电刺激猫小脑顶核对动脉血压和肾交感神经放电的影响

在38只麻醉及人工呼吸的猫,观察到电刺激小脑顶核嘴侧部能引起动脉血压显著升高;肾交感神经放电于刺激期间显著增加。去缓冲神经对刺激顶核所引起的血压反应的幅度和肾交感神经放电均无明显影响,但可明显延长血压反应升高相以及血压恢复期的时间。静脉注射氯庄定引起血压降低、心率减慢及肾交感神经放电的抑制,并能减弱刺激顶核引起的血压反应,但增强了刺激顶核引起的肾神经放电的变化。电解损毁延髓腹外侧面引起血压降低及肾交感神经放电的抑制,然而无论单侧还是双侧损毁延髓腹外侧面都不能阻断刺激顶核所引起的血压和肾交感神经放电的反应。以上结果表明,电刺激顶核能引起明显的心血管反应,其反应的下行性通路可能不通过延髓腹外侧面。     

北京市5种园林树木蒸腾作用模拟研究

通过对北京市园林5种常用乔木,国槐（Sophora japonica）、银杏（Ginkgo biloba）、白蜡（Fraxinus chinensis）、杜仲（Eucommia ulmoides）和臭椿（Ailanthus altissima）等植物蒸腾作用与周围环境气象因子（温度、湿度、太阳有效辐射）及植株叶面积指数相关关系的研究,利用Javis公式计算冠层气孔阻力,同时采用PM公式计算冠层蒸腾速率和植株日蒸腾量,并分析不同乔木的冠层气孔导度对环境主要驱动因子的响应规律。结果表明：5种被观测乔木中,国槐耗水量最大,白蜡耗水量最小,植株蒸腾量大小依次为国槐〉银杏〉杜仲〉臭椿〉白蜡（P＜0．01）。植物叶片气孔导度及蒸腾量与环境驱动因子太阳辐射及水气压亏缺的相关关系表明,在土壤水分条件较好时,国槐长势优于其它4种乔木,但是其对水分的利用不够经济,在干旱的情况下不能有效节水。     

A synthetic wheat with 56 chromosomes derived fromTriticum turgidum andAegilops tauschii

By colchicine treatment of hybrids between Triticum turgidum and Aegilops tauschii (as seedlings), a fertile wheat plant (SHW-L2) carrying 56 chromosomes was artificially synthesized. At metaphase I of 50 pollen mother cells, the 56 chromosomes of the new wheat SHW-L2 showed a mean pairing configuration of 2.82 univalents, 6.18 rod bivalents, 19.39 ring bivalents, 0.5 trivalents, and 0.14 quadrivalents. Cytological analyses suggested that SHW-L2 had additional 7 pairs of chromosomes from the A and D genome besides the 42 chromosomes of common wheat. The special chromosome constitution of SHW-L2 may be derived from the chromosome doubling by the colchicine treatment of seedlings and then spontaneous doubling of gametes.     

Glial cell line-derived neurotrophic factor (GDNF) is a neurotrophic factor for sensory neurons: Comparison with the effects of the neurotrophins

We compared the effects of glial cell line-derived neurotrophic factor (GDNF) on dorsal root ganglion (DRG) sensory neurons to that of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin 3 (NT-3). All of these factors were retrogradely transported to sub-populations of sensory neuron cell bodies in the L4/L5 DRG of neonatal rats. The size distribution of ¹²⁵I-GDNF-labeled neurons was variable and consisted of both small and large DRG neurons (mean of 506.60 μm²). ¹²⁵I-NGF was preferentially taken up by small neurons with a mean cross-sectional area of 383.03 μm². Iodinated BDNF and NT-3 were transported by medium to large neurons with mean sizes of 501.48 and 529.27 μm², respectively. A neonatal, sciatic nerve axotomy-induced cell death model was used to determine whether any of these factors could influence DRG neuron survival in vivo. GDNF and NGF rescued nearly 100% of the sensory neurons. BDNF and NT-3 did not promote any detectable level of neuronal survival despite the fact that they underwent retrograde transport. We examined the in vitro survival-promoting ability of these factors on neonatal DRG neuronal cultures derived from neonatal rats. GDNF, NGF, and NT-3 were effective in vitro, while BDNF was not. The range of effects seen in the models described here underscores the importance of testing neuronal responsiveness in more than one model. The biological responsiveness of DRG neurons to GDNF in multiple models suggests that this factor may play a role in the development and maintenance of sensory neurons. © 1997 John Wiley & Sons, Inc. J Neurobiol 32: 22–32, 1997.     

圈养大熊猫野化培训期的生境选择特征

大熊猫(Ailuropoda melanoleuca)是我国特有的珍稀物种,也是世界上最濒危的野生动物之一。为了将人工繁育的部分大熊猫个体重引入其历史分布区或复壮野生种群,中国保护大熊猫研究中心从2003年开始进行圈养大熊猫的野外放归工作,通过野化培训以提高圈养大熊猫适应和选择野外环境的能力。对野化培训大熊猫"淘淘"的生境选择研究表明:该野化培训大熊猫幼仔经常活动于新笋密度较大的区域[生境与对照:(2.68±1.14)对(1.58±0.66)],却避开成竹密度过大[(9.91±2.51)对(12.18±4.68)]、竹子较高[(4.57±1.09) m对(4.98±0.66) m]以及枯死竹过多[(2.52±0.86)对(3.39±1.33)]的区域;喜欢活动于离水源[(1.59±0.67)对(2.19±0.87)]和隐蔽场所较近[(5.37±2.14) m对(8.35±7.76)m],以及距离乔木较远[(3.09±0.69) m对(2.70±0.42) m]和郁闭度较低[(1.85±0.57)对(2.10±0.47)]的区域(P < 0.05),新笋密度大小是该栖息地在整个野化培训期间是否被利用的最重要因素。该野化培训大熊猫幼仔保持着与带仔母兽相近的生境选择特征,对竹子环境的选择也与卧龙野生大熊猫相似,野化培训对该大熊猫幼仔产生了积极的作用。野化培训大熊猫幼仔形成的家域和核域面积分别为9.21 hm² 和1.93 hm²,占野化培训圈面积的51.95%和10.89%,其中家域面积仅有卧龙野生大熊猫的1.4%-2.4%,所以在以后的野化培训过程中需要采取增加野化培训圈中环境丰富度等方式,促进野化培训大熊猫形成较大的家域面积。     

Comparison of Expression of Inflammatory Cytokines in the Spinal Cord Between Young Adult and Aged Beagle Dogs

Aging is an inevitable process that occurs in the whole body system accompanying with many functional and morphological changes. Inflammation is known as one of age-related factors, and inflammatory changes could enhance mortality risk. In this study, we compared immunoreactivities of inflammatory cytokines, such as interleukin (IL)-2 (a pro-inflammatory cytokine), its receptor (IL-2R), IL-4 (an anti-inflammatory cytokine), and its receptor (IL-4R) in the cervical and lumbar spinal cord of young adult (2–3 years old) and aged (10–12 years old) beagle dogs using immunohistochemistry and western blotting. IL-2 and IL-2R-immunoreactive nerve cells were found throughout the gray matter of the cervical and lumbar spinal cord of young adult and aged dogs. In the spinal cord neurons of the aged dog, immunoreactivity and protein levels were apparently increased compared with those in the young adult dog. Change patterns of IL-4- and IL-4R-immunoreactive cells and their protein levels were also similar to those in IL-2 and IL-2R; however, IL-4 and IL-4R immunoreactivity in the periphery of the neuronal cytoplasm in the aged dog was much stronger than that in the young adult dog. These results indicate that the increase of inflammatory cytokines and their receptors in the aged spinal cord might be related to maintaining a balance of inflammatory reaction in the spinal cord during normal aging.     

Tumor necrosis factor regulates intestinal epithelial cell migration by receptor-dependent mechanisms

Altered mucosal integrity andincreased cytokine production, including tumor necrosis factor (TNF),are the hallmarks of inflammatory bowel disease (IBD). In this study,we addressed the role of TNF receptors (TNFR) on intestinal epithelialcell migration in an in vitro wound closure model. With mouse TNFR1 orTNFR2 knockout intestinal epithelial cells, gene transfection, andpharmacological inhibitors, we show a concentration-dependentreceptor-mediated regulation of intestinal cell migration by TNF. Aphysiological TNF level (1 ng/ml) enhances migration through TNFR2,whereas a pathological level (100 ng/ml) inhibits wound closure through TNFR1. Increased rate of wound closure by TNFR2 or inhibition by TNFR1cannot be explained by either increased proliferation orapoptosis, respectively. Furthermore, inhibiting Src tyrosine kinase decreases TNF-induced focal adhesion kinase (FAK) tyrosine phosphorylation and cellular migration. We therefore conclude thatTNFR2 activates a novel Src-regulated pathway involving FAK tyrosinephosphorylation that enhances migration of intestinal epithelial cells.

     

Cytosolic prion protein is not toxic and protects against Bax-mediated cell death in human primary neurons

Recently, it was observed that reverse-translocated cytosolic PrP and PrP expressed in the cytosol induce rapid death in neurons (Ma, J., Wollmann, R., and Lindquist, S. (2002) Science 298, 1781-1785). In this study, we investigated whether accumulation of prion protein (PrP) in the cytosol is toxic to human neurons in primary culture. We show that in these neurons, a single PrP isoform lacking signal peptide accumulates in the cytosol of neurons treated with epoxomicin, a specific proteasome inhibitor. Therefore, endogenously expressed PrP is subject to the endoplasmic reticulum-associated degradation (ERAD) pathway and is degraded by the proteasome in human primary neurons. In contrast to its toxicity in N2a cells, reverse-translocated PrP (ERAD-PrP) is not toxic even when neurons are microinjected with cDNA constructs to overexpress either wild-type PrP or mutant PrPD178N. We found that ERAD-PrP in human neurons remains detergent-soluble and proteinase K-sensitive, in contrast to its detergent-insoluble and proteinase K-resistant state in N2a cells. Furthermore, not only is microinjection of a cDNA construct expressing CyPrP not toxic, it protects these neurons against Bax-mediated cell death. We conclude that in human neurons, ERAD-PrP is not converted naturally into a form reminiscent of scrapie PrP and that PrP located in the cytosol retains its protective function against Bax. Thus, it is unlikely that simple accumulation of PrP in the cytosol can cause neurodegeneration in prion diseases.