MoMa脑保护装置在颈动脉狭窄支架置人术中的作用

目的 探讨颈动脉狭窄支架置人术中使用MoMa脑保护装置的作用.方法 回顾性分析2008年12月-2010年5月,对6例颈内动脉重度狭窄的患者行颈动脉支架置人术并使用MoMa脑保护装置的临床资料.结果 ①6例患者的临床症状均获得改善,NIHSS评分较术前提高1-2分.②保护装置的滤网中均可见捕获的小斑块,无一例患者发生栓子脱落事件,颈内动脉重度狭窄均得到改善（残余狭窄率均〈30%）.③术后3d及3个月复查头部MRI,均未发现新发的缺血病灶.有1例在使用Moma脑保护装置过程中,血液从颈外动脉逆流而加用远端脑保护装置;1例术后出现急性冠状动脉综合征,经积极治疗后好转.6例患者术后3个月复查颈部血管彩超均未发现再狭窄.结论 对颈动脉重度狭窄的患者行支架置人术时,使用MoMa脑保护装置是相对安全、有效的,但尚需大样本病例的进一步研究.     

肉苁蓉花粉生活力测定研究

目的了解肉苁蓉花粉在自然条件下的寿命。方法采用花粉离体萌发法，对自然生长的肉苁蓉花粉生活力进行测定研究。结果肉苁蓉花粉萌发的最佳条件为初花期花粉，在恒温25℃，以0．6％琼脂 10％蔗糖 0．1％硼酸为离体培养基进行培养，有利于花粉的萌发和花粉管的生长；低温(4℃)条件下可进行短期的花粉贮藏，延长花粉的寿命。结论为采用肉苁蓉花粉进行优良种质资源的保存和人工育种工作提供了理论依据。     

肉苁蓉多糖对衰老小鼠脂质过氧化的影响

目的:研究肉苁蓉多糖(polysacchridesofcistanchedeserticolaY.C.Ma,PCD)对亚急性衰老小鼠的抗 脂质过氧化作用。方法:使用D 半乳糖造成小鼠亚急性衰老模型,观察PCD对亚急性衰老小鼠血液和肝脏组 织中超氧化物岐酶(SOD)、脂质过氧化物(LPO)的含量的影响。结果:灌服肉苁蓉多糖衰老小鼠的血液和肝脏 组织中SOD明显高于模型组(P<0.05);LPO的含量明显低于模型组(P<0.05)。结论:肉苁蓉多糖具有明显 的抗脂质过氧化功能,防止亚急性衰老小鼠的组织脂质过氧化损伤。     

荒漠肉苁蓉茎腐病的初步研究

目的分离和鉴定肉苁蓉茎腐病病原菌,研究其生物学特性,并室内筛选对该病原菌有效的杀菌剂。方法组织分离法和菌丝尖端纯化法得到主要病原菌,通过测量不同营养条件下菌落生长直径研究其生物学特性,平皿菌丝生长抑制法进行杀菌剂的生物测定。结果接骨木镰刀菌Fusariumsambucinum是肉苁蓉茎腐病的主要病原菌,为首次记录;适合其生长的培养基为PSA培养基,对碳和氮的吸收主要以蔗糖和蛋白胨为主,适宜生长温度为10～30℃,适宜生长pH为6～8;多菌灵、菌线威、绿享二号在室内可以有效地抑制病原菌。结论该病原菌的分离鉴定可以为该病害原的防治提供理论依据。     

多波长线性回归法同时测定安痛定注射液中的三组分

目的：对安痛定注射液中的三组分实行分光光度法同时测定。方法：对传统的多波长线性回归分光光度法进行改进,使其不需要等吸收波长。结果：９份模拟样品中氨基比林、安替比林、巴比妥的平均回收率分别为９９．９％、９９．８％、１００．３％,相对标准偏差分别为０．５％、１．０％、１．７％。对３个批号实际样品的测定结果与标准方法一致。结论：方法简便快捷,适于安痛定注射液的制剂分析。     

来自于肉苁蓉的一个新天然产物(英)

从中药肉苁蓉（CistanchedeserticolaY.C.Ma）中得到一个新天然产物,2,5-二氧-4-咪唑烷基-氨基甲酸,经光谱鉴定和X-射线衍射推定其化学结构和立体构型。     

肉苁蓉化学成分的研究

从列当科植物肉苁蓉Ｃｉｓｔａｎｃｈｅ ｄｅｓｅｒｔｉｃｏｌａ中分得１０个化合物,通过理化常数,光谱数据及Ｘ－衍射分别鉴定为苁蓉素,梓醇,丁香苷,红景天苷,２,５－二氧－４－咪唑烷基－氨基甲酸,甘露醇,硬脂酸,β－谷甾醇,胡萝卜苷和甜菜碱。其中Ⅴ为新的天然产物,Ⅱ为首次从本属植物中分得,Ⅰ,Ⅲ,Ⅳ为首次从该种植物中分得。     

Lactobacillus acidophilus Induces a Strain-specific and Toll-Like Receptor 2–Dependent Enhancement of Intestinal Epithelial Tight Junction Barrier and Protection Against Intestinal Inflammation

Defective intestinal tight junction (TJ) barrier is an important pathogenic factor of inflammatory bowel disease. To date, no effective therapies that specifically target the intestinal TJ barrier are available. The purpose of this study was to identify probiotic bacterial species or strains that induce a rapid and sustained enhancement of intestinal TJ barrier and protect against the development of intestinal inflammation by targeting the TJ barrier. After high-throughput screening of >20 Lactobacillus and other probiotic bacterial species or strains, a specific strain of Lactobacillus acidophilus, referred to as LA1, uniquely produced a marked enhancement of the intestinal TJ barrier. LA1 attached to the apical membrane surface of intestinal epithelial cells in a Toll-like receptor (TLR)-2–dependent manner and caused a rapid increase in enterocyte TLR-2 membrane expression and TLR-2/TLR-1 and TLR-2/TLR-6 hetero-complex–dependent enhancement in intestinal TJ barrier function. Oral administration of LA1 caused a rapid enhancement in mouse intestinal TJ barrier, protected against a dextran sodium sulfate (DSS) increase in intestinal permeability, and prevented the DSS-induced colitis in a TLR-2– and intestinal TJ barrier–dependent manner. In conclusion, we report for the first time that a specific strain of LA causes a strain-specific enhancement of intestinal TJ barrier through a novel mechanism that involves the TLR-2 receptor complex and protects against the DSS-induced colitis by targeting the intestinal TJ barrier.

Intestinal epithelial tight junctions (TJs) are the apical-most junctional complexes and act as a functional and structural barrier against the paracellular permeation of harmful luminal antigens, which promote intestinal inflammation.¹ The increased intestinal permeability caused by defective intestinal epithelial TJ barrier or a leaky gut is an important pathogenic factor that contributes to the development of intestinal inflammation in inflammatory bowel disease (IBD) and other inflammatory conditions of the gut, including necrotizing enterocolitis and celiac disease.^2,3 Clinical studies in patients with IBD have found that a persistent increase in intestinal permeability after clinical remission is predictive of poor clinical outcome and early recurrence of the disease, whereas normalization of intestinal permeability correlates with a sustained long-term clinical remission.4, 5, 6 Accumulating evidence has found that a defective intestinal TJ barrier plays an important role in exacerbation and prolongation of intestinal inflammation in IBD. Currently, no effective therapies that specifically target the tightening of the intestinal TJ barrier are available.Intestinal microbiota play an important role in modulating the immune system and in the pathogenesis of intestinal inflammation.⁷ Patients with IBD have bacterial dysbiosis in the gut, characterized by a decrease in bacterial diversity and an aberrant increase in some commensal bacteria, which are an important factor in the pathogenesis of intestinal inflammation.^8,9 Normal microbial flora of the gastrointestinal tract consists both of bacteria that are known to have beneficial effects (probiotic bacteria) on intestinal homeostasis and bacteria that could potentially have detrimental effects on gut health (pathogenic bacteria).¹⁰ The modulation of intestinal microflora affects the physiologic and pathologic states in humans and animals. For example, fecal transplantation from healthy, unaffected individuals to patients with refractory Clostridium difficile colitis is curative in up to 94% of the treated patients, and transfer of stool microbiome from obese mice induces obesity in previous lean mice, whereas transfer of microbiome from lean mice preserves the lean phenotype.11, 12, 13 The beneficial effects of gut microbiota are host and bacterial species-specific.¹⁴ Although multiple studies indicate that some commensal bacteria play a beneficial role in gut homeostasis by preserving or promoting the intestinal barrier function, because of conflicting reports, it remains unclear which probiotic species cause a persistent predictable enhancement in the TJ barrier and could be used to treat intestinal inflammation by targeting the TJ barrier. For example, some studies suggest that Lactobacillus acidophilus, Lactobacillus casei, Lactobacillus plantarum, or Lactobacillus rhamnosus cause a modest enhancement in the intestinal epithelial TJ barrier, whereas others have found minimal or no effect of these probiotic species on the intestinal TJ barrier.15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25 The major aim the current study was to perform a high-throughput screening of Lactobacillus and other bacterial species to identify probiotic species that induce a rapid, predictable, and marked increase in the intestinal epithelial TJ barrier and protect against the development of intestinal inflammation by preserving the intestinal TJ barrier.In the studies described herein, most of the probiotic species tested (>20 species or strains) had a modest or minimal effect on intestinal TJ barrier function. L. acidophilus uniquely caused a rapid and marked increase in intestinal TJ barrier function. Further analysis indicated that the effect of L. acidophilus was strain-specific, limited to a specific strain of L. acidophilus, and did not extend to other L. acidophilus strains. The L. acidophilus enhancement of the intestinal TJ barrier was mediated by live bacterial-enterocyte interaction that involved Toll-like receptor (TLR)-2 heterodimeric complexes on the apical membrane surface of intestinal epithelial cells. Our animal studies also found that L. acidophilus causes a marked enhancement in mouse intestinal barrier function and protects against the dextran sodium sulfate (DSS)–induced colitis by preserving and augmenting the mouse intestinal barrier function in a strain-specific manner.     

巴马小型猪脑死亡状态下血清炎症介质的改变及在肝脏损伤中的作用

目的：探讨巴马小型猪在脑死亡状态下血清炎症介质的变化及对肝脏损伤的作用。方法:巴马小型猪10只，随机分脑死亡组与对照组，每组5只。用颅内加压法建立脑死亡模型，对照组仅开颅麻醉维持，分别于3、6、12、18和24h取血清测丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）及IL-1β、IL-6和TNF-α水平。结果:（1）炎症介质变化：脑死亡组动物血清IL-1β、IL-6和TNF-α水平均自脑死亡后3h开始升高，并随时间的延长而继续升高；脑死亡后3、6、12、18和24 h脑死亡组明显高于对照组（P<0.05）。（2）肝脏酶学变化：血清ALT、AST水平自脑死亡后12 h开始升高，并随时间的延长而继续升高；脑死亡后12、18和24 h脑死亡组明显高于对照组（P<0.05）。结论：巴马小型猪脑死亡状态下血清炎症介质升高，并随时间的延长而继续升高。脑死亡状态下肝脏功能的损伤可能与这些炎症介质的水平升高有关。     

马加爵仇恨杀友的行为及心理过程研究

目的为了探讨和预防类似马加爵仇恨杀友的行为和心理规律，加强对大学生的心理和思想政治教育．使他们健康成长为社会主义事业的接班人和建设者。方法通过社会、学校调查，依据相关的理论，借鉴相关的文献、资料以及定性、定量分析等方法研究马加爵仇恨杀友的行为和心理过程。结果马加爵仇恨杀友的行为过程：预谋策划阶段，周密实施阶段，精心逃跑阶段。马加爵仇恨杀友的心理过程：萌发阶段——自卑心理，发展阶段——压抑心理，爆发阶段——绝望心理。从马加爵残酷杀害学友中得到的启示。结论只要大学生的心理健康和思想政治教育等工作到位，马加爵杀人犯罪的行为是完全可以预防和避免的。