八肽胆囊收缩素(CCK-8)对抗电针镇痛及电针耐受机理的初步探讨

本文采用电生理学方法,以大鼠丘脑束旁核痛兴奋神经元(PEN)和痛抑制神经元(PIN)的电活动变化为才旨标,在细胞水平上研究八肽胆囊收缩素(CCK-8)与电针镇痛和电针耐受机理的关系.结果表明:电针大鼠“足三里”穴位可抑制PEN和兴奋PIN的电活动,产生镇痛效应;脑室注射CCK-8可取消电针对PEN和PIN放电的影响;而无硫CCK-8对呈现电针效应的PEN和PIN的电活动无影响.长时间电针(六小时)可使PEN和PIN的放电对再次电针无明显变化,亦即产生对电针镇痛的耐受效应.推测,内源性CCK-8可能参与电针耐受的形成.     

电针对佐剂性关节炎大鼠炎症局部阿片肽基因表达的影响

以佐剂性关节炎大鼠为炎症痛模型，选择悬钟，昆仑穴位，采用原位杂交组织化学方法，观察电针（ＥＡ）对大鼠炎症局部阿片肽前体物质前阿黑皮素（ＰＯＭＣ）和前脑啡肽原（ＰＥＮＫ）ｍＲＮＡ的表达，结果ＥＡ可以促进炎症局部免疫细胞中ＰＯＭＣ和ＰＥＮＫ ｍＲＮＡ的表达，使阿片肽的合成和释放增加，以实现外周炎症局部的镇痛作用。     

外源GA对垂柳茎部次生木质部和次生韧皮部发生的影响(简报)

外源ＧＡ对垂柳茎部次生木质部和次生韧皮部发生的影响（简报）张凤娟（河北农业技术师范学院基础部，昌黎，０６６６００ＥＦＦＥＣＴＳＯＦＥＸＴＥＲＮＡＬＧＡＯＮＳＥＣＯＮＤ－ＸＹＬＥＭＡＮＤＳＥＣＯＮＤ－ＰＨＬＯＥＭＯＦＷＥＥＰＩＮＧＷＩＬＬＯＷＳＴＥＭＳ...     

暴发性鱼病防治的试验

暴发性鱼病防治的试验华建权，叶松林　　（浙江省慈溪市水产技术推广站慈溪３１５３００）ＡＮＥＸＰＥＲＩＭＥＮＴＯＮＴＲＥＡＴＭＥＮＴＯＦＳＵＤＤＥＮＡＴＴＡＣＫＯＦＦＩＳＨＤＩＳＥＡＳＥＨｕａＪｉａｎｑｕａｎＹｅＳｏｎｇｌｉｎ（ＣｉｘｉＦｉｓｈｅｒｉｅ...     

低氧应激下β-内啡呔对大鼠免疫功能的作用

本实验选用成年雄性ｗｉｓｔａｖ大鼠,就急性低氧应激性对β－内啡呔（β－ＥＰ）参与免疫调节的机制进行了探讨。结果表明：与对照（２．３ｋｍ）相比,急性低氧（７ｋｍ,２４ｈｒ）使大鼠肾上皮质酮（ＣＳ）和去甲肾上肾腺素（ＮＥ）明显升高（Ｐ〈０．０５）;正常大鼠侧脑室注射外源性（ＩＣＶ）β－ＥＰ（．ｎｍｏｌ,４ｍｌ）再给预低氧刺激较单纯低氧组ＣＳ和血浆ＮＥ升高更为明显（Ｐ〈０．０１）;急性低氧对大鼠脑室注射     

THE RISE AND DECLINE OF THE UNITED STATES SHIPPING AND SHIPBUILDING INDUSTRIES

ＴＨＥＲＩＳＥＡＮＤＤＥＣＬＩＮＥＯＦＴＨＥＵＮＩＴＥＤＳＴＡＴＥＳＳＨＩＰＰＩＮＧＡＮＤＳＨＩＰＢＵＩＬＤＩＮＧＩＮＤＵＳＴＲＩＥＳ￥（ＣａｐｔａｉｎＪａｍｅｓＳ．Ｃ．Ｃｈａｏ，ＤＣＳ，ＬＬ．Ｄ．ＪｏｈｎＪ．Ｃｌａｒｋ，Ｐｈ．Ｄ．）Ａｂｓｔｒａｃｔ...     

PVC／NBR／SBS三元共混物的形态结构与性能

本文通过冲击试验、动态力学分析（ＭＭＡ）、透射电镜（ＴＥＭ）和扫描电镜（ＳＥＭ）观察，研究了聚氯乙烯／丁腈橡胶／苯乙烯。丁二烯。苯乙烯嵌段共聚物（ＰＶＣ／ＮＢＲ／ＳＢＳ）三元共混物的形态结构和性能，并且讨论了两者之间的关系。ＮＢＲ－２９对ＰＶＣ和ＳＢＳ有较好的增容作用，与ＳＢＳ一起对ＰＶＣ有协同增韧效应。     

POLYCYCLE－COMPOUNDING STRUCTURES AND REGIONAL LAYERSLIP－DIPSLIP SYSTEMS：IMPLICATIONS FOR THE TARIM BASIN，XINJIAN

ＰＯＬＹＣＹＣＬＥ－ＣＯＭＰＯＵＮＤＩＮＧＳＴＲＵＣＴＵＲＥＳＡＮＤＲＥＧＩＯＮＡＬＬＡＹＥＲＳＬＩＰ－ＤＩＰＳＬＩＰＳＹＳＴＥＭＳ：ＩＭＰＬＩＣＡＴＩＯＮＳＦＯＲＴＨＥＴＡＲＩＭＢＡＳＩＮ，ＸＩＮＪＩＡＮ￥ＳｕｎＹａｎ；ＪｉａＣｈｅｎｇｚａｏ（Ｄｅ...     

电针对佐剂性关节炎大鼠炎症局部c-fos表达的影响

目的：观察电针（ＥＡ）对炎症痛模型佐剂性关节炎（ＡＡ）大鼠炎症局部ｃ－ｆｏｓ表达的影响,以探讨针刺对炎症痛的外周镇痛机制。方法：以福氏完全佐剂造成炎症痛模型ＡＡ、选取悬钟、昆仑穴ＥＡ治疗,采用免疫组织化学方法检测ｃ－ｆｏｓ表达。结果：ＥＡ可以抑制ＡＡ大鼠炎症局部ｃ－ｆｏｓ的表达。结论：ｃ－ｆｏｓ可能参与了ＥＡ对炎症痛的外周镇痛作用。     

重视泛读课课堂上的听说教学

重视泛读课课堂上的听说教学ＡＴＴＡＣＨＩＭＰＯＲＴＡＮＣＥＴＯＬＩＳＴＥＮＩＮＧ－ＡＮＤ－ＳＰＥＡＫＩＮＧＩＮＳＴＲＵＣＴＩＯＮＩＮＥＸＴＥＮＳＩＶＥＲＥＡＤＩＮＧＬＥＣＴＵＲＥ刘雅儿ＬｉｕＹａ＇ｅｒ（浙江水产学院基础课部，舟山３１６１０１）（Ｚｈｅ...     

Relationship between the analgesic effect of electroacupuncture and CCK-8 content in spinal perfusate in rats

There exists significant individual variation in electroacupuncture (EA) induced analgesia. Rats may be classified as high- and lowresponders according to their response to EA analgesia. The content of cholecystokinin octapeptide like immunoreactivity (CCK-8-ir) in the spinal perfusate of highresponder (HR) and low-responder (LR) rats was measured with radioimmunoassay. The result showed that the CCK-8-ir content in LR rats was significantly lower than that in HR rats. There exists a negative correlation between the EA effect and the CCK-8-ir content during EA stimulation. It is concluded that the spinal release of CCK-8 may be one of the key factors determining the effect of EA analgesia.     

Inhibiting pain with pain— A basic neuromechanism of acupuncture analgesia

(i) The structure and function of the meridian (channel and collateral) described by ancient medical doctors may correspond to the blood circulation, nerve control and neurohumoral modulation of modern medicine. (ii) The needling, which can injure the tissue, is a noxious stimulation inducing pain. Acupuncture manipulation, such as lifting and thrusting, twisting and twirling, or electroacupuncture (EA) with the sufferable biggest intensity for patients should be a stronger pain stimulation. The needling sensation of soreness, numbness, distension and heaviness is a deep pain. (iii) There is an intrinsic analgesic system in brain, which centers around the periventricular and periaqueductal grey matter, contains endorphins as possible mediators, goes through the descending inhibition system in medulla oblon-gata, and acts on the gating mechanism in spinal cord. Itcould be producing analgesia while the system is activated. (iv) NRM might be a supraspinal center modulating pain, and the R-S neurons could form a basic circuit of negative feedback modulating pain. The discovery of excitatory-inhibitory reversible R-S neurons may give a neuro-physiological explanation for the double direction modulation of acupuncture at acupoint. (v) Non-noxious stimulation such as massage or stroking could excite type I and n afferent fibers, producing a weaker and transient analgesia through the spinal mechanism. When the acupoint is near the pain area, the afferent information from them could be converged on the same and neighboring spinal segments, the light acupuncture or low intensity of EA also has analgesic effects, showing acupoint specificity. But the acupoint specificity is not limited in a specially designated channel line, and it is closely related to the segment of innervation. (vi) While acupuncture manipulation of lifting and thrusting, twisting and twirling or a high intensity of EA is used, because the intensities of these stimulations exceed the threshold of afferent C fibers, they could fully excite Ⅲ(Aδ) and Ⅳ (C) afferent fibers, producing a strong and lasting analgesia, mainly through the supraspinal negative feedback mechanism modulating pain, it has curative effects. Therefore, the essence of acupuncture analgesia may chiefly be inhibiting pain with pain.     

不同间隔时间电针对佐剂性关节炎大鼠炎症局部前阿黑皮素和前脑啡肽原mRNA表达的影响

目的:观察不同间隔时间电针对佐剂性关节炎(AA)大鼠的镇痛效应,以探讨针刺镇痛的最佳间隔时间和作用机制。方法:将96只大鼠随机分为对照组、模型组和电针组,每组再分为3 h、6 h、12 h和24 h小组,以Freund’s完全佐剂造成AA大鼠模型,电针选取悬钟和昆仑穴,分别以3 h、6 h、12 h和24 h作为治疗间隔时间,连续治疗6 d,以痛阈、炎症局部前阿黑皮素(POMC)mRNA和前脑啡肽原(PENK)mRNA表达作为观察指标。结果:间隔24 h电针能显著提高AA大鼠的痛阈;不同间隔时间电针均能促进炎症局部POMC mRNA和PENK mRNA的表达。结论:间隔24 h电针可明显提高对AA大鼠的镇痛效应;不同间隔时间电针镇痛效应与促进炎症局部阿片肽基因表达有关。     

Orphanin FQ antagonizes the analgesic effect of 5-HT in rat brain

Orphanin FQ (OFQ) is a new modulatory peptide which was found in 1994. It mediates in morphine analgesia and electroacupuncture analgesia. The interaction between OFQ and 5-hydroxytryptamine (5-HT) on analgesia was observed using the method of intracere-broventricular microinjection. The results showed that cumulative i. c. v. administration of gradually increasing doses of 5-HT produced a dose-dependent analgesia, and administration of different doses of OFQ separateness had no significant effect on tail flick latency, but 1 or 10 μg OFQ could reverse the analgesia induced by 5-HT, suggesting that OFQ could antagonize the analgesia induced by 5-HT in rat brain.     

Effect of nocistatin in pain modulation

Using tail-flick latency as the nociceptive index and von Frey hair to measure the mechanical allodynia, the aim of the present study is to determine whether nocistatin, injected intracerebroventricularly (i.c.v.), would reverse the anti-morphine effect of orphanin FQ (OFQ), and, injected i.c.v. or intrathecally (Lt.), would inhibit the mechanical allodynia in a L5 and L6 spinal nerve ligation model of neuropathic pain in rats. The results show that i.c.v. injection of nocistatin produces no significant changes in the TFL, nor does it affect morphine analgesia. In addition, i.c.v. or i.t. nocistatin produces no significant changes in withdrawal threshold of the nerve-lesioned hind paw. However, nocistatin significantly reverses the antagonistic effect of OFQ on morphine analgesia when it was coinjected i.c.v. with OFQ. The results suggest that nocistatin can reverse the anti-morphine effect of OFQ in rat brain, but cannot inhibit the mechanical allodynia of neuropathic pain in rat brain and spinal cord.     

Analgesia and hyperalgesia from GABA-mediated modulation of the cerebral cortex

It is known that pain perception can be altered by mood, attention and cognition, or by direct stimulation of the cerebral cortex, but we know little of the neural mechanisms underlying the cortical modulation of pain. One of the few cortical areas consistently activated by painful stimuli is the rostral agranular insular cortex (RAIC) where, as in other parts of the cortex, the neurotransmitter gamma-aminobutyric acid (GABA) robustly inhibits neuronal activity. Here we show that changes in GABA neurotransmission in the RAIC can raise or lower the pain threshold--producing analgesia or hyperalgesia, respectively--in freely moving rats. Locally increasing GABA, by using an enzyme inhibitor or gene transfer mediated by a viral vector, produces lasting analgesia by enhancing the descending inhibition of spinal nociceptive neurons. Selectively activating GABA(B)-receptor-bearing RAIC neurons produces hyperalgesia through projections to the amygdala, an area involved in pain and fear. Whereas most studies focus on the role of the cerebral cortex as the end point of nociceptive processing, we suggest that cerebral cortex activity can change the set-point of pain threshold in a top-down manner.     

电针对AD大鼠学习记忆能力及神经元凋亡的影响

目的:探讨电针对AD模型大鼠学习记忆能力和神经元凋亡的影响.方法:将40只健康SD大鼠随机分为正常组、假手术组、模型组和电针组,采用A1-40注入大鼠双侧Meynert核建立AD模型,电针组采用电针治疗,治疗一个月后用水迷宫试验测定各组大鼠学习记忆能力,然后处死大鼠检测海马及皮质的神经元凋亡百分比.结果:模型组出现学习记忆障碍,呈渐进性加重,4周时更为显著,而且在海马区和皮质区神经元有较高的凋亡比例,电针组有明显改善(P<0.01).结论:Meynert核注射A可使大鼠发生较持久的学习记忆功能障碍及胆碱能神经元凋亡,电针治疗可改善AD大鼠学习记忆能力,抑制神经元凋亡.     

Stimulation of food intake in rats by centrally administered hypothalamic growth hormone-releasing factor

Hypothalamic growth hormone-releasing factors (GRFs) have been purified recently from human pancreatic (hp) tumours and from rat hypothalamus (rh). GRF peptides have strong homology with peptides of the glucagon, vasoactive intestinal polypeptide and PHI-27 family. Aside from their potent actions on release of somatotropin, no other biological actions of GRFs have been reported. GRF has been localized in neurones bordering the ventromedial hypothalamic nucleus, a region associated frequently with experimental analysis of feeding behaviour. We now report that intracerebroventricularly (i.c.v.)-administered rhGRF and hpGRF(1-40) in doses of 0.2, 2.0 and 20.0 pmol, produced an increase in food intake in hungry rats. This effect seemed to be specific to GRF as i.c.v. injections of a structurally related but physiologically inactive peptide in the same doses had no effect on feeding. In addition, peripheral injections of rhGRF or growth hormone had no effect on food intake, suggesting that the present effects may be mediated centrally. Injections (i.c.v.) of rhGRF (0.2, 2.0 and 20.0 pmol) had no effect on general activity, suggesting that GRF does not produce nonspecific arousal.