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  • 1
    Online Resource
    Online Resource
    A multicentre, prospective, double-blind study comparing the accuracy of autoantibody diagnostic assays in myasthenia gravis: the SCREAM study
    Elsevier BV ; 2023
    In:  The Lancet Regional Health - Western Pacific Vol. 38 ( 2023-09), p. 100846-
    Details
    In: The Lancet Regional Health - Western Pacific, Elsevier BV, Vol. 38 ( 2023-09), p. 100846-
    Type of Medium: Online Resource
    ISSN: 2666-6065
    URL: Article
    DOI: 10.1016/j.lanwpc.2023.100846
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 3052289-4
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  • 2
    Online Resource
    Online Resource
    Tissue plasminogen activator mobilizes neutrophils and T cells that exacerbate hemorrhagic transformation in stroke
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 64.21-64.21
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 64.21-64.21
    Abstract: Hemorrhagic complications represent a major limitation of thrombolytic therapy with tissue plasminogen activator (tPA) in patients with ischemic stroke. Here we report that tPA induces a swift surge of circulating neutrophils and T cells in both ischemic stroke patients and a rat model of focal embolic stroke. tPA exacerbates endothelial injury and increases adhesion and migration of neutrophils and T cells, which are associated with brain hemorrhage in rats subjected to embolic stroke. Genetic ablation of annexin A2 in neutrophils and T cells diminishes the effect of tPA on these cells. Decoupling the interaction between mobilized neutrophils/T cells and the neurovascular unit, achieved by using a sphingosine-1-phosphate receptor 1 modulator RP101075 and a CCL2 synthesis inhibitor bindarit, which block lymphocyte egress and myeloid cell recruitment, respectively, attenuates hemorrhagic transformation and improves neurological function after tPA thrombolysis. Our study suggests that immune invasion of the neurovascular unit represents a previously unrecognized mechanism governing the emergence of tPA-mediated brain hemorrhage, which can be overcome by precise immune modulation during thrombolytic therapy.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.64.21
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    tPA Mobilizes Immune Cells That Exacerbate Hemorrhagic Transformation in Stroke
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Research Vol. 128, No. 1 ( 2021-01-08), p. 62-75
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 128, No. 1 ( 2021-01-08), p. 62-75
    Abstract: Hemorrhagic complications represent a major limitation of intravenous thrombolysis using tPA (tissue-type plasminogen activator) in patients with ischemic stroke. The expression of tPA receptors on immune cells raises the question of what effects tPA exerts on these cells and whether these effects contribute to thrombolysis-related hemorrhagic transformation. Objective: We aim to determine the impact of tPA on immune cells and investigate the association between observed immune alteration with hemorrhagic transformation in ischemic stroke patients and in a rat model of embolic stroke. Methods and Results: Paired blood samples were collected before and 1 hour after tPA infusion from 71 patients with ischemic stroke. Control blood samples were collected from 27 ischemic stroke patients without tPA treatment. A rat embolic middle cerebral artery occlusion model was adopted to investigate the underlying mechanisms of hemorrhagic transformation. We report that tPA induces a swift surge of circulating neutrophils and T cells with profoundly altered molecular features in ischemic stroke patients and a rat model of focal embolic stroke. tPA exacerbates endothelial injury, increases adhesion and migration of neutrophils and T cells, which are associated with brain hemorrhage in rats subjected to embolic stroke. Genetic ablation of annexin A2 in neutrophils and T cells diminishes the effect of tPA on these cells. Decoupling the interaction between mobilized neutrophils/T cells and the neurovascular unit, achieved via a S1PR (sphingosine-1-phosphate receptor) 1 modulator RP101075 and a CCL2 (C-C motif chemokine ligand 2) synthesis inhibitor bindarit, which block lymphocyte egress and myeloid cell recruitment, respectively, attenuates hemorrhagic transformation and improves neurological function after tPA thrombolysis. Conclusions: Our findings suggest that immune invasion of the neurovascular unit represents a previously unrecognized mechanism underlying tPA-mediated brain hemorrhage, which can be overcome by precise immune modulation during thrombolytic therapy.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.120.317596
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1467838-X
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  • 4
    Online Resource
    Online Resource
    Diagnosis of Early Bacterial Pneumonia and Sepsis After Cardiovascular Surgery: A Diagnostic Prediction Model Based on LASSO Logistic Regression
    Informa UK Limited ; 2023
    In:  Journal of Inflammation Research Vol. Volume 16 ( 2023-09), p. 3983-3996
    Details
    In: Journal of Inflammation Research, Informa UK Limited, Vol. Volume 16 ( 2023-09), p. 3983-3996
    Type of Medium: Online Resource
    ISSN: 1178-7031
    URL: Article
    DOI: 10.2147/JIR.S423683
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2023
    detail.hit.zdb_id: 2494878-0
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  • 5
    Online Resource
    Online Resource
    CFHR1-Modified Neural Stem Cells Ameliorated Brain Injury in a Mouse Model of Neuromyelitis Optica Spectrum Disorders
    The American Association of Immunologists ; 2016
    In:  The Journal of Immunology Vol. 197, No. 9 ( 2016-11-01), p. 3471-3480
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 197, No. 9 ( 2016-11-01), p. 3471-3480
    Abstract: A major hurdle for effective stem cell therapy is ongoing inflammation in the target organ. Reconditioning the lesion microenvironment may be an effective way to promote stem cell therapy. In this study, we showed that engineered neural stem cells (NSCs) with complement factor H–related protein 1, a complement inhibitor protein, can attenuate inflammatory infiltration and immune-mediated damage of astrocytes, an important pathogenic progress in patients with neuromyelitis optica spectrum disorders. Furthermore, we demonstrated that transplantation of the complement factor H–related protein 1–modified NSCs effectively blocked the complement activation cascade and inhibited formation of the membrane attack complex, thus contributing to the protection of endogenous and transplanted NSC-differentiated astrocytes. Therefore, manipulation of the lesion microenvironment contributes to a more effective cell replacement therapeutic strategy for autoimmune diseases of the CNS.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1600135
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2016
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Augmentation of Circulating Follicular Helper T Cells and Their Impact on Autoreactive B Cells in Myasthenia Gravis
    The American Association of Immunologists ; 2016
    In:  The Journal of Immunology Vol. 197, No. 7 ( 2016-10-01), p. 2610-2617
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 197, No. 7 ( 2016-10-01), p. 2610-2617
    Abstract: Myasthenia gravis (MG) is a chronic humoral immunity–mediated autoimmune disorder of the neuromuscular junction characterized by muscle weakness. Follicular helper T (Tfh) cells may be the key Th cell subset that promotes MG development, as their major function is helping B cell activation and Ab production. Aberrance of thymus-derived Tfh cells might be implicated in autoimmune diseases including MG; just how circulating Tfh cells, especially those from patients with a normal thymus, contribute to MG pathogenesis remains to be uncovered. In this article, we characterize a population of circulating CD4+CXCR5+PD-1+ Tfh cells in ocular and generalized MG patients without thymic abnormalities and demonstrate that the circulating Tfh cells are significantly enriched in generalized MG patients but not in ocular MG patients compared with healthy subjects, whereas a proportion of follicular regulatory T cells decreased in MG patients. In addition, the frequency of plasma cells and B cells was higher and the serum levels of IL-6/IL-21 were also elevated in these MG patients. The activated Tfh1 and Tfh17 in Tfh cells are the major source for IL-21 production in MG patients. A strong correlation between Tfh cells and the plasma cell frequency and anti–acetylcholine receptor Ab titers was evident in generalized MG patients. In particular, we found that Tfh cells derived from MG patients promoted B cells to produce Abs in an IL-21 signaling–dependent manner. Collectively, our results suggest that circulating Tfh cells may act on autoreactive B cells and thus contribute to the development of MG in patients without thymic abnormalities.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1500725
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2016
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    Fingolimod enhances the efficacy of delayed alteplase administration in acute ischemic stroke by promoting anterograde reperfusion and retrograde collateral flow
    Wiley ; 2018
    In:  Annals of Neurology Vol. 84, No. 5 ( 2018-11), p. 717-728
    Details
    In: Annals of Neurology, Wiley, Vol. 84, No. 5 ( 2018-11), p. 717-728
    Abstract: The present study was undertaken to determine the efficacy of coadministration of fingolimod with alteplase in acute ischemic stroke patients in a delayed time window. Methods This was a prospective, randomized, open‐label, blinded endpoint clinical trial, enrolling patients with internal carotid artery or middle cerebral artery proximal occlusion within 4.5 to 6 hours from symptom onset. Patients were randomly assigned to receive alteplase alone or alteplase with fingolimod. All patients underwent pretreatment and 24‐hour noncontrast computed tomography (CT)/perfusion CT/CT angiography. The coprimary endpoints were the decrease of National Institutes of Health Stroke Scale scores over 24 hours and the favorable shift of modified Rankin Scale score (mRS) distribution at day 90. Exploratory outcomes included vessel recanalization, anterograde reperfusion, and retrograde reperfusion of collateral flow. Results Each treatment group included 23 patients. Compared with alteplase alone, patients receiving fingolimod plus alteplase exhibited better early clinical improvement at 24 hours and a favorable shift of mRS distribution at day 90. In addition, patients who received fingolimod and alteplase exhibited a greater reduction in the perfusion lesion accompanied by suppressed infarct growth by 24 hours. Fingolimod in conjunction with alteplase significantly improved anterograde reperfusion of downstream territory and prevented the failure of retrograde reperfusion from collateral circulation. Interpretation Fingolimod may enhance the efficacy of alteplase administration in the 4.5‐ to 6‐hour time window in patients with a proximal cerebral arterial occlusion and salvageable penumbral tissue by promoting both anterograde reperfusion and retrograde collateral flow. These findings are instructive for the design of future trials of recanalization therapies in extended time windows. Ann Neurol 2018;84:725–736
    Type of Medium: Online Resource
    ISSN: 0364-5134 , 1531-8249
    URL: Issue
    URL: Article
    DOI: 10.1002/ana.v84.5
    DOI: 10.1002/ana.25352
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2037912-2
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  • 8
    Online Resource
    Online Resource
    Non-invasive tracking of CD4 + T cells with a paramagnetic and fluorescent nanoparticle in brain ischemia
    SAGE Publications ; 2016
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 36, No. 8 ( 2016-08), p. 1464-1476
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 36, No. 8 ( 2016-08), p. 1464-1476
    Abstract: Recent studies have demonstrated that lymphocytes play a key role in ischemic brain injury. However, there is still a lack of viable approaches to non-invasively track infiltrating lymphocytes and reveal their key spatiotemporal events in the inflamed central nervous system (CNS). Here we describe an in vivo imaging approach for sequential monitoring of brain-infiltrating CD4 + T cells in experimental ischemic stroke. We show that magnetic resonance imaging (MRI) or Xenogen imaging combined with labeling of SPIO-Molday ION Rhodamine-B (MIRB) can be used to monitor the dynamics of CD4 + T cells in a passive transfer model. MIRB-labeled CD4 + T cells can be longitudinally visualized in the mouse brain and peripheral organs such as the spleen and liver after cerebral ischemia. Immunostaining of tissue sections showed similar kinetics of MIRB-labeled CD4 + T cells when compared with in vivo observations. Our results demonstrated the use of MIRB coupled with in vivo imaging as a valid method to track CD4 + T cells in ischemic brain injury. This approach will facilitate future investigations to identify the dynamics and key spatiotemporal events for brain-infiltrating lymphocytes in CNS inflammatory diseases.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1177/0271678X15611137
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2016
    detail.hit.zdb_id: 2039456-1
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  • 9
    Online Resource
    Online Resource
    Abstract WP277: Non-invasive Tracking of CD4 + T Cells With a Paramagnetic and Fluorescent Nanoparticle in Brain Ischemia
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Stroke Vol. 47, No. suppl_1 ( 2016-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 47, No. suppl_1 ( 2016-02)
    Abstract: Introduction: Recent studies have demonstrated that lymphocytes play a key role in ischemic brain injury. However, there is still a lack of viable approaches to non-invasively track infiltrating lymphocytes and reveal their key spatiotemporal events in the inflamed central nervous system (CNS). In the present study, we describe an in vivo imaging approach for sequential monitoring of brain-infiltrating CD4 + T cells in experimental ischemic stroke. Methods: CD4 + T cells were obtained from splenocytes of C57BL/6 mice. After in vitro incubation with SPIO-Molday ION Rhodamine-B (MIRB) for 24 h, CD4 + Rh-B + T cells were sorted and purified with FACS followed by subsequent passive transfer into Rag2 -/- recipient mice (lack of T and B cells). After sham or 60 min of MCAO procedures with designated time of reperfusion, MIRB-labeled cells were sequentially visualized using 7T-MRI and Xenogen imaging. In separate groups of Rag2 -/- mice that received MIRB-labeled CD4 + T cells prior to sham or MCAO surgeries, brain, liver and spleen sections were obtained from these animals after MRI scans and immunostained with CD4 specific antibody, and the images were captured by a fluorescence microscopy. Results: We show that MRI or Xenogen imaging combined with labeling of MIRB can be used to monitor the dynamics of CD4 + T cells in a passive transfer model (Figure 1). MIRB-labeled CD4 + T cells can be longitudinally visualized in the mouse brain and peripheral organs such as the spleen and liver after cerebral ischemia. Immunostaining of tissue sections showed similar kinetics of MIRB-labeled CD4 + T cells when compared with in vivo observations. Conclusion: Our results demonstrated the use of MIRB coupled with in vivo imaging as a valid method to track CD4 + T cells in ischemic brain injury. This approach will facilitate future investigations to identify the dynamics and key spatiotemporal events for brain-infiltrating lymphocytes in CNS inflammatory diseases.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.47.suppl_1.wp277
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467823-8
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  • 10
    Online Resource
    Online Resource
    Selective Sphingosine-1-Phosphate Receptor 1 Modulation Attenuates Experimental Intracerebral Hemorrhage
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Stroke Vol. 47, No. 7 ( 2016-07), p. 1899-1906
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 47, No. 7 ( 2016-07), p. 1899-1906
    Abstract: Preclinical studies and a proof-of-concept clinical study have shown that sphingosine-1-phosphate receptor (S1PR) modulator, fingolimod, improves the clinical outcome of intracerebral hemorrhage (ICH). However, the specific subtype of the S1PRs through which immune modulation provides protection in ICH remains unclear. In addition, fingolimod-induced adverse effects could limit its use in patients with stroke because of interactions with other S1PR subtypes, particularly with S1PR3. RP101075 is a selective S1PR1 agonist with superior cardiovascular safety profile. In this study, we investigated the impact of RP101075 treatment in a mouse model of ICH. Methods— ICH was induced by injection of autologous blood in 294 male C57BL/6J and Rag2 −/− mice. ICH mice randomly received vehicle, RP101075, or RP101075 plus S1PR1 antagonist W146 by daily oral gavage for three consecutive days, starting from 30 minutes after surgery. Neurodeficits, brain edema, brain infiltration of immune cells, blood–brain barrier integrity, and cell death were assessed after ICH. Results— RP101075 significantly attenuated neurological deficits and reduced brain edema in ICH mice. W146 blocked the effects of RP101075 on neurodeficits and brain edema. RP101075 reduced the counts of brain-infiltrating lymphocytes, neutrophils, and microglia, as well as cytokine expression after ICH. Enhanced blood–brain barrier integrity and alleviated neuronal death were also seen in ICH mice after RP101075 treatment. Conclusions— S1PR1 modulation via RP101075 provides protection in experimental ICH. Together with the advantageous pharmacological features of RP101075, these results warrant further investigations of its mechanisms of action and translational values in ICH patients.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.115.012236
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467823-8
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