Follow-up of subjects occupationally exposed to asbestos: MRI and PET scans

MRI and PET scans are not normally used for screening and follow-up of patients following occupational exposure to asbestos. These examinations usually complement the investigation of a parenchymal mass, an effusion or pleural thickening. PET and MRI have an excellent ability to define a parenchymal lesion as malignant (cancer versus rounded atelectasis) or a pleural lesion (mesothelioma versus plaque). MRI distinguishes perfectly the involvement of sub-pleural fat by bronchial carcinoma or mesothelioma. MRI, taking account of its lack of irradiation, could be regarded as suitable for potentially repeated examinations following initial screeing by CT scan. A comparative study of multidetector scanner versus MRI, including diffusion MRI could be, nevertheless, interesting. PET cannot be proposed for the follow up or for screening on account of the irradiation induced and the difficulty of access. Pleural plaques do not take up FDG. There is no specific study of asbestos related fibrosis and there is discordance between studies of other types of pulmonary fibrosis.     

Sur une polioencéphalopathie progressive avec dégénérescences neurofibrillaires

Resumé Une affection neurologique caracterisée par l'atteinte de nombreux nerfs craniens, des signes pyramidaux, des troubles de la sensibilité profonde, de la torpeur et de la désorientation, se présente chez une femme alcoolique âgée de 46 ans. Evolution en sept mois. Histologiquement: polioencéphalopathie avec plaques argyrophiles, dégénérescences neurofibrillaires et lipopigmentaires, sans raréfaction neuronale. Les formations les plus intéressées sont l'écorce hippocampique et les noyaux de la calotte mésencéphalique. La substance blanche du centre ovale et les faisceaux pyramidaux et postérieurs participent au processus.

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Progressive polioencephalopathy with neurofibrillary degeneration

Summary A case is presented of an alcoholic woman aged 46, with a progressive impairment of cranial nerves, bilateral pyramidal signs and involvement of deep sensation, clouding of the sensorium and loss of orientation. The disease run a fatal course in seven months. Histological examination disclosed a polioencephalopathy with argyrophilic plaques, neurofibrillary degeneration and accumulation of lipofuscin, without neuronal loss. Such changes were mostly evident in the hippocampal cortex and tegmental nuclei at midbrain level. White substance of centrum ovale, pyramidal tracts and posterior columns were also affected.

Nous tenons à remercier le Dr. Ludo van Bogaert pour son aide critique et disinteressée dans la formulation de ce travail, Mme Zunino et Mlle Janssens pour l'histologie, et M. Camusso pour la photographie.     

彩色多普勒超声诊断糖尿病患者颈动脉粥样硬化斑块的价值

目的探讨彩色多普勒超声诊断糖尿病患者颈动脉粥样硬化斑块的价值。方法对124例糖尿病患者（研究组）及100例健康人群（对照组）行颈动脉超声检查,测量颈动脉内-中膜厚度（IMT）和斑块指标,进行对比分析。结果研究组颈动脉IMT、斑块发生率均高于对照组（均P〈0．05）。两组斑块发生部位差异无统计学意义（P〉0．05）,均主要出现在颈动脉分叉处。结论2型糖尿病患者颈动脉粥样硬化的发病率较高,颈动脉彩色多普勒超声是动脉粥样硬化性病变筛选和诊断的理想方法。     

Age-dependent decline of blood-brain barrier P-glycoprotein expression in the canine brain

The efflux transporter P-glycoprotein serves as a major molecular gatekeeper at the blood-brain barrier. It has been suggested that a reduction of P-glycoprotein activity with aging might enhance exposure of brain tissue to exogenous and endogenous compounds thereby contributing to the development of neurodegenerative diseases.Brain tissue from owner-kept dogs renders an excellent tool to study the impact of aging on the background of variable environmental and genetic influencing factors. Therefore, we determined expression rates of P-glycoprotein in canine post-mortem tissue from 23 non-laboratory dogs. P-glycoprotein expression in the parahippocampal cortex exhibited a negative correlation with age. Analysis of the area labeled for P-glycoprotein in dogs aged >100 months revealed a 72% drop in P-glycoprotein expression as compared to young adults aged 23-36 months. Respective data from the dentate hilus and dentate gyrus indicated an earlier drop with a reduction by 77 and 80% in dogs aged 37-99 months in comparison with younger individuals. In contrast to the decline observed with aging in dogs without plaques, P-glycoprotein expression rates rather tended to increase with further aging in dogs with plaque formation.In conclusion, the thorough analysis of P-glycoprotein expression rates in non-laboratory dogs revealed a significant decline with aging. The data strongly support the concept that age-dependent changes might predispose to neurodegenerative diseases. In the early pathogenesis of Alzheimer's disease which is modelled by diffuse plaques in the canine brain, an up-regulation of P-glycoprotein might act as a compensatory mechanism to enhance Abeta efflux from the brain. Future studies are necessary to further evaluate the correlation between Abeta deposits and P-glycoprotein expression in different phases of the disease.     

微量元素锶对实验性兔动脉粥样硬化斑块形成的影响

目的研究微量元素锶对高脂喂养实验性兔动脉粥样硬化进程中斑块形成的影响。方法71只新西兰兔适应性饲养1周后,随机分为A～E五组,分别是纯水对照组15只,锶水浓度3 mg/L组14只,锶水浓度9 mg/L组16只,锶水浓度18 mg/L组12只,锶水浓度36 mg/L组14只。各组均给予高脂饲料,120 g/（只.d）喂养12周。实验开始及结束时,检测血脂四项总胆固醇（total cholesterol,TC）、三酰甘油（triglyceride,TG）、高密度脂蛋白胆固醇（high-densitylipoprotein cholesterol,HDL-C）及低密度脂蛋白胆固醇（low-density lipoprotein cholesterol,LDL-C）,Elisa法检测血清炎性因子高敏C反应蛋白（high sensitive C reactive protein,hs-CRP）、内皮素-1（endothelin-1,ET-1）、白细胞介素-2（interleukin-2,IL-2）及白细胞介素-6（interleukin-6,IL-6）。图像处理软件计算动脉粥样硬化斑块面积百分比。普通光镜观察主动脉HE染色切片,根据动脉粥样硬化四级分类标准将其分为轻、中、重度及无明显变化者,比较各组差异。结果①高脂喂养12周（第13周）后,A～E组血脂四项升高幅度呈大致递减趋势,D、E组血脂四项升高幅度明显小于A组;②锶水喂养后各组hs-CRP、ET-1、IL-2、IL-6均较喂养前显著升高（P〈0.01）,但各组间比较差异无统计学意义（P〉0.05）;③随锶水浓度增高,A～E组动脉粥样硬化斑块面积逐渐减小（P〈0.05,P〈0.01）;④病理结果示：各组实验性兔主动脉均有轻、中、重度动脉粥样硬化及无明显变化者,A组以重度者最多,E组以轻度及无明显变化者居多,总体趋势A～E组逐渐减轻。结论微量元素锶可延缓动脉粥样硬化进程中斑块形成,且锶水浓度越高,效果越显著,其作用与改善脂质代谢有关。     

Benign asbestos-related pleuropulmonary diseases

Among the non malignant diseases related to asbestos exposure, pleural plaques are the most frequent. Pleural effusion and diffuse pleural thickening, as well as asbestosis, are uncommon nowadays in asbestos-exposed screened populations. Despite the absence of any useful treatment, accurate diagnoses of these diseases are needed for two reasons: on the one hand in order to save patients from anxiety related to diagnostic and prognostic discrepancies, and on the other hand in order to ensure a proper attribution of the high social and financial compensations which are provided in France for asbestos affected patients. CT scan of the thorax is the most sensitive and specific tool for a precise diagnosis of these lesions, but it often displays minute abnormalities which may give rise to major diagnostic discordances, owing to the absence of any tomodensitometric reference in populations proved to be free from any asbestos exposure. There is a need to seek for a suitable standardization of imaging technique and interpretation, for a consensus in the characterization of CTscan abnormalities that warrant compensation, and for a careful medico-psychologic assistance for patients affected by asbestos-related benign diseases.     

Intraneuronal Aβ immunoreactivity is not a predictor of brain amyloidosis-β or neurofibrillary degeneration

Amyloid β (Aβ) immunoreactivity in neurons was examined in brains of 32 control subjects, 31 people with Down syndrome, and 36 patients with sporadic Alzheimer’s disease to determine if intraneuronal Aβ immunoreactivity is an early manifestation of Alzheimer-type pathology leading to fibrillar plaque formation and/or neurofibrillary degeneration. The appearance of Aβ immunoreactivity in neurons in infants and stable neuron-type specific Aβ immunoreactivity in a majority of brain structures during late childhood, adulthood, and normal aging does not support this hypothesis. The absence or detection of only traces of reaction with antibodies against 4–13 aa and 8–17 aa of Aβ in neurons indicated that intraneuronal Aβ was mainly a product of α- and γ-secretases (Aβ_17–40/42). The presence of N-terminally truncated Aβ_17–40 and Aβ_17–42 in the control brains was confirmed by Western blotting and the identity of Aβ_17–40 was confirmed by mass spectrometry. The prevalence of products of α- and γ -secretases in neurons and β- and γ-secretases in plaques argues against major contribution of Aβ-immunopositive material detected in neuronal soma to amyloid deposit in plaques. The strongest intraneuronal Aβ_17–42 immunoreactivity was observed in structures with low susceptibility to fibrillar Aβ deposition, neurofibrillary degeneration, and neuronal loss compared to areas more vulnerable to Alzheimer-type pathology. These observations indicate that the intraneuronal Aβ immunoreactivity detected in this study is not a predictor of brain amyloidosis or neurofibrillary degeneration. The constant level of Aβ immunoreactivity in structures free from neuronal pathology during essentially the entire life span suggests that intraneuronal amino-terminally truncated Aβ represents a product of normal neuronal metabolism. This study was supported in part by funds from the New York State Office of Mental Retardation and Developmental Disabilities and grants from the National Institutes of Health (The National Institute of Child Health and Human Development R01 HD43960 and PO1 HD35897; and the National Institute of Aging P30 AG08051, AG03051, and PO1 AG11531).     

Levels of dietary sodium intake: diverging associations with arterial stiffness and atheromatosis

BackgroundRecent epidemiological evidence suggests a J-shaped, rather than the classical linear, association between dietary sodium (Na) intake and cardiovascular (CV) disease. Numerous animal studies have shown the acceleration of atheromatosis in a low-salt diet but data in humans are scarce. Our aim was to test the hypothesis that in a cohort of patients who are CV-free, yet at increased CV risk, moderate Na intake is associated with lower prevalence of atheromatosis and arterial stiffening than those at very low Na intake.MethodsTwo 24-h dietary recalls were conducted to estimate Na intake. Atheromatosis (carotid and femoral plaques) was assessed by B-mode ultrasonography and arterial stiffness through tonometry (carotid-to-femoral pulse wave velocity, cf-PWV).ResultsIn 901 individuals (age: 52.4 ± 13.8 years, 45.2% males), only females at 3rd and 4th quartile of total Na intake (derived from food and discretionary salt) had significantly lower probability to present femoral plaques than those at 1st quartile (751.0 ± 215.5 mg/day), even in the full-adjusted model [0.462(0.229-0.935) and p = 0.032 3rd quartile; 0.274(0.118-0.638) and p = 0.003 4th quartile]. On the contrary, male and female individuals at 3rd quartile had significantly higher probability to present arterial stiffness (PWV >10 m/s) than those at 1st quartile [1.991(1.047-3.785) and p = 0.036].ConclusionsOverall, the present data suggest that very low Na intake is associated with: a) accelerated atheromatosis, verifying findings from animal models, and providing a possible explanation of the modern epidemiology and b) lower arterial stiffness, which is in line with previous human findings, therefore suggesting a diverging effect of Na in the two major arterial pathologies.