芦沙坦的降压效应和内、外侧缰核神经元单位放电的关系

目的和方法 :观察腹腔注射 (i.p) 2mg kg和 10mg kg芦沙坦 (losartan)对大鼠股动脉血压 (aterialbloodpressure ,AP)和心率 (heartrate,HR)的影响以及与缰核 (Hb)神经元活动的关系。用玻璃微电极记录内侧缰核 (MHb)、外侧缰核(LHb)神经元单位放电活动 ,观察 10mg kg芦沙坦对其放电频率的影响。结果 :2mg kg芦沙坦对大鼠AP和HR无明显影响 ;(10mg kg芦沙坦可显著降低大鼠动脉血压 ,但对心率无明显影响。 10mg kg芦沙坦可使LHb内 6 6 6 6 % 12 18)神经元单位放电频率增加 ,使MHb内 6 1 90 % (13 2 1)神经元单位放电频率减少。结论 :10mg kg芦沙坦可明显地降低大鼠AP ,但 2mg kg芦沙坦对AP无明显影响 ;10mg kg芦沙坦可兴奋LHb和抑制MHb,产生降压效应     

缰核神经元阿片受体的分布特征

目的: 用膜片钳方法探索内侧缰核(MHb),外侧缰核(LHb)阿片受体的类型.方法: 急性分离出生后10～15 d的大鼠缰核神经元,用全细胞电压钳记录方式记录其K 通道电流.以DAGO(μ受体激动剂),DPDPE(σ受体激动剂)区分MHb,LHb分别含有的阿片受体类型.结果: 在缰核可记录到两种类型的K 通道,快(瞬时)整流 K 通道(IA)和慢(延时)整流 K 通道(IK).DAGO,DPDPE使两种类型的K 通道电流增加.结论: MHb有较高密度的σ受体的分布;LHb以μ受体类型分布为主.     

可卡因对外侧缰核神经元的作用及机制初探

目的：探讨可卡因对外侧缰核神经元的作用及可能机制。方法：腹腔注射可卡因,观察内、外侧缰核神经元c—Fos蛋白的表达;在外侧缰核微电泳可卡因,观察其痛相关神经元自发及痛诱发放电的改变：应用全细胞膜片钳技术观察可卡因对外侧缰核神经元延迟整流K^＋电流的影响：结果：①可卡因明显增加外侧缰核c—Fos蛋白表达,但不明显增加内侧缰核c—Fos蛋白表达。②微电泳可卡因至外侧缰核,引起外侧缰核痛兴奋神经元放电增加和痛诱发反应增强,痛抑制神经元放电减少和痛诱发反应减弱.③膜片钳研究显示,可卡因抑制外侧缰核延迟整流K^＋通道,导致K^＋电流减少。结论：外侧缰核神经元对可卡因有较高的敏感性,可卡因能兴奋多数外侧缰核神经元,可能是由于其抑制神经元延迟整流K^＋通道开放产生的.     

八肽胆囊收缩素对抗吗啡对丘脑束旁核痛反应神经元放电的影响

已知脑室注射硫化八肽胆囊收缩素(CCK-8)对吗啡镇痛效应(用辐射热甩尾反应的潜伏期作测痛指标)有对抗作用。本工作研究了脑室注射CCK-8对吗啡引起的大鼠丘脑两侧束旁核痛反应神经元同时电变化的影响。结果如下:(1)腹腔注射吗啡(10mg/kg)可抑制痛兴奋神经元(PEN)和加强痛抑制神经元(PIN)的电活动。(2)脑室注射CCK-8(15ng/15μl)能对抗吗啡引起PEN放电的抑制作用和PIN电活动的加强作用。无硫CCK-8对吗啡的效应没有对抗作用。(3)注射CCK-8可同时对抗吗啡对束旁核中一个PEN的抑制作用和一个PIN的加强作用。上述结果与甩尾阈测痛的结果一致,即CCK-8对吗啡引起的镇痛效应有明显的对抗作用。     

损毁缰核对应激性高血压形成的影响

目的和方法 :运用核团损毁和微量注射的方法观察损毁缰核 (Hb)对应激性高血压 (SIH)形成进程的影响及SIH大鼠Hb内神经元对L 谷氨酸 (Glu)反应性的变化。结果 :①损毁双侧Hb延缓了SIH的形成进程 ;②在SIH大鼠内侧Hb(MHb)微量注射不同浓度的CIu ,血压明显升高 ,呈浓度依赖性 ,升高值与正常大鼠MHb注入等量GIu引起的升高值相比 ,有显著性差异 (P <0 .0 5 ) ;③在SIH大鼠外侧Hb(LHb)注入不同浓度的Glu ,血压明显下降 ,也呈浓度依赖性 ,下降值与正常大鼠LHb注入等量Glu引起的下降值相比 ,有显著性差异 (P <0 .0 5 )。结论 :损毁Hb延缓了SIH的形成进程 ,SIH大鼠Hb对Glu的敏感性提高了 ,Hb参与SIH的形成 ,且其作用有部位特异性。     

大鼠扣带回前部对外侧缰核单位放电的抑制作用

电刺激扣带回前部,对75％的外侧缰核痛兴奋神经元(pain-excitative neuron of lateral habenular nucleus,LHPE)和75％的痛抑制神经元(pain-inhibitive neuron of lateral habenular nucleus,LHPI)的自发放电均产生抑制作用,并取消躯体和内脏伤害性刺激对外侧缰核(lateral habenular nucleus,LHN)单位放电的影响。扣带回内微量注射吗啡可以抑制LHPE的自发放电,并取消伤害性刺激对LHPE的增频效应。注射纳洛酮则使LHPE的自发放电增多,加强伤害性刺激对LHPE的增频作用,并可拮抗电针对LHPE伤害性刺激反应的抑制作用。     

褪黑色素对缰核痛神经元单位放电的影响及可能机制

目的通过观察褪黑色素对缰核痛神经元单位放电的影响,进一步证明褪黑色素的中枢镇痛作用及可能机制。方法：应用细胞外神经元单位放电记录方法,记录缰核神经元痛相关神经元放电,并观察外侧缰核痛神经元在褪黑色素作用下电活动的改变,及对伤害性刺激痛敏感性的改变,在此基础上观察纳洛酮的翻转作用。结果：褪黑色素影响外侧缰核痛神经元的电活动,并使外侧缰核痛神经元对伤害性刺激敏感性降低,此种作用可被纳洛酮翻转。结论：褪黑色素可通过作用于外侧缰核的阿片受体而影响其痛相关神经元对痛刺激的反应,这可能是褪黑色素中枢镇痛机制之一。     

刺激大鼠伏核和伏核内微量注射纳洛酮对外侧缰核“痛”单位放电的影响

在清醒、肌肉麻痹状态下的大鼠,观察到重复电刺激伏核对外侧缰核痛兴奋单位(LHPE)自发放电和痛诱发放电有明显的抑制作用。腹腔注射纳洛酮(6mg/kg体重)可阻断这种抑制作用。而电刺激伏核对外侧缰核痛抑制单位放电有兴奋作用。双侧伏核内微量注射纳洛酮(1.8ug,4min注完)使 LHPE 放电增加,注射吗啡(15ug,4min注完)可抑制 LHPE 放电。本文就以上结果在针刺镇痛中的意义进行了讨论。     

八肽胆囊收缩素对吗啡成瘾大鼠中枢痛觉的调制

目的:观察八肽胆囊收缩素(CCK-8)对正常及吗啡成瘾大鼠尾核中痛兴奋神经元(PEN)电活动的影响,从而进一步探讨中枢CCK-8和尾核在吗啡成瘾大鼠痛觉调制中的作用.方法:70只Wistar大鼠随机分为2组:正常对照组35只(又分为生理盐水组巧只和CCK-8组20只)及吗啡成瘾组35只、(又分为生理盐水组15只和CCK-8组20只).大鼠背部皮下注射递增剂量吗啡,依次为5、10、20、40、50、60mg/kg,3次/d(8:00,12:00,16:00),连续给药6d,建立吗啡成瘾大鼠的模型.正常对照组大鼠背部皮下注射生理盐水,时间、剂量均与吗啡成瘾组相同.第7天8:00观察大鼠的自然戒断症状30min后开始实验.实验以电脉冲刺激大鼠的坐骨神经作为伤害性痛刺激,用玻璃微电极记录尾核中PEN的放电,观察尾核内注入CCK-8对PEN电活动的影响.结果:实验结果表明:①CCK-8可提高正常大鼠尾核中PEN的兴奋性,即25个PEN平均秒净增值由注射CCK-8前(100%)增加到(224.34±10.81)5,潜伏期缩短到(54.69±5.62)%.②CCK-8使吗啡成瘾大鼠尾核中PEN的兴奋性也增高,22个PEN的平均秒净增值比注药前(100%)提高了(118.93±8.50)%,潜伏期缩短了(33.96±7.23)%.结论:CCK-8可使吗啡成瘾与正常大鼠尾核中PEN对电刺激的兴奋性增强,均呈易化疼痛作用,证明中枢CCK-8系统和尾核在吗啡成瘾过程和疼痛的调节中都起到了一定的作用.     

孕烷醇酮对应激性高血压大鼠血压的影响

实验探讨了孕烷醇酮(pregnanolone,PGN)对应激性高血压(stress-induced hypertension,SIH)大鼠血压影响的可能机制。采用电击足底结合噪声应激刺激的方法制备应激性高血压大鼠模型,观察每天应激刺激前腹腔注射PGN(0.24 mg/kg)对应激大鼠血压的影响,并观察PGN对应激刺激引起大鼠血中血管紧张素Ⅱ(angiotensin Ⅱ,Ang Ⅱ)含量和大鼠脑内Fos蛋白样免疫反应(FLI)神经元表达的影响。将动物随机分为正常对照组、应激1 h组、应激1 h PGN组、应激15 d组和应激15 d PGN组。实验结果如下:应激15 d PGN组大鼠尾动脉收缩压升高幅值较应激15 d组大鼠尾动脉收缩压升高幅值明显降低(P<0.001)。同时,应激1 h组及应激15 d组血中Ang Ⅱ含量与对照组相比有显著升高(均P<0.001);应激1 h PGN组及应激15 d PGN组大鼠血中Ang Ⅱ含量分别显著低于应激1 h组及应激15 d组(均P<0.05);应激15 d组血中Ang Ⅱ含量较应激1 h组高(P<0.05)。正常对照组、应激15 d组、应激15 d PGN组大鼠脑内仅见少数FLI神经元。与对照组相比,应激1 h组大鼠脑内外侧缰核(LHb)、内侧缰核(MHb)、室旁核(PVN)、杏仁中央核(CeA)和下丘脑外侧区(LH)等部位可见FLI神经元显著增加,而腹腔注射PGN后再应激1 h,可抑制上述效应。结果提示,PGN可抑制SIH大鼠血压升高的程     

Recent advances in the study of Kaposi's sarcoma-associated herpesvirus replication and pathogenesis

It has now been over twenty years since a novel herpesviral genome was identified in Kaposi's sarcoma biopsies. Since then, the cumulative research effort by molecular biologists, virologists, clinicians, and epidemiologists alike has led to the extensive characterization of this tumor virus, Kaposi's sarcoma-associated herpesvirus(KSHV; also known as human herpesvirus 8(HHV-8)), and its associated diseases. Here we review the current knowledge of KSHV biology and pathogenesis, with a particular emphasis on new and exciting advances in the field of epigenetics. We also discuss the development and practicality of various cell culture and animal model systems to study KSHV replication and pathogenesis.     

The structure, reproduction and taxonomy of Vidalia and Osmundaria (Rhodophyta, Rhodomelaceae)

Comprises species occurring mostly in subtidal habitats in tropical, subtropical and warm-temperate areas of the world. An analysis of the type species, V. spiralis (Sonder) Lamouroux ex J. Agardh, a species from Australia, establishes basic characters for distinguishing species in the genus. These characters are (1) branching patterns of thalli, (2) flat blades that may be spiralled on their axis, (3) width of the blade, (4) primary or secondary derivation of sterile and fertile branchlets and (5) position of sterile and fertile branchlets on the thalli. Application of the latter two characters provides an important basic method for separation of species into three major groups. Osmundaria , a genus known only in southern Australia, was studied in relation to Vidalia , and its separation from the Vidalia assemblage is not accepted. Species of Vidalia therefore are transferred to the older genus name, Osmundaria. Two new species, Osmundaria papenfussii and Osmundaria oliveae are described from Natal. Confusion in the usage of the epithet, Vidalia fimbriala Brown ex Turner has been clarified, and Vidalia gregaria Falkenberg, described as an epiphyte on Osmundaria pro/ifera Lamouroux, is revealed to be young branches of the host, Osmundaria prolifera.     

New or rare chromosome counts in Artemisia L. (Asteraceae, Anthemideae) and related genera from Kazakhstan

Fifteen chromosome counts of six Artemisia taxa and one species of each of the genera Brachanthemum, Hippolytia, Kaschgaria, Lepidolopsis and Turaniphytum are reported from Kazakhstan. Three of them are new reports, two are not consistent with previous counts and the remainder are confirmations of very scarce (one to four) earlier records. All the populations studied have the same basic chromosome number, x = 9, with ploidy levels ranging from 2x to 6x. Some correlations between ploidy level, morphological characters and distribution are noted.     

肝癌中HBV和HCV基因和抗原的分布及意义

采用原位分子杂交方法检测HCV RNA及HBV X基因;采用免疫组织化学方法研究HCV核心抗原,非结构区C33c抗原及HBxAg在肝细胞肝癌中的定位及分布.结果表明(1)HCV RNA、HBV X基因在肝细胞肝癌组织检出率分别为40%(55/136)和82%(112/136).HCV RNA定位于癌细胞的胞浆内,阳性细胞呈散在、灶状及弥漫分布三种形式;HBV X基因在肝癌细胞中的分布呈胞浆型、核型及核浆型,阳性细胞也呈上述三种分布形式;(2)HCV C33c抗原、核心抗原在肝细胞肝癌中的阳性率为81%(133/164)及86%(141/164).C33c抗原定位于癌细胞及肝细胞的胞浆内;核心抗原既定位于癌细胞核中,又可定位于胞浆中.C33c抗原阳性细胞以灶状分布为主;而核心抗原阳性细     

Selection with two alleles and complete dominance

For a plant selection model with frequency-independent viabilities, fertilities and selfing rates, it is shown that apart from global fixation, for certain parameter combinations a protected polymorphism and facultative fixation (either allele may become fixed according to initial frequencies) may both occur. Facultative fixation requires different selling rates for the dominant and recessive type. Protection of the polymorphism requires resource allocation for male and female function. In this connection the problem of purely genetically caused population extinction is discussed.
For general frequency dependence and regular segregation, the chances for establishment of a completely recessive gene are compared to those of a completely dominant gene. It is proven that the process of establishment of the recessive gene, despite a fitness advantage, may be considerably endangered by drift effects if random mating prevails. The recessive gene may reach the same effectivity in establishment as a dominant gene, only if the recessive homozygote mates exclusively with its own type during the period of establishment.