Reversed palmaris longus muscle on MRI: report of four cases

Muscle anomalies around the wrist, in particular the palmaris longus muscle, may cause effort-related median nerve compression. A search of the medical records at our university hospital between 1994 and 1999 revealed four patients with an effort-related median nerve compression due to a reversed palmaris longus muscle. Magnetic resonance imaging was used in the patient work-up and showed an anomalous muscle in each case that had been missed initially. All four patients were free of pain after simple excision of the anomalous muscle. Awareness of muscle anomalies at the wrist on MR imaging is essential in evaluating patients with nerve compressions at the wrist. The purpose of this article is to heighten this awareness in radiologists. Received: 23 June 1999; Revised: 30 September 1999; Accepted: 24 December 1999     

用彗星试验研究低剂量辐射对荷瘤鼠放疗后DNA损伤的影响

目的　研究低剂量辐射对荷瘤鼠放疗后外周血淋巴细胞DNA损伤的影响。方法　采用中性单细胞凝胶电泳检测低剂量辐射对荷瘤鼠放疗后外周血淋巴细胞DNA双链断裂的情况。观察了尾长、彗星长、头DNA%、尾DNA%、尾矩、Olive尾矩等指标的变化。结果　2.0 Gy局部放疗前 6 h接受 5 cGy低剂量全身照射并连续 5d组, 其尾长、尾DNA%、尾矩、Olive尾矩均较单纯局部放疗组明显减小, 各项指标差异均有显著性(P<0.01)。结论　局部放疗前荷瘤鼠预先接受低剂量全身照射能减轻荷瘤鼠放疗后外周血淋巴细胞DNA损伤。     

县级综合医院工作人员针刺伤害状况的回顾性调查分析

目的了解县级综合医院工作人员针刺伤害的发生频率和特征,为制定安全注射对策提供依据。方法采用回顾性调查方法,对山东省4所县级综合医院过去1年间发生的针刺伤害事件进行登记,分析其发生特征。结果30.6%的调查对象曾发生过针刺伤害,年人均0.44次,每百病床平均每年发生针刺伤害46.7次。助产士、麻醉师、检验技师为针刺伤害的高发职业。针刺伤害主要发生在器材使用后的分解、消毒、废弃过程中(43.7%),最主要的原因器材为翼状针(37.2%)。结论所调查医院针刺伤害的发生频率与欧美等国基本相同;我国医疗单位注射等操作规范尚有待进一步完善。     

手法治疗神经根型颈椎病的X线椎体位移观察及分析

目的：观察手法治疗后神经根型颈椎病的X线椎体位移改变方法：收集140例神经根型颈椎病的病人，对治疗前后X线椎体位移改变进行观察，并与70例正常人群进行比较。结果：两组颈4、5、6椎体位移治疗前比较，有显著性差异（P〈0．05，P〈0．01）；手法治疗后能够改善椎体的水平及角度位移，治疗前比较有显著性差异（P〈0．05．P〈0．01）；治疗后临床控制69．3％，好转22．9％，总有效率92．1％。结论：神经根型颈椎病椎体位移改变可能是其发病原因之一，手法治疗改善颈椎椎体异常位移，提高颈椎的稳定性是手法治疗神经根型颈椎病取得较好疗效的因素之一。     

脉络宁注射液治疗半面痉挛的实验研究

目的:探讨脉络宁对半面痉挛脱髓鞘面神经的保护作用,为半面痉挛的治疗提供依据。方法:将24只新西兰大白兔随机分为对照组、脉络宁组和生理盐水组,在手术显微镜下分离出其茎乳孔处的面神经主干和颞浅动脉,使二者密切接触,以制备半面痉挛动物模型;术后第5周起对脉络宁组和生理盐水组分别自耳缘静脉推注脉络宁注射液和生理盐水持续2周;第7周取3组动物血清测定丙二醛(MDA)和超氧化物歧化酶(SOD),并处死取材行面神经光、电镜观察。结果:脉络宁组血清MDA明显低于生理盐水组(P<0.05),SOD明显高于生理盐水组(P<0.01),而与对照组比较变化不明显(P>0.05)。生理盐水组面神经纤维溃变明显,髓鞘松解分离,轴突肿胀有空泡或全部消失;脉络宁组面神经病变较轻。结论:脉络宁注射液对半面痉挛脱髓鞘面神经有明显的保护作用,对半面痉挛的治疗具有极其重要的应用价值。     

The pineal gland is not essential for circadian expression of rat period homologue (rper2) mRNA in the suprachiasmatic nucleus and peripheral tissues

To investigate the functional involvement of the pineal gland in circadian expression of the rat period homolog gene (rPer2) in the suprachiasmatic nucleus (SCN) and peripheral tissues, we performed Northern blot analysis in tissues from pinealectomized rats. The ectomy did not have any significant effects on rPer2 mRNA expression patterns both in a daily light-dark condition and in a constant darkness. These results suggest that the rhythmic secretion of pineal melatonin is not essential for the circadian expression of clock genes in the SCN and other peripheral tissues of rats.     

Early and selective pathology of light chain neurofilament in the spinal cord and sciatic nerve of G86R mutant superoxide dismutase transgenic mice

Pathologic accumulation of neurofilament protein (NF), both within spheroids of the proximal axon and within inclusions of motor neuron somata, is a hallmark of neurodegeneration in amyotrophic lateral sclerosis (ALS). Transgenic mice that express mutations in superoxide dismutase (SOD-1), which were genetically linked to familial ALS, develop symptomatology and pathology that strongly resemble ALS and therefore provide a useful model for studying the disease. Examining NF in the G86R mutant SOD-1 transgenic mice, we previously demonstrated that phosphorylated NF accumulates in motor neuron somata of symptomatic transgenic mice. In the present study, we expand these results by examining the immunocytochemical distribution of the three subunits of NF (i.e., light, medium, and heavy chains) as well as tubulin in presymptomatic and symptomatic SOD-1 transgenic mice. Although all NF subunits, but not tubulin, accumulate along with phosphorylated NF in the spinal cord inclusions of symptomatic mice, numerous inclusions containing only light chain NF are found in the spinal cord of presymptomatic SOD-1 transgenic mice. In addition to these results in the spinal cord, intensely immunoreactive aggregates of NF-L, but not the other NF subunits or tubulin, were observed in the sciatic nerve of both symptomatic and presymptomatic mutant SOD-1 transgenic mice. These results suggest that the mechanism of NF alteration in SOD-1 transgenic mice, and also perhaps in ALS patients, originates with the disruption of NF-L, only later involving the other subunits.     

Central leptin suppresses splenic lymphocyte functions through activation of the corticotropin-releasing hormone-sympathetic nervous system

Leptin is one of the key afferent signals that regulate food intake and energy expenditure by acting on specific receptors in the hypothalamus. Recently, leptin was reported to activate the peripheral immune system by acting directly on lymphocytes. To elucidate the brain-mediated participation of leptin in the modulation of peripheral immune functions, we examined the effects of intracerebroventricular (icv) injection of murine recombinant leptin on the proliferative response to Concanavalin A (ConA response) of splenic lymphocytes in rats. The ConA response of splenic lymphocytes was markedly reduced 30 min after icv injection of leptin. The suppressive effect of leptin was abolished completely either by surgical severing of the splenic nerves or by icv injection of an antibody against corticotropin-releasing hormone (CRH), but only partially by an anti-urocortin antibody. Icv injection of CRH and urocortin also suppressed the ConA response of splenic lymphocytes, and the effect of urocortin was prevented by the anti-CRH antibody, while that of CRH was not prevented by the anti-urocortin antibody. These results suggest that leptin suppresses peripheral lymphocyte functions, in contrast to the direct activating effects, indirectly through the activation of the CRH (urocortin)-sympathetic nervous system.     

Netrin-1 and peripheral nerve regeneration in the adult rat

Axonal guidance during development of the nervous system is thought to be highly regulated through interactions of axons with attractive, repulsive, and trophic cues. Similar mechanisms regulate axonal regeneration after injury. The netrins have been shown to influence the guidance of several classes of developing axons. Although netrins have been implicated as axonal guidance cues in the developing peripheral nervous system, there has been no direct evidence of netrin-1 expression in either developing or adult peripheral nerve. The present study utilized competitive PCR and immunohistochemistry to demonstrate the localization of netrin-1 within adult rat sciatic nerve. The expression of netrin-1 mRNA and protein was compared for normal or regenerated sciatic nerve 2 weeks following either a crush or a transection and repair injury. The PCR data show that netrin-1 mRNA is normally expressed at low levels in peripheral nerve, and similar low levels are found 2 weeks following a crush injury. However, 2 weeks following nerve transection and repair there is approximately a 40-fold increase in netrin-1 mRNA levels. Immunohistochemistry data show that Schwann cells are the major source of netrin-1 protein in peripheral nerve. Our results suggest that netrin-1 mRNA levels are profoundly affected during peripheral nerve injury and regeneration. The localization of netrin-1 to Schwann cells suggests that this protein is strategically situated to influence axon regeneration in adult peripheral nerve.     

Truncated TrkB mediates the endocytosis and release of BDNF and neurotrophin-4/5 by rat astrocytes and schwann cells in vitro

Binding and cross-linking studies with radiolabeled neurotrophins demonstrate that cultured rat hippocampal astrocytes lack full-length TrkB, but do express high levels of truncated TrkB (tTrkB). In astrocytes and Schwann cells, tTrkB appears to have the novel function of mediating the endocytosis of neurotrophins into an acid-stable, Triton X-100 resistant intracellular pool that is released back into the medium in a temperature-dependent manner. Chloroquine treatment, trichloroacetic acid solubility, and sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis revealed that when incubated with astrocytes or Schwann cells for at least 48 h neither the intracellular nor the released neurotrophins were significantly degraded. The endocytosis and release of neurotrophins may represent a novel mechanism whereby neuroglia can regulate the local concentration of these neurotrophic factors for extended periods of time.