高压氧治疗急性脑梗死的疗效以及对患者血清血管内皮生长因子、促血管生成素Ⅱ的影响

目的  观察高压氧治疗对急性脑梗死的临床疗效及其血清中血管内皮生长因子（VEGF）、促血管生成素Ⅱ（Ang-2）含量的影响。方法  选取200例急性脑梗死患者随机分为高压氧治疗组（治疗组）114例、非高压氧治疗组（对照组）86例,两组患者均进行30 d治疗。分别比较两组治疗前后神经功能缺损（NIHSS）评分,日常生活活动能力（ADL）评分及血清中Ang-2、VEGF水平的变化。结果  治疗后两组患者临床神经功能缺损程度评分均有所减少,与治疗前比较,两组均在治疗后24 h内评分差异有统计学意义（P <0.05）,治疗组较对照组评分显著减少,且随着时间延长,评分呈时间依赖性降低;治疗后两组患者ADL评分均有所提高,与治疗前比较,两组在治疗后24 h评分差异无统计学意义（P >0.05）,治疗15 d后评分差异有统计学意义（P <0.05）,治疗组较对照组评分显著增高,且随着时间延长,评分呈时间依赖性升高;两组治疗后血清VEGF及Ang-2含量的比治疗前患者血清中VEGF及Ang-2含量均有不同程度增加,治疗组较对照组VEGF及Ang-2含量显著增加,VEGF及Ang-2含量15 d时达到高峰,30 d时有所下降,与治疗前比较,两组在治疗后24 h VEGF及Ang-2含量差异无统计学意义（P >0.05）。治疗15 d后及30 d后VEGF及Ang-2含量差异有统计学意义（P <0.05）。结论  高压氧治疗可调节脑梗死患者血清中Ang-2 、VEGF的含量,改善神经功能缺损及提高日常生活活动能力,值得进一步研究及应用。

     

Effect of disodium cromoglycate on inflammatory cells bearing the Fc epsilon receptor type II (FcϵRII)

Disodium cromoglycate (DSCG) has well-established stabilizing properties on mast cells and basophils. However, the potential inhibitory effect of DSCG has been little demonstrated on the IgE stimulation of cell populations expressing epsilon receptors type II, (Fc_ϵRII), such as mononuclear phagocytes, eosinophils or platelets. Therefore, using various parameters of IgE-mediated triggering, we demonstrated the inhibitory role of DSCG on: (i) the release of neutrophil chemotactic factor by human alveolar macrophages, (ii) the oxygen metabolite-dependent chemiluminescence of human alveolar macrophages, rat peritonal macrophages, human eosinophils, human and rat platelets, and (iii) the β-glucuronidase release and synthesis by human alveolar macrophages.The inhibition of IgE-dependent stimulation ranged from 60% to 80%, according to the cells and to the measured parameter.It could therefore be considered that the action of DSCG was not restricted to its effects on mast cells and basophils, but also on other cells expressing Fc_ϵR leading to a potential reduction of the physiopathological consequences of allergic asthma and, possibly, of the late phase reaction sometimes associated with the disease, insofar as these cells are involved.     

Solving a myth: Does boric acid stabilize aldosterone in urine at typical clinical laboratory storage conditions?

Aldosterone is produced by the adrenal gland and plays an important role in blood pressure regulation and electrolyte hemostasis. Clinically, measurement of urine aldosterone provides evidence for the diagnosis of hyper- and hypo-aldosteronism. Urine specimen that is collected in consecutive 24 h is preferred, which mitigates the risk of misdiagnosis due to large diurnal variation in aldosterone secretion. Preservatives such as boric acid are routinely added to the collection containers prior to urine collection. However, little is known of the effectiveness of these preservatives on stabilizing aldosterone in urine. In the current study, we examined the stability of urine aldosterone under typical clinical laboratory storage conditions with and without the supplementation of boric acid. Our result demonstrated that the addition of boric acid is unnecessary.