Abstract Anterior clinoidal meningiomas (ACMs) remain a major neurosurgical challenge. The skull base techniques, including extradural clinoidectomy and optic unroofing performed at the early stage of surgery, provide advantages for improving the extent of resection, and thereby enhancing overall outcome, and particularly visual function. Additionally, when the anterior clinoidal meningiomas encase neurovascular structures, particularly the supraclinoid internal carotid artery and its branches, this further increases morbidity and decreases the extent of resection. Although it might be possible to remove the tumor from the artery wall despite complete encasement or narrowing, the decision of whether the tumor can be safely separated from the arterial wall ultimately must be made intraoperatively. The patient is a 75-year-old woman with right-sided progressive vision loss. In the neurological examination, she only had light perception in the right eye without any visual acuity or peripheral loss in the left eye. MRI showed a homogeneously enhancing right-sided anterior clinoidal mass with encasing and narrowing of the supraclinoid internal carotid artery (ICA). Computed tomography (CT) angiography showed a mild narrowing of the right supraclinoid ICA with associated a 360-degree encasement. The decision was made to proceed using a pterional approach with extradural anterior clinoidectomy and optic unroofing. The surgery and postoperative course were uneventful. MRI confirmed gross total resection (Figs. 1 and 2). The histopathology was a meningothelial meningioma, World Health Organization (WHO) grade I. The patient continues to do well without any recurrence and has shown improved vision at 15-month follow-up. This video demonstrates important steps of the microsurgical skull base techniques for resection of these challenging tumors. The link to the video can be found at https://youtu.be/vt3o1c2o8Z0
Objective
To determine the intervention of mycophenolate mofetil(MMF) in glial scar formation and learning and memory function in a rat model of diffuse axonal injury(DAI).
Methods
Ninety-six SD rats were randomly divided into sham group, normal saline (NS) group and mycophenolate mofetil (MMF) group according to the random number table, with 32 rats per group. Immunohistochemistry was used to detect activated microglia cells, activated astrocytes and chondroitin sulphate proteoglycanns (CSPGs) in the hippocampus. Image-Pro Plus software was used to quantitatively assess the changes of activated microglia cells, activated astrocytes and CSPGs. Morris water maze was applied for testing rat learning and memory function. Integrated absorbance (IA) of major constituents (microglia, astrosyte, chondroitin sulphate proteoglycan) of the glial scar was determined and analyzed for the correlation with the parameters of MWM.
Results
At 7, 14 and 28 days after injury, MMF group showed decreased IA of activated microglia in the hippocampus compared to sham and NS groups (P<0. 05). At 7-11 days after injury, percent distance and percent time in the target quadrant of Morris water maze did not differ significantly among the three groups and were not related to the IA of glial scar. At 28-32 days after injury, percent distance and percent time in the target quadrant of Morris water maze lowered significantly in MMF group. At 28 days after injury, IA of the glial scar had a positive correlation with mean speed and mean escape latency, but negative correlation with percent distance and time in the target quadrant that measured in Morris water maze at 28-32 days after injury.
Conclusion
MMF significantly attenuates glial scar formation into the hippocampus and improves learning and memory function in rats during the recovery stage when administered in the early stage after DAI.
Key words:
Diffuse axonal injury; Hippocampus; Mycophenolate mofetil
With the rapid development of the Internet of vehicles, there is a huge amount of multimedia data becoming a hidden trouble in the Internet of Things. Therefore, it is necessary to process and store them in real time as a way of big data curation. In this paper, a method of real-time processing and storage based on CDN in vehicle monitoring system is proposed. The MPEG-DASH standard is used to process the multimedia data by dividing them into MPD files and media segments. A real-time monitoring system of vehicle on the basis of the method introduced is designed and implemented.
The molecular and cellular mechanisms underlying the anti-proliferative effects of preoptic regulator factor 2 (Porf-2) on neural stem cells (NSCs) remain largely unknown. Here, we found that Porf-2 inhibits the activity of ras-related C3 botulinum toxin substrate 1 (Rac1) protein in hippocampus-derived rat NSCs. Reduced Rac1 activity impaired the nuclear translocation of β-catenin, ultimately causing a repression of NSCs proliferation. Porf-2 knockdown enhanced NSCs proliferation but not in the presence of small molecule inhibitors of Rac1 or Wnt. At the same time, the repression of NSCs proliferation caused by Porf-2 overexpression was counteracted by small molecule activators of Rac1 or Wnt. By using a rat optic nerve crush model, we observed that Porf-2 knockdown enhanced the recovery of visual function. In particular, optic nerve injury in rats led to increased Wnt family member 3a (Wnt3a) protein expression, which we found responsible for enhancing Porf-2 knockdown-induced NSCs proliferation. These findings suggest that Porf-2 exerts its inhibitory effect on NSCs proliferation via Rac1-Wnt/β-catenin pathway. Porf-2 may therefore represent and interesting target for optic nerve injury recovery and therapy.
Background Micronuclei (MN) in mammalian cells serve as a reliable biomarker of genomic instability and genotoxic exposure. Elevation of MN is commonly observed in cells bearing intrinsic genomic instability and in normal cells exposed to genotoxic agents. DNA double-strand breaks are marked by phosphorylation of H2AX at serine 139 (γ-H2AX). One subclass of MN contains massive and uniform γ-H2AX signals. This study tested whether this subclass of MN can be induced by replication stress. Principal Findings We observed that a large proportion of MN, from 20% to nearly 50%, showed uniform staining by antibodies against γ-H2AX, a marker of DNA double-strand breaks (DSBs). Such micronuclei were designated as MN-γ–H2AX (+). We showed that such MN can be induced by chemicals that are known to cause DNA replication stress and S phase arrest. Hydroxyurea, aphidicolin and thymidine could all significantly induce MN-γ–H2AX (+), which were formed during S phase and appeared to be derived from aggregation of DSBs. MN-γ–H2AX (−), MN that were devoid of uniform γ-H2AX signals, were induced to a lesser extent in terms of fold change. Paclitaxel, which inhibits the disassembly of microtubules, only induced MN-γ–H2AX (−). The frequency of MN-γ–H2AX (+), but not that of MN-γ–H2AX (−), was also significantly increased in cells that experience S phase prolongation due to depletion of cell cycle regulator CUL4B. Depletion of replication protein A1 (RPA1) by RNA interference resulted in an elevation of both MN-γ–H2AX (+) and MN-γ–H2AX (−). Conclusions/Significance A subclass of MN, MN-γ–H2AX (+), can be preferentially induced by replication stress. Classification of MN according to their γ-H2AX status may provide a more refined evaluation of intrinsic genomic instabilities and the various environmental genotoxicants.
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