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Systems analysis of intracranial pressure

Comparison with volume-pressure test and CSF-pulse amplitude analysis

Michael Chopp and Harold D. Portnoy

N eurosurgeons are well aware that simply measuring intracranial pressure (ICP) fails to differentiate those patients with intracranial hypertension who have a benign course from those who may go on to fulminating intracranial hypertension. To differentiate these patients, several investigators 15, 24 have utilized the volume-pressure test (VPT), in which the intracranial system is provoked by the rapid introduction of a small volume of fluid and the immediate change in ICP determined (volume-pressure response, VPR). The test establishes an exponential volume

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Dunyue Lu, Asim Mahmood, Changsheng Qu, Anton Goussev, Mei Lu and Michael Chopp

were cut on a vibratome. To evaluate hemorrhage volume, five sections with a 200-µm interval were analyzed with the aid of a light microscope with a 203 objective. Quantitative Measurements of Hemorrhage To measure the extent of hemorrhage, five tissue sections from each rat were digitized under a 20× objective (BX40; Olympus Optical Co., Ltd., Nagano, Japan) by using a 3-charge-coupled device color video camera (DXC-970MD; Sony Corp., Tokyo, Japan) interfaced with the MicroComputer Imaging Device image analysis system (Imaging Research, Inc., St. Catharine's, ON

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Harold D. Portnoy, Michael Chopp, Craig Branch and Michael B. Shannon

. With the onset of hypercapnia, there is a beginning loss of vasomotor tone with an increase in cerebral blood volume. As T A of the precapillary vessels decreases, the CSFPW increases in amplitude and begins to show the influence of increasing transmission of the fundamental frequency, with rounding of the waveform. Because vascular expansion is more rapid than CSF absorption, Pcsf rises, which results in compression of the lateral lacunae and suppression of the fundamental frequency of the CSFPW. The SSPW thus initially remains fairly normal. As CSF absorption

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Ye Xiong, Asim Mahmood, Yanlu Zhang, Yuling Meng, Zheng Gang Zhang, Changsheng Qu, Thomas N. Sager and Michael Chopp

lesion volume and cell loss after TBI remains unknown. In addition, there have been no studies of the effects of CEPO on angiogenesis and neurogenesis after TBI or any comparing the efficacy of multiple doses of CEPO with a single dose for treatment of TBI. Accordingly, using a CCI model of TBI in rats, we investigated the effects of posttraumatic administration of CEPO on cortical and hippocampal injury, cell proliferation, neurogenesis, angiogenesis, long-term sensorimotor function, and spatial learning recovery. We compared the efficacy of a single dose of CEPO with

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Asim Mahmood, Dunyue Lu, Yi Li, Jae Li Chen and Michael Chopp

were mounted on a stereotactic frame. Using an aseptic procedure, a burr hole 1 mm in diameter was made on the left side of the scalp. Semisuspended donor cells (10 6 BM cells in a total fluid volume of 10 µl, including BM stroma and PBS) were injected using a 10-µl Hamilton syringe, which was inserted vertically through the burr hole into the left cortex and striatum at the following coordinates: 0 mm anterior and 2 mm to the right of the bregma, at a depth of 4.5 mm. 52 This position approximates the boundary zone of cerebral contusion. Each injection was divided

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Asim Mahmood, Hongtao Wu, Changsheng Qu, Ye Xiong and Michael Chopp

group underwent transplantation of scaffolds impregnated with hMSCs (3 × 10 6 hMSCs/scaffold) into the lesion cavity. The total volume injected in all 3 groups was 60 μl, and all treatments were performed 7 days after TBI. Seeding hMSCs Onto Scaffolds Collagen scaffolds were obtained from commercial sources (Davol Inc.). Scaffolds were pre-wet in culture medium consisting of DMEM supplemented with 10% fetal calf serum, 100 U/ml penicillin, 100 μg/ml streptomycin, 0.1 mM nonessential amino acids, and 1 ng/ml basic fibroblast growth factor (Life Technologies). 24

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Dunyue Lu, Asim Mahmood, Ruilan Zhang, Yi Li and Michael Chopp

, which differs morphologically from the surrounding normal tissue. Cell proliferation was also calculated as the density (cell number per square millimeter), which was used for analysis. For cell phenotyping, 100 BrdU-positive cells per animal were analyzed for colocalization with the Hu protein marker for neurons, 39 GFAP for astrocytes, 67 and MBP for oligodendrocytes 76 by using a fluorescence microscope with an objective lens at × 40. To estimate the volume of the hippocampus, sections were stained with H & E and analyzed using an objective lens at × 10 and a

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Ye Xiong, Yanlu Zhang, Asim Mahmood, Yuling Meng, Zheng Gang Zhang, Daniel C. Morris and Michael Chopp

-TBI does not reduce cortical lesion volume but reduces hippocampal cell loss and promotes endogenous neurorestorative effects, which potentially contribute to improved functional recovery. 77 However, the therapeutic efficacy of early Tβ4 treatment for TBI has not been investigated. Although human TBI is a complex and multifaceted disease, pharmacological compounds delivered in a clinically relevant time window may improve the outcome of patients with TBI. 37 In the present study, we tested the hypothesis that Tβ4 treatment initiated 6 hours postinjury provides

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Yuxia Han, Don Seyfried, Yuling Meng, Dongmei Yang, Lonni Schultz, Michael Chopp and Donald Seyfried

were randomly divided into 3 groups (8 rats per group): group 1 received exosomes derived from 3 × 10 6 MSCs (in 0.5 ml phosphate-buffered saline [PBS]); group 2 was treated with equal volume (0.5 ml) of PBS; and group 3 (sham group) had surgery without blood infusion into the brain and was treated with 0.5 ml PBS. The exosome solution or PBS was administered intravenously over 5 minutes via the tail vein, starting 24 hours after the ICH; this protocol was chosen based on our ischemic stroke and TBI studies with exosomes in rats. 55 All rats were killed at 28 days

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Dunyue Lu, Yi Li, Asim Mahmood, Lei Wang, Tahir Rafiq and Michael Chopp

, the lesion volumes of all rats were calculated and analyzed. The mean lesion volume (16.8 ± 3.4% of the ipsilateral hemisphere) of the TBI/NMSCS group was significantly decreased when compared with the TBI/saline (23.4 ± 4.8%), TBI/neurosphere (21.1 ± 3.2%), and TBI/MSC (22.6 ± 5.6%) groups (p < 0.05). No significant difference was detected between the TBI/saline group and the TBI/neurosphere group ( Fig. 4 ). All rats receiving NMSCS had surviving transplants and these grafts appeared to attach to the wall of the lesion cavity ( Fig. 5a–c ). Some cells labeled by