脊髓手术中体感诱发电位监测的临床研究

报告３０例脊髓手术中体感诱发电位（ＳＥＰ）连续监测的临床研究结果。ＳＥＰ记录包括脊髓ＳＥＰ（ＳＳＥＰ）和皮层ＳＥＰ（ＳＣＥＰ）。麻醉药物对ＳＥＰ有一定程度影响，ＳＣＥＰ相对较大。认为，至少术中ＳＥＰ潜伏期延长不超过８％和波幅降低不超过５０％，不会引起术后并发症，超过该范围由于病例较少，尚不能肯定与预后的关系，需进一步探讨。     

适应社会主义市场经济 发展妇幼保健机构

本文在分析黑龙江省妇幼保健机构设置现状的基础上,论述了在社会主义市场经济新形势下,妇幼保健机构发展的指导思想、模式与对策。     

不同术后镇痛模式对红细胞免疫功能的影响

目的探讨不同术后镇痛模式对红细胞免疫功能的影响。方法50例妇科手术患者,按术后不同镇痛模式分为硬膜外自控镇痛(PCEA)组和静脉自控镇痛(PCIA)组。并分别于术前、术后1、3、7 d采静脉血样检测红细胞C3b受体花环率(RCR)、红细胞免疫复合物花环率(RICR)、红细胞免疫粘附促进因子(RFER)和红细胞免疫粘附抑制因子(RFIR)。结果与术前比,PCEA组术后1 d RCR、RFER显著上升(P<0.05),RFIR显著下降(P<0.05),术后3 d RCR、RFER仍显著上升(P<0.05),而RICR显著下降(P<0.05);PCIA组术后1 d RCR、RFER显著下降(P<0.05),RFIR、RICR显著上升(P<0.05);PCIA组术后1、3 d RCR、RFER比PCEA组显著降低(P<0.05),而RICR显著上升(P<0.05);两组各参数在术后7 d基本恢复至术前水平。结论PCEA对红细胞免疫功能的稳定和恢复作用明显强于PCIA。     

不典型脑转移瘤CT和MR的诊断分析

目的：提高CT与MR对不典型脑转移瘤的诊断准确性。方法：回顾性分析58例经临床手术证实的有完整资料的不典型脑转移瘤的CT和MR表现。结果：病变大部分位于幕上，有钙化者较多，约2／3有强化和水肿，且多发。部分有出血和囊变。结论：不典型脑转移瘤的CT和MR表现多种多样，多发者相对容易诊断，单发者诊断不易。颅外肿瘤的检查有助于鉴别诊断。肺部的影像学检查是必不可少的。     

Mirizzi综合征的影像学诊断

目的:探讨Mirizzi综合征的发病机理、临床表现、影像学诊断及术前诊断的重要价值.方法:查阅了大量的相关资料文献,进行对比、分析、总结归纳.结果:Mirizzi综合征是胆道系统感染的一种特殊类型,临床少见,极易造成漏诊和误诊,在术中造成不必要的胆道损伤和胆总管探查,影像学检查在诊断此综合征方面有较多的独特优势.结论:Mirizzi综合征术前可以通过影像学检查尤其是超声检查明确诊断.     

有效控制与控制不佳的MRI阴性的GTCS病人发作间期SPECT对照研究

目的:利用单光子发射计算机断层摄影(SPECT)半定量分析有效控制与控制不良的MRI阴性的全面性强直阵挛发作癫(GTCS)病人的局部脑血流差异,探讨脑血流灌注与其预后的关系.材料和方法:对29例有效控制的和12例控制不佳的MRI阴性的GTCS病人进行发作间期99mTc-ECD-SPECT脑血灌流显像,10例年龄匹配的健康人作对照,用感兴趣区(ROI)的不对称指数(%AI)进行半定量分析.将SPECT分析结果与病人的临床表现与EEG相比较.结果:①控制不佳组与有效控制组在丘脑和基底节区的%AI存在显著性差异(P<0.05);②控制不佳组SPECT脑显像的异常率(83.3%,10/12)明显高于有效控制组的异常率(17.2%,5/29),两组具有显著性差异(P<0.01);而两组病人的EEG异常率分别为58.3%、44.8%(7/12、13/29),无显著性差异(P>0.05).结论:控制不佳的MRI阴性的GTCS病人往往存在发作间期的低血流灌注脑区,提示癫的难治性;而控制良好的病人多无明显异常发现,可能预后较好.     

影响脐血IgE值因素的研究

目的　本研究对影响脐血IgE值的可疑因素进行分析 ,探讨影响儿童食物过敏的可疑因素。方法　选取孕期妇女 10 5名及其所生婴儿 ,采用标准问卷调查获取资料 ,对影响脐血IgE的因素进行分析。 结果　母亲的过敏性疾病史、父亲过敏性疾病史中的皮炎表现型、孕期妇女过敏性疾病发作史、有过敏史妇女孕后期摄入过量的牛奶和鸡蛋均与脐血IgE值的上升有关 ,且上述 5个因素对脐血IgE水平的影响依次降低。 结论　母亲的过敏性疾病史和父亲过敏性疾病史中的皮炎表现型是导致新生儿脐血IgE值升高的主要危险因素 ;同时 ,妊娠期加强对有过敏史妇女的保护 ,防止过敏性疾病的复发 ,在孕后期控制有过敏史妇女牛奶、鸡蛋等大分子食物致敏原的摄入 ,有助于降低脐血IgE值。     

Calcification and ossification of chronic encapsulated intracerebral haematoma: case report.

We report a case of calcified chronic encapsulated intracerebral haematoma (ICH) in a 29-year-old female who presented with progressive left sided weakness and intermittent seizures since childhood. The preoperative magnetic resonance (MR) imaging of the head initially suggested that a partially thrombosed aneurysm or vascular malformation was present. However, no vascular stain was found on the digital subtraction angiography (DSA) of both the carotid and vertebral arteries. The excised mass was histologically diagnosed as a chronic ICH. We traced the patient's medical history and found that at the age of one she sustained a head injury after a fall. So far, to our knowledge, no case of epilepsy secondary to a calcified chronic encapsulated ICH occurring 28 years after head injury has been reported. Calcified chronic encapsulated ICH concomitant with new bone formation within is even rarer. The possible pathogenesis of this case is discussed.     

Outcome after traumatic frontal intracerebral haemorrhage: a comparison of unilateral and bilateral haematomas

Frontal intracerebral haemorrhage (ICH) is a common result of cranial trauma. Outcome differences between bilateral and unilateral frontal ICH are not well studied but would be valuable to predict prognosis in clinical practice. Two aims are proposed in this study: first to compare the risk of developing delayed ICH after bilateral or unilateral frontal ICH, and second to determine the variables helpful to predict outcome according to the Glasgow Outcome Scale (GOS). Between January 1993 and December 1997, 694 consecutive patients with traumatic ICH were admitted to the Chang Gung Medical Center within 24 h of the trauma. Patients with ICH in sites other than the frontal lobes were excluded. A total of 161 cases (mean age 46.3+/-20.3 years), including 57 bilateral (mean age 52.5+/-18.7 years) and 104 unilateral (mean age 42.9+/-20.5 years) traumatic frontal ICH were studied. Twenty-eight of 57 patients (49%) with bifrontal ICH versus 17 of 104 patients (16%) with unilateral frontal ICH had a further, delayed ICH. In 42 of 45 patients (93%) with delayed ICH, this occurred within 5 days of the initial trauma. Multivariate logistic regression was used to select significant predictors of outcome. We found that delayed ICH (p<0.001), age (p=0.004) and mechanism of injury (p=0.001) explained the worse outcome in patients with bifrontal ICH. The best-fitting logistic regression model included three variables: delayed ICH (p=0.011), initial GCS (p=0.023), and a sum score of clinical and radiological variables (p=0.003). Bifrontal ICH tended to occur in older patients after a fall and was associated with a higher risk of developing delayed ICH or brain stem compression compared to unilateral ICH damage. Using these three variables - delayed ICH, initial GCS, and the sum score - in a logistical regression model is useful to predict outcome in patients with traumatic frontal ICH and may aid patient management.     

Skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) by inhibiting activation of the IGF-I signaling pathways.

We showed that unloading markedly diminished the effects of IGF-I to activate its signaling pathways, and the disintegrin echistatin showed a similar block in osteoprogenitor cells. Furthermore, unloading decreased alphaVbeta3 integrin expression. These results show that skeletal unloading induces resistance to IGF-I by inhibiting activation of the IGF-I signaling pathways at least in part through downregulation of integrin signaling. INTRODUCTION: We have previously reported that skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) with respect to bone formation. However, the underlying mechanism remains unclear. The aim of this study was to clarify how skeletal unloading induces resistance to the effects of IGF-I administration in vivo and in vitro with respect to bone formation. MATERIALS AND METHODS: We first determined the response of bone to IGF-I administration in vivo during skeletal unloading. We then evaluated the response of osteoprogenitor cells isolated from unloaded bones to IGF-I treatment in vitro with respect to activation of the IGF-I signaling pathways. Finally we examined the potential role of integrins in mediating the responsiveness of osteoprogenitor cells to IGF-I. RESULTS: IGF-I administration in vivo significantly increased proliferation of osteoblasts. Unloading markedly decreased proliferation and blocked the ability of IGF-I to increase proliferation. On a cellular level, IGF-I treatment in vitro stimulated the activation of its receptor, Ras, ERK1/2 (p44/42 MAPK), and Akt in cultured osteoprogenitor cells from normally loaded bones, but these effects were markedly diminished in cells from unloaded bones. These results were not caused by altered phosphatase activity or changes in receptor binding to IGF-I. Inhibition of the Ras/MAPK pathway was more impacted by unloading than that of Akt. The disintegrin echistatin (an antagonist of the alphaVbeta3 integrin) blocked the ability of IGF-I to stimulate its receptor phosphorylation and osteoblast proliferation, similar to that seen in cells from unloaded bone. Furthermore, unloading significantly decreased the mRNA levels both of alphaV and beta3 integrin subunits in osteoprogenitor cells. CONCLUSION: These results indicate that skeletal unloading induces resistance to IGF-I by inhibiting the activation of IGF-I signaling pathways, at least in part, through downregulation of integrin signaling, resulting in decreased proliferation of osteoblasts and their precursors.