HPLC和1HNMR分析确定cis-A-和cis-B-羟甲芬太尼的组成和构型

羟甲芬太尼(1)是一个强效的镇痛剂和高亲和、高选择性的阿片μ受体激动剂。通过HPLC和¹HNMR分析,cis-A-l被确定为由等量的cis-(+)-(3R,4S,2'S)-l和:cis-(—)-(3S,4R,2'R)-1组成的外消旋体,cis-B-l被确定为由等量的cis-(—)-(3R,4S,2'R)-1和cis-(+)-(3S/,4R,2'S)-1组成的外消旋体。     

激素敏感型肾病综合征小儿的HLA

为了解中国汉族儿童激素敏感型肾病综合征与ＨＬＡ的关系，研究了３７名该病患儿的ＨＬＡ－Ａ，Ｂ，ＤＲ，ＤＱ抗原频率，ＨＬＡ－Ａ，Ｂ抗原与本病无关联，ＨＬＡ－ＤＲ７抗原频率（３７．８４％）较对照组（１１．２３％）有显著性增高（Ｐｃ＝１．７×１０－３），ＨＬＡ一ＤＱ抗原较对照组低（３２．４３％与６１．４０％，Ｐｃ＝７．７×１０－３），频复发或频反复病人与ＨＬＡ－ＤＲ９抗原相关（Ｐｃ＝２．９×ｌ０－２）。支持该病有免疫遗传基础的假说     

欧芹素乙和异欧芹素乙对小鼠腹腔巨噬细胞体外释放肿瘤坏死因子的抑制作用

研究了欧芹素乙（Ｉｍｐｅｒａｔｏｒｉｎ，Ｉｍｐ）和异欧芹素乙（Ｉｓｏ－ｉｍｐｅｒａｔｏｒｉｎ，Ｉｓｉ）及对照药物维拉帕米（Ｖｅｒａｐａｍｉｌ，Ｖｅｒ）对小鼠腹腔巨噬细胞体外释放肿瘤坏死因子（Ｔｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒ，ＴＮＦ）的影响。结果表明：Ｉｍｐ、Ｉｓｉ及Ｖｅｒ对小鼠腹腔巨噬细胞体外释放ＴＮＦ具有显著的抑制作用。药物浓度在１０－６～１０－４ｍｏｌ／Ｌ范围内，该抑制作用呈剂量依赖性：药物浓度达１０－４ｍｏｌ／Ｌ时，则可完全抑制ＴＮＦ的释放。     

微创经皮钢板骨桥接术联合锁定加压钛板治疗胫骨远端骨折

目的探讨微创经皮钢板骨桥接术（minimallyi nvasive percutaneous plate osteosynthesis，MIPPO）联合锁定加压钛板（locking compression plate，LCP）治疗胫骨远端骨折的近期疗效。方法2004年6月～2006年3月采用MIPPO联合LCP治疗胫骨远端骨折16例，AO分型：43A1型7例，43A3型5例，43B1型2例，43C3型2例。采用3种方法复位胫骨骨折后插入LCP，用锁定螺钉固定。结果16例随访5～20个月，平均11，5月。16例切口一期愈合，骨折无延迟愈合、畸形愈合、断钉、断板等并发症。术后X线检查4～12周（平均7．6周）骨痂形成并开始部分负重，8～20周骨性愈合（平均16周），此时开始完全负重。3例出现胫骨远端内植物局部不适。根据美国足踝骨科学会评分系统对踝关节功能评分，优14例（87．5％），良2例（12，5％）。结论MIPPO具有创伤小、固定牢靠、可早期功能锻炼等优点，近期疗效满意，是治疗胫骨远端骨折的有效方法。     

<Emphasis Type="Italic">p</Emphasis>-Glycoprotein ABCB5 and YB-1 expression plays a role in increased heterogeneity of breast cancer cells: correlations with cell fusion and doxorubicin resistance

Background  

Cancer cells recurrently develop into acquired resistance to the administered drugs. The iatrogenic mechanisms of induced chemotherapy-resistance remain elusive and the degree of drug resistance did not exclusively correlate with reductions of drug accumulation, suggesting that drug resistance may involve additional mechanisms. Our aim is to define the potential targets, that makes drug-sensitive MCF-7 breast cancer cells turn to drug-resistant, for the anti-cancer drug development against drug resistant breast cancer cells.     

推拿并牵引治疗腰椎间盘突出症230例

笔者2006年3月～2008年5月应用牵引配合手法推拿治疗腰椎间盘突出症230例，收到满意疗效，总结如下。     

The adverse effect of treatment prolongation in cervical cancer by high-dose-rate intracavitary brachytherapy.

BACKGROUND AND PURPOSE: The potential risk of prolongation of treatment time in cervical cancer has been reported for many low-dose rate (LDR) studies, with an estimated loss of local control ranging from 0.3 to 1.6% per day of treatment prolongation. Since the treatment schedule for fractionated high-dose rate intracavitary brachytherapy (HDRICB) is not directly comparable with that for low-dose rate studies, this report aims to evaluate the adverse effect of treatment prolongation specifically for cervical cancer treated with HDRICB. MATERIAL AND METHODS: From September 1992 to December 1997, 257 patients diagnosed with uterine cervical cancer (35 Ib, 26 IIa, 122 IIb, 10 IIIa, 57 IIIb, 7 IVa), who underwent external radiotherapy combined with between two and four courses of HDRICB and a minimum of 3 years of follow-up (median 57 months), were analyzed. Treatment consisted of irradiation of the whole pelvis with 44-45 Gy consisting of 22-25 fractions by 5 weeks, with the dose boosted to 54-58 Gy (with central shielding) for patients diagnosed as FIGO stage IIb-IVa bilateral parametrial disease. HDRICB was performed using an Ir-192 remote afterloading technique at 1-week intervals. The standard prescribed dose for each course of HDRICB was 7.2 Gy to point A for three insertions (before July 1995), or 6.0 Gy to point A for four insertions (after July 1995). Total prescribed point A doses (external beam radiotherapy+HDRICB) ranged from 58 to 71.6 Gy (median, 65.6 Gy) for stage IB-IIA, while analogous dosage for larger lesions (stage IIb-IVa) ranged from 59 to 75.6 Gy (median, 65.6 Gy). Kaplan-Meier and multivariate analyses were used to test the effect of treatment time on pelvic control rate (PCR) and cause-specific survival (CSS) at 5 years. RESULTS: Median treatment time was 63 days. For all stages of disease, the 5-year CSS and PCR were significantly different comparing treatment times of less than and greater than or equal to 63 days [83% and 65% (P=0.004], 93% and 83% (P=0.02), respectively]. These associations were also significant for stage Ib/IIa [97% and 79% (P=0.01), and 100% and 87% (P=0.02), respectively), but not for stage IIb [75% and 72% (P=0.79), and 93% and 87% (P=0.83), respectively] or stage III [66% and 49% (P=0.2), and 83% and 72% (P=0.21), respectively]. Multivariate analysis identified three prognostic factors for CSS, stage (P<0.001), tumor response to external RT (P=0.001), and overall treatment time (OTT; P=0.006). Prognostic factors for pelvic failure were stage (P<0.001), tumor response to external RT (P=0.001), and OTT (P=0.03). Prolongation of treatment time resulted in a daily decrease in pelvic control rate of 0.67% overall, and 0.43% for stage Ib-IIa, 0.57% for stage IIb, and 0.73% for stage III patients. CONCLUSION: Analysis of the data from the current study demonstrates that the adverse effect of treatment prolongation was observed later in the treatment course for the high-dose rate (HDR) series compared to the LDR analog, however, treatment-time prolongation still negatively influenced the cause-specific survival and pelvic control rate for both dosage groups.     

von Willebrand factor binding to platelet glycoprotein Ib-IX-V stimulates the assembly of an α-actinin-based signaling complex

Summary. Background: Pathological shear stress induces platelet aggregation that is dependent on von Willebrand factor (VWF) binding to glycoprotein (Gp)Ib‐IX‐V and phosphatidylinositol 3‐kinase activation. We tested the hypothesis that pathological shear stress stimulates phosphatidylinositol 3,4,5‐trisphosphate (PIP₃) synthesis by directing the assembly of a molecular signaling complex that includes class IA phosphatidylinositol 3‐kinase (PI 3‐KIA). Methods: Platelets were subjected to 120 dynes cm^?2 shear stress in a cone‐plate viscometer. Resting and sheared platelets were lyzed, immunoprecipitations of PI 3‐KIA performed, or lipids extracted for PIP₃ measurements. α‐Actinin was incubated with phosphatidylinositol 4,5‐bisphosphate (PIP₂), immunoprecipitated, and used as a substrate for in vitro PI 3‐KIA activity. Results: Pathological shear stress induces biphasic PIP₃ production. In resting platelets, PI 3‐KIA associates with α‐actinin and PIP₂. After exposure to shear stress, α‐actinin and PIP₂ rapidly disassociate from PI 3‐KIA. PI 3‐KIA then gradually re‐associates with PIP₂ and α‐actinin, and this complex becomes linked to GpIbα through the cytoskeleton. PIP₃ production and the observed changes in the association between α‐actinin, PIP₂, and PI 3‐KIA are inhibited when VWF binding to GpIbα is blocked. In a cell‐free system, α‐actinin binds PIP₂ and when the α‐actinin–PIP₂ complex is added to platelet PI 3‐KIA, PIP₃ production is stimulated. Conclusions: These results suggest that pathological shear‐induced VWF binding to GpIb‐IX‐V stimulates PIP₃ production through the assembly of an α‐actinin‐based complex that colocalizes PI 3‐KIA with substrate PIP₂.     

第一、二鳃弓综合征颜面不对称的整形外科矫治

目的探讨第一、二鳃弓综合征面部不对称畸形的整形外科矫治方法。方法根据第一、二鳃弓综合征患者临床及X线所示面部双侧不对称情况,采用健侧下颌骨外板去除、颧骨截骨降低;患侧下颌体、颧骨应用健侧下颌骨外板贴附植骨或高密度多孔聚乙烯(Medpor)假体置入等术式,配合颏部水平截骨颏成形术,以缩小面部双侧宽度的差异,矫治颜面不对称畸形。结果共矫治23例,经6个月至3年的术后随访观察,双侧面部宽度差异明显缩小,正面观面部不对称明显改善。结论第一、二鳃弓综合征面部骨骼发育畸形是三维方向的,双侧面骨宽度的差异,是造成正面观面部不对称的重要因素,根据受术者的具体情况,采用以上术式的组合,扩充患侧或同时缩窄健侧骨骼,进行面部骨性支架重建,可以取得良好的矫治效果。