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- Escartin, C., et al.
(författare)
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Reactive astrocyte nomenclature, definitions, and future directions
- 2021
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Ingår i: Nature Neuroscience. - : Springer Science and Business Media LLC. - 1097-6256 .- 1546-1726. ; 24, s. 312-325
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Tidskriftsartikel (refereegranskat)abstract
- Reactive astrocytes are astrocytes undergoing morphological, molecular, and functional remodeling in response to injury, disease, or infection of the CNS. Although this remodeling was first described over a century ago, uncertainties and controversies remain regarding the contribution of reactive astrocytes to CNS diseases, repair, and aging. It is also unclear whether fixed categories of reactive astrocytes exist and, if so, how to identify them. We point out the shortcomings of binary divisions of reactive astrocytes into good-vs-bad, neurotoxic-vs-neuroprotective or A1-vs-A2. We advocate, instead, that research on reactive astrocytes include assessment of multiple molecular and functional parameters-preferably in vivo-plus multivariate statistics and determination of impact on pathological hallmarks in relevant models. These guidelines may spur the discovery of astrocyte-based biomarkers as well as astrocyte-targeting therapies that abrogate detrimental actions of reactive astrocytes, potentiate their neuro- and glioprotective actions, and restore or augment their homeostatic, modulatory, and defensive functions. Good-bad binary classifications fail to describe reactive astrocytes in CNS disorders. Here, 81 researchers reach consensus on widespread misconceptions and provide definitions and recommendations for future research on reactive astrocytes.
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| 2. |
- Klaastad, Ö, et al.
(författare)
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Distribution of local anesthetic in axillary brachial plexus block : A clinical and magnetic resonance imaging study
- 2002
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Ingår i: Anesthesiology. - : Ovid Technologies (Wolters Kluwer Health). - 0003-3022 .- 1528-1175. ; 96:6, s. 1315-1324
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Tidskriftsartikel (refereegranskat)abstract
- Background: There is an unsettled discussion about whether the distribution of local anesthetic is free or inhibited when performing brachial plexus blocks. This is the first study to use magnetic resonance imaging (MRI) to help answer this question. Methods: Thirteen patients received axillary block by a catheter-nerve stimulator technique. After locating the median nerve, a total dose of 50 ml local anesthetic was injected via the catheter in four divided doses of 1, 4, 15, and 30 ml. Results of sensory and motor testing were compared with the spread of local anesthetic as seen by MRI scans taken after each dose. The distribution of local anesthetic was described with reference to a 20-mm diameter circle around the artery. Results: Thirty minutes after the last dose, only two patients demonstrated analgesia or anesthesia in the areas of the radial, median, and ulnar nerve. At that time, eight of the patients had incomplete spread of local anesthetic around the artery, as seen by MRI. Their blocks were significantly poorer than those of the five patients with complete filling of the circle, although incomplete blocks were also present in the latter group. Conclusion: This study demonstrated that MRI is useful in examining local anesthetic distribution in axillary blocks because it can show the correlation between MRI distribution pattern and clinical effect. The cross-sectional spread of fluid around the brachial-axillary artery was often incomplete-inhibited, and the clinical effect often inadequate.
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| 8. |
- Hol, P K, et al.
(författare)
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MRI-guided celiac plexus block
- 2000
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Ingår i: Magnetic Resonance Imaging. - 0730-725X .- 1873-5894. ; 12, s. 562-564
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Tidskriftsartikel (refereegranskat)
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| 9. |
- van Dijk, B. J., et al.
(författare)
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Complement C5 Contributes to Brain Injury After Subarachnoid Hemorrhage
- 2020
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Ingår i: Translational Stroke Research. - : Springer Science and Business Media LLC. - 1868-4483 .- 1868-601X. ; 11, s. 678-688
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Tidskriftsartikel (refereegranskat)abstract
- Previous studies showed that complement activation is associated with poor functional outcome after aneurysmal subarachnoid hemorrhage (SAH). We investigated whether complement activation is underlying brain injury after aneurysmal SAH (n=7) and if it is an appropriate treatment target. We investigated complement expression in brain tissue of aneurysmal SAH patients (n =930) and studied the role of common genetic variants in C3 and C5 genes in outcome. We analyzed plasma levels (n =229) to identify the functionality of a single nucleotide polymorphism (SNP) associated with outcome. The time course of C5a levels was measured in plasma (n =31) and CSF (n =10). In an SAH mouse model, we studied the extent of microglia activation and cell death in wild-type mice, mice lacking the C5a receptor, and in mice treated with C5-specific antibodies (n=15 per group). Brain sections from aneurysmal SAH patients showed increased presence of complement components C1q and C3/C3b/iC3B compared to controls. The complement component 5 (C5) SNP correlated with C5a plasma levels and poor disease outcome. Serial measurements in CSF revealed that C5a was >1400-fold increased 1 day after aneurysmal SAH and then gradually decreased. C5a in plasma was 2-fold increased at days 3–10 after aneurysmal SAH. In the SAH mouse model, we observed a ≈40% reduction in both microglia activation and cell death in mice lacking the C5a receptor, and in mice treated with C5-specific antibodies. These data show that C5 contributes to brain injury after experimental SAH, and support further study of C5-specific antibodies as novel treatment option to reduce brain injury and improve prognosis after aneurysmal SAH.
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