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The 1.7- and 2.43-MeV levels in 9Be were populated with the reaction 11B(d, α)9Be* by bombarding thin boron on carbon foils with 1.7-MeV deuterons. The alpha particles were analyzed in energy with a surface-barrier counter set at the unique kinematically determined angle and the recoiling 9Be nuclei at 90o were analyzed in rigidity with a magnetic spectrometer, in energy by a surface-barrier counter at the spectrometer focus, and in velocity by the time delay between an alpha and a 9Be count. When a pulse from the spectrometer counter was in the appropriate delayed coincidence with a pulse from the alpha counter, the two pulses were recorded in a two-dimensional pulse height analyzer. Most of the 9Be* decay by particle breakup. Only those that gamma decay are detected by the spectrometer counter. Thus the experiment provides a direct measurement of Γrad/Γ. Analysis of 384 observed events gives Γrad/Γ = (1.16 ± 0.14) X 10-4 for the 2.43-MeV level. Combining this ratio with the value of Γrad = 0.122 ± 0.015 eV found from inelastic electron scattering gives Γ = (1.05 ± 0.18) keV. For the 1.7-MeV level, an upper limit, Γrad/Γ ≤ 2.4 = 10-5, was determined.

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Ang 1-7-ak duen eragina giza espermatozoideen mugikortasunean aztertu dugu, baita molekula honek Akt-ren fosforilazioan dituen efektuak ere. Bestalde, Mas hartzailearen presentzia espermatozoideetan ikertu dugu.

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本发明提供化合物5,6-二羟基-2-(4-羟苯基)-4-酮-4H-1-苯并吡喃基-7-羟基-β-D-葡萄糖醛酸在制备抗艾滋病药物中和在制备逆转录酶抑制剂药物中的应用。

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用卢瑟福背散射沟道技术研究了1MeVSi~+在衬底加温和室温下以不同剂量注入Al_(0.3)Ga_(0.7)As/GaAs超晶格和GaAs后的晶格损伤。在衬底加温下, 观察到Al_(0.3)Ga_(0.7)As/GaAs超晶格和GaAs都存在一个动态退火速率与缺陷产生速率相平衡的剂量范围, 以及两种速率失去平衡的临界剂量。用热尖峰与碰撞模型解释了晶格损伤积累与注入剂量和衬底温度的关系。

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以开顶箱内经过6个生长季高浓度CO2处理的原位土壤种植的红松幼树为实验对象,研究了500μmolmol-1CO2对针叶光合作用及相应光合参数的影响。实地条件下测定了净光合速率(PN)对光合有效辐射(PAR)及胞间CO2浓度(Ci)的响应曲线,根据光合作用的生化模型,推算出了Rubisco活性或数量限制的最大羧化速率(VCmax)和光饱和条件下由RuBP再生能力限制的最大电子传递速率(Jmax),以及表观量子产量(AQY)和最大净光合速率(Pmax)等。500μmolmol-1CO2使红松针叶的VCmax降低了4%,Jmax和Jmax/VCmax比分别增加了27%和18%,均与对照差异不显著,所以红松针叶经过6个生长季高浓度CO2处理仍未发生光合驯化。在各自生长条件下测定的PN-PAR响应曲线表明,500μmolmol-1CO2使Pmax增加了94%,AQY增加了21%,Pmax增长高于AQY和Jmax的增加比例,说明500μmolmol-1CO2使红松针叶对光的利用效率增强。500μmolmol-1CO2下的最大气孔导度(gsmax)和最大蒸腾速率(Emax)与对照比增加了一倍,与Pmax增加的幅度接近。500μmol mol-1CO2下和对照条件下的Ci/Ca比均随环境CO2浓度(Ca)增加呈非线性下降趋势,在较低Ca处(Ca≤200μmol mol-1),500μmol mol-1CO2使Ci/Ca比下降了1%~7%,较高Ca处(Ca≥300μmol mol-1),500μmol mol-1CO2使Ci/Ca比增加了5%~20%。CO2浓度变化会改变Ci/Ca比,由于气孔的调节作用,Ci/Ca比最终还是要维持在一恒定范围,且气孔对较低的CO2浓度更敏感。

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Random multimode lasers are achieved in 4-(dicyanomethylene)-2-tert-butyl-6(1,1,7,7-tetramethyljulolidyl-9-enyl)-4H-pyran (DCJTB) doped polystyrene thin films by introducing silicon dioxide (SiO2) nanoparticles as scatterers. The devices emit a resonance multimode peak at a center wavelength of 640 nm with a mode linewidth less than 0.87 nm. The threshold excitation intensity is as low as 0.25 mJ pulse(-1) cm(-2). It can be seen that the microscopic random resonance cavities can be formed by multiple scattering of SiO2 nanoparticles.

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1,7-Diaminoheptane (DAH) had been covalently grafted on glassy carbon electrode by amino cation radical formation, which resulted in a stable cationic monolayer under proper pH conditions. Dawson-type tungstodiphosphate anion, P2W18O626- and small molecule, Ru(NH3)(6)(3+) were alternately assembled on the DAH modified electrode through layer-by-layer electrostatic interaction. Thus-prepared multilayer film had been characterized by cyclic voltammetry and X-ray photoelectron spectroscopy. The P2W18O626- multilayers exhibit high electrocatalytic response and sensitivity towards the reduction of iodate. With the increase of the number of P2W18O626- the catalytic current was enhanced and the catalytic potential shifted positively. Iodate in table salt was determined at the modified electrode containing three layers of P2W18O626- with satisfactory results. The multilayer electrode is promising as an electrochemical sensor for the detection of trace iodate.

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目的 通过对比观察藏药1号与藏药7号水提液对大鼠离体胸动脉条收缩作用的影响,研究藏药1号与藏药7号的降压机制。方法 以生理盐水作为对照组,观察藏药1号与藏药7号水提液(6mg/ml)和维拉帕米(Ver 0.013 mg/ml)对高K~+液引起的主动脉条收缩的时效影响,观察对KCl,NE及CaCl_2引起的大鼠主动脉条收缩的量效曲线的影响,以及对NE引起的依赖于细胞内钙及细胞外钙的收缩的影响。结果 藏药1号与藏药7号水提液抑制高K~+液引起的主动脉收缩(P<0.001);而且可以使KCl,NE及CaCl_2引起的大鼠主动脉条收缩的量效曲线非平行右移,最大效应降低,呈非竞争性拮抗作用(P<0.05),与维拉帕米相似,并且对NE引起的依赖于细胞内钙及细胞外钙的收缩均有抑制作用(P<0.05)。从pD'2值分析,藏药1号的药效作用要强于藏药7号,但比Ver的弱。结论 提示藏药1号与藏药7号的降压机制与钙离子通道拮抗剂一致,而且其作用效果比Ver延迟、平缓,其最大作用与Ver相近。而且藏药1号药效更加显著。

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Initial studies have demonstrated that intra- renal infusion of Ang (1-7) caused a diuresis and natriuresis that was proportional to the degree of activation of the Renin Angiotensin Aldosterone System (RAAS). This raised the question as why the magnitude of this diuresis and natriuresis was compromised in rats receiving a high sodium diet (suppressed RAAS) and enhanced in low sodium fed rats (activated RAAS)? Could the answer lie with changes in intra-renal AT1 or Mas receptor expression? Interestingly, the observed Ang (1-7) induced increases in sodium and water excretion in rats receiving either a low or normal sodium diet were and blocked in the presence of the AT 1 receptor antagonist (Losartan) in the presence of the, 'Mas' receptor antagonist (A-779). These data suggest that both AT1 and 'Mas' receptors need to be functional in order to fully mediate the renal responses to intra-renal Ang (1-7) infusion. Importantly, further experimentation also revealed that there is a proportional relationship between AT 1 receptor expression in the rat renal cortex and the magnitude of the excretory actions of intra renal Ang (1-7) infusion, which is only partially dependent on the level of 'Mas' receptor expression. These observations suggest that although Ang (1-7) induced increases in sodium and water excretion are mediated by the Mas receptor, the magnitude of these excretory responses appear to be dependent upon the level of AT 1 receptor expression and more specifically Ang II/ AT 1 receptor signalling. Thus in rats receiving a low sodium diet, Ang (1-7) acts via the Mas receptor to inhibit Ang II/ AT 1 receptor signalling. In rats receiving a high sodium diet the down regulated AT 1 receptor expression implies a reduction in Ang II/ AT 1 receptor signalling which renders the counter-regulatory effects of intra-renal Ang (1-7) infusion redundant.

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Glucagon-like peptide-1(7-36)amide (GLP-1) possesses several unique and beneficial effects for the potential treatment of type 2 diabetes. However, the rapid in-activation of GLP-1 by dipeptidyl peptidase IV (DPP IV) results in a short half-life in vivo (less than 2 min) hindering therapeutic development. In the present study, a novel His(7)-modified analogue of GLP-1, N-pyroglutamyl-GLP-1, as well as N-acetyl-GLP-1 were synthesised and tested for DPP IV stability and biological activity. Incubation of GLP-1 with either DPP IV or human plasma resulted in rapid degradation of native GLP-1 to GLP-1 (9-36),amide, while N-acetyl-GLP-1 and N-pyroglutamyl-GLP-1 were completely resistant to degradation. N-acetyl-GLP-1 and N-pyroglutamyl-GLP-1 bound to the GLP-1 receptor but had reduced affinities (IC50 values 32(.)9 and 6(.)7 nM, respectively) compared with native GLP-1 (IC50 0(.)37 nM). Similarly, both analogues stimulated cAMP production with EC50 values of 16(.)3 and 27 nM respectively compared with GLP-1 (EC50 4(.)7 nM). However, N-acetyl-GLP-1 and N-pyroglutamyl-GLP-1 exhibited potent insulinotropic activity in vitro at 5(.)6 mM glucose (P

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Although the incretin hormone glucagon-like peptide-1 (GLP-1) is a potent stimulator of insulin release, its rapid degradation in vivo by the enzyme dipeptidyl peptidase IV (DPP IV) greatly limits its potential for treatment of type 2 diabetes. Here, we report two novel Ala(8)-substituted analogues of GLP-1, (Abu(8))GLP-1 and (Val(8) GLP-1 which were completely resistant to inactivation by DPP IV or human plasma. (Abu(8))GLP-1 and (Val(8))GLP-1 exhibited moderate affinities (IC50: 4.76 and 81.1 nM, respectively) for the human GLP-1 receptor compared with native GLP-1 (IC50: 0.37 nM). (Abu(8))GLP-1 and (Val(8))GLP-1 dose-dependently stimulated cAMP in insulin-secreting BRIN BD11 cells with reduced potency compared with native GLP-1 (1.5- and 3.5-fold, respectively). Consistent with other mechanisms of action, the analogues showed similar, or in the case of (Val(8))GLP-1 slightly impaired insulin releasing activity in BRIN BD11 cells. Using adult obese (ob/ob) mice, (Abu(8))GLP-1 had similar glucose-lowering potency to native GLP-1 whereas the action of (Val(8))GLP-1 was enhanced by 37%. The in vivo insulin-releasing activities were similar. These data indicate that substitution of Ala(8) in GLP-1 with Abu or Val confers resistance to DPP IV inactivation and that (Val(8))GLP-1 is a particularly potent N-terminally modified GLP-1 analogue of possible use in type 2 diabetes.