疑核内有关神经元在机体细胞免疫调节中的作用

研究了疑核内胆碱能神经元、去甲肾上腺素能神经元、脑啡肽能神经元对机体细胞免疫机能的影响 ,并对疑核内 3种神经元之间的相互关系进行了探讨。实验用麻醉家兔 ,分 6组进行 ,分别在疑核处通过微量注射器注入氯化乙酰胆碱 ( Ach)、密胆碱 -3( HC-3)、酒石酸去甲肾上腺素 ( NA)、6-羟基多巴胺 ( 6-OHDA)、盐酸吗啡 ( MP)、盐酸纳络酮 ( NX) ,并分别于注射前和注射后不同时间取外周血 ,测定 T细胞百分率及PHA诱导的有丝分裂原反应。结果 :Ach组上述免疫指标比注射前明显升高 ;HC-3组上述免疫指标比注射前明显降低 ;NA组上述免疫指标在注射后 30、60 min时明显低于注射前 ;6-OHDA组上述免疫指标在注射后 1 0～ 1 2 0 min时明显升高 ;MP组上述免疫指标在注射后 60、1 2 0 min时明显降低 ;NX组上述免疫指标注射前、后无明显变化。提示 :疑核增强机体细胞免疫的作用可能是通过胆碱能神经元实现的 ;疑核内的去甲肾上腺素能神经元与胆碱能神经元的作用相拮抗 ;而疑核内的脑啡肽能神经元可能对前两者的活动起一种调整作用     

疑核在下丘脑外侧区微量注射IL-6调节机体细胞免疫过程中的作用

为探索外源性ＩＬ－６可否通过反馈作用调节机体的免疫反应,选用３～４月龄、体重１．５～２．５ｋｇ的健康青紫蓝家兔,麻醉后固定于脑立体定位仪上。试验组Ⅰ动物（ｎ＝８）在下丘脑外侧区注射２．５ｐｍｏｌ／ＬＩＬ－６２μＬ;试验组Ⅱ动物（ｎ＝５）在疑核处注入２％盐酸利多卡因０．５μＬ后,再在下丘脑外侧区注射２．５ｐｍｏｌ／ＬＩＬ－６２μＬ;对照组动物（ｎ＝４）在下丘脑外侧区注射人工脑脊液２μＬ。分别在注射前及注射后不同时间无菌采血作细胞免疫指标测定。结果：试验组Ⅰ动物的Ｔ细胞百分率和ＰＨＡ诱导的淋巴细胞转化率,在注射ＩＬ－６后６０ｍｉｎ显著升高;试验组Ⅱ动物的Ｔ细胞百分率和ＰＨＡ诱导的淋巴细胞转化率,在注射ＩＬ－６后１２０ｍｉｎ出现显著升高;对照组动物在注射前后无明显变化;由此证明,下丘脑外侧区一定量的ＩＬ－６具有增强机体细胞免疫功能的作用,而这种细胞免疫的调节作用至少有一部分是通过疑核到达免疫系统的。疑核是下丘脑外侧区ＩＬ－６调节机体细胞免疫的通路之一。     

偏型、粘型和易型小麦雄性不育系的初步研究

调查了10种不同山羊草(Aegilops)细胞质的异质小麦品种 Chris 与1B /1R 小黑麦易位系77(2)杂交 F_1及回交后代的育性表现,结果表明:1.在同核背景下,山羊草不同种的细胞质在对77(2)的育性反应上明显不同,依此差异进行特定的质核组配,能得到更宜于培育杂种小麦的新型不育系;2.不同的不育胞质在同核背景下虽都能产生雄性不育,但     

北京鸭前庭核和耳蜗核的解剖

用火棉胶包埋,Ｎｉｓｓｌ,Ｌｕｘｏｌ固蓝－克紫和Ｗｅｉｌ氏染色方法,对成年北京鸭的前庭核和耳蜗核各亚核的位置,细胞构筑进行了研究。测量和计算出前庭核和耳蜗核各亚核的长度,细胞胞体的直径,并按胞体直径大小将细胞分型,统计出各亚核不同类型细胞所有占百比,结果如下：前庭核各亚核的长度分别是前庭背内侧核（２．７５±０．１２）ｍｍ,前庭降核（２．０３±０．１５）ｍｍ,前庭腹外侧核（１．７７±０．１８）ｍｍ前     

LH422细胞质对广亲和基因表达的影响

水稻籼粳亚种间杂交一代在一定程度上表现不育,这是利用亚种间杂种优势的主要障碍。多年来许多学者对舢粳杂种的部分不育性的遗传机理做了大量的研究,认为这种不育性受核基因控制。在育性基因作用的方式上,Oka[7,8]认为籼粳杂种F1的不育性由不同座位的配于重复致死基因引起。Ikehashi[10,12]则认为这种不育性受同一位点上一组复等位基因的控制,并提出单座位抱子体一配子体互作致死模式。这些解释都没有涉及细胞质与育性的关系。已有报道「“认为,细胞质对籼粳杂种后代的育性有着明显的影响。1994年,我们发现在LH422参与的某些杂交组…     

Effect of the density on the growth and survival of the Caribbean scallops Argopecten nucleus and Nodipecten nodosus in suspended culture

Juveniles of the Caribbean scallops Argopecten nucleus and Nodipecten nodosus were suspended in pearl nets at densities of 25%, 30% and 50% coverage of the bottom of the net (BC) during days. Additionally, adults of A. nucleus (>35 mm) were placed in lantern nets at densities of 40%, 50% and 65% BC during days. Stocking density affected the growth of animals, with higher growth rates obtained at the lower densities. Although the survival of the two scallops was not influenced at the densities studied, the 15-day net changes, and culture in water of <28 °C produced better survival of A. nucleus and N. nodosus respectively. Predators of the families Cymatiidae, Grapsidae, Portunidae, Majidae and Xanthidae were found in the culture nets of juvenile A. nucleus , but during the adult phase they were absent. Predators exhibited a dense-independent behaviour in relation to scallops. There was not any association between predator frequency and survival of A. nucleus .     

三氯生对红白鲫的急性毒性及遗传毒性研究

研究三氯生对红白鲫的急性毒性和遗传毒性作用,为分析评价三氯生对鱼类的生态安全性提供相应的毒理学资料。试验在规格为58 cm×28 cm×36 cm的玻璃水族箱中进行,红白鲫体长6.8~7.5 cm。采用半静态染毒法,设置不同浓度梯度的三氯生染毒组以及空白对照组和二甲基亚砜溶剂对照组,分别进行为期96 h的急性毒性试验和14 d的遗传毒性试验,观察记录死亡数,统计血红细胞微核率和核异常率。三氯生对红白鲫的96 h LC50为1 111.9μg/L。TCS染毒处理14 d后,红白鲫红细胞核异常的情况明显增多,主要是细胞质中有1~2个微核,其他常见核异常为红细胞核质外凸、核质内凹及核内空泡化;空白对照组和溶剂对照组之间核异常比率无显著差异(P0.05),而三氯生暴露各浓度组(600.0、690.0、793.5μg/L)核异常比率均极显著高于对照组(P0.01),且呈现明显的剂量-效应关系。研究表明,三氯生对红白鲫具有潜在的遗传毒性,且毒性效应在特定条件下随着暴露浓度的增加而增强。     

疑核对细胞免疫机能调节作用的研究

实验用3～4月龄1.5～2.5kg灰色家兔22只,麻醉后于疑核内插入同心圆电极,在刺激前和刺激后采血检测PHA诱导的淋巴细胞转化率、T细胞百分率,并测定全血葡萄糖浓度;刺激疑核后0.5h,采6例胸腺组织作超微结构观察;刺激疑核后3.5h,采胸腺作石蜡切片ANAE阳性率检测。电极位置均作组织学检查。结果:刺激疑核后T细胞百分率、PHA诱导的淋巴细胞转化率持续升高(P<0.05);胸腺各部位ANAE阳性淋巴细胞百分率升高,胸腺后微静脉内淋巴细胞增多,均与对照组及非刺激对照组相差非常显著(P<0.005);胸腺髓质ANAE阳性淋巴细胞率与外周血液T细胞百分率相关显著;胸腺超微结构示上皮性网状细胞机能活跃,分泌旺盛,皮质处于分裂状态的淋巴细胞增多,髓质淋巴细胞活动能力增强。由此认为,疑核与外周细胞免疫存在机能联系,刺激疑核可引起细胞免疫机能增强。本实验还证明,刺激疑核引起血糖浓度降低,因而除神经途径外,疑核还通过体液途径调节免疫机能。实验结果提示,疑核可能是大脑皮层、下丘脑调节免疫机能的中继核。实验确定了疑核定位坐标是AP_(20～21),L_(1～1.5),H_(20～21)。     

哺乳动物体细胞核移植中供体细胞的研究进展

本文对哺乳动物核移植供体细胞的研究进展进行了综述。主要涉及细胞类型、细胞年龄和细胞所处的周期时相对核移植胚胎发育的影响，以及目前核移植技术存在的问题等。     

Role of central PGE2 on sympathetic excitation in chronic heart failure

AIM: To observe the effect of central prostaglandin E₂ (PGE₂) on sympathetic activation in chronic heart failure (CHF) and to explore the underlying mechanism. METHODS: Male SD rats were subjected to coronary artery ligation to induce heart failure (HF), and the intracerebroventricular infusion was performed by osmotic pump continuously. The rats in sham group and HF group were given artificial cerebrospinal fluid (0.25 μL/h). The rats in HF plus treatment group was given celecoxib (CLB; 20 mg/h). After 4 weeks, the levels of PGE₂ in cerebrospinal fluid (CSF), the sympathetic nerve excitability and cardiac function were measured, and the changes of corticotropin-hormone releasing hormone (CRH)-containing neurons activation and neurotransmitter contents in the hypothalamic paraventricular nucleus (PVN) were also determined. RESULTS: Compared with the sham-operated rats, the HF rats had raised level of PGE₂ in CSF, up-regulated renal sympathetic nerve activity and plasma norepinephrine, increased left ventricular end diastolic pressure, lung-to-body weight and right ventricular-to-body weight ratios, and decreased maximal increase and decreased rate of left ventricular pressure (P<0.05). In addition, the number of CRH positive neurons in PVN and the level of plasma adrenocorticotropic hormone were higher in HF rats than those in sham-operated rats (P<0.05). After administration of CLB into the lateral ventricle of HF rats, the contents of PGE₂ in CSF were significantly reduced, the number of activation CRH neurons in PVN was decreased, the excitability of sympathetic nerves was down-regulated and cardiac function was improved (P<0.05). Compared with the sham-operated rats, the content of glutamic acid in PVN of HF rats was increased, the content of γ-aminobutyric acid and the number of glutamate decarboxylase 67-positive neurons were decreased (P<0.05). After the CLB was given, the above indexes were reversed (P<0.05). CONCLUSION: These findings indicate that in CHF, the increased central PGE₂ may activate CRH-containing PVN neurons and contribute to the augmented sympathetic drive possibly by modulating the neurotransmitters within the PVN.