应用Ilizarov技术治疗手腕部瘢痕挛缩畸形临床观察

目的 观察Ilizarov技术治疗手腕部瘢痕挛缩畸形的临床效果。 方法 2017年4月~2020年1月,应用Ilizarov技术治疗7例手腕部瘢痕挛缩畸形患者,男3例,女4例;年龄12~52岁,平均24岁;左手部2例,左腕关节1例,右腕关节4例;创面感染致瘢痕增生2例,开水烫伤致瘢痕增生1例,火焰烧伤致瘢痕增生4例。瘢痕形成6月~34年,平均7年。根据Mayo评分法评估手腕部功能,术前患者手腕部功能可5例,差2例。 结果 腕关节畸形均获得矫正,以腕关节中立位为0°测量,腕关节掌屈可达到55~70°,背伸可达0~55°,无明显疼痛及麻木感,手指活动灵活。患者均无针道感染、肢端感觉麻木等并发症。术后随访5月~24月（平均15月）,末次随访时评估手腕部功能,良4例、可3例,较术前显著改善。 结论 应用Ilizarov技术治疗手腕部瘢痕挛缩畸形安全有效,可为烧伤后肢体功能重建提供一种新的疗法。     

蒙娜丽莎之谜

<正>500多年前,意大利人达芬奇创作出历史上最负盛名的肖像画杰作《蒙娜丽莎》。19世纪中叶,"她"正式入驻世界上最著名的艺术博物馆——法国的卢浮宫,刚开始被该馆收藏,"她"的知名度还不是很高,后来到了1911年,该馆的一个油漆     

个体人格类型与气味偏好的关系

目的：探讨气味偏好与个体人格之间的初步关系。为在行为层面上研究人格提供新的路径。方法：以艾森克的现代人格理论模型为框架，采用人格问卷和实验结合的方法进行研究，通过实验法在控制的条件下得到个体的气味偏好数据，通过人格问卷得到同一群体的人格各维度分值。结果：不同人格特征的个体在气味偏好上存在显著差异。结论：气味偏好和人格之间存在一定的联系。     

肾结核病灶中淋巴细胞趋化因子的表达

目的:探讨淋巴细胞趋化因子在正常肾脏和肾结核中的表达以及淋巴细胞趋化因子和浸润CD4 、D8 T细胞在肾脏结核病灶中的分布特点.方法:6例正常肾脏和10例肾结核病变组织,经匀浆后,采用RT-PCR法扩增人淋巴细胞趋化因子(hLptn)的含编码区序列的cDNA;扩增cDNA的克隆至pGM-T Easy T载体,测序;应用免疫组织化学方法检测正常肾脏和肾结核中的hLptn的表达和结核病灶中的CD4、CD8分子的表达.结果:正常肾脏和肾结核组织均表达hLptn mRNA,应用RT-PCR法克隆的cDNA序列与GenBank中U23772的序列一致;hLptn在正常的肾小球、肾小管中和结核病变中残存的肾小球、肾小管中均有表达;结核病变中有散在的CD4和CD8分子阳性细胞,与hLptn的分布无重叠.结论:淋巴细胞趋化因子在肾脏的肾小球和肾小管中呈结构性表达,肾结核肉芽肿中淋巴细胞的募集可能非依赖于hLptn的作用.     

GKT测谎模式研究

犯罪知识测试（Guilty Knowledge Test，简称GKT），是Lykken在1959年引入的一种测谎测试程序。本文就GKT测试的认知原理一定向反应有关理论的发展及其与GKT测试的关系进行了介绍，并以此为起点，对GKT测谎研究的四种范式进行了分析与探讨，最后指出GKT测谎模式还存在的问题、相关的扩展性研究以及发展趋势。     

非实验因素对人体核磁共振代谢组学检测结果的影响

代谢组学被认为是未来诊断疾病和评价患者机能状况的有力手段,但目前的研究结果表明,很多非实验因素,如饮食、运动、环境以及个体差异等均会影响临床实验结果,为保证不同核磁共振(Nuclear magnetic resonance,NMR)实验数据之间的可比性,很有必要在实验设计和数据分析过程中对这些因素进行合理的控制.     

腺病毒介导的肝癌靶向SEA-CD80基因治疗及免疫学机制的初步研究

目的: 观察肝癌靶向性葡萄球菌肠毒素A (SEA)/CD80基因重组腺病毒载体对肝癌的疗效,并对其免疫学机制进行初步研究.方法: 利用AdEasy腺病毒系统分别构建并制备甲胎蛋白(AFP)启动子和增强子Ⅰ调控的SEA和/或CD80基因重组腺病毒载体, 然后采用瘤体内直接注射的方式对小鼠皮下移植性肝癌进行治疗, 采用RT-PCR和Western blot方法检测腺病毒注射部位的SEA和CD80 mRNA和蛋白的表达情况; 采用ELISpot方法和LDH释放实验分别检测脾脏淋巴细胞中肝癌特异性IFN-γ分泌细胞的频数和细胞毒性T细胞(CTLs)对Hepa1-6细胞的特异杀伤活性; 通过观察荷瘤小鼠经治疗后肿瘤体积的变化及生存时间, 评价重组腺病毒对肝癌的治疗作用.结果: 我们构建的腺病毒能够使SEA和/或CD80 mRNA和蛋白靶向地在肝癌组织中表达; 与空载体组和PBS对照组相比, 双基因组和单基因组分泌IFN-γ的T细胞数量均明显增多, CTL对Hepa1-6细胞的特异性杀伤作用均明显增强, 荷瘤小鼠肿瘤体积明显减小, 生存期明显延长; 双基因组的疗效和对免疫系统的激活作用明显高于单基因组; CD80 和SEA的组之间、空载体和PBS组之间无明显差异.结论: 我们制备的肝癌靶向性重组腺病毒对肝癌有良好的治疗作用, 联合基因治疗优于单个基因治疗.     

联系我们

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敬告作者

本刊编辑部自2011年6月起不再向论著类作者提供纸质单行本,如有需要者可向本刊索取文稿的电子版数据(PDF格式),或登录本刊网站(http://www.cjcep.com)自行下载。     

太行山猕猴距骨的性别判别分析

太行山猕猴主要分布在太行山南坡中条山南端,是我国黄河以北分布最集中、数量最多、面积最大的猕猴自然分布种群。在形态、行为、遗传、食性、骨学方面均具有其特殊性。踝关节的距骨作为最坚固的骨骼之一,在国内有关该部位的研究报道较少。本研究主要对太行山猕猴距骨进行测量统计分析,找出两性间差异较大的变量,建立判别函数,为太行山猕猴的基础研究和生物学研究积累资料。     

Colocalization of CB1 receptors with L1 and GAP-43 in forebrain white matter regions during fetal rat brain development: evidence for a role of these receptors in axonal growth and guidance

There is recent evidence supporting the notion that the cannabinoid signaling system plays a modulatory role in the regulation of cell proliferation and migration, survival of neural progenitors, neuritic elongation and guidance, and synaptogenesis. This assumption is based on the fact that cannabinoid 1-type receptors (CB₁ receptors) and their ligands emerge early in brain development and are abundantly expressed in certain brain regions that play key roles in these processes. We have recently presented in vivo evidence showing that this modulatory action might be exerted through regulating the synthesis of the cell adhesion molecule L1 that is also a key element for those processes. To further explore this issue, we conducted here immunohistochemical studies aimed at determining the cellular substrates of CB₁ receptor–L1 interactions in the rat brain during late fetal development. In this period, we previously found that the activation of CB₁ receptors increased L1 synthesis in several forebrain white matter regions but not in gray matter areas. Using double labeling studies, we observed here colocalization of both proteins in fiber tracts including the corpus callosum, the adjacent subcortical white matter, the internal capsule and the anterior commissure. Experiments conducted with cultures of fetal rat cortical nerve cells revealed that L1 is present mainly in neurons but not in glial cells. This fact, together with the results obtained in the double labeling studies, would indicate that L1 and CB₁ receptors should possibly be present in axons elongating through these white matter tracts, or, alternatively, in migrating neurons. Further experiments confirmed the presence of CB₁ receptors in elongating axons, since these receptors colocalized with growth-associated protein 43 (GAP-43), a marker of growth cones, but not with synaptophysin, a marker of active synaptic terminals, in the same forebrain white matter regions. Lastly, using cultured fetal rat cortical neurons, we also observed that the activation of cannabinoid receptors increased the levels of the full-length L1 and altered those of some active proteolytic fragments of this protein whose generation has been associated with specific steps in the process of neuritic elongation in cultured neurons. In summary, we have demonstrated that the effects caused by cannabinoid agonists on L1 are facilitated by the colocalization of this cell adhesion molecule with CB₁ receptors in several forebrain white matter regions during fetal brain development. We have provided strong evidence that this phenomenon occurs in axons elongating through these white matter tracts, and we have explored in vitro how cannabinoid receptors influence L1 levels. Considering the role played by L1 in different events related to neural development, our observations support the occurrence of a physiological mechanism by which the cannabinoid system might regulate the process of axonal growth and guidance through regulating the synthesis and function of L1.     

Cannabinoid receptor CB2 modulates the CXCL12/CXCR4-mediated chemotaxis of T lymphocytes

Cannabinoids have been shown to influence the immune system. However, their immunomodulatory effects have not been extensively studied. In this investigation, we have observed that both primary and Jurkat T cells express a functional cannabinoid receptor 2 (CB₂). Furthermore, both the synthetic cannabinoids CP55,940 and WIN55,212-2, as well as the CB₂-selective agonist JWH-015, caused a significant inhibition of the chemokine CXCL12-induced and CXCR4-mediated chemotaxis of Jurkat T cells, as well as their transendothelial migration. Involvement of the CB₂ receptor was further confirmed by partial reversal of the inhibition using the CB₂-specific antagonist, AM630. Similarly, CP55,940 and JWH-015 inhibited the CXCL12-induced chemotaxis of primary CD4⁺ and CD8⁺ T lymphocytes. Further investigation of signaling studies to delineate the mechanism of inhibition revealed that cannabinoids enhance CXCL12-induced p44/42 MAP kinase activity. However, enhanced MAP kinase activity was not responsible for the inhibition of chemotaxis. This suggests that cannabinoids differentially regulate CXCR4-mediated migration and MAP kinase activation in T cells. Cannabinoids were also found to downregulate the PMA-enhanced enzyme activity of matrix metalloproteinase-9, which is known to play an important role in transendothelial migration. This study provides novel information regarding cannabinoid modulation of functional effects in T cells.     

The D1 dopamine agonist SKF 38393, but not the D2 agonist LY 171555, decreases the affinity of type II corticosteroid receptors in rat hippocampus and ventral striatum

Type I and type II brain corticosteroid receptors are regulated by adrenal hormones as well as being under neural control. Recent studies have indicated that neurotransmitters such as serotonin and noradrenaline are also involved in the regulation of corticosteroid receptors. In a previous study, we showed that dopamine also modulates activity of the corticosteroid receptor system. In the present study, we examined the roles of the dopamine D₁ and D₂ receptor subtypes in the regulation of corticosteroid receptors. Adrenalectomized rats whose corticosterone levels were maintained within normal limits by corticosterone replacement implants, were injected intraperitoneally with the D₁ agonist SKF 38393 or the D₂ agonist LY 171555. Corticosteroid receptors were assayed in the ventral striatum and hippocampus. We have shown that the D₁ agonist SKF 38393 decreased type II receptor affinity in both regions, whereas the D₂ agonist LY 171555 had no effects.

The results show that the influence of the dopaminergic system on corticosteroid receptors appears to be mediated by D₁ receptors.     

Decline in striatal dopamine D1 and D2 receptor activation in aged F344 rats

Aging differentially affects receptor function. In the present electrophysiological study we compared neuronal responsiveness to locally applied dopamine D₁ and D₂ receptor agonist in the striatum of female Fischer 344 rats aged 3 and 26–27 months. In a subgroup of the old rats, the nigrostriatal dopamine bundle was destroyed unilaterally with 6-hydroxydopamine (6-OHDA) to assess receptor plasticity in response to denervation. Spontaneous firing rate of striatal neurons was higher in aged compared to young rats. Higher doses of the D₁ agonist SKF 38393 or the D₂ agonist quinpirole were required to elicit a 50% change in firing rate in aged compared to young rats. No difference with SKF 38393 or quinpirole was detected between 6-OHDA denervated and control (nonlesioned) striatum in aged rats. Supersensitivity to D₂ agonists has been reported following 6-OHDA lesions in young rats. These observations suggest that D₂ receptors in aged rat striatum might not be as plastic as in younger rats.     

Central CRF, urocortins and stress increase colonic transit via CRF1 receptors while activation of CRF2 receptors delays gastric transit in mice

Recently characterized selective agonists and developed antagonists for the corticotropin releasing factor (CRF) receptors are new tools to investigate stress-related functional changes. The influence of mammalian CRF and related peptides injected intracerebroventricularly ( i.c.v. ) on gastric and colonic motility, and the CRF receptor subtypes involved and their role in colonic response to stress were studied in conscious mice. The CRF₁/CRF₂ agonists rat urocortin 1 (rUcn 1) and rat/human CRF (r/h CRF), the preferential CRF₁ agonist ovine CRF (oCRF), and the CRF₂ agonist mouse (m) Ucn 2, injected i.c.v. inhibited gastric emptying and stimulated distal colonic motor function (bead transit and defecation) while oCRF_9–33OH (devoid of CRF receptor affinity) showed neither effects. mUcn 2 injected peripherally had no colonic effect. The selective CRF₂ antagonist astressin₂-B ( i.c.v. ), at a 20 : 1 antagonist: agonist ratio, blocked i.c.v. r/hCRF and rUcn 1 induced inhibition of gastric transit and reduced that of mUcn 2, while the CRF₁ antagonist NBI-35965 had no effect. By contrast, the colonic motor stimulation induced by i.c.v. r/hCRF and rUcn 1 and 1h restraint stress were antagonized only by NBI-35965 while stimulation induced by mUcn 2 was equally blocked by both antagonists. None of the CRF antagonists injected i.c.v. alone influenced gut transit. These data establish in mice that brain CRF₁ receptors mediate the stimulation of colonic transit induced by central CRF, urocortins (1 and 2) and restraint stress, while CRF₂ receptors mediate the inhibitory actions of these peptides on gastric transit.     

去泛素化酶USP14调控H_2O_2诱导的H9c2细胞氧化应激损伤

目的:观察抑制泛素特异性蛋白酶14(ubiquitin-specific protease 14,USP14)的活性对H_2O_2诱导的H9c2细胞氧化应激损伤的影响。方法:体外培养H9c2心肌细胞,用H_2O_2(25μmol/L)处理2 h,建立心肌细胞氧化应激损伤模型。将细胞分为对照(control,CON)组、模型组(H_2O_2组)、USP14抑制剂IU1处理组(IU1组)和IU1处理后建模组(IU1+H_2O_2组)。MTS法检测H9c2心肌细胞活力;流式细胞术检测细胞内活性氧簇(ROS)的产生和细胞存活率;Western blot法检测丝裂原活化蛋白激酶家族相关蛋白的表达变化。结果:与CON组相比,H_2O_2组细胞活力、细胞存活率显著降低,细胞内ROS含量、Bax/Bcl-2、P53、p-ERK1/2、p-JNK和p-P38的蛋白水平显著增加(P0.05);与H_2O_2组比较,IU1+H_2O_2组细胞活力、细胞存活率显著增加,细胞内ROS含量、Bax/Bcl-2、P53、p-ERK1/2、p-JNK和p-P38蛋白水平显著降低(P0.05)。结论:抑制USP14活性可以减轻氧化应激条件下H9c2心肌细胞的损伤,其机制可能与抑制丝裂原活化蛋白激酶信号活化和下调凋亡相关蛋白有关。     

Cannabinoid CB2-Selective Inverse Agonist Protects Against Antigen-Induced Bone Loss

Work to improve the therapeutic properties of cannabinoid CB₂ receptor-selective inverse agonists has led to the development of Sch.036, an aryl substituted triaryl bis-sulfone with improved oral pharmacokinetic parameters. In this report, we show that this compound blocks in vivo trafficking of various leukocyte populations, a property consistent with other members of this chemical series. This CB₂-selective compound also shows efficacy in leukocyte recruitment models when added in concert with suboptimal doses of selected anti-inflammatory agents, consistent with its unique function and indicative of its potential therapeutic utility. Finally, studies with Sch.036 show that this cannabinoid CB₂-specific inverse agonist can ameliorate bone damage in a rat model of relapsing-remitting arthritis. This result suggests that a cannabinoid CB₂-selective inverse agonist may help ameliorate a particularly harmful property of this inflammatory joint disease.     

Adenosine inhibition via A1 receptor of N-type Ca2+ current and peptide release from isolated neurohypophysial terminals of the rat

Effects of adenosine on voltage-gated Ca²⁺ channel currents and on arginine vasopressin (AVP) and oxytocin (OT) release from isolated neurohypophysial (NH) terminals of the rat were investigated using perforated-patch clamp recordings and hormone-specific radioimmunoassays. Adenosine, but not adenosine 5'-triphosphate (ATP), dose-dependently and reversibly inhibited the transient component of the whole-terminal Ba²⁺ currents, with an IC₅₀ of 0.875 μ m. Adenosine strongly inhibited, in a dose-dependent manner (IC₅₀= 2.67 μ m ), depolarization-triggered AVP and OT release from isolated NH terminals. Adenosine and the N-type Ca²⁺ channel blocker ω-conotoxin GVIA, but not other Ca²⁺ channel-type antagonists, inhibited the same transient component of the Ba²⁺ current. Other components such as the L-, Q- and R-type channels, however, were insensitive to adenosine. Similarly, only adenosine and ω-conotoxin GVIA were able to inhibit the same component of AVP release. A₁ receptor agonists, but not other purinoceptor-type agonists, inhibited the same transient component of the Ba²⁺ current as adenosine. Furthermore, the A₁ receptor antagonist 8-cyclopentyltheophylline (CPT), but not the A₂ receptor antagonist 3, 7-dimethyl-1-propargylxanthine (DMPGX), reversed inhibition of this current component by adenosine. The inhibition of AVP and OT release also appeared to be via the A₁ receptor, since it was reversed by CPT. We therefore conclude that adenosine, acting via A₁ receptors, specifically blocks the terminal N-type Ca²⁺ channel thus leading to inhibition of the release of both AVP and OT.     

Activity-dependent bidirectional regulation of GABAA receptor channels by the 5-HT4 receptor-mediated signalling in rat prefrontal cortical pyramidal neurons

Emerging evidence has implicated a potential role for 5-HT₄ receptors in cognition and anxiolysis. One of the main target structures of 5-HT₄ receptors on 'cognitive and emotional' pathways is the prefrontal cortex (PFC). As GABAergic signalling plays a key role in regulating PFC functions, we examined the effect of 5-HT₄ receptors on GABA_A receptor channels in PFC pyramidal neurons. Application of 5-HT₄ receptor agonists produced either an enhancement or a reduction of GABA-evoked currents in PFC neurons, which are both mediated by anchored protein kinase A (PKA). Although PKA phosphorylation of GABA_A receptor β3 or β1 subunits leads to current enhancement or reduction respectively in heterologous expression systems, we found that β3 and β1 subunits are co-expressed in PFC pyramidal neurons. Interestingly, altering PKA activation levels can change the direction of the dual effect, switching enhancement to reduction and vice versa. In addition, increased neuronal activity in PFC slices elevated the PKA activation level, changing the enhancing effect of 5-HT₄ receptors on the amplitude of GABAergic inhibitory postsynaptic currents (IPSCs) to a reduction. These results suggest that 5-HT₄ receptors can modulate GABAergic signalling bidirectionally, depending on the basal PKA activation levels that are determined by neuronal activity. This modulation provides a unique and flexible mechanism for 5-HT₄ receptors to dynamically regulate synaptic transmission and neuronal excitability in the PFC network.