OBJECTIVE: To analyze whether ICG can
be used to analyze and confirm perfusion Selumetinib order changes early after SAH.
METHODS: We prospectively enrolled 11 patients with acute SAH within the past 24 hours and 14 patients undergoing surgery for unruptured aneurysms. Cortical ICG videography was performed, and offline analysis included the arterial, parenchymal, and venous cortical compartment. Transit times, signal gradient, maximum of fluorescence intensity, and the area under the curve were calculated as surrogate markers for perfusion characteristics.
RESULTS: Arterial, parenchymal, and venous transit times were comparable in both groups. The velocity of signal change in SAH patients was significantly lower in all 3 compartments
(P < .001, P < .01, P < .001, respectively), as was the peak fluorescence intensity (P < .001). In SAH patients, fluorescence intensity did not vary between areas with and without diffuse cortical blood. Area under the curve analysis showed significantly lower Selleck PD0325901 values in SAH patients compared with the control group (P < .001).
CONCLUSION: Cortical ICG videography and analysis are feasible during surgery. Patients early after SAH have a significantly lower velocity of signal change, lower peak of fluorescence intensity, and lower overall area under the curve, but similar transit times. This technique can be used to quantify perfusion alteration, in this case, acute SAH, and may be used as an adapted
measurement tool for intraoperative therapy.”
“The papillomavirus E1 helicase is recruited by E2 to the viral Aprepitant origin, where it assembles into a double hexamer that orchestrates replication of the viral genome. We previously identified the cellular WD40 repeat-containing protein p80/UAF1 as a novel interaction partner of E1 from anogenital human papillomavirus (HPV) types. p80 was found to interact with the first 40 residues of HPV type 31 (HPV31) E1, and amino acid substitutions within this domain abrogated the maintenance of the viral episome in keratinocytes. In this study, we report that these p80-binding substitutions reduce by 70% the ability of E1 to support transient viral DNA replication without affecting its interaction with E2 and assembly at the origin in vivo. Microscopy studies revealed that p80 is relocalized from the cytoplasm to discrete subnuclear foci by E1 and E2. Chromatin immunoprecipitation assays further revealed that p80 is recruited to the viral origin in an E1- and E2-dependent manner. Interestingly, overexpression of a 40-amino- acid-long p80-binding peptide, derived from HPV31 E1, was found to inhibit viral DNA replication by preventing the recruitment of endogenous p80 to the origin. Mutant peptides defective for p80 interaction were not inhibitory, demonstrating the specificity of this effect.