2023 |
Hood RJ, Beard DJ, McLeod DD, Murtha LA, Spratt NJ, 'Intracranial pressure elevation post-stroke: Mechanisms and consequences', Frontiers in Stroke, 2 [C1]
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Nova |
2023 |
Beard D, Murtha L, McLeod D, 'Editorial: Intracranial Pressure Regulation in Stroke', Frontiers in Stroke, (2023)
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2021 |
Chen O, Michlíková S, Eckhardt L, Wondrak M, De Mendoza AM, Krause M, et al., 'Efficient heat shock response affects hyperthermia-induced radiosensitization in a tumor spheroid control probability assay', Cancers, 13 (2021) [C1]
Hyperthermia (HT) combined with irradiation is a well-known concept to improve the curative potential of radiotherapy. Technological progress has opened new avenues for thermoradi... [more]
Hyperthermia (HT) combined with irradiation is a well-known concept to improve the curative potential of radiotherapy. Technological progress has opened new avenues for thermoradio-therapy, even for recurrent head and neck squamous cell carcinomas (HNSCC). Preclinical evaluation of the curative radiosensitizing potential of various HT regimens remains ethically, economically, and technically challenging. One key objective of our study was to refine an advanced 3-D assay setup for HT + RT research and treatment testing. For the first time, HT-induced radiosensitization was systematically examined in two differently radioresponsive HNSCC spheroid models using the unique in vitro ¿curative¿ analytical endpoint of spheroid control probability. We further in-vestigated the cellular stress response mechanisms underlying the HT-related radiosensitization process with the aim to unravel the impact of HT-induced proteotoxic stress on the overall radiore-sponse. HT disrupted the proteome¿s thermal stability, causing severe proteotoxic stress. It strongly enhanced radiation efficacy and affected paramount survival and stress response signaling networks. Transcriptomics, q-PCR, and western blotting data revealed that HT + RT co-treatment critically triggers the heat shock response (HSR). Pre-treatment with chemical chaperones intensified the radiosensitizing effect, thereby suppressing HT-induced Hsp27 expression. Our data suggest that HT-induced radiosensitization is adversely affected by the proteotoxic stress response. Hence, we propose the inhibition of particular heat shock proteins as a targeting strategy to improve the outcome of combinatorial HT + RT.
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2021 |
De Mendoza AM, Michlikova S, Berger J, Karschau J, Kunz-Schughart LA, McLeod DD, 'Mathematical model for the thermal enhancement of radiation response: thermodynamic approach', SCIENTIFIC REPORTS, 11 (2021) [C1]
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Nova |
2020 |
Ferrara F, Zeisig V, Pietsch S, Ruetten R, Dreyer AY, Pieper L, et al., 'Hypothesis and Theory: A Pathophysiological Concept of Stroke-Induced Acute Phase Response and Increased Intestinal Permeability Leading to Secondary Brain Damage', FRONTIERS IN NEUROSCIENCE, 14 (2020) [C1]
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Nova |
2019 |
Boltze J, Ferrara F, Hainsworth AH, Bridges LR, Zille M, Lobsien D, et al., 'Lesional and perilesional tissue characterization by automated image processing in a novel gyrencephalic animal model of peracute intracerebral hemorrhage', Journal of Cerebral Blood Flow and Metabolism, 39 2521-2535 (2019) [C1]
Intracerebral hemorrhage (ICH) is an important stroke subtype, but preclinical research is limited by a lack of translational animal models. Large animal models are useful to comp... [more]
Intracerebral hemorrhage (ICH) is an important stroke subtype, but preclinical research is limited by a lack of translational animal models. Large animal models are useful to comparatively investigate key pathophysiological parameters in human ICH. To (i) establish an acute model of moderate ICH in adult sheep and (ii) an advanced neuroimage processing pipeline for automatic brain tissue and hemorrhagic lesion determination; 14 adult sheep were assigned for stereotactically induced ICH into cerebral white matter under physiological monitoring. Six hours after ICH neuroimaging using 1.5T MRI including structural as well as perfusion and diffusion, weighted imaging was performed before scarification and subsequent neuropathological investigation including immunohistological staining. Controlled, stereotactic application of autologous blood caused a space-occupying intracerebral hematoma of moderate severity, predominantly affecting white matter at 5 h post-injection. Neuroimage post-processing including lesion probability maps enabled automatic quantification of structural alterations including perilesional diffusion and perfusion restrictions. Neuropathological and immunohistological investigation confirmed perilesional vacuolation, axonal damage, and perivascular blood as seen after human ICH. The model and imaging platform reflects key aspects of human ICH and enables future translational research on hematoma expansion/evacuation, white matter changes, hematoma evacuation, and other aspects.
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Nova |
2017 |
Demuth HU, Dijkhuizen RM, Farr TD, Gelderblom M, Horsburgh K, Iadecola C, et al., 'Recent progress in translational research on neurovascular and neurodegenerative disorders', Restorative Neurology and Neuroscience, 35 87-103 (2017) [C1]
The already established and widely used intravenous application of recombinant tissue plasminogen activator as a re-opening strategy for acute vessel occlusion in ischemic stroke ... [more]
The already established and widely used intravenous application of recombinant tissue plasminogen activator as a re-opening strategy for acute vessel occlusion in ischemic stroke was recently added by mechanical thrombectomy, representing a fundamental progress in evidence-based medicine to improve the patient's outcome. This has been paralleled by a swift increase in our understanding of pathomechanisms underlying many neurovascular diseases and most prevalent forms of dementia. Taken together, these current advances offer the potential to overcome almost two decades of marginally successful translational research on stroke and dementia, thereby spurring the entire field of translational neuroscience. Moreover, they may also pave the way for the renaissance of classical neuroprotective paradigms. This review reports and summarizes some of the most interesting and promising recent achievements in neurovascular and dementia research. It highlights sessions from the 9th International Symposium on Neuroprotection and Neurorepair that have been discussed from April 19th to 22nd in Leipzig, Germany. To acknowledge the emerging culture of interdisciplinary collaboration and research, special emphasis is given on translational stories ranging from fundamental research on neurode- and -regeneration to late stage translational or early stage clinical investigations.
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Nova |
2017 |
Rostas JAP, Hoffman A, Murtha LA, Pepperall D, McLeod DD, Dickson PW, et al., 'Ischaemia- and excitotoxicity-induced CaMKII-Mediated neuronal cell death: The relative roles of CaMKII autophosphorylation at T286 and T253', Neurochemistry International, 104 6-10 (2017) [C1]
Ischaemia/excitotoxicity produces persistent activation of CaMKII (Ca2+-calmodulin stimulated protein kinase II) that initiates cell death. This study investigated the involvement... [more]
Ischaemia/excitotoxicity produces persistent activation of CaMKII (Ca2+-calmodulin stimulated protein kinase II) that initiates cell death. This study investigated the involvement of CaMKII phosphorylation at T286 and T253 in producing this persistent activation. In T286A-aCaMKII transgenic mice that lack the ability to phosphorylate aCaMKII at T286, transient occlusion of the middle cerebral artery for 90¿min resulted in no significant difference in infarct size compared to normal littermate controls. Overexpression of the phospho-mimic mutant T286D-aCaMKII in differentiated neuroblastoma cell lines did not enhance excitotoxicity-induced cell death compared to overexpression of wild type aCaMKII. By contrast, overexpression of the phospho-mimic mutant T253D-aCaMKII significantly enhanced excitotoxicity-induced cell death whereas overexpression of the phospho-null mutant T253V-aCaMKII produced no enhancement. These results indicate that T286 phosphorylation does not play a significant role in ischaemia/excitotoxicity induced CaMKII-mediated cell death and suggest that T253 phosphorylation is required to produce the persistent activation of CaMKII involved in ischaemia/excitotoxicity induced cell death.
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Nova |
2017 |
Diehl R, Ferrara F, Müller C, Dreyer AY, McLeod DD, Fricke S, Boltze J, 'Immunosuppression for in vivo research: State-of-The-Art protocols and experimental approaches', Cellular and Molecular Immunology, 14 146-179 (2017) [C1]
Almost every experimental treatment strategy using non-Autologous cell, tissue or organ transplantation is tested in small and large animal models before clinical translation. Bec... [more]
Almost every experimental treatment strategy using non-Autologous cell, tissue or organ transplantation is tested in small and large animal models before clinical translation. Because these strategies require immunosuppression in most cases, immunosuppressive protocols are a key element in transplantation experiments. However, standard immunosuppressive protocols are often applied without detailed knowledge regarding their efficacy within the particular experimental setting and in the chosen model species. Optimization of such protocols is pertinent to the translation of experimental results to human patients and thus warrants further investigation. This review summarizes current knowledge regarding immunosuppressive drug classes as well as their dosages and application regimens with consideration of species-specific drug metabolization and side effects. It also summarizes contemporary knowledge of novel immunomodulatory strategies, such as the use of mesenchymal stem cells or antibodies. Thus, this review is intended to serve as a state-of-The-Art compendium for researchers to refine applied experimental immunosuppression and immunomodulation strategies to enhance the predictive value of preclinical transplantation studies.
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Nova |
2016 |
Schmidt B, Reinhard M, Lezaic V, McLeod DD, Weinhold M, Mattes H, Klingelhöfer J, 'Autoregulation monitoring and outcome prediction in neurocritical care patients: Does one index fit all?', Journal of Clinical Monitoring and Computing, 30 367-375 (2016) [C1]
Indexes PRx and Mx have been formerly introduced to assess cerebral autoregulation and have been shown to be associated with 3-month clinical outcome. In a mixed cohort of neurocr... [more]
Indexes PRx and Mx have been formerly introduced to assess cerebral autoregulation and have been shown to be associated with 3-month clinical outcome. In a mixed cohort of neurocritical care patients, we retrospectively investigated the impact of selected clinical characteristics on this association. Forty-one patients (18¿77¿years) with severe traumatic (TBI, N¿=¿20) and non-traumatic (N¿=¿21) brain injuries were studied. Cerebral blood flow velocity, arterial blood pressure and intracranial pressure were repeatedly recorded during 1-h periods. Calculated PRx and Mx were correlated with 3-month clinical outcome score of modified Rankin Scale (mRS) in different subgroups with specific clinical characteristics. Both PRx and Mx correlated significantly with outcome (PRx: r¿=¿0.38, p¿<¿0.05; AUC¿=¿0.64, n.s./Mx: r¿=¿0.48, p¿<¿0.005; AUC¿=¿0.80, p¿<¿0.005) in the overall group, and in patients with hemicraniectomy (N¿=¿17; PRx: r¿=¿0.73, p¿<¿0.001; AUC¿=¿0.89, p¿<¿0.01/Mx: r¿=¿0.69, p¿<¿0.005; AUC¿=¿0.87, p¿<¿0.05). Mx, not PRx, correlated significantly with mRS in patients with heart failure (N¿=¿17; r¿=¿0.69, p¿<¿0.005; AUC¿=¿0.92, p¿<¿0.005), and in non-traumatic patients (r¿=¿0.49, p¿<¿0.05; AUC¿=¿0.79, p¿<¿0.05). PRx, not Mx, correlated significantly with mRS in TBI patients (r¿=¿0.63, p¿<¿0.01; AUC¿=¿0.89, p¿<¿0.01). Both indexes did not correlate with mRS in diabetes patients (N¿=¿15), PRx failed in hypocapnic patients (N¿=¿26). Both PRx and Mx were significantly associated with 3-month clinical outcome, even in patients with hemicraniectomy. PRx was more appropriate for TBI patients, while Mx was better suited for non-traumatic patients and patients with heart failure. Prognostic values of indexes were affected by diabetes (both Mx and PRx) and hypocapnia (PRx only).
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Nova |
2016 |
Beard DJ, Murtha LA, McLeod DD, Spratt NJ, 'Intracranial Pressure and Collateral Blood Flow', Stroke, 47 1695-1700 (2016) [C1]
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Nova |
2016 |
Beard DJ, Logan CL, McLeod DD, Hood RJ, Pepperall D, Murtha LA, Spratt NJ, 'Ischemic penumbra as a trigger for intracranial pressure rise - A potential cause for collateral failure and infarct progression?', J Cereb Blood Flow Metab, 36 917-927 (2016) [C1]
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Nova |
2016 |
Murtha LA, Beard DJ, Bourke JT, Pepperall D, McLeod DD, Spratt NJ, 'Intracranial Pressure Elevation 24 h after Ischemic Stroke in Aged Rats Is Prevented by Early, Short Hypothermia Treatment.', Front Aging Neurosci, 8 124 (2016) [C1]
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Nova |
2015 |
Murtha LA, McLeod DD, Pepperall D, McCann SK, Beard DJ, Tomkins AJ, et al., 'Intracranial pressure elevation after ischemic stroke in rats: Cerebral edema is not the only cause, and short-duration mild hypothermia is a highly effective preventive therapy', Journal of Cerebral Blood Flow and Metabolism, 35 592-600 (2015) [C1]
In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equa... [more]
In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equates to higher ICP. We recently demonstrated a dramatic ICP elevation 24 hours after small ischemic strokes in rats, with minimal edema. This ICP elevation was completely prevented by short-duration moderate hypothermia soon after stroke. Here, our aims were to determine the importance of edema in ICP elevation after stroke and whether mild hypothermia could prevent the ICP rise. Experimental stroke was performed in rats. ICP was monitored and short-duration mild (35 °C) or moderate (32.5 °C) hypothermia, or normothermia (37 °C) was induced after stroke onset. Edema was measured in three studies, using wet-dry weight calculations, T 2-weighted magnetic resonance imaging, or histology. ICP increased 24 hours after stroke onset in all normothermic animals. Short-duration mild or moderate hypothermia prevented this rise. No correlation was seen between ¿ICP and edema or infarct volumes. Calculated rates of edema growth were orders of magnitude less than normal cerebrospinal fluid production rates. These data challenge current concepts and suggest that factors other than cerebral edema are the primary cause of the ICP elevation 24 hours after stroke onset.
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Nova |
2015 |
Beard DJ, Mcleod DD, Logan CL, Murtha LA, Imtiaz MS, Van Helden DF, Spratt NJ, 'Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke', Journal of Cerebral Blood Flow and Metabolism, 35 861-872 (2015) [C1]
Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite st... [more]
Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arterial occlusion. The cause for 'collateral failure' is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by >450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.
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Nova |
2015 |
Mcleod DD, Parsons MW, Hood R, Hiles B, Allen J, Mccann SK, et al., 'Perfusion computed tomography thresholds defining ischemic penumbra and infarct core: Studies in a rat stroke model', International Journal of Stroke, 10 553-559 (2015) [C1]
Background: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (ischemic penumbra) after ischemic stro... [more]
Background: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (ischemic penumbra) after ischemic stroke and guide reperfusion therapies. Aims: The study aims to determine whether there are important changes in perfusion computed tomography thresholds defining ischemic penumbra and infarct core over time following stroke. Methods: Permanent middle cerebral artery occlusion was performed in adult outbred Wistar rats (n=6) and serial perfusion computed tomography scans were taken every 30 mins for 2h. To define infarction thresholds at 1h and 2h post-stroke, separate groups of rats underwent 1h (n=6) and 2h (n=6) of middle cerebral artery occlusion followed by reperfusion. Infarct volumes were defined by histology at 24h. Co-registration with perfusion computed tomography maps (cerebral blood flow, cerebral blood volume, and mean transit time) permitted pixel-based analysis of thresholds defining infarction, using receiver operating characteristic curves. Results: Relative cerebral blood flow was the perfusion computed tomography parameter that most accurately predicted penumbra (area under the curve=0·698) and also infarct core (area under the curve=0·750). A relative cerebral blood flow threshold of <75% of mean contralateral cerebral blood flow most accurately predicted penumbral tissue at 0·5h (area under the curve=0·660), 1h (area under the curve=0·659), 1·5h (area under the curve=0·636), and 2h (area under the curve=0·664) after stroke onset. A relative cerebral blood flow threshold of <55% of mean contralateral most accurately predicted infarct core at 1h (area under the curve=0·765) and at 2h (area under the curve=0·689) after middle cerebral artery occlusion. Conclusions: The data provide perfusion computed tomography defined relative cerebral blood flow thresholds for infarct core and ischemic penumbra within the first two hours after experimental stroke in rats. These thresholds were shown to be stable to define the volume of infarct core and penumbra within this time window.
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Nova |
2014 |
Beard DJ, McLeod DD, Murtha LA, Spratt NJ, 'Elevation of intracranial pressure reduces leptomeningeal collateral and watershed blood flow during experimental stroke', CEREBROVASCULAR DISEASES, 37 65-65 (2014)
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2014 |
Murtha LA, McLeod DD, Beard DJ, Pepperall DG, Spratt NJ, 'Short duration mild hypothermia prevents delayed intracranial pressure rise following experimental ischaemic stroke', CEREBROVASCULAR DISEASES, 37 340-340 (2014)
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2014 |
Spratt NJ, Tomkins AJ, Pepperall D, McLeod DD, Calford MB, 'Allopregnanolone and its precursor progesterone do not reduce injury after experimental stroke in hypertensive rats - role of postoperative temperature regulation?', PLoS One, 9 e107752 (2014) [C1]
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Nova |
2014 |
Murtha LA, Mcleod DD, Mccann SK, Pepperall D, Chung S, Levi CR, et al., 'Short-duration hypothermia after ischemic stroke prevents delayed intracranial pressure rise', International Journal of Stroke, 9 553-559 (2014) [C1]
Background: Intracranial pressure elevation, peaking three to seven post-stroke is well recognized following large strokes. Data following small-moderate stroke are limited. Thera... [more]
Background: Intracranial pressure elevation, peaking three to seven post-stroke is well recognized following large strokes. Data following small-moderate stroke are limited. Therapeutic hypothermia improves outcome after cardiac arrest, is strongly neuroprotective in experimental stroke, and is under clinical trial in stroke. Hypothermia lowers elevated intracranial pressure; however, rebound intracranial pressure elevation and neurological deterioration may occur during rewarming. Hypotheses: (1) Intracranial pressure increases 24h after moderate and small strokes. (2) Short-duration hypothermia-rewarming, instituted before intracranial pressure elevation, prevents this 24h intracranial pressure elevation. Methods: Long-Evans rats with two hour middle cerebral artery occlusion or outbred Wistar rats with three hour middle cerebral artery occlusion had intracranial pressure measured at baseline and 24h. Wistars were randomized to 2·5h hypothermia (32·5°C) or normothermia, commencing 1h after stroke. Results: In Long-Evans rats (n=5), intracranial pressure increased from 10·9±4·6mmHg at baseline to 32·4±11·4mmHg at 24h, infarct volume was 84·3±15·9mm3. In normothermic Wistars (n=10), intracranial pressure increased from 6·7±2·3mmHg to 31·6±9·3mmHg, infarct volume was 31·3±18·4mm3. In hypothermia-treated Wistars (n=10), 24h intracranial pressure did not increase (7·0±2·8mmHg, P<0·001 vs. normothermia), and infarct volume was smaller (15·4±11·8mm3, P<0·05). Conclusions: We saw major intracranial pressure elevation 24h after stroke in two rat strains, even after small strokes. Short-duration hypothermia prevented the intracranial pressure rise, an effect sustained for at least 18h after rewarming. The findings have potentially important implications for design of future clinical trials. © 2013 The Authors. International Journal of Stroke © 2013 World Stroke Organization.
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Nova |
2014 |
Murtha LA, Yang Q, Parsons MW, Levi CR, Beard DJ, Spratt NJ, McLeod DD, 'Cerebrospinal fluid is drained primarily via the spinal canal and olfactory route in young and aged spontaneously hypertensive rats', Fluids and Barriers of the CNS, 11 (2014) [C1]
Background: Many aspects of CSF dynamics are poorly understood due to the difficulties involved in quantification and visualization. In particular, there is debate surrounding the... [more]
Background: Many aspects of CSF dynamics are poorly understood due to the difficulties involved in quantification and visualization. In particular, there is debate surrounding the route of CSF drainage. Our aim was to quantify CSF flow, volume, and drainage route dynamics in vivo in young and aged spontaneously hypertensive rats (SHR) using a novel contrast-enhanced computed tomography (CT) method.Methods: ICP was recorded in young (2-5 months) and aged (16 months) SHR. Contrast was administered into the lateral ventricles bilaterally and sequential CT imaging was used to visualize the entire intracranial CSF system and CSF drainage routes. A customized contrast decay software module was used to quantify CSF flow at multiple locations.Results: ICP was significantly higher in aged rats than in young rats (11.52 ± 2.36 mmHg, versus 7.04 ± 2.89 mmHg, p = 0.03). Contrast was observed throughout the entire intracranial CSF system and was seen to enter the spinal canal and cross the cribriform plate into the olfactory mucosa within 9.1 ± 6.1 and 22.2 ± 7.1 minutes, respectively. No contrast was observed adjacent to the sagittal sinus. There were no significant differences between young and aged rats in either contrast distribution times or CSF flow rates. Mean flow rates (combined young and aged) were 3.0 ± 1.5 µL/min at the cerebral aqueduct; 3.5 ± 1.4 µL/min at the 3rd ventric= and 2.8 ± 0.9 µL/min at the 4th ventricle. Intracranial CSF volumes (and as percentage total brain volume) were 204 ± 97 µL (8.8 ± 4.3%) in the young and 275 ± 35 µL (10.8 ± 1.9%) in the aged animals (NS).Conclusions: We have demonstrated a contrast-enhanced CT technique for measuring and visualising CSF dynamics in vivo. These results indicate substantial drainage of CSF via spinal and olfactory routes, but there was little evidence of drainage via sagittal sinus arachnoid granulations in either young or aged animals. The data suggests that spinal and olfactory routes are the primary routes of CSF drainage and that sagittal sinus arachnoid granulations play a minor role, even in aged rats with higher ICP. © 2014 Murtha et al.; licensee BioMed Central Ltd.
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Nova |
2013 |
McLeod DD, Beard DJ, Parsons MW, Levi CR, Calford MB, Spratt NJ, 'Inadvertent Occlusion of the Anterior Choroidal Artery Explains Infarct Variability in the Middle Cerebral Artery Thread Occlusion Stroke Model', PLOS ONE, 8 (2013) [C1]
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Nova |
2012 |
Murtha L, McLeod D, Spratt N, 'Epidural intracranial pressure measurement in rats using a fiber-optic pressure transducer.', Journal of visualized experiments : JoVE, (2012) [C1]
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Nova |
2012 |
McLeod DD, Parsons G, Gunther R, Quail AW, Cottee DB, White SW, 'Differential effects of inhaled methacholine on circumferential wall and vascular smooth muscle of third-generation airways in awake sheep', Journal of Applied Physiology, 113 1233-1242 (2012) [C1]
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Nova |
2011 |
McLeod DD, Parsons MW, Levi CR, Beautement S, Buxton D, Roworth B, Spratt NJ, 'Establishing a rodent stroke perfusion computed tomography model', International Journal of Stroke, 6 284-289 (2011) [C1]
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Nova |
2011 |
McIlveen SA, White SW, Quail AW, McLeod DD, Parsons G, 'Integration of baroreflex and autoregulation control of bronchial blood flow in awake dogs', Acta Physiologica, 203 299-310 (2011) [C1]
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Nova |
2011 |
Spratt NJ, Donnan GA, McLeod DD, Howells DW, ''Salvaged' stroke ischaemic penumbra shows significant injury: Studies with the hypoxia tracer FMISO', Journal of Cerebral Blood Flow and Metabolism, 31 934-943 (2011) [C1]
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2007 |
Parsons G, White SW, Quail AW, McIlveen SA, Bishop R, McLeod DD, et al., 'Autonomic control of bronchial blood flow and airway dimensions during strenuous exercise in sheep', Pulmonary Pharmacology & Therapeutics, 20 190-199 (2007) [C1]
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Nova |
2007 |
Bishop R, McLeod DD, McIlveen SA, Blake RJ, Gunther R, Davis J, et al., 'Effects of graded exercise on bronchial blood flow and airway dimensions in sheep', Pulmonary Pharmacology & Therapeutics, 20 178-189 (2007) [C1]
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Nova |
2003 |
Quail A, Cottee D, McLeod D, Blake R, Bishop R, McIlveen S, White S, 'Analysis of bronchovascular downstream blood pressure changes in exercising sheep.', Arch Physiol Biochem, 111 309-313 (2003)
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2003 |
Bishop R, McLeod D, McIlveen S, Blake R, Gunther R, Davis J, et al., 'Long-term measurement of bronchial vascular resistance in awake sheep and dogs.', Arch Physiol Biochem, 111 315-316 (2003)
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2003 |
Quail AW, Cottee DB, McLeod DD, Blake RJ, Bishop R, McIlveen SA, White SW, 'Analysis of Bronchovascular Downstream Blood Pressure Changes in Exercising Sheep', Archives of Physiology and Biochemistry, 111 309-313 (2003) [C1]
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Nova |
2003 |
Bishop R, McLeod DD, McIlveen SA, Blake RJ, Gunther R, Davis J, et al., 'Long-Term Measurement of Bronchial Vascular Resistance in Awake Sheep and Dogs', Archives of Physiology and Biochemistry, 111 315-315 (2003) [C1]
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Nova |
2003 |
White S, McIlveen S, Parsons G, Quail A, Cottee D, Gunther R, et al., 'Neural control of the bronchial circulation.', Archives of physiology and biochemistry, 111 305-308 (2003)
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2003 |
White SW, McIlveen SA, Parsons G, Quail AW, Cottee DB, Gunther R, et al., 'Neural Control of the Bronchial Circulation', Archives of the Physiology and Biochemistry, 111 305-308 (2003) [C1]
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Nova |
2003 |
S W, S M, G P, A Q, D C, R G, et al., 'Neural Control of the Bronchial Circulation', Archives of Physiology and Biochemistry, 111 305-308 (2003)
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