Some studies on the mechanism of action of antibodies to nerve growth factor.

The effects of antibodies to the nerve growth factor from mouse salivary gland were examined in vitro and in vivo. Treatment of explants of receptive ganglia with antibody and complement did not produce cell damage as judged by the ability of the tissue to respond to nerve growth factor. New-born mice experimentally depleted of or genetically deficient in key complement components were susceptible to the action of the antiserum.These results show that the effect of the antibody is independent of complement and are consistent with the view that it acts by neutralization of endogenous nerve growth factor.     

Expression and localization of heat shock proteins in rat basophilic leukemia cells: differential modulation by degranulation,thermal or oxidative stress

BACKGROUND: Rat basophilic leukemia (RBL-2H3) cells are well characterized in terms of morphological and biochemical changes upon activation, and have been extensively used as a model system for studying the mechanisms of the immediate hypersensitivity reaction. To investigate whether overexpression of heat shock/stress proteins (HSP) is involved in the mast cell-dependent reactivity, we examined the adaptive responses of RBL-2H3 cells to classical stress conditions such as heat shock or oxidative injury produced by an aqueous extract of tobacco smoke. METHODS: HSP were determined by flow cytometry and immunocytochemistry. Degranulation was confirmed as the release of beta-hexosaminidase, determined spectrophotometrically, and by electron microscopy experiments. RESULTS: We found that RBL-2H3 cells respond to heat shock or oxidative injury by the synthesis of both the inducible 72 kDa HSP (Hsp70), and the oxidation-specific 32 kDa heme oxygenase (HO)-1. Heat shock induced mainly Hsp70 in a cell growth-dependent manner, whereas oxidative stress induced mainly HO-1 in a cell growth-independent manner. However, heat shock or oxidative stress had no significant effects on degranulation. CONCLUSION: Stress-mediated synthesis of HSP was not associated with RBL-2H3 degranulation and likewise, degranulation did not induce HSP.     

Endoscopic ultrasound-guided fine-needle aspiration cytology of peripheral nerve-sheath tumors

Endoscopic ultrasound (EUS) has allowed for the fine-needle aspiration and diagnosis of many different gastrointestinal neoplasms, including mesenchymal tumors. Although most mesenchymal tumors of the gastrointestinal tract are gastrointestinal stromal tumors (GISTs), other mesenchymal tumors, including neural tumors, do occur. Proper diagnosis and differentiation of these tumors from GISTs are important because of their different prognoses and treatment regimens. We encountered three peripheral nerve-sheath tumors of the gastrointestinal tract aspirated by EUS (two schwannomas and a granular-cell tumor). We report on the endoscopic ultrasound, cytologic, histologic, and immunohistochemical findings of these cases.     

Differential effects of scopolamine on neuronal survival in ischemia and glutamate neurotoxicity: relationships to the excessive vulnerability of the dorsoseptal hippocampus

The neurodegeneration in the CA1 subfield of hippocampus exhibited a dorsal-ventral gradient of susceptibility in global ischemia (82% dorsoseptally and only 16% ventrotemporally). Scopolamine (SCOP) did not improve the neuronal damage caused by the global ischemic challenge in rats and did not reduce the infarct area after the focal MCA-occlusion in mice. No differences were observed between saline and SCOP-treated animals in the physiologic parameters, except for a slight increase in rectal temperature. In contrast, treatment of hippocampal cultures with increasing concentrations of SCOP (1 nM to 1 mM) under glutamate incubation had a beneficial effect on neuronal viability. These data show that (1) there is substantial gradient of vulnerability of the hippocampus from dorsal to ventral in global ischemia and (2) that interactions between the NMDA, muscarinic receptors and their corresponding neurotransmitter inputs to hippocampal neurons are evident in vitro and may play a crucial role in neuronal neurodegeneration. However, the mechanisms underlying the high vulnerability of dorsal hippocampus still remain enigmatic.     

骶骨骨折的动态冲击试验研究

目的:探讨骶骨在冲击载荷作用下发生骨折的机理。方法:采集人体新鲜骨盆标本10具,分别行动态冲击试验和静态破坏试验,测量动态骨折时的一系列动力学参数,确定骨折的动力学特性。结果:⑴骶骨受垂直冲击时按应力波的传递方向发生骨折,其动力学性质呈粘弹性,应力波呈周期性衰减,得到了骶骨的载荷响应曲线与应变响应曲线;骶骨骨折的平均冲击载荷为(9366±514) N,冲击时间为(2.78±1.02) s,动荷系数为1.21。⑵骶骨的动态破坏机制与静态破坏机制有很大的不同,不但极限载荷不同,而且前者随应变速率的提高而快速增加,冲击能量在25 J以上时呈脆性劈裂状通过骶孔或骶髂关节骨折,并累及神经根损伤,而静态大多为骶髂关节骨折。结论:骶骨骨折大都在高速冲击下发生,与其动力学特性、力的传导以及动载荷响应等诸多因素相关。     

The hippocampus and neurotransplantation

The present article is a review of our own results from histological and electron microscopic studies of hippocampal neurotransplants with different levels of integration with recipient brains. A model providing complete isolation from the brain was obtained using transplants developing in the anterior chamber of the eye. The growth, development, and cytological composition of transplanted tissue was found to depend on factors such as the age of the donor embryo tissue, the genetic compatibility between the donor and recipient, and the level of integration with the brain. Ultrastructural analysis of intraocular and intracortical transplants showed that overall, nerve and glial cells have the characteristics of highly differentiated, mature elements; the numerical density and structures of synaptic contacts were similar to those in normal conditions. However, transplanted tissues contained morphological features providing evidence of continuing growth of several nerve processes and increases in non-synaptic and transport-metabolic intercellular interactions. The ultrastructural deviations observed here are regarded as the manifestations of compensatory-adaptive changes during the development of tissues in conditions deficient in natural afferent synaptic influences. It is also demonstrated that the axons of transplanted neurons lacking adequate cellular targets can establish functional synaptic contacts with neuronal elements in the recipient brain which are not their normal targets.Translated from Zhurnal Vysshei Nervnoi Deyatelnosti, Vol. 54, No. 2, pp. 149–162, March–April, 2004.     

心肌肽素对大鼠心脏缺血-再灌注损伤的治疗作用

目的:研究多肽类物质心肌肽素对大鼠心脏缺血-再灌注损伤的治疗作用。方法:在大鼠冠脉结扎致心肌缺血-再灌注损伤模型上,观察心肌肽素治疗性给药对缺血大鼠血浆中肌酸磷酸激酶(CPK)、乳酸脱氢酶(LDH)活性及脂质过氧化终产物(MDA)含量的影响。结果:心肌肽素治疗性给药能明显降低血浆CPK、LDH的活性与MDA含量,其作用具有明显的量效关系。结论:心肌肽素对心脏缺血-再灌注损伤有治疗作用,提示可能与其抗脂质过氧化和影响心肌酶的活性有关。     

Investigation on the Maternal-Infantile Infection with Human Parvovirus B19

With the investigations on pregnant women and newbornsinfected withToxoplasma, rubella virus, cytomegalovirus,herpes simplex virus (TORCH), it was found that humanparvovirus B19 (B19 virus), which belongs to the familyParvoviridae and the genus Erythrovir…     

内洋地黄素拮抗剂上调缺血再灌注损伤大鼠心肌细胞膜钠泵亚基的表达

目的： 观察内洋地黄素特异性拮抗剂地高辛抗血清对心肌缺血再灌注（MIR）损伤大鼠心肌组织内洋地黄素水平、钠泵活性、线粒体总钙浓度以及钠泵各亚基基因表达的影响，探讨内洋地黄素在心肌缺血再灌注损伤中的作用及其机制。方法: 将56只雄性SD大鼠随机分成7组，每组8只。假手术对照组（sham）：丝线穿过左冠状动脉前降支，但不结扎；缺血再灌注组（MIR）：结扎左冠状动脉前降支30 min，再灌注45 min；生理盐水组（NS）、维拉帕米组（Ver）、小剂量、中剂量、大剂量地高辛抗血清组（ADA）：于再灌注前5 min经股静脉分别注射生理盐水、维拉帕米5 mg·kg^-1、地高辛抗血清8.6 mg·kg^-1、 17.3 mg·kg^-1、34.5 mg·kg^-1，容积均为5 mL·kg^-1，5 min内注射完毕，其余同MIR模型组。再灌注结束后，立即取缺血区左室心肌检测心肌匀浆内洋地黄素水平、心肌细胞膜Na+ K+_ATP酶和Ca2+_Mg2+_ATP酶活性、线粒体总钙浓度；分别采用RT-PCR及Western blotting方法和免疫组化方法检测心肌钠泵α₁、α₂、α₃和β₁亚基mRNA及蛋白水平基因表达的改变。结果: 心肌缺血再灌注损伤时，心肌组织内洋地黄素水平明显升高，心肌细胞膜钠泵和Ca2+_Mg2+_ATP酶活性显著下降，线粒体总钙浓度升高，钠泵α₁、α₂、α₃和β₁亚基在mRNA及蛋白水平基因表达均明显下降；维拉帕米除具有降低线粒体总钙浓度外，对其它各项指标无明显影响。地高辛抗血清呈剂量依赖性地显著降低心肌组织内洋地黄素水平，恢复细胞膜钠泵和Ca2+_Mg2+_ATP酶活性，降低线粒体总钙浓度，上调钠泵α₁、α₂、α₃和β₁亚基mRNA及蛋白水平的基因表达。结论: 心肌缺血再灌注促进机体内洋地黄素分泌增加，后者通过下调心肌细胞膜上的钠泵α₁、α₂、α₃和β₁亚基基因表达抑制钠泵活性，进而抑制Ca2+_Mg2+_ATP酶活性，导致线粒体内钙超载，介导心肌缺血再灌注损伤。内洋地黄素特异性拮抗剂地高辛抗血清通过阻断内洋地黄素的生物学作用，上调钠泵各亚基的基因表达，发挥其抗心肌缺血再灌注损伤的作用。     

Axonal and glial currents activated during the post-tetanic hyperpolarization in non-myelinated nerve

 Changes in membrane potential and potassium concentration in the extracellular space ([K⁺]_e) of rabbit vagus nerve were measured simultaneously during electrical activity and during the period of recovery using a modified sucrose-gap method and potassium-sensitive microelectrodes. After stimulation for 15 s at 15 Hz the main activity-induced increase in [K⁺]_e reached 16.9 mM. This increase in [K⁺]_e was paralleled by a depolarization of the preparation. The period of activity was followed by a post-tetanic hyperpolarization (PTH) lasting tens of seconds, generated by the axonal electrogenic Na⁺-K⁺ pump and to a lesser extent by the pump of the surrounding Schwann cells. The amplitude of the PTH dramatically increased in experiments in which inward currents were blocked by removal of Cl^– or after application of Cs⁺ or Ba²⁺, indicating that under normal conditions the current generated by the Na⁺-K⁺ pump is strongly short-circuited. A pharmacological and kinetic study showed that these currents are: (1) the hyperpolarization-activated current I _h, and (2) the inwardly rectifying I _KIR current. The results show that the latter originates from Schwann cells. Our data indicate that in non-myelinated nerves there is a subtle association of inward ionic channels which (1) helps the cell to maintain an optimal membrane potential after a period of activity, and (2) contributes to the removal of excess K⁺ from the extracellular space. Received: 7 August 1997 / Received after revision 6 April 1998 / Accepted: 15 April 1998