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Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the levels of Abeta40 and Abeta42 in the CSF of patents with intracerebral hemorrhage (ICH) and their correlations with the hemorrhagic volume and the volume of perihematomal hypodensity. Methods: Enzyme-linked immuno sorbent assay (Elisa) was used to investigate the levels of Abeta40 and Abeta42 in CSF of 73 ICH patients and 72 normal controls (NC). Results: The levels of Abeta40 and Abeta42 in CSF were significantly increased in ICH patients when compared with NC group (P<0.01). The levels of Abeta40 in CSF (r=0.549, P<0.01; r=0.791, P<0.01) and Abeta42 (r=0.450, P<0.01; r=0.440, P<0.01) were positively correlated with the hemorrhagic volume and the volume of perihematomal hypodensity. Conclusions: As the levels of Abeta proteins in CSF reflect the status of neuronal degeneration, the increased levels of Abeta in CSF indicate that ICH patients experience significant neuronal degeneration. In this regard, the Abeta levels in CSF might be valuable for estimation of the disease severity of ICH patients. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the levels of total Tau (t-Tau) and phosphorylated Tau (p-Tau) in the CSF of patents with hepatic encephalopathy (HE) and to investigate their correlations with the severity of the disease. Methods: Enzyme-linked immuno sorbent assay (Elisa) was used to investigate the CSF levels of total Tau, Tau181, Tau231 in 32 HE patients and 27 normal controls (NC). Results: The CSF levels of t-Tau and p--Tau were significantly increased in HE patients when compared with normal controls (P<0.01). The CSF levels of t-Tau and p-Tau were positively correlated with the Child-Pugh Scores and West Haven Yale of the disease. Conclusions: As the levels of Tau proteins in CSF reflect the status of neuronal degeneration and the status of stress, the increased levels of Tau proteins in CSF indicate that HE patients experience significant neuronal degenerations and stress. [ABSTRACT FROM AUTHOR]