36 h完全睡眠剥夺对客体工作记忆相关电位的影响

目的:采用事件相关电位(ERP)技术探讨36 h完全睡眠剥夺对客体工作记忆的影响。方法:本研究采用自身前后对照设计,16名睡眠质量良好的健康大学生(平均年龄为23岁,年龄范围21～28岁)分别在清醒状态下及36 h完全睡眠剥夺后接受2-back客体工作记忆任务,同时采集脑电数据。选用重复测量方差分析的方法比较睡眠剥夺前后与客体工作记忆有关的P2、N2、P3成分的波幅和潜伏期的差异。结果:在36 h完全睡眠剥夺后,与客体工作记忆加工相关的N2波的潜伏期显著延长(P<0.05),波幅减少但未见统计学差异(P>0.05); P2波潜伏期显著延长(P<0.05),波幅未见明显变化(P>0.05)。P3波波幅、潜伏期未见统计学差异(P>0.05)。结论:36h的完全睡眠剥夺影响了客体工作记忆相关电位,损害了个体的客体工作记忆加工能力。     

不同睡眠剥夺时间对大鼠下丘脑内单胺类神经递质的影响

目的:探讨不同睡眠剥夺时间对大鼠认知功能的影响以及对下丘脑内单胺类神经递质去甲肾上腺素、多巴胺、五羟吲哚乙酸、五羟色胺的含量的影响。方法:32只健康雄性wistar大鼠随机分为4组,即96 h、120 h、144 h睡眠剥夺,正常对照组。利用睡眠剥夺箱建立大鼠SD模型,避暗穿梭法测试大鼠认知功能,高效液相电化学检测法测定下丘脑内单胺类神经递质含量。结果:大鼠避暗穿梭实验,与对照组比较,96 h、120 h组大鼠潜伏期显著缩短(P0.05);与对照组比较,各组大鼠下丘脑内NA含量均有下降(P0.05);与对照组比较,各组大鼠下丘脑内DA含量均显著下降,(P0.01),96 h、120 h、144 h组间比较,表现出含量逐渐减少的趋势;与对照组比较,各组5-HIAA含量均有上升,且120 h组明显高于其他各组(P0.05),其他组无显著性差异(P0.05);与对照组比较,各组5-HT含量均有升高,120 h、144 h组显著升高(P0.01),96 h组无显著性(P0.05)。结论:睡眠剥夺可以使大鼠中枢NA、DA含量下降,5-HIAA、5-HT含量升高,且随着睡眠剥夺时间的延长,变化更为明显,这可能是睡眠剥夺损害认知功能的原因之一。     

慢性睡眠剥夺加重APP/PS1/tau小鼠学习记忆能力和病理损伤

睡眠在认知功能和情绪的调节过程中发挥重要作用。近年研究显示,睡眠障碍是阿尔茨海默病(Alzheimer’s disease,AD)重要的危险因素之一,但慢性睡眠剥夺对于AD模型小鼠认知功能的影响及其机制尚不明确。本研究采用改良多平台法对8月龄雄性APP/PS1/tau三转基因AD模型(3xTg-AD)小鼠和野生型(wild type, WT)小鼠(每组8只)进行连续21天、每天20 h的睡眠剥夺。睡眠剥夺结束后,采用旷场、高架十字迷宫、糖水偏好、物体识别、Y迷宫和条件恐惧记忆实验等多种行为学手段观察慢性睡眠剥夺对3xTg-AD小鼠的焦虑和抑郁样行为以及多种认知功能的影响,并通过免疫组织化学染色观察小鼠海马区β淀粉样蛋白(amyloidβprotein, Aβ)斑块沉积、神经原纤维缠结和小胶质细胞的活化程度。结果显示:(1)慢性睡眠剥夺未影响3xTg-AD小鼠的焦虑(P=0.539)和抑郁样行为(P=0.874);(2)慢性睡眠剥夺加重了3xTg-AD小鼠的识别记忆(P 0.001)、工作记忆(P=0.002)和条件恐惧记忆能力(P=0.039)损伤;(3)慢性睡眠剥夺增加了3xTg-AD小鼠海马区Aβ斑块的沉积(P 0.001)和小胶质细胞的过度活化(P 0.001),但并未导致tau蛋白异常磷酸化和神经原纤维缠结出现。以上结果表明,慢性睡眠剥夺加重了3xTg-AD小鼠的识别记忆、工作记忆和条件恐惧记忆能力损伤,且其损伤作用与3xTg-AD小鼠海马区Aβ斑块沉积增加和小胶质细胞过度活化密切相关。     

大鼠海马CA1区GABA能神经元在睡眠调节中的作用

采用脑立体定位技术确定Sprague-Dawley大鼠(Rattus norregicus)双侧海马CA1区插管位置并进行核团埋管,同时安装脑电和肌电电极,用于记录大鼠皮层脑电活动和肌电活动。运用睡眠描记技术观察海马CA1区微量注射药物后对大鼠睡眠-觉醒周期的影响。发现海马内微量注射0.75μg、1.0μg的γ-氨基丁酸(GABA)后觉醒时间增加,分别为(120.7±13.3)min和(124.6±19.2)min(P0.05),睡眠时间减少,分别为(119.4±13.3)min与(115.4±19.2)min(P0.05),其中,深慢波睡眠时间(SWS2)分别减少53.3%(t=2.451,P0.05)和63.5%(t=3.367,P0.01);而微量注射1.0μgGABAA受体阻断剂荷包牡丹碱(Bic)后,睡眠时间增加(165.5±20.8)min(P0.01),觉醒时间减少(74.5±20.8)min(P0.01),其中,SWS2时间增加79.6%(t=2.600,P0.05),并可对抗GABA的促醒效应;微量注射GABAB受体激动剂氯苯氨基丁酸(Bac)对睡眠-觉醒周期无直接影响,亦不能阻断GABA的促醒效应。结果提示,GABA在海马参与大鼠睡眠-觉醒周期的调节且具有促觉醒作用,GABA对睡眠的影响主要是通过改变深慢波睡眠成分实现的,GABAA受体参与介导了这一过程。     

丁苯酞对睡眠剥夺大鼠脑额叶HMGB1和RAGE表达的影响

目的:探讨丁苯酞对睡眠剥夺大鼠脑额叶高迁移率族蛋白1(HMGB1)和晚期糖基化终产物受体(RAGE)表达的影响。方法:建立Sprague Dawley(SD)大鼠慢性睡眠剥夺和丁苯酞干预模型,共分为3组(n=6):大平台对照组、慢性睡眠剥夺组、慢性睡眠剥夺+丁苯酞组,慢性睡眠剥夺组采用睡眠剥夺箱对大鼠进28 d, 18 h/d的睡眠剥夺,慢性睡眠剥夺+丁苯酞组在睡眠剥夺28 d后腹腔注射丁苯酞100 mg/(kg·d),共14 d。各组大鼠取脑部标本,免疫组化检测额叶高迁移率族蛋白1 (HMGB1)、核转录因子kappB(NF-κB) p65表达,Western blot检测大鼠额叶HMGB1、沉默信息调节因子1(SIRT1)、晚期糖基化终产物(RAGE)、NF-κB表达。结果:与大平台对照组比较,慢性睡眠剥夺组大鼠额叶HMGB1、RAGE、细胞核NF-κBp65表达显著增多(P均<0.05),而SIRT1表达显著减少(P<0.05);与慢性睡眠剥夺组比较,慢性睡眠剥夺+丁苯酞组大鼠额叶HMGB1、RAGE、细胞核NF-κBp65表达显著减少(P均<0.05),而SI...     

NUCB2/nesfatin-1对小鼠摄食行为的调控及机制

目的:探讨NUCB2/nesfatin-1对小鼠摄食行为的调控及机制。方法:利用侧脑室埋管,免疫组化染色等方法,探讨侧脑室和外周注射nesfatin-1对小鼠摄食行为的影响。结果:侧脑室注射不同剂量nesfatin-1(0.3μg,1μg,3μg),注药后4 h夜间进食量明显减少,且呈显著剂量依赖关系(t=2.61~4.78,P0.05~0.01),侧脑室注射3μg nesfatin-1,小鼠前3小时累积摄食量明显降低(t=8.69~10.73,P0.01),且持续降低12小时(t=2.64,P0.05),同时餐间间隔时间明显延长(t=2.66,P0.05),每分钟/1-4 h进食量明显降低(t=2.63,P0.05),且进食每克食物所用时间明显增加(t=3.02,P0.05)。在下丘脑弓状核,外侧区和背内侧核均有NUCB2/nesfatin-1免疫阳性神经元表达。皮下或腹腔注射nesfatin-1,小鼠进食量和进食行为均无显著改变(P0.05)。结论:中枢nesfatin-1可抑制小鼠摄食行为。     

产后与非产后抑郁症患者事件相关电位P300的对比研究

目的:探讨产后抑郁症与非产后抑郁症患者事件相关电位P300的差异,为产后抑郁症的预防提供参考指标。方法:选择2011年1月~2012年10月解放军第三医院精神科收治的35例产后抑郁症患者(产后组)和36例非产后抑郁症患者(非产后组)为研究对象,并检测其事件相关电位P300,并与36名健康志愿者(对照组)的结果进行比较。结果:(1)与对照组相比,产后组、非产后组P2、N2、P3潜伏期均显著延迟,P2、N2、P3波幅均明显降低,差异均有统计学意义(P0.05)。(2)与产后组相比,非产后组P2、N2、P3潜伏期差异均无统计学意义(P0.05)。P2、N2波幅均偏高,差异均有统计学意义(P2[(5.0±2.1)ms vs.(3.9±1.8)μV],N2[(3.2±1.7)μV vs.(2.1±1.0)μV],P0.05),P3波幅差异无统计学意义(P0.05)。结论:产后与非产后抑郁症患者认知功能均受损,非产后抑郁患者受损程度大于产后抑郁患者;产后抑郁的外界感知能力和早期注意受损程度大于非产后抑郁患者。     

补充支链氨基酸对睡眠剥夺大鼠行为和血清游离脂肪酸水平的影响

探讨补充支链氨基酸 (branched -chainaminoacids ,BCAA)对睡眠剥夺 (sleepdeprivation ,SD)大鼠的行为和血清游离脂肪酸 (freefattyacids,FFA)水平的影响。采用小站台水环境 (flower -pot)睡眠剥夺模型对大鼠进行睡眠剥夺。成年、雄性Sprague-Dawley大鼠 5 6只 ,按体重随机分为C(对照组、自由睡眠 )、2 4hSD(剥夺睡眠 2 4h)、2 4hSDB(睡眠剥夺 2 4h ,进食添加BCAA的饲料 )、4 8hSD、4 8hSDB、72hSD、72hSDB组 ,每组 8只。睡眠剥夺结束后 ,采用旷场实验 (openfieldtest,OPT)评价大鼠的精神行为。结果各睡眠剥夺组大鼠的OFT得分均显著高于对照组 (P <0 .0 5 ) ;其中以 4 8hSD组最高 ,72hSD组的OFT得分又显著低于 72hSDB组 (P <0 .0 5 )。睡眠剥夺各组大鼠血清FFA水平均显著高于非剥夺组 ,72hSDB组显著高于 72hSD组 (P <0 .0 5 )。结论为补充支链氨基酸可以改善睡眠剥夺大鼠的旷场实验行为 ,降低睡眠剥夺大鼠血清FFA水平。     

中枢nesfatin-1对大鼠夜间摄食和胃排空的影响

目的:观察中枢nesfatin-1对大鼠夜间摄食和胃排空的影响。方法:大鼠经腹腔注射硫酸仲丁巴比妥(100~150 mg/kg)麻醉,侧脑室、第四脑室或小脑延髓池注射nesfatin-1或CRF受体拮抗剂astressin-B或astressin2-B,观察对摄食、胃排空的影响。结果:侧脑室注射nesfatin-1后大鼠第3-6 h夜间进食量(t=3.05~3.58,P0.01)和3 h和6 h的累积进食量(t=5.90~12.1,P0.01)明显减少,nesfatin-1的该抑制效应可被预先侧脑室注射astressin-B或astressin2-B阻断(t=1.06~2.22,P0.05)。第四脑室或小脑延髓池注射nesfatin-1后大鼠夜间摄食量在第1h就明显减少(t=2.59~6.26,P0.05~0.01),持续减少至5-6h(t=1.69~7.42,P0.05~0.01)。侧脑室注射不同剂量nesfatin-1(0.05或0.5μg)20 min后GE率明显降低,且随注射剂量增大,GE率越低(t=3.25~4.67,P0.01)。若预先给予大鼠CRF受体拮抗剂astressin2-B(30μg)再注射nesfatin-1(0.5μg),nesfatin-1抑制大鼠胃排空效应明显减弱(t=2.45~2.85,P0.05)。禁食24 h后再喂食2 h,大鼠下丘脑中nesfatin-1表达明显增加(t=2.87,P0.05),禁食24 h后血浆nesfatin-1水平明显降低(t=1.51,P0.05)。结论:Nesfatin-1抑制摄食作用可能由nesfatin-1和CRF2信号系统共同调节。     

不同时间睡眠剥夺对大鼠运动能力及谷氨酰胺的影响

目的：探索睡眠剥夺对大鼠运动能力及谷氨酰胺含量变化的影响,为睡眠剥夺后的运动训练等提供一定的实验依据。方法：将30只雄性SD大鼠按体重随机分安静对照组、0h睡眠剥夺力竭运动组（SDE）、24h SDE、48h SDE和72h SDE组（n=6）,采用轻柔刺激法建立睡眠剥夺模型和依据Bedford建立的大鼠运动模型。结果：24h SDE睡眠剥夺组与0h SDE组比较。大鼠后蹬跑时间明显长（P〈0．05）,48h SDE睡眠剥夺组和72h SDE睡眠剥夺与0h SDE睡眠剥夺组比较,后蹬跑时间显著性减少（P〈0．01）;24h SDE睡眠剥夺组与c组比较大鼠胸腺谷氨酰胺含量显著升高（P〈0．05）,48h SDE睡眠剥夺组和72h SDE睡眠剥夺组与C组比较大鼠胸腺谷氨酰胺含量降低（P〈0．01）;睡眠剥夺组与C组比较,血清谷氨酰胺含量的变化均具有高度显著性差异（P〈0．01）,睡眠剥夺24h后血清谷氨酰胺含量显著增多,却在睡眠剥夺48h、72h后血清谷氨酰胺含量明显下降。结论：①睡眠剥夺24h能提高大鼠运动能力,睡眠剥夺48h甚至是72h后大鼠运动能力开始降低。②睡眠剥夺24h后大鼠胸腺谷氨酰胺含量和血清谷氨酰胺含量升高,而睡眠剥夺48h后大鼠胸腺和血清的谷氨酰胺含量下降明显,睡眠剥夺72h后胸腺和血清谷氨酰胺含量显著性降低。     

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.