抗瘤升白超微饮片治疗白细胞减少症的临床观察及药物经济学分析

目的：对比观察抗瘤升白超微饮片、传统汤剂及片剂治疗恶性肿瘤化疗所致骨髓损伤的疗效及药物经济学差异。方法：将90例化疗后出现白细胞减少症的患者随机分为抗瘤升白超微饮片组（超微组）、抗瘤升白片剂组（片剂组）和抗瘤升白汤剂组（汤剂组）。其中片剂组和汤剂组药物剂量相等,超微组剂量为汤剂、片剂剂量的1/2,各组均口服给药,连续给药4周,观察3组白细胞逐周变化、治疗白细胞减少症疗效、显效时间、生存质量,采用成本-效果分析法比较各组药物经济学性能。结果：在进行4周治疗后,超微组与片剂组、汤剂组白细胞数均较治疗前升高,差异有统计学意义（P〈0.01）,各组间白细胞逐周变化差异无统计学意义（P〉0.05）。超微组、片剂组、汤剂组治疗白细胞减少症的总有效率分别为86.7%、80.0%、83.3%,差异无统计学意义（P〉0.05）。超微组显效时间为（13.2±1.5）d,较片剂组、汤剂组短,差异有统计学意义（P〈0.05）。生存质量比较,3组差异无统计学意义（P〉0.05）。超微组、片剂组、汤剂组成本效果比分别为4.55、4.62、4.37,3组比值接近。结论：抗瘤升白超微饮片在治疗白细胞减少症及改善患者生活质量方面与抗瘤升白片及抗瘤升白传统汤药疗效相同,不增加治疗成本,起效更快。     

Perioperative cognitive decline in the aging population

Elderly patients who have an acute illness or who undergo surgery often experience cognitive decline. The pathophysiologic mechanisms that cause neurodegeneration resulting in cognitive decline, including protein deposition and neuroinflammation, also play a role in animal models of surgery-induced cognitive decline. With the aging of the population, surgical candidates of advanced age with underlying neurodegeneration are encountered more often, raising concerns that, in patients with this combination, cognitive function will precipitously decline postoperatively. This special article is based on a symposium that the University of California, San Francisco, convened to explore the contributions of surgery and anesthesia to the development of cognitive decline in the aged patient. A road map to further elucidate the mechanisms, diagnosis, risk factors, mitigation, and treatment of postoperative cognitive decline in the elderly is provided.     

七氟醚抑制脑干吸气前运动神经元的作用机制

研究背景:位于延髓尾部腹侧髓质的神经元是与吸气相关的前运动神经元,它们是支配呼吸肌如膈肌、肋间外肌、肋间内肌等运动神经元的上一级神经元。这些神经元的兴奋状态由NMDA受体,AM PA受体调控,也受抑制性AGBAA能神经调节。作者在去大脑狗的模型上探讨七氟醚对这些突触机制的影响。方法:实验在去大脑狗上进行,并应用迷走神经切断术使其处于瘫痪状态,通过机械通气维持高氧、高碳酸血症。局部微量注射AGBAA受体阻断剂荷包牡丹碱及谷氨酸受体激动剂AMPA、NMDA后,用细胞外记录技术,观测1MAC七氟醚对单个神经元活性的影响。用神经元…     

Effects of RNAi-mediated silencing of PEN-2, APH-1a, and nicastrin on wild-type vs FAD mutant forms of presenilin 1

The gamma-secretase complex consists of PS1/PS2, nicastrin, APH-1a, and PEN-2. PS1 undergoes endoproteolytic processing to yield two fragments: PS1-NTF and PS1-CTF. Changes in PEN-2 levels have been shown previously to affect the endoproteolytic processing of wild-type (wt)-PS1. However, the effects of PEN-2 on the proteolytic processing of familial Alzheimer's disease (FAD) mutant forms of PS1 have not yet been reported. To determine whether PEN-2 affects the proteolytic processing of mutant PS1 in the same manner as that of wt-PS1, we established RNA interference (RNAi) for PEN-2 in H4 human neuroglioma cells stably transfected to express wt or FAD mutant forms of PS1 including L286V, A246E, and that lacking exon 9 (Delta9). As expected, in H4 cells expressing wt-PS1, RNAi for PEN-2 increased levels of PS1-FL and attenuated PS1 endoproteolysis. Likewise, in cells expressing PS1 with the FAD missense mutations, L286V and A246E, RNAi for PEN-2 increased PS1-FL and reduced PS1 endoproteolysis. However, in H4 cells stably transfected to express the FAD-linked Delta9 mutation (PS1 lacking exon 9), RNAi for PEN-2 did not increase but, instead, decreased PS1-FL. In contrast, RNAi for nicastrin and APH-1a decreased PS1-FL in H4 cells expressing either wt-PS1 or Delta9-PS1. In summary, the metabolism of wt-PS1 and FAD-linked Delta9-PS1 is specifically and differentially affected by loss of function of PEN-2.