丹参酮ⅡA对神经祖细胞系C17．2的保护作用

目的:了解丹参酮ⅡA对神经祖细胞系C17.2的保护作用,探讨其可能的作用机制。方法:本实验于2005年起在广州血液中心器官移植配型中心实验室进行。C17.2祖细胞系由澳大利亚新南威尔士大学解剖教研室David Walsh博士惠赠。将C17.2细胞以1×109L-1的密度接种,用含10%胎牛血清IMDM,37℃、体积分数为0.05CO2、饱和湿度的CO2培养箱培养,接近融合的C17.2细胞用含0.1mmol/LEDTA的胰酶室温消化,按1∶3的比例传代。C17.2细胞以5×107L-1的密度接种于96孔板或25cm2的培养瓶中,用含10%胎牛血清IMDM培养过夜后,加入含4g/L AAPH(水溶性偶氮引发剂2,2'-偶氮二(2-脒基丙烷)二盐酸盐)无血清的IMDM培养基培养建立神经细胞凋亡模型。C17.2细胞以5×103/孔的密度接种于96孔板中,用含10%胎牛血清IMDM培养过夜后,加入含4g/LAAPH无血清的IMDM培养基培养。对照组不加入丹参酮ⅡA,实验组分别加入0.02,0.05,0.1,0.2mg/L丹参酮ⅡA培养8h,噻唑蓝法检测细胞活性:细胞活性的相对值=(实验组吸光度值/对照组吸光度值)×100%,流式细胞仪检测细胞凋亡。结果:①AAPH处理8h后,C17.2细胞被过氧化损害,大多数细胞失去正常的形态,细胞呈圆形,脱落。加入丹参酮ⅡA后,细胞形态基本保持正常,少数细胞呈圆形。②C17.2细胞在IMDM的培养液中,细胞数量是含4g/L AAPH无血清的IMDM培养基条件下的2.5～3倍。浓度为0.02,0.05,0.1mg/L的丹参酮ⅡA对C17.2细胞有保护作用,质量浓度大于0.2mg/L丹参酮ⅡA对C17.2细胞保护作用降低。③AAPH作用前大部分C17.2细胞的线粒体完整,有少量的早期凋亡细胞和凋亡细胞,AAPH作用后凋亡细胞总数、凋亡细胞明显增加。丹参酮ⅡA处理组可以明显减少早期凋亡细胞。结论:在体外丹参酮ⅡA对神经细胞具有抗凋亡的作用,可以保护神经细胞。     

马兜铃酸的倍半萜的酯类化合物VI.绵毛马兜铃中马兜铃酸萜酯I的结构鉴定

从绵毛马兜铃(Aristolocha mannisima Hance)中分得一个马兜铃酸倍半萜的酯类化合物,经红外、紫外、高分辩质谱和多种一维和二维核磁共振谱鉴定,确定了其骨架结构及顺反构型,命名为马兜铃酸萜酯I。     

In situ preservation of cadaver kidneys for transplantation: laboratory observations and clinical application.

Many kidneys obtained from cadaver donors undergoing sudden cardiac arrest cannot be transplanted due to the long periods of warm ischemia from the moment of arrest to nephrectomy. A double-ballon-triple-lumen catheter for the rapid in situ preservation of cadaver kidneys has been designed. Used in combination with equipment routinely found in any hospital, it can cool human kidneys in situ to 10-15 C and maintain this temperature until nephrectomy can be performed. Kidenys preserved with this catheter have functioned after transplantation into suitable recipients. This report describes the design and laboratory evaluation of this new device, its clinical effectiveness and technique of insertion.     

What price support? Ventricular assist device induced systemic response

Use of ventricular support systems has been associated with myriad systemic complications. Engendered by the blood-biomaterial interface of a unique host/device relationship, these complications include diverse humoral dyscrasias that frequently culminate in episodes of bleeding, hemolysis and thrombogenicity, heightened susceptibility to inflammation and infection, and transient immunal compromise. Recent endeavor in biocompatibility research has served to illustrate the critical role played by cellular, humoral, and neurohormonal components in regulating cytokine expression and has provided insight into the complexities involved in such biomechanical juxtapositions. The following is intended as a review of current literature attempting to address the many aspects of this host/device interaction and their consequences for the supported patient.     

Correlation between plasma neurohormone levels and left ventricular functional and morphological improvement in LVAD patients

Objective: Certain neurohormones (e.g., brain natriuretic peptide (BNP), endothelin-1 (ET-1)) have demonstrated reliability as clinical markers of left ventricular (LV) function. The aim of this study was to examine the relationship between plasma levels of these neurohormones, LV function and histological evidence of morphological improvement in left ventricular assist device (LVAD) recipients to determine whether serial hormonal expression may be used to assess cardiac status in the LVAD setting. Methods: Plasma levels of BNP and ET-1 were measured in 19 end-stage congestive heart failure patients directly before and up to 18 weeks after implantation with various devices (DeBakeyVAD, Novacor, TCI HeartMate). Echocardiographic indices corresponding to the time-points of serial hormonal measurement were evaluated. Immunohistochemical collagen staining of LV tissue samples derived from LVAD patients at the time of device insertion and removal were then contrasted. Patients were grouped according to device employed and etiology (ischemic/dilated cardiomyopathy, ICMP/DCMP). Results: LVAD therapy significantly enhanced LV ejection fraction (EF%: 21% ± 3.8% to 37% ± 11.39%) and cardiac output (CO: 3.49 ± 1.3 to 7.3 ± 0.2 l/m) in all patients; other parameters were not appreciably altered. Absolute BNP and ET-1 plasma levels remained significantly lower in all patients after LVAD implantation (both: p < 0.001). The NOV group exhibited the most BNP reduction and EF% increase (p < 0.0004 and p < 0.038, respectively), whereas ET-1 was lower in the DVAD group (p < 0.06). In all categories, the ICMP group experienced more significant change when compared to those in the DCMP grouping. Collagen levels were sharply reduced in all patients (p < 0.0005); however, while those in the DVAD demonstrated the most evident change (p < 0.0036), there was little difference between the DCMP/ICMP groups (p < 0.012 vs p < 0.022). Both BNP and ET-1 manifested bi-phasic tendencies and an inverse proportionality to EF% measurements. Conclusions: Plasma BNP and ET-1 levels appear to correlate both with device-related LV functional and myocardial morphological improvement and may be of potential use as therapeutic indicators.