Resistin is elevated in cystic fibrosis sputum and correlates negatively with lung function

Background

Resistin is an immunometabolic mediator that is elevated in several inflammatory disorders. A ligand for Toll-like receptor 4, resistin modulates the recruitment and activation of myeloid cells, notably neutrophils. Neutrophils are major drivers of cystic fibrosis (CF) lung disease, in part due to the release of human neutrophil elastase- and myeloperoxidase-rich primary granules, leading to tissue damage. Here we assessed the relationship of resistin to CF lung disease.

含有黄嘌呤衍生物的N-杂环卡宾金属配合物的生物活性研究进展

N-杂环卡宾(NHC)是一类多功能的配体,能够与过渡金属形成稳定的配位化合物,在催化、药学和材料科学等领域有着广泛的应用。黄嘌呤衍生物具有抗肿瘤转移和抗血管生成等生物活性,且结构易于修饰。将黄嘌呤衍生的NHC配体与过渡金属相结合有望得到具有全新生物活性的金属配合物。综述黄嘌呤衍生物的生物活性,以及黄嘌呤衍生的NHC金属配合物的结构特点和生物活性,并对黄嘌呤NHC金属配合物的研究进行了总结和展望,以期为进一步的研究提供参考。     

骨外固定器行胫骨迁移治疗血栓闭塞性脉管炎的护理

目的总结利用骨外固定器行胫骨迁移治疗血栓闭塞性脉管炎的护理经验.方法对35例血栓闭塞性脉管炎37条患肢应用骨外固定器迁移胫骨治疗.术前积极处理患肢、有效的心理护理,术后严密观察,做好骨外固定器迁移胫骨的护理.结果 32例间歇性跛行距离增加;27例夜间静息痛均得到缓解;7例足趾缺血坏死中除3例术后患肢缺血加重截肢外,余4例患肢供血改善,坏死区域结痂愈合;总有效率91.9%.结论全面、准确地评估患者,完善术前准备及术后正确迁移指导可提高骨外固定器行胫骨迁移治疗血栓闭塞性脉管炎的有效性.     

PPD为丝裂源作淋巴细胞转化试验对结核性胸膜炎的诊断价值

以结核菌素纯蛋白衍生物(PPD)为丝裂源作淋巴细胞转化试验,检测结核性(17例)和非结核性(14例)胸膜炎患者的外周血淋巴细胞(PBL)和胸腔积液淋巴细胞(PEL)对PPD 的反应性。结果显示:结核性胸膜炎患者无论PPD 皮试是阳性还是阴性,其PEL 的PPD 刺激指数(PPD-SI)都显著高于PBL(P 分别<0.001与<0.01);结核性PEL 的PPD-SI 显著高于非结核性PEL(P<0.001)。提示PPD 胸腔积液淋巴细胞转化试验可作为诊断结核性胸膜炎的有效方法。     

一阶导数高速脉冲极谱法用于盐酸普鲁卡因的定量分析

研究了一阶导数高速脉冲极谱法,并运用于盐酸普鲁卡因及其注射制剂的定量分析。在-0.04 V(对 Ag/AgCl)处出现的良好导数峰,于1.0～6.0×10~(-4)mol/L 范围内,导数峰电流与浓度呈线性关系。检测限为3.0×10~(-8)mol/L。操作简便、快速、灵敏,结果准确。     

第2足趾腓侧皮瓣移植的应用解剖及在手部皮肤缺损中的应用

目的探讨第2足趾腓侧皮瓣移植的应用解剖及临床应用的适应证、手术方法和优缺点等。方法新鲜成人尸体足左、右各10只,经灌注、解剖、测量,了解皮瓣的血供范围和相关血管、神经的外径。临床应用17例修复手部皮肤缺损,了解皮瓣的成活及功能恢复情况。结果灌注剂可达整个第2足趾及相邻趾蹼,测得第2足趾跖趾关节处腓侧固有动脉、趾背静脉分别为(1.0±0.2)mm、(0.9±0.2)mm;临床应用17例移植皮瓣全部成活,手、足部均无感染。经半年以上随访,被修复手指外观、颜色接近正常,供足无疼痛和植皮破溃现象发生。结论第2足趾腓侧皮瓣血供可靠,口径适于吻合,质地好,适于手指皮肤确实的修复。     

幼兔缺血预处理在心肌保护第二窗期对未成熟心肌Bcl-2基因mRNA表达的影响

目的　观察幼兔心脏缺血预处理 2 4h对未成熟心肌缺血 /再灌注后Bcl -2mRNA表达的影响 ,探讨未成熟心肌保护第二窗形成的作用机理。方法　 18只 3～ 4周龄幼兔 ,随机分为 3组 ,每组 6只 :Ⅰ组 ,正常对照组 ;Ⅱ组 ,缺血 /再灌注损伤组 ;Ⅲ组 ,缺血预处理组。建立活体心脏缺血 /再灌注损伤模型 ,Maclab/8s系统监测左心室发展压 (LVDP)、左室压上升及下降最大速率 (+dp/dtmax,-dp/dtmax)变化 ,原位免疫杂交 (ISH)方法检测心肌细胞内Bcl-2mRNA的表达。结果　缺血再灌注前 ,各组间LVDP、±dp/dtmax无显著性差异 (P >0 .0 5) ;再灌注 1h后 ,Ⅱ组的LVDP、+dp/dtmax和 -dp/dtmax恢复率分别为 (42 .81± 12 .56) %、(3 0 .67± 16.2 2 ) %和 (2 9.49± 10 .13 ) % ;Ⅲ组LVDP、+dp/dtmax及 -dp/dtmax恢复率分别为 (84.15± 13 .56) %、(69.49± 10 .3 6) %和 (58.3 7± 12 .45) % ,两组间有显著性差异 (P <0 .0 1)。Ⅱ组、Ⅲ组Bcl -2mRNA表达阳性细胞面积百分数分别为 (8.3± 2 .5) %、(76.3±13 .5) % ,两组间有显著性差异 (P <0 .0 1)。结论　缺血预处理可上调Bcl -2mRNA表达 ,参与未成熟心肌保护第二窗的形成 ,促进未成熟心肌缺血 /再灌注后心室功能恢复     

Electrophysiological properties of the propafenone-analogue GE 68 (1-[3-(phenylethyl)-2-benzofuryl]-2-(propylamino)-ethanol) in isolated preparations and ventricular myocytes of guinea-pig hearts

GE 68 ((Rac.)-1-[3-(Phenylethyl)-2-benzofuryl]-2-(propylamino)-ethanol hydrochloride) is structurally related to propafenone, and exerts negative inotropic and negative chronotropic effects similar to the parent drug, but lacks any β-adrenoceptor blocking activity contrary to propafenone. Thus, the electrophysiological effects of GE 68 were studied in papillary muscles, left atria, Purkinje fibres, sinoatrial nodes and ventricular myocytes of the guinea-pig heart with the intracellular microelectrode technique and the patch-clamp technique in the cell-attached mode. The decrease of the maximum upstroke velocity (V˙_max) by GE 68 (1 to 10 μM) was use- and frequency-dependent. V˙_max recovered from the use-dependent block with a time constant of 4.1 ± 0.6 s. In papillary muscles and Purkinje fibres action potential duration was shortened, while it was prolonged in left atria and sinoatrial nodes. Half-maximal steady-state inactivation of the sodium channels was shifted to more negative membrane potentials (control: –91.5 ± 0.8 mV, 10 μM GE 68: –97.9 ± 2.5 mV). The peak of the current-voltage relationship and the reversal potential were not changed by GE 68. The amplitude of the unitary current remained unaltered, while open state probability was decreased. The most striking effect of GE 68 was an increase of the number of sweeps without single channel openings (1 μM: 2 fold, 10 μM: 6 fold). GE 68 also caused a decrease of the mean open times, and an increase of the mean closed times in unmodified and pronase-modified sodium channels. Besides the lack of β-adrenoceptor blocking activity, data present a faster recovery from the use-dependent block by GE 68 and a lower affinity to inactivated sodium channels compared to the reference drug propafenone, as well as differences in the effect on single channel kinetics. Received: 25 July 1996 / Accepted: 14 October 1996     

喉症丸鉴定方法的研究

对不同批号喉症丸的二阶导数紫外谱线组图谱进行了测绘分析，发现不同批号的喉症丸其四溶剂二阶导数紫外吸收光谱特征数据，λmax或λsh具有很好的重现性，其分辨率高，特征性强，因此，以二阶导数紫外谱线组法控制喉症丸质量，鉴别喉症丸真伪优劣具有良好的重现性和准确性。     

Effect of KB-2796, a new diphenylpiperazine Ca antagonist, on voltage-dependent Ca currents and oxidative metabolism in dissociated mammalian CNS neurons

The effects of KB-2796, 1-[bis(4-fluorophenyl)methyl]-4-(2,3,4-trimethoxybenzyl)piperazine-2HCl, on the low- and high-voltage activated Ca²⁺ currents (LVA and HVA I_Ca, respectively) and on oxidative metabolism were studied in neurons freshly dissociated from rat brain. KB-2796 reduced the peak amplitude of LVA I_Ca in a concentration-dependent manner with a threshold concentration of 10⁻⁷ M when the LVA I_Ca was elicited every 30 s in the external solution with 10 mM Ca²⁺. The concentration for half-maximum inhibition (IC₅₀) was 1.9 × 10⁻⁶M. At 10⁻⁵ M or more of KB-2796, a complete suppression of the LVA I_Ca was observed in the majority of neurons tested. There was no apparent effect on the current-voltage (I-V) relationship and the current kinetics. KB-2796 delayed the reactivation and enhanced the inactivation of the Ca²⁺ channel for LVA I_Ca voltage- and time-dependently, suggesting that KB-2796 preferentially binds to the inactivated Ca²⁺ channel. KB-2796 at a concentration of3.0 × 10⁻⁶M also decreased the peak amplitude of the HVA I_Ca without shifting the I-V relationship. In addition, KB-2796 reduced the oxidative metabolism (the formation of reactive oxygen species) of the neuron in a concentration-dependent manner with a threshold concentration of3 × 10⁻⁶M. It is suggested that the inhibitory action of KB-2796 on the neuronal Ca²⁺ influx and the oxidative metabolism, in combination with a cerebral vasodilatory action, may reduce ischemic brain damage.