Fatal haemorrhage in medulloblastoma following ventricular drainage. Case report and review of the literature

Haemorrhage in medulloblastoma is reported to be very rare. The authors report a case of a 13-year-old boy who presented with headache, unsteadiness, diplopia and papilloedema due to posterior fossa medulloblastoma causing obstructive hydrocephalus. Six hours following placement of an external ventricular drain, he suddenly became comatose with respiratory arrest. The cause was marked upward herniation of the anterior vermis and downward herniation of the cerebellar tonsils due to massive spontaneous intratumoural haemorrhage extended into the ventricular system. This atypical clinical course of fatal haemorrhage in medulloblastoma after insertion of external ventricular drainage is reported and the literature discussed.     

O等位基因引起ABO基因型与表现型定型差异

保证输血时血清学方面的安全,首要的是对受血者与献血者ABO血型定型,血清学检查通常分两个步骤.正定型通常使用鼠源单克隆抗体检测红细胞表面是否存在A或B抗原.互补的实验即反定型,利用当红细胞上缺乏A或B抗原时,人群可天然产生相对应的抗体的原理,检测血清中是否存在抗-A或者抗-B抗体.确定了受血者红细胞表面的ABO抗原以及血浆中的抗体,便能确定血型,为其提供相合的血液.     

Complete recovery of severe tetraparesis after excision of large C1-osteochondroma

Severe tetraparesis resulting from cervical cord compression due to osteochondroma of the Atlas is a rare condition, especially in young children. In this report, the author discusses the clinical presentation, and outcome of surgical excision of a large C1 osteochondroma presenting with severe myelopathic tetraparesis, in a 10-year-old girl. Computed tomography and magnetic resonance images revealed a large bony lump arising from the posterior arch of atlas, filling most of the spinal canal, and compressing the cervical spinal cord. Another histologically proven exostosis was incidentally found at the spinous process of T1. There was no history of exostosis in the family, and the patient improved dramatically after removal of the C1 osteochondroma.     

Seronegative and seropositive rheumatoid arthritis: radiographic differences

Patients with seronegative and patients with seropositive rheumatoid arthritis (RA) have clinical, genetic, and immunologic differences. This study was undertaken to determine whether the two populations differ radiologically. Seventeen patients with seronegative RA were closely matched with seropositive control subjects. Radiographs of the hands and wrists were studied blindly, and disease severity was quantified with use of a modification of the Beaver Creek grading sheet. The following distinguishing features were also evaluated: osteosclerosis, new bone formation, carpal predominance, ankylosis (fusion), symmetry, and classical erosions. Seropositive patients had more severe disease, with larger and more numerous erosions, while the seronegative group had more osteosclerosis, carpal predominance, fusion, and new bone formation. Symmetry was equal in both groups. Although there were definite quantitative and qualitative differences between the two populations, radiologists should be cautious in using these criteria because of the great deal of overlap between the two groups.     

神经细胞营养（诱向）因子与运动神经元疾病

本文从神经营养（诱向）因子有选择地保障运动神经元健康存活和执行功能，防止它凋亡和损伤所引起的神经元退变及促进其再生等生物学效应，结合运动神经元病的病理退变的主要特点及本实验室对运动神经元营养（诱向）因子的工作，综述了这方面的新进展，期望对探索运动神经元病的病因和治疗提供新的线索和可能性。     

Blood coagulation and the risk of atherothrombosis: a complex relationship

The principles of Virchov's triad appear to be operational in atherothrombosis or arterial thrombosis: local flow changes and particularly vacular wall damage are the main pathophysiological elements. Furthermore, alterations in arterial blood composition are also involved although the specific role and importance of blood coagulation is an ongoing matter of debate. In this review we provide support for the hypothesis that activated blood coagulation is an essential determinant of the risk of atherothrombotic complications. We distinguish two phases in atherosclerosis: In the first phase, atherosclerosis develops under influence of "classical" risk factors, i.e. both genetic and acquired forces. While fibrinogen/fibrin molecules participate in early plaque lesions, increased activity of systemic coagulation is of no major influence on the risk of arterial thrombosis, except in rare cases where a number of specific procoagulant forces collide. Despite the presence of tissue factor - factor VII complex it is unlikely that all fibrin in the atherosclerotic plaque is the direct result from local clotting activity. The dominant effect of coagulation in this phase is anticoagulant, i.e. thrombin enhances protein C activation through its binding to endothelial thrombomodulin.The second phase is characterized by advancing atherosclerosis, with greater impact of inflammation as indicated by an elevated level of plasma C-reactive protein, the result of increased production influenced by interleukin-6. Inflammation overwhelms protective anticoagulant forces, which in itself may have become less efficient due to down regulation of thrombomodulin and endothelial cell protein C receptor (EPCR) expression. In this phase, the inflammatory drive leads to recurrent induction of tissue factor and assembly of catalytic complexes on aggregated cells and on microparticles, maintaining a certain level of thrombin production and fibrin formation. In advanced atherosclerosis systemic and vascular wall driven coagulation becomes more important and elevated levels of D-dimer fragments should be interpreted as markers of this hypercoagulability.