运动对骨骼－肌腱界面愈合组织的影响

利用纽西兰兔作体内实验，来分析手术后石膏固定，笼内活动，连续被动性活动三种不同的复健方法对肌腱－骨骼间界面愈合组织的影响。结果显示在术后第１５天愈合组织所能承受的最大张力，笼内活动组为０．８７５ｋｇ，石膏固定组为２．０１４ｋｇ，是笼内活动组的２３１．５２％，而连续被动性活动组为２．６３８ｋｇ，是笼内活动组的２６１．３５％。石膏固定组虽有很高的张力，但关节内粘连也较多。     

低心室容量负荷未能影响兔离体心肌的氧耗反应时间

为了解心肌容量负荷是否影响心肌的氧化磷酸化过程,采用兔离体灌流心肌线粒体氧耗反应时间测定方法,对一下正常心室容量负荷和低心室容量负荷时的心肌线粒体氧耗反应时间进行比较,结果提示心肌作功负荷变化未能影响心肌线粒体的能量代谢动态调节过程。     

Effect of vagotomy on acute pancreatitis in rats

Acute pancreatitis ( AP) is a common surgicalabdomen,which has a high mortality,especiallyhemorrhagic necrotic pancreatitis.Many things areunknown for its pathogen,pathogenesis and clinicaltreatment.Restraining secretion of pancreatin so asto decrease its complication is used now in clinicalpractice[1] .A lot of information indicates that vagushas directdomination on exocrine of pancreas[2 ] .Thepurpose of this study was to investigate whether thevagotomy ( VG) had effect on AP in rats.1　M…     

电针肾俞、膈俞、百会穴对拟血管性痴呆学习记忆障碍小鼠水迷宫实验的影响

目的　观察电针肾俞、膈俞、百会穴对拟血管性痴呆小鼠学习记忆障碍的影响。方法　复制脑缺血再灌注拟血管性痴呆小鼠模型 ,并电针肾俞、膈俞、百会穴 ,分别于术后 7天、15天、30天 ,与药物喜德镇对照 ,采用水迷宫法 ,记录游全程时间、错误次数。结果　造模导致了小鼠学习与记忆能力下降 ,表现为游全程时间延长 ,错误次数增加 ,且随着观察时间的延长 ,这种改变逐渐加重。电针和喜德镇均可使模型小鼠的游全程时间缩短 ,错误次数减少 ,但电针组于 7天和 30天时 ,成绩显著优于药物组。结论　电针肾俞、膈俞、百会穴对模型小鼠学习与记忆能力下降有改善和提高作用     

An outline of spreading of Western mediciine into Yantai in modern age

At the turn of the last century, side by side with the infiltration of religious culture from Western countries, western medicine spread into Yantai. The religious force, headed by American Presbyterian Mission, carried out charitable activities in the process of preaching and laid down the foundation for western medicine rooted in Yantai by establishing schools, education and training followers. They cultivated local physicians by first setting up clinics which had later transformed into hospitals. These are their major measures for building bases for spreading Christianity by foreigners. The Temple Hill Hospital set up by the American physician Oscar F. Hills in Yantai was a successful example of mutual promotion of missionary and medical activities which pushed forward the spreading and development of western medicine in Yantai.     

GABA(A) receptors mediate inhibition of T cell responses

We describe the presence of functional GABA(A) receptors on T cells. GABA inhibited anti-CD3 and antigen-specific T cell proliferation in vitro in a dose-dependent manner that was 1) mimicked by the GABA(A) receptor agonist muscimol (but not the GABA(B) receptor agonist baclofen), 2) blocked by GABA(A) receptor antagonists and a GABA(A) receptor Cl- channel blocker (picrotoxin) and 3) enhanced by pentobarbital. These data suggest that GABA(A) receptors mediate this immune inhibition and that these receptors can be modulated in a similar fashion to their neuronal counterparts. Finally, GABA inhibited DTH responses in vivo. Thus, pharmacological modulation of GABA(A) receptors may provide new approaches to modulate T cell responses in inflammation and autoimmune disease.     

Analysis of differential effects of Pb2+ on protein kinase C isozymes

Protein kinase C has been implicated as a cellular target for Pb2+ toxicity. We have previously proposed that Pb2+ modulates PKC activity by interacting with multiple sites within the enzyme. In order to further characterize the Pb-PKC interactions we compared the effects of Pb2+ on the CA-dependent and -independent protein kinase C isozymes using recombinant human PKC-alpha, PKC-epsilon, and PKC-zeta as well as the catalytic fragment of bovine brain protein kinase C, the PKC-M. The results demonstrate that, whereas at pM concentrations Pb2+ activates PKC-alpha half maximally (KAct approximately 2 pM), it has no effect on PKC-epsilon, PKC-zeta, or PKC-M activities. The activation of PKC-alpha by Pb2+ is additive with Ca2+ in a manner indicating interaction with half of the calcium activation sites. In the micromolar range of concentrations, Pb2+ inhibits all PKCs with estimated K0.5 of 1.0, 2.3, 28, and 93 microM for PKC-M, PKC-alpha, PKC-epsilon, and PKC-zeta, respectively. Examination of Pb2+ effects on PKC-M kinetics indicates a mixed type inhibition with respect to ATP and noncompetitive inhibition with respect to histone. Taken together with the results of our previous study (Tomsig and Suszkiw, J. Neurochem. 64, 2667-2673, 1995) and the evidence for the existence of two Ca2+ coordination sites Ca1 and Ca2 within the C2 domain (Shao et al., Science [Washington, D.C.] 273, 248-251, 1996), the results of the current study provide further support for a multisite Pb-PKC interaction scheme wherein lead (1) partially activates the enzyme through pM-affinity interactions with the Ca1 site and inhibits the divalent cation-dependent activity through nM-affinity interactions with Ca2 site in the C2 domain and (2) inhibits the constitutive kinase activity through microM-affinity interactions with the catalytic domain. The concentration dependence of the differential effects of Pb2+ on the calcium-dependent and -independent PKCs underscores the importance of the C2 motif as a high affinity molecular target for Pb2+.