Surgical management of symptomatic cavum septum pellucidum cysts: systematic review of the literature

Neurosurgical Review - Cavum septum pellucidum (CSP) and cavum vergae (CV) cysts are commonly found incidentally. They are usually asymptomatic but may present with symptoms related to obstructive...     

Human platelets after their contact with influenza virus activate the complement system in autologous serum

Guinea pig erythrocytes that have been exposed to influenza virus activate the alternative pathway through virus-induced desialation of the cells. Neuraminidase treatment of rabbit platelets enhance their clearancein vivo. Washed human platelets were labeled with⁵¹Cr exposed to Influenza virus, and resuspended in autologous serum that had been dialyzed against Veronal-buffered saline containing Ca⁺⁺ and Mg⁺⁺ (VBS⁺⁺), VBS containing 8 mM EGTA and 2 mM Mg⁺⁺ (VBS-MgEGTA) or VBS containing 20 mM EDTA (VBS-EDTA) for 60 min at 37°C. Three per cent⁵¹Cr release and no complement consumption were observed in VBS-EDTA serum. In contrast, 6%⁵¹Cr release with 37 and 54% decrease in C3 and B hemolytic activities respectively occurred in VBS-MgEGTA serum and 14%⁵¹Cr release with 50% decrease in C2 hemolytic activity occurred in VBS⁺⁺ serum. These results suggest that influenza virus may alter the platelet surface in such a way that both complement pathways might be recruited and the cells be lyzed in autologous serum.The human complement system is activated by a number of viruses and virus-infected cells through antibody-dependent and independent mechanisms. Guinea pig erythrocytes that have been treated with influenza virus are lyzed in human serum through activation of the classical and of the alternative pathways: activation of the alternative pathway is dependent on an acquired resistance of the cell-bound C3 amplification convertase to control mechanisms that are directly related to desialation of the cells by viral neuraminidase [1]. Since,in vivo, clearance of desialated platelets is enhanced in animal models and since human platelets do not express the C3b receptor-associated inhibitory activity of the complement system, we investigated whether human platelets, after contact with influenza virus, acquire the ability to activate complement in autologous serum.     

Normal and abnormal p21 h-ras posttranslational products in human neoplastic and nonneoplastic liver-tissues

Using two-dimensional Western blot analysis with a pan-ras antibody, we previously defined conditions that allow to resolve the four post-translational p21-H-ras products expressed in normal mature rat tissues. Using the same approach, we conducted experiments that sometimes revealed deviations from the normal basal p21-H-ras pattern in primary human liver tumors. One type of alteration encountered was indicative of modifications in the relative rate of accomplishment of the different steps in the post-translational metabolisation of the protein, resulting in the accumulation of precursors of the fully-processed p21-H-ras product. This was also observed during ontogenesis and might thus be correlated with either cellular growth potential or differentiation. The second type of altered pattern is defined by the detection of abnormal spots and probably corresponds to the presence of mutant p21-ras products.