周围剂量当量仪的研制

周围剂量当量仪研制是根据国际辐射单位和测量委员会（ＩＣＲＵ）３９号报告推荐的周围剂量当量而设计的一种数字化智能型辐射防护仪。方法采用能量补偿对探测器进行能响校正。结果补偿结果使得探测器在４７～２３０ｋｅＶ与ＩＳＯ推荐的Ｈ＊（１０）／Ｋａ值误差在５％以内。本文重点描述了周围剂量当量仪探测器部分的工艺结构和剂量学性能以及电子学测量部分的主要功能。结论通过实际应用我们初步获得的结论是由于该仪器可直接测量周围剂量当量，稳定性好且具有自动取平均值特点，它可做为实验室校准用测量仪器，又由于该仪器体积小，电池供电，读数面板又有背光功能，它也可以做为现场仪器用于辐射防护实践的现场测量     

Imaging of shifted stimulated echoes and multiple spin echoes

It is shown that a repetitive pulse sequence consisting of two 90° pulses and gradients in a 1:2 ratio around the second 90° pulse generates interscan shifted stimulated echoes (SSTEs) and intrascan multiple spin echoes (MSEs). Separation of these two types of signals is accomplished using specific gradient crusher schemes. The intensity of the SSTEs is an order of magnitude larger than that of the MSEs and determines the signal contrast if both effects are selected simultaneously. The SSTE sequence generates improved contrast between gray and white matter, even at high field, which is explained in terms of increased inverse T₁-weighting for the interscan echo. The MSE image has low signal to noise and no detectable contrast. The effect of interscan diffusion weighting is also discussed.     

脑梗死后再发缺血性卒中与脑出血患者微血管病变及预后的比较

【目的】探讨脑梗死后再发缺血性卒中与脑出血患者的临床特点、影像学上微血管病变及预后的异同。【方法】连续收集急性复发性卒中的住院病例（初发事件为脑梗死，复发事件包括脑梗死或脑出血），详细记录临床资料。观察脑内微出血及自质病变的严重程度，随访有无严重血管事件及死亡的发生。【结果】175例再发脑梗死患者。19例复发事件为脑出血的患者进入本研究。155例（88．6％）再发脑梗死患者，以及18例（94．7％）脑出血患者存在自质病变。77例（44％）再发脑梗死患者和16例（84．2％）脑出血患者存在脑内微出血。脑出血组自质病变的严重程度及微出血的数目均明显高于再发脑梗死组（P=0．033，0．016），脑出血组的死亡率及再发脑出血的危险性明显增高（P=0．034，0．036）。【结论】严重的脑自质病变及微出血的出现与脑梗死后再发脑出血有关。多发微出血提示出血风险增高。如复发事件为脑出血，则其死亡率及再次复发脑出血的风险均明显增加。     

Binswanger's disease in the absence of chronic arterial hypertension

Summary The cerebral changes are described in a woman of 54 who suffered from Binswanger's encephalopathy: there were no signs or symptoms of chronic arterial hypertension. The disease presented as dementia of about 3 years duration. Computed tomography of the brain 2. 5 years before her death showed bilateral widespread hypodense lesions in the cerebral white matter. She died of an asthmatic attack. Autopsy disclosed extensive bilateral degeneration of the central white matter, lacunes and gliosis. Severe obliterative arteriolosclerosis occurred in the meningeal vessels and those supplying the affected parts of the brain. Light microscopy showed that the most severe lesions occurred in the arterioles. Immunohistochemistry demonstrated profound extravasation of plasma proteins chiefly albumin, indicating dysfunction of the blood-brain barrier. Thus, the lesions characteristic of Binswanger's encephalopathy may develop in the absence of chronic arterial hypertension. Additional pathogenic factors, possibly genetic predisposition to vascular injury may play a role in the development of this condition.Supported by grants from the Swedish Medical Research Council, Project No 12X-03020 and 1987 Års Stiftelse för Strokeforskning     

An Autopsied Case of Interferon Encephalopathy

Abstract: A 78-year-old male with renal carcinoma was treated with a high dose infusion of interferon-alpha (IFN-alpha) for eight months. The patient had evidence of organlc brain syndrome such 88 : dysfunction of memory, slowing of behavior, and development of mental confusion that appeared eight months after the treatment. MRI at the time of mental confusion revealed difise white matter lesions. Neuropathologic findings were compatible to Binswanger's disease and Senile Dementia of Alzheimer Type (SDAT), Preexisting neurologic abnormalities including intracerebral arteriosclerosis and cerebral atrophy may increase susceptibility to unacceptably severe IFN neurotoxicity.     

Mapping corpus callosum deficits in autism: an index of aberrant cortical connectivity.

BACKGROUND: Volumetric studies have reported reductions in the size of the corpus callosum (CC) in autism, but the callosal regions contributing to this deficit have differed among studies. In this study, a computational method was used to detect and map the spatial pattern of CC abnormalities in male patients with autism. METHODS: Twenty-four boys with autism (aged 10.0 +/- 3.3 years) and 26 control boys (aged 11.0 +/- 2.5 years) underwent a magnetic resonance imaging (MRI) scan at 3 Tesla. Total and regional areas of the CC were determined using traditional morphometric methods. Three-dimensional (3D) surface models of the CC were also created from the MRI scans. Statistical maps were created to visualize morphologic variability of the CC and to localize regions of callosal thinning in autism. RESULTS: Traditional morphometric methods detected a significant reduction in the total callosal area and in the anterior third of the CC in patients with autism; however, 3D maps revealed significant reductions in both the splenium and genu of the CC in patients. CONCLUSIONS: Statistical maps of the CC revealed callosal deficits in autism with greater precision than traditional morphometric methods. These abnormalities suggest aberrant connections between cortical regions, which is consistent with the hypothesis of abnormal cortical connectivity in autism.     

Occupational chronic exposure to metals

Summary Stainless steel welders (n = 103) were examined. To estimate external exposure, personal air sampling was used. Internal exposure was quantified by the determination of nickel levels in erythrocytes, plasma and urine. Men and women (n = 123) were examined for control purposes. In the plasma and erythrocytes of the controls the nickel concentration was below the level of detection (< 1.81 μg/l). The element concentrations in urine were between < 0.1 and 13.3 μg/l. Of the controls 95% showed nickel levels in urine below 2.2 μg/l (reference value). The average concentration of nickel in the air was 93 ± 81 μg/m³. The average concentration of nickel in the plasma samples was 4.9 ± 4.0 μg/l (95th percentile 12.8 μg/L). In erythrocytes nickel could not be detected. The nickel concentrations in the urine of the welders were 18.5 ± 28.5 μg/l on average (95th percentile 52.5 μg/l). Only a weak correlation between the nickel levels of plasma and urine could be detected (C_urine = 2.07 + 8.45 C_plasma; r = 0.294; p < 0.01). Based on our results and on the reported literature a future limit value for the nickel concentration in urine should lay between 30 and 50 μg/l. This value corresponds to an external exposure of 500 μg nickel per cubic metre.     

Blood-brain barrier dysfunction in Binswanger’s disease; an immunohistochemical study

Binswanger’s disease is pathologically characterized by a combination of diffuse cerebrovascular white matter lesions and lacunar infarcts in the basal ganglia and white matter. Although a blood-brain barrier (BBB) dysfunction has been implicated in the pathogenesis of these white matter (WM) lesions, few authors have addressed this problem. In the present study, we describe BBB dysfunction and its regional differences in the brains of Binswanger’s disease patients. Twelve brains from Binswanger’s disease patients (group III) were examined and compared with those from five patients with non-neurological disease (group I) and five cortical infarct patients without significant WM lesions (group II). Immunohistochemistry was performed for glial fibrillary acidic protein and vimentin as astroglial cell markers, and for immunoglobulins, complements and fibrinogen as extravasated serum protein markers. The grading scores for IgG extravasation were significantly higher in group III as compared to group I, in both the periventricular WM and the subcortical WM (P < 0.01). In group III, the scores in the periventricular WM and subcortical WM were significantly higher than in the subcortical U fibers and cerebral cortex (P < 0.01 for the periventricular WM; P < 0.001 for the subcortical WM), respectively. Clasmatodendritic astroglia, which had swollen cell bodies and large cytoplasmic vacuoles with disintegrated processes, incorporated the serum components IgG, IgM, C3d, C1q and fibrinogen, both in the periventricular WM and subcortical WM in 5 out of 12 (42%) Binswanger’s disease brains. These results indicate that WM lesions in Binswanger’s disease are accompanied by BBB dysfunction, although it remains uncertain whether BBB dysfunction is secondary to either chronic cerebral ischemia or arterial hypertension. Received: 25 April 1997 / Revised, accepted: 21 July 1997     

Magnetization Transfer and T2 Relaxation Components in Tissue

T₂ relaxation makes an important contribution to tissue contrast in magnetic resonance (MR) imaging. Many tissues are known to exhibit multicomponent T₂ relaxation that suggests some compartmental segregation of mobile protons on a T₂ timescale. Magnetization transfer (MT) is another relaxation mechanism that can be used to produce tissue contrast in MR imaging. The MT process depends strongly on water-macromolecular interactions. To investigate the relationship between multicomponent T₂ relaxation and the MT process, multiecho T₂ measurements have been combined with MT measurements for freshly excised samples of cardiac muscle, striated muscle, and white matter. For muscle, short T₂ components show greater MT than long T₂ components, consistent with the belief that they represent distinct water environments. For white matter, quantitative MT measurements were identical for the two major T₂ components, apparently because of exchange between the T₂ compartments on a timescale characteristic of the MT experiment. Implications for accurate modeling of MT in tissue and the use of MT for MR image contrast are discussed.     

Magnetization transfer imaging of multiple sclerosis

While conventional magnetic resonance imaging (MRI) measures signal primarily from the hydrogen nuclei of water, magnetization transfer (MT) MRI indirectly detects macromolecular associated hydrogen nuclei via their magnetic interaction with the observable water. In the normal adult CNS, white matter exhibits the largest MT effect due to the macromolecular content of the highly structured and lipid rich myelin. Pathologies which alter the structural integrity and the relative macromolecular-water composition, such as multiple sclerosis (MS), therefore show abnormal MT. Conventional MRI, which has a high MS lesion detection sensitivity but poor specificity in terms of differentiating the pathological state of a plaque, can thus be supplemented by MT to provide more specific information on the extent of demyelination and axonal loss. In this paper we review the basic concepts of MT imaging and its role in MS lesion characterization.Financial support was provided by the Medical Research Council of Canada, Fonds de la Recherche en Santé du Québec, and the Killam Foundation.