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The article presents an abstract of the paper titled "Characterization of Astrocytic Proliferation in Rat Denate Gyrus." It investigates the glial cells of hippocampus with respect to their functional properties. The results suggest that glial proliferation and its neurite outgrowth factor could play a role in the pathogenesis of epilepsy.

Traumatic brain injury (TBI) is associated with poor clinical outcomes; autopsy studies of TBI victims demonstrate significant oligodendrocyte progenitor cell (OPC) death post TBI; an observation, which may explain the lack of meaningful repair of injured axons. Whilst high-mobility group box-1 (HMGB1) and its key receptors TLR2/4 are identified as key initiators of neuroinflammation post-TBI, they have been identified as attractive targets for development of novel therapeutic approaches to improve post-TBI clinical outcomes. In this report we establish unequivocal evidence that HMGB1 released in vitro impairs OPC response to mechanical injury; an effect that is pharmacologically reversible. We show that needle scratch injury hyper-acutely induced microglial HMGB1 nucleus-to-cytoplasm translocation and subsequent release into culture medium. Application of injury-conditioned media resulted in significant decreases in OPC number through anti-proliferative effects. This effect was reversed by co-treatment with the TLR2/4 receptor antagonist BoxA. Furthermore, whilst injury conditioned medium drove OPCs towards an activated reactive morphology, this was also abolished after BoxA co-treatment. We conclude that HMGB1, through TLR2/4 dependant mechanisms, may be detrimental to OPC proliferation following injury in vitro, negatively affecting the potential for restoring a mature oligodendrocyte population, and subsequent axonal remyelination. Further study is required to assess how HMGB1-TLR signalling influences OPC maturation and myelination capacity. [ABSTRACT FROM AUTHOR]

It is generally recommended that, in cases of difficulty in removing a ventricular catheter during a shunt revision, it is best left alone to avoid intraventricular haemorrhage. Retained ventricular catheters (RVCs) are usually safe, although in the presence of ventriculitis they may become colonized by organisms and become a source of persistent or recurrent infection. The authors present a case of persistent and intractable ventriculitis due to an old retained ventricular catheter. A 23-year-old female, who had a RVC and a functioning shunt, was admitted for a suspected blocked shunt. At surgery the shunt was found to be infected and external drainage was instituted. Over the next 4 months, she developed intractable and persistent staphylococcal ventriculitis, despite undergoing 10 further surgical procedures, and appropriate intravenous and intrathecal antibiotic therapy. She responded rapidly only after surgical removal of the old RVC via a craniotomy. The staphylococcus cultured from the RVC had an identical antibiogram to the organism responsible for the intractable ventriculitis. This case emphasizes the point that, although RVC are generally considered safe, removal becomes imperative in the presence of concurrent CSF infection that fails to respond quickly to intrathecal antibiotic therapy. [ABSTRACT FROM AUTHOR]