Carotid-cavernous sinus fistula associated with a primitive trigeminal artery

Carotid-cavernous sinus fistulas are not rare, but they have never been reported in association with persistent primitive trigeminal artery. We recently encountered such a case. The Jaeger-Hamby procedure was employed, with mandatory occlusion of the primitive trigeminal artery.     

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.     

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.     

纸质病案保存期限的思考

本文作者比较了不同时期的纸质病案的使用率,讨论了旧病案的缺点,如难于保存,占用空间及实用价值不大.作者提出了改进保存病案的办法.     

PTCA及支架植入术治疗心肌梗死并重症泵功能衰竭近期效果观察

OBJECTIVE: To evaluate the short-term therapeutic effect of percutaneous transluminal coronary angioplasty (PTCA) with stent implantation in the treatment of myocardial infarction with severe pump failure. METHODS: The clinical data of 73 patients receiving PTCA and stent implantation for myocardial infarction with severity pump failure were analyzed and grouped according the occurrence of complications, degree of the vascular lesions and the complexity of the surgical procedures. Preoperative and postoperative ventricular ejection fractions (LVEF) were compared in each case. RESULTS: The degree of vascular lesions and surgical complexity were not shown to relate to the occurrence of the complications. Except in cases complicated by chronic renal dysfunction, significant improvement was achieved in the patients 7 d after the operation (P<0.05), regardless of different degrees of vascular lesions and surgical complexity. CONCLUSION: PTCA with stent implantation is effective to improve the short-term cardiac function of patients with myocardial infarction and severe pump failure.     

Dose-rate scaling factor estimation of THOR BNCT test beam.

In 1998, an epithermal neutron test beam was designed and constructed at the Tsing Hua Open-Pool Reactor (THOR) for the purpose of preliminary dosimetric experiments in boron neutron capture therapy (BNCT). A new epithermal neutron beam was designed at this facility, and is currently under construction, with clinical trials targeted in late 2004. Depth dose-rate distributions for the THOR BNCT test beam have been measured by means of activation foil and dual ion chamber techniques. Neutron and structure-induced gamma spectra measured at the test beam exit were configured into a source function for the Monte Carlo-based treatment planning code NCTPlan. Dose-rate scaling factors (DRSFs) were determined to normalize computationally derived dose-rate distributions with experimental measurements in corresponding mathematical and physical phantoms, and to thus enable accurate treatment planning using the NCTPlan code. A similar approach will be implemented in characterizing the new THOR epithermal beam in preparation for clinical studies. This paper reports the in-phantom calculated and experimental dosimetry comparisons and derived DRSFs obtained with the THOR test beam.