF(1 alpha)) by colorimetry and radioimmunoassay, as appropriate. We found that STP could inhibit ADP-induced platelet aggregation, and the inhibitory ratio was 91.50% at the STP concentration of 4.0 mg/mL. Furthermore, STP markedly affected AA metabolism by decreasing the synthesis of MDA (P < 0.01) and increasing the synthesis of 6-keto-PGF(1 alpha), thus changing the plasma TXB2/6-keto-PGF(1 alpha) balance when the platelets were activated (P < 0.01). Therefore, STP altered AA metabolism and these findings
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Six deep-sea proteolytic bacteria taken from Aleutian margin sediments were screened; one of them produced a cold-adapted neutral halophilic protease. These bacteria belong to Pseudoalteromonas spp., which were identified by the 16S rDNA sequence. Of the six proteases produced, two were neutral cold-adapted proteases that showed their optimal activity at pH 7-8 and at temperature close to 35 degrees C, and the other four were alkaline proteases that showed their optimal activity at pH 9 and at temperature of 40-45 degrees C. The neutral cold-adapted protease E1 showed its optimal activity at a sodium chloride concentration of 2 M, whereas the activity of the other five proteases decreased at elevated sodium chloride concentrations. Protease E1 was purified to electrophoretic homogeneity and its molecular mass was 34 kDa, as estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The molecular weight of protease E1 was determined to be 32,411 Da by mass spectrometric analysis. Phenylmethyl sulfonylfluoride (PMSF) did not inhibit the activity of this protease, whereas it was partially inhibited by ethylenediaminetetra-acetic acid sodium salt (EDTA-Na). De novo amino acid sequencing proved protease E1 to be a novel protein.
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There is excess nitrate (NO3) in the Pearl River coastal plume in the southern waters of Hong Kong in summer. We hypothesize that phosphorus (P) limitation controls the utilization of excess NO3 due to the high N:P ratio in the Pearl River. To test this hypothesis, we conducted two 1-day cruises on July 13 and 19, 2000 to examine the response of the phytoplankton to P additions with respect to changes in biomass, uptake of nutrients and nutrient uptake ratios using a batch incubation of natural water samples collected from the Pearl River estuary and adjacent coastal waters. At a station (E1, salinity =5) in the Pearl River estuary, the N/P ratio at the surface was 46:1, (64 muM DIN: 1.3 muM PO4) and decreased to 24:1 (12 muM DIN: 0.5 muM PO4) downstream at a station (Stn 26, salinity =26) in the coastal plume south of Hong Kong. Without a P addition, NO3 in the water samples collected at E1 could not be depleted during a 9 day incubation (similar to20 muM NO3 remaining). With a P addition, NO3 disappeared completely on day 6 with the depletion of the added PO4 (2-3 muM). This was also true for a station, E4 (salinity= 15) further downstream, but within the estuary. At Stn 26, in the coastal plume south of Hong Kong, NO3 (similar to11.5 muM) was eventually depleted without the addition of PO4, but it took 8 days instead of 5 days for Stn E4. The uptake ratio of dissolved inorganic nitrogen (DIN) to PO4, without a P addition was 51:1, 43:1 and 46:1 for Stns E1, E4 and 26, respectively. With a P addition, the DIN/PO4 uptake ratio decreased to 20:1, 14:1 and 12:1, respectively, for the 3 stations. These results clearly indicate potential P limitation to utilization of NO3 in the Pearl River estuary, resulting in excess NO3 in waters of the coastal plume downstream of the estuary, some of which would eventually be transported offshore. High uptake ratios of N:P without a P addition (43N:1P) suggest that phytoplankton have a nitrogen uptake capacity in excess of the Redfield ratio of 16N: 1P by 2.5-3 times. The value of 2.5-3 times was likely a maximum that should have contained a contribution of P released from desorption of P from sediments or from regeneration by zooplankton grazing and bacterial activity during the incubation of natural water samples. Without a P addition, however, phytoplankton biomass did not increase. This means that P turnover rates or regeneration may allow phytoplankton to take up additional N in excess of the Redfield ratio and store it, but without increasing the algal biomass. Therefore, high ambient N:P ratios in excess of the Redfield ratio do indicate potential P limitation to phytoplankton biomass in this estuarine coastal ecosystem. (C) 2004 Elsevier Ltd. All rights reserved.
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以江河源区退化高寒草甸为对象,利用层次分析法,探讨了高寒草地的退化原因和恢复治理措施的有效性.结果表明:长期超载过牧和暖干化气候是导致高寒草甸退化的主导因子,贡献率为65.99%;伴随草地初始退化出现的鼠虫和毒杂草泛滥危害是加速高寒草甸退化的重要因子,贡献率为15.03%;人类不合理干扰造成的高寒草甸退化也不应忽视,贡献率为9.64%.各个恢复治理措施组合权重的分配格局相对均衡,其中围栏封育和划区轮牧(E2)与控制放牧强度(E1),效益较好,组合权重达0.3007.层次分析法可为草原管理,防止草地退化、恢复治理退化草地、优化利用草地资源提供定量依据.
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The West Shandong Uplift and its adjacent basins, with same evolutional history before Mesozoic, are an important basin-orogenic systems in North China. After late Mesozoic, tectonic differentiation between basin and orogenic belt gradually displayed in the study area. The Boxing sag is a part of Jiyang Depression near to West Shandong Uplift, in which the whole Mesozoic and Cenozoic strata are preserved. Based on the analysis of sedimentary records in the Boxing sag, the Cenozoic structural and sedimentary evolutions in Boxing Sag and its response to Western Shandong uplift are discussed in this dissertation. The main conclusions in this research are presented as follows. Based on Seismic and well logging profile interpretation, fault growth index, thickness difference between bottom wall and top wall and fault activity rate from Eocene to Pliocene are studied. Boxing sag had three main faults, NE, NW and NEE trending faults. Research shows that the activity of the NW trending fault in the Boxing sag became weaken from E1-2S4 to N2m gradually. The evolution of NE and the NEE trending fault can be divided into three episodes, from E1-2k to E2s4, from E2s3 to E3s1, from N2m to E3d. The analysis of Paleogene samples of heavy mineral assemblages shows that metamorphic rocks represented by garnet, intermediate-acid igneous rocks represented by the assemblage of apatite, zircon and tourmaline became less from E1-2k to N2g, and sedimentary rocks represented by the assemblage of pyrite, barite and limonite also became less. Intermediate-basic igneous rocks represented by the assemblage of leucoxene, rutile and ilmenite and metamorphic rocks represented by epidote became more and more. Electronic microprobe analysis shows that glaucophane and barroisite are existed in Kongdian Formation and the 4th member of Shahejie Formation, and they demonstrate that Western Shandong and Eastern Shandong are all the source regions of the Boxing Sag, and they also indicate that oceanic crust existed before the collision between the Yangtze and North China continent. The fact that Eastern Shandong is the source region of Boxing Sag also indicates that Western Shandong was not high enough to prevent sediment from Eastern Shandong at E1-2k and E2s4. The results of the dating of five detrital zircons of Boxing Sag show Kongdian Formation and the 4th member of Shahejie Formation have the age peaks of 2800Ma and 700-800. It means that Eastern Shandong is the source region of Boxing Sag at early Paleogene and Western Shandong is not high enough to prevent the sediment from Eastern Shandong. The ages of 160-180 and 220-260 Ma, which exist in the Guantao Formation and Paleogene, are common in Eastern Shandong and rare in Western Shandong,and it implied that Western Shandong is a low uplift at 24Ma. The Paleogene strata have almost same age groups, while the Guantao Formation has significant variations of age groups, and this indicates that Boxing Sag and Western Shandong uplift had taken place tremendous changes. The results of apatite fission track in Boxing sag show that three times uplifts happened at the source region at 60 Ma, 45Ma and 15Ma respectively, and the Boxing sag experienced two subsidences at 60Ma, 45Ma and one uplift at 20Ma.
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Gough, John, (2004) 'Holevo-Ordering and the Continuous-Time Limit for Open Floquet Dynamics', Letters in Mathematical Physcis 67(3) pp.207-221 RAE2008
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Despite studies demonstrating that inhibition of cyclooxygenase-2 (COX-2)-derived prostaglandin E2 (PGE2) has significant chemotherapeutic benefits in vitro and in vivo, inhibition of COX enzymes is associated with serious gastrointestinal and cardiovascular side effects, limiting the clinical utility of these drugs. PGE2 signals through four different receptors (EP1–EP4) and targeting individual receptor(s) may avoid these side effects, while retaining significant anticancer benefits. Here, we show that targeted inhibition of the EP1 receptor in the tumor cells and the tumor microenvironment resulted in the significant inhibition of tumor growth in vivo. Both dietary administration and direct injection of the EP1 receptor-specific antagonist, ONO-8713, effectively reduced the growth of established CT26 tumors in BALB/c mice, with suppression of the EP1 receptor in the tumor cells alone less effective in reducing tumor growth. This antitumor effect was associated with reduced Fas ligand expression and attenuated tumor-induced immune suppression. In particular, tumor infiltration by CD4+CD25+Foxp3+ regulatory T cells was decreased, whereas the cytotoxic activity of isolated splenocytes against CT26 cells was increased. F4/80+ macrophage infiltration was also decreased; however, there was no change in macrophage phenotype. These findings suggest that the EP1 receptor represents a potential target for the treatment of colon cancer.
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STUDY DESIGN: The inflammatory responses of primary human intervertebral disc (IVD) cells to tumor necrosis factor α (TNF-α) and an antagonist were evaluated in vitro. OBJECTIVE: To investigate an ability for soluble TNF receptor type II (sTNFRII) to antagonize TNF-α-induced inflammatory events in primary human IVD cells in vitro. SUMMARY OF BACKGROUND DATA: TNF-α is a known mediator of inflammation and pain associated with radiculopathy and IVD degeneration. sTNFRs and their analogues are of interest for the clinical treatment of these IVD pathologies, although information on the effects of sTNFR on human IVD cells remains unknown. METHODS: IVD cells were isolated from surgical tissues procured from 15 patients and cultured with or without 1.4 nmol/L TNF-α (25 ng/mL). Treatment groups were coincubated with varying doses of sTNFRII (12.5-100 nmol/L). Nitric oxide (NO), prostaglandin E₂ (PGE₂), and interleukin-6 (IL6) levels in media were quantified to characterize the inflammatory phenotype of the IVD cells. RESULTS: Across all patients, TNF-α induced large, statistically significant increases in NO, PGE₂, and IL6 secretion from IVD cells compared with controls (60-, 112-, and 4-fold increases, respectively; P < 0.0001). Coincubation of TNF-α with nanomolar doses of sTNFRII significantly attenuated the secretion of NO and PGE₂ in a dose-dependent manner, whereas IL6 levels were unchanged. Mean IC₅₀ values for NO and PGE₂ were found to be 35.1 and 20.5 nmol/L, respectively. CONCLUSION: Nanomolar concentrations of sTNFRII were able to significantly attenuate the effects of TNF-α on primary human IVD cells in vitro. These results suggest this sTNFR to be a potent TNF antagonist with potential to attenuate inflammation in IVD pathology.
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High-sensitivity studies of E1 and M1 transitions observed in the reaction 138Ba(gamma,gamma{'}) at energies below the one-neutron separation energy have been performed using the nearly monoenergetic and 100% linearly polarized photon beams of the HIgammaS facility. The electric dipole character of the so-called "pygmy" dipole resonance was experimentally verified for excitations from 4.0 to 8.6 MeV. The fine structure of the M1 "spin-flip" mode was observed for the first time in N=82 nuclei.
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Nicotinic acid is one of the most effective agents for both lowering triglycerides and raising HDL. However, the side effect of cutaneous flushing severely limits patient compliance. As nicotinic acid stimulates the GPCR GPR109A and Gi/Go proteins, here we dissected the roles of G proteins and the adaptor proteins, beta-arrestins, in nicotinic acid-induced signaling and physiological responses. In a human cell line-based signaling assay, nicotinic acid stimulation led to pertussis toxin-sensitive lowering of cAMP, recruitment of beta-arrestins to the cell membrane, an activating conformational change in beta-arrestin, and beta-arrestin-dependent signaling to ERK MAPK. In addition, we found that nicotinic acid promoted the binding of beta-arrestin1 to activated cytosolic phospholipase A2 as well as beta-arrestin1-dependent activation of cytosolic phospholipase A2 and release of arachidonate, the precursor of prostaglandin D2 and the vasodilator responsible for the flushing response. Moreover, beta-arrestin1-null mice displayed reduced cutaneous flushing in response to nicotinic acid, although the improvement in serum free fatty acid levels was similar to that observed in wild-type mice. These data suggest that the adverse side effect of cutaneous flushing is mediated by beta-arrestin1, but lowering of serum free fatty acid levels is not. Furthermore, G protein-biased ligands that activate GPR109A in a beta-arrestin-independent fashion may represent an improved therapeutic option for the treatment of dyslipidemia.