在清醒家兔中电针对刺激下丘脑引起的防御反应的抑制作用

在清醒家兔中电刺激下丘脑背内侧区可引起血压升高、肾交感神经放电增加、心率减慢等一系列防御反应的表现。用低频电脉冲刺激一侧“足三里”穴20min,可明显抑制刺激下丘脑引起的防御反应。这种抑制效应在停止电针后仍能持续一段时间,但可被静脉内注射纳洛酮(0.4mg/kg)翻转。预先注射纳洛酮也能防止电针的抑制效应。损毁下丘脑基底部包括弓状核在内的局部区域后,电针对防御反应的抑制作用基本消失。在弓状核区微量注射 L-谷氨酸钠(50mM,1μl)也可抑制刺激下丘脑引起的防御反应。这种抑制效应同样可被静脉内注射纳洛酮翻转。以上实验结果表明,电针可抑制刺激下丘脑引起的防御反应,弓状核区的内啡肽神经元可能在电针对防御反应的抑制效应中起重要的作用。     

伏核在躯体传入冲动抑制防御性心血管反应中的作用及机制

损毁伏核可明显削弱电刺激腓深神经（ＤＰＮ）对兴奋下丘脑背内侧核诱发的升压反应和心肌缺血的抑制作用（Ｐ＜０．０５,Ｐ＜０．０１）。电刺激伏核可引起明显的降压效应。中脑中央灰质腹侧部（ｖＰＡＧ）微量注射纳洛酮可明显衰减伏核的减压效应;损毁ｖＰＡＧ甚至可翻转伏核的减压效应,引起轻度升压（Ｐ＜０．０１）。损毁弓状核后伏核的减压效应基本消失,弓状核内微量注射纳洛酮明显衰减伏的的减压效应。故ＤＰＮ传入冲动可能     

兔下丘脑弓状核区在躯体传入冲动抑制刺激下丘脑诱发的期前收缩中的作用

实验在62只乌拉坦、氯醛醣麻醉兔上进行,用三碘季铵酚制动,由人工呼吸机维持通气。电解损毁下丘脑弓状核区或者在该区微量注射纳洛酮(2μg/1μl)可消除刺激腓深神经对刺激下丘脑诱发的期前收缩的抑制作用。在下丘脑弓状核区微量注射吗啡(2μg/1μl)可减少刺激下丘脑诱发的期前收缩次数,而注射纳洛酮(2μg/1μl)则使期前收缩数增多。无论损毁延髓中线区或在中央灰质内微量注射纳洛酮(2μg/1μl),均可消除下丘脑弓状核区微量注射吗啡(2μg/1μl)对刺激下丘脑诱发的期前收缩的抑制作用。因而,在下丘脑弓状核区微量注射吗啡,可能经中脑中央灰质而发挥对刺激下丘脑诱发的期前收缩的抑制作用。     

家兔延髓腹侧区内注射吗啡对刺激下丘脑诱发室性期前收缩的抑制作用

家免63只,用乌拉坦(700mg/kg)和氯醛醣(35mg/kg)静脉麻醉,三碘季铵酚制动,在人工呼吸下进行实验。用电刺激下丘脑近中线区的方法诱发定性期前收缩(HVE)。双侧延髓腹侧区内微量注射吗啡(5μg 溶于0.5—1μl 中)可抑制 HVE。在双侧延髓腹侧区微量注射纳洛酬(2μg 溶于0.5—1μl 中)能阻断电刺激中缝核尾端或中缝核尾端内微量注射 L-谷氨酸钠(50mmol/L,0.5—1μl)对 HVE 的抑制效应,也能减少或消除刺激腓深神经对 HVE 的抑制作用。上述结果提示,延髓腹侧部阿片受体的激活可抑制 HVE;另外,腓深神经传入冲动也可能通过中缝核尾端激活延髓腹侧区的阿片受体而抑制 HVE。     

下丘脑弓状核区参与由中脑导水管周围灰质到伏核的上行镇痛通路

在家兔中脑导水管周围灰质(PAG)内微量注射吗啡产生的镇痛作用可被伏核内注射β-内啡肽抗体所对抗,在损毁下丘脑弓状核区(ARH)后该对抗效应消失。但损毁ARH并不影响PAG注射吗啡所引起的镇痛作用,也不影响伏核注射纳洛酮对于PAG内注射吗啡引起镇痛的对抗作用,以上结果提示,(1)从PAG到伏核的上行镇痛通路中有ARH及β-内啡肽能纤维参与;(2)除β-内啡肽以外,伏核内尚有其它阿片肽发挥镇痛作用。     

兴奋黑质对中缝大核神经元的抑制作用及其机制

本工作观察到在清醒、麻痹大鼠,电刺激黑质致密部(SN_C)或网状部(SN_R)均明显抑制中缝大核(NRM)神经元的自发放电;电针刺激双侧“足三里-三阴交”的同时,电刺激SN_C或SN_R可完全翻转电针对NRM神经元的兴奋效应,NRM神经元放电受抑制。将谷氨酸钠微量注入黑质,对中缝大核神经元亦具有抑制作用,电解损毁双侧中脑导水管周围灰质(PAG)腹外侧部或将多巴胺受体阻断剂氟哌啶醇注入该处,均可阻断此抑制效应。提示黑质对抗电针镇痛机制之一是通过其DA能投射纤维作用于PAG内的DA受体,进而抑制PAG-NRM系统而实现的。     

兔隔核刺激及隔核阿片受体在镇内脏痛中的作用

本工作以电刺激内脏大神经测定清醒家兔的内脏痛阈。实验观察到,以弱电流刺激隔核对内脏痛阈有升高、降低和无明显变化三种效应;向家兔双侧隔核注入阿片受体激动剂埃托啡(etorphine)2μg/2μl,注药后 5min,内脏痛阈即升高,维持 40min;静脉注射纳洛酮O.2mg/kg或 2μg/2μl纳洛酮注入中脑导水管周围灰质(PAG)均能阻断隔核内注入埃托啡的镇痛作用;电针刺激能抑制内脏痛,静脉注射纳洛酮 0.4mg/kg 能阻断这一效应,但对电针后效应无明显影响,向隔核内注入纳洛酮 2μg/2μl亦能阻断针效,而且后效应消失。结果提示,镇内脏痛与内阿片肽活动有关,隔核的阿片受体被激活即有明显抑制内脏痛的作用,其作用的传出通路可能通过 PAG;隔核的阿片受体参与电针镇内脏痛过程。     

蓝斑复合核区内微量注射去甲肾上腺素对刺激兔下丘脑诱发室性期前收缩的影响

在72只乌拉坦、氯醛糖麻醉兔,静脉注射三碘季铵酚后,在人工呼吸下进行实验。结果观察到,在家兔蓝斑复合核(Lo-So)区微量注射去甲肾上腺素(NE)或可乐宁(Clonidine)能减少刺激下丘脑诱发的室性期前收缩(HVE)数。而微量注射β-肾上腺素能受体阻断剂心得安、α_1肾上腺素激动剂甲氧胺(Methoxamine)或苯肾上腺素(Phenylephrine)、α肾上腺素能阻断剂育亨宾(Yohimbine)或阿片受体阻断剂纳洛酮则对 HVE 无明显影响。在 Lo-So 区微量注射 NE 对 HVE 的抑制效应不能被事先在该区注射心得安所阻断但能被事先静脉或 Lo-So 区注射育亨宾所阻断。NE 或可乐宁的抑制效应也均可被育亨宾所翻转。可乐宁的抑制效应还可被纳洛酮所翻转。电解损毁延髓中缝大核区可消除在 Lo-So 区微量注射 NE 或可乐宁对HVE 的抑制效应。上述结果提示,Lo-So 区α_2受体的兴奋可减少 HVE 数,这些作用可能依赖于延髓中缝大核区的完整。可乐宁对 HVE 的抑制作用可能有阿片受体的参与。     

兔孤束核腹外侧区微量注射谷氨酸钠及甘氨酸对弓状核诱发电位的影响

实验在６６只麻醉、制动,断双侧颈迷走神经和人工通气的家兔上进行。通过微量注射神经元胞体兴奋剂谷氨酸钠和神经元胞体抑制剂甘氨酸,改变孤束核腹外侧区神经元兴奋活动,探讨对下丘脑弓状核诱发电位的影响及其可能的机制和意义。实验结果如下：（１）孤束核腹外侧区微量注射谷氨酸钠,可使膈神经放电显著增加和使弓状核诱发电位Ｐ２及Ｎ２波幅显著降低;而微量注射甘氨酸则使膈神经放电显著减少和使弓状核诱发电位Ｐ２及Ｎ２波幅显著增大。（２）静脉注射纳洛酮对谷氨酸钠引起的膈神经放电兴奋效应无明显影响,但能翻转谷氨酸钠对弓状核诱发电位Ｐ２及Ｎ２波幅的抑制效应。提示：孤束核腹外侧区呼吸神经元的兴奋活动可扩散至弓状核,并对弓状核诱发电位产生影响,此影响可能是由内源性阿片系统参与而实现的。     

大鼠下丘脑弓状核对导水管周围灰质—中缝大核系统的兴奋机制及其在电针效应中的作用

清醒箭毒化雄性大白鼠,在人工呼吸维持下,1.分析下丘脑弓状核(AR)兴奋中缝大核(NRM)的机制:观察到电刺激 AR 对 NRM 的兴奋效应,可因切断双侧 AR 至导水管周围灰质(PAG)的β-内啡肽(β-End)能束、PAG 内双侧注射纳洛酮或抗β-End 血清而绝大部分消失,提示 AR 对 NRM 的兴奋效应,主要通过 AR 区β-End 能神经元轴突与 PAG-NRM 系统的直接联系而实现;2.检验 AR 至 PAG-NRM 的神经通路在电针效应中的作用:实验显示上丘水平去大脑后,电针兴奋 NRM 的效应完全消失,表明此效应主要依赖中脑以上结构实现;进一步分别用 Halász 氏刀游离 AR、切断 AR 至 PAG 的β-End 能束、PAG 内注射纳洛酮或抗β-End 血清后,也使电针效应基本上完全消失,说明电针使 NRM神经元兴奋的效应,主要通过 AR 与 PAG-NRM 间的β-End 能神经通路实现。     

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.