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  • Ovid Technologies (Wolters Kluwer Health)  (16)
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  • Ovid Technologies (Wolters Kluwer Health)  (16)
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  • 1
    Online Resource
    Online Resource
    Pharmacological Induction of Heme Oxygenase-1 by a Triterpenoid Protects Neurons Against Ischemic Injury
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Stroke Vol. 43, No. 5 ( 2012-05), p. 1390-1397
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 5 ( 2012-05), p. 1390-1397
    Abstract: Heme oxygenase-1 (HO-1) is an inducible Phase 2 enzyme that degrades toxic heme; its role in cerebral ischemia is not fully understood. We hypothesize that chemically induced HO-1 upregulation with the novel triterpenoid CDDO-Im (2-cyano-3,12 dioxooleana-1,9 dien-28-oyl imidazoline), a robust inducer of Phase 2 genes, protects neurons against ischemic injury. Methods— Using 3 different models of ischemia, including oxygen–glucose deprivation in neuronal cultures, global ischemia in rats, and focal ischemia in mice, we determined (1) whether CDDO-Im induces HO-1 expression and protects against ischemic injury; and (2) whether HO-1 inhibition disrupts the neuroprotective effect of CDDO-Im. Results— CDDO-Im treatment (50–300 nmol/L) resulted in 8-fold HO-1 upregulation in cultured neurons and protected against oxygen–glucose deprivation. The protection was abolished when the cultures were transfected with nuclear factor (erythroid-derived 2) like-2–shRNA or coincubated with tin protoporphyrin IX, a specific HO-1 inhibitor. In the rat model of global ischemia, intracerebroventricular infusion of CDDO-Im (0.5–1.5 μg) augmented HO-1 expression in hippocampal neurons and resulted in significant increases in CA1 neuronal survival after global ischemia. To further strengthen the clinical relevance of the CDDO-Im treatment, we tested its effects in the mouse model of temporary focal ischemia (60 minutes). Postischemic intraperitoneal injection of CDDO-Im (10–100 μg) enhanced HO-1 expression and significantly reduced neurological dysfunction and infarct volume. Intracerebroventricular infusion of tin protoporphyrin IX reduced the neuroprotective effect of CDDO-Im against global and focal ischemia. Conclusions— CDDO-Im confers neuroprotection against ischemic injury by upregulating HO-1, suggesting that enhance of HO-1 expression may be a legitimate strategy for therapeutic intervention of stroke.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.111.647420
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1467823-8
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  • 2
    Online Resource
    Online Resource
    Sirtuin 5-Mediated Lysine Desuccinylation Protects Mitochondrial Metabolism Following Subarachnoid Hemorrhage in Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Stroke Vol. 52, No. 12 ( 2021-12), p. 4043-4053
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 52, No. 12 ( 2021-12), p. 4043-4053
    Abstract: Sirt5 (Sirtuin 5) desuccinylates multiple metabolic enzymes and plays an important role in maintaining energy homeostasis. The goal of this study was to determine whether Sirt5-mediated desuccinylation restores the energy metabolism and protects brain against subarachnoid hemorrhage (SAH). Methods: Male C57BL/6 or Sirt5 −/− mice were used. The endovascular perforation SAH model was applied. Protein lysine succinylation in the brain cortex was examined using liquid chromatography-tandem mass spectrometry analysis. The brain metabolism was evaluated by measurement of brain pH as well as ATP and reactive oxygen species level. Neuronal cell death and neurobehavioral deficits were assessed 24 hours after SAH. The expression and desuccinylation activity of Sirt5, lysine succinylation of citrate synthase and ATP synthase subunits were investigated by Western blot, immunohistochemistry, and ELISA in SAH mice and patients. Furthermore, the benefits of resveratrol-mediated Sirt5 activation were investigated. Results: A total of 211 lysine succinylation sites were differentially expressed on 170 proteins in mice brain after SAH. Thirty-nine percent of these succinylated proteins were localized in mitochondria and they are related to energy metabolism. SAH caused a decrease of Sirt5 expression and succinylated citrate synthase as well as the subunits of ATP synthase, subsequently lowered brain pH, reduced ATP and increased reactive oxygen species production, leading to neuronal cell death, and neurological deficits. Knockdown of Sirt5 aggravated SAH-induced effects, mentioned above. Administration of resveratrol resulted in activation of Sirt5. The activation was accompanied both with restoration of the mitochondrial metabolism and alleviation of early brain injury as well as with desuccinylating citrate synthase and ATP synthase. Conclusions: Protein lysine succinylation is a biochemical hallmark of metabolic crisis after SAH, and disruption of lysine succinylation through activation of Sirt5 might be a promising therapeutic strategy for the treatment of SAH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.121.034850
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
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  • 3
    Online Resource
    Online Resource
    Cytotoxic and antiangiogenic paclitaxel solubilized and permeation-enhanced by natural product nanoparticles
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Anti-Cancer Drugs Vol. 26, No. 2 ( 2015-02), p. 167-179
    Details
    In: Anti-Cancer Drugs, Ovid Technologies (Wolters Kluwer Health), Vol. 26, No. 2 ( 2015-02), p. 167-179
    Type of Medium: Online Resource
    ISSN: 0959-4973
    URL: Article
    DOI: 10.1097/CAD.0000000000000173
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2025803-3
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  • 4
    Online Resource
    Online Resource
    Heme oxygenase modulates small intestine leukocyte adhesion following hindlimb ischemia/reperfusion by regulating the expression of intercellular adhesion molecule-1*
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Critical Care Medicine Vol. 33, No. 11 ( 2005-11), p. 2563-2570
    Details
    In: Critical Care Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 11 ( 2005-11), p. 2563-2570
    Type of Medium: Online Resource
    ISSN: 0090-3493
    URL: Article
    DOI: 10.1097/01.CCM.0000186765.61268.FC
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 2034247-0
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  • 5
    Online Resource
    Online Resource
    CHARACTERISTICS OF PERIPAPILLARY INTRACHOROIDAL CAVITATION IN HIGHLY MYOPIC EYES : The Zhongshan Ophthalmic Center–Brien Holden Vision Institute High Myopia Cohort Study
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Retina Vol. 41, No. 5 ( 2021-05), p. 1057-1062
    Details
    In: Retina, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. 5 ( 2021-05), p. 1057-1062
    Abstract: To characterize peripapillary intrachoroidal cavitation (PICC) in highly myopic participants and its associated risk factors. Methods: This observational, cross-sectional study recruited 890 Chinese participants with bilateral high myopia, defined as ≤−6.00 diopters spherical power. Fundus photography and spectral-domain optical coherence tomography were used to determine the presence of PICC, defined as a yellow–orange lesion adjacent to the disc border with a corresponding intrachoroidal hyporeflective space. Results: Among 890 participants, 884 right eyes were included for analysis. The rate of PICC was 3.6% (32 eyes). Peripapillary intrachoroidal cavitation was observed in two eyes without myopic retinal lesions, nine eyes with tessellated fundus only, 16 eyes with diffuse chorioretinal atrophy, and five eyes with patchy chorioretinal atrophy. The most commonly affected area was inferior disc border (87.5%), followed by multiple (9.4%) and superior (3.1%) disc borders. The multiple linear logistic regression model showed that older age, more myopic spherical equivalent, and longer axial length were associated with the presence of PICC. Conclusion: Peripapillary intrachoroidal cavitation was present in 3.6% of highly myopic eyes. It was more common in eyes with a higher myopic maculopathy category. Older age, more myopic spherical equivalent, and longer axial length were risk factors for the presence of PICC.
    Type of Medium: Online Resource
    ISSN: 0275-004X
    URL: Article
    DOI: 10.1097/IAE.0000000000002963
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2071014-8
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  • 6
    Online Resource
    Online Resource
    Subarachnoid Extension of Intracerebral Hemorrhage and 90-Day Outcomes in INTERACT2
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Stroke Vol. 45, No. 1 ( 2014-01), p. 258-260
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 45, No. 1 ( 2014-01), p. 258-260
    Abstract: The prognostic significance of subarachnoid extension of intracerebral hemorrhage was determined in the INTEnsive blood pressure Reduction in Acute Cerebral hemorrhage Trial (INTERACT2) study. Methods— INTERACT2 was an open randomized controlled trial of early intensive compared with guideline-recommended blood pressure lowering in patients with elevated systolic blood pressure within 6 hours of intracerebral hemorrhage. Independent predictors of death or major disability (scores 3–6 on the modified Rankin Scale) at 90 days were analyzed in logistic regression models. Results— Of 2582 participants, 192 (7%) had subarachnoid extension, which was associated with larger hematoma volumes ( P 〈 0.0001) and higher National Institute of Health Stroke Scale score ( P 〈 0.0001). Subarachnoid extension predicted death or major disability at 90 days (71% versus 53%; unadjusted odds ratio, 2.25; 95% confidence interval, 1.63–3.10; P 〈 0.0001). The association remained significant after adjusting for age, region, lipid-lowering therapy, systolic blood pressure, glucose, location of hematoma, intraventricular extension, and randomized treatment (odds ratio, 2.17; 95% confidence interval, 1.50–3.14; P 〈 0.0001), but not after further adjustment for baseline hematoma volume ( P =0.62). Conclusions— Subarachnoid extension of intracerebral hemorrhage is associated with poor prognosis, which is determined by a larger volume of the underlying intraparenchymal hematoma. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00716079.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.113.003524
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1467823-8
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  • 7
    Online Resource
    Online Resource
    Abstract 3856: Adoptive Transfer Of Regulatory T Cells Confers Long Term Neuroprotection Against Cerebral Ischemic Stroke
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Stroke Vol. 43, No. suppl_1 ( 2012-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. suppl_1 ( 2012-02)
    Abstract: Stroke is the leading cause of serious long-term disability in adults. Activation and mobilization of CD4+CD25+ regulatory T cells (Tregs) is an intrinsic mechanism the body uses to restrict pro-inflammatory response, one of the well-established contributing factors for secondary neuronal injury and long-term neurological deficits after stroke. The current study explores the protective effect of Tregs adoptive therapy against post-ischemic brain damage and investigated the mechanisms underlying the action of Tregs. Using a mouse model of focal transient ischemia, we found that intravenous injections of Tregs (2 x 10 6 /animal) within 24 hours (2, 6, and 24 hours) after ischemia resulted in marked reduction of brain infarct. The maximal protection occurred upon earlier Tregs transfer with 2-hour delay after MCAO, which resulted in approximately 30% reduction of infarct volume. Post-ischemic sensorimotor dysfunction significantly improved during both the acute and late recovery after MCAO in Treg-treated mice as assessed by corner test, forelimb placing and cylinder test up to 28 days after ischemic stroke. Furthermore, Tregs treatment inhibited the up-regulation of IL-6, IL-1β, IL-17 and TNF-α in the ischemic brain and mitigated the cerebral infiltration of peripheral immune cells, including neutrophil, macrophage and T cells early after MCAO. Taken together, our study demonstrates that adoptive therapy with Tregs is a novel and potent cell-based therapy targeting post-stroke inflammatory dysregulation.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.43.suppl_1.A3856
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 8
    Online Resource
    Online Resource
    n -3 Polyunsaturated Fatty Acids Reduce Neonatal Hypoxic/Ischemic Brain Injury by Promoting Phosphatidylserine Formation and Akt Signaling
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Stroke Vol. 46, No. 10 ( 2015-10), p. 2943-2950
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 46, No. 10 ( 2015-10), p. 2943-2950
    Abstract: Omega-3 polyunsaturated fatty acids ( n-3 PUFAs) attenuate neonatal hypoxic/ischemic (H/I) brain damage, but the underlying mechanisms are not fully understood. This study tested the hypothesis that n-3 PUFAs enhance Akt-dependent prosurvival signaling by promoting the biosynthesis of phosphatidylserine in neuronal cell membranes. Methods— Dietary n-3 PUFA supplementation was initiated on the second day of pregnancy in dams. H/I was induced in 7-day-old rat pups by ipsilateral common carotid artery occlusion followed by hypoxia (8% oxygen for 2.5 hours). Neurological outcomes, brain tissue loss, cell death, and the activation of signaling events were assessed after H/I. The effects of n-3 PUFAs (docosahexaenoic acid and eicosapentaenoic acid) on oxygen-glucose deprivation–induced cell death and the underlying mechanism of protection were also examined in primary cortical neuron cultures. Results— n-3 PUFAs reduced brain tissue loss at 7 days after H/I and improved neurological outcomes, whereas inhibition of PI3K/Akt signaling by LY294002 partially abrogated this neuroprotective effect. Docosahexaenoic acid/eicosapentaenoic acid also prevented ischemic neuronal death through the Akt prosurvival pathway in vitro. Furthermore, docosahexaenoic acid/eicosapentaenoic acid increased the production of phosphatidylserine, the major membrane-bound phospholipids, after ischemia both in vitro and in vivo. A reduction in membrane phosphatidylserine by shRNA-mediated knockdown of phosphatidylserine synthetase-1 attenuated Akt activation and neuronal survival after docosahexaenoic acid/eicosapentaenoic acid treatment in the oxygen-glucose deprivation model. Conclusions— n-3 PUFAs robustly protect against H/I-induced brain damage in neonates by activating Akt prosurvival pathway in compromised neurons. In addition, n-3 PUFAs promote the formation of membrane phosphatidylserine, thereby promoting Akt activity and improving cellular survival.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.115.010815
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
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  • 9
    Online Resource
    Online Resource
    Abstract WP168: Regulatory T Cell Transplantation Inhibits Cerebral Endothelial Inflammation In Mice Transient Focal Ischemia.
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Stroke Vol. 44, No. suppl_1 ( 2013-02)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 44, No. suppl_1 ( 2013-02)
    Abstract: INTRODUCTION: Cerebral endothelial cells express large amounts of adhesion molecules, attracting peripheral immune cells to infiltrate into brain parenchyma. Regulatory T cell (Treg) was recently reported as a key cerebroprotective immunomodulator in ischemic stroke. HYPOTHESIS: We assessed the hypothesis that Treg transplantation could protect the ischemic brain from endothelial inflammation via cell-cell interaction. METHODS: Transient focal cerebral ischemia was induced in C57/BL6 mice by unilateral middle cerebral artery occlusion (MCAO) for 60 minutes. Tregs (2x10 6 /mouse) or same numbers of splenocytes were injected intravenously at 2 hours after MCAO. RESULTS: We found that Treg transplantation could inhibit ICAM-1 expression on endothelial cells in vitro by 3.86±0.04 folds (P 〈 0.01) and also at 24 hours after ischemia in vivo, resulting in ameliorated blood brain barrier damage and reduced infiltration of peripheral immune cells, such as T cells, macrophage, and neutrophils. Further study showed that depletion of CCR5 on Tregs reduced the protective effect of Treg transplantation. Real-time PCR demonstrated 134±46 folds (P 〈 0.05) increase of CCL3, the ligand of CCR5 in the ischemic brain at 24 hours after stroke. Immunofluorescence showed that CCL3, possibly released from activated microglia, was closely associated with inflamed endothelial cells. In vitro migration test further revealed that widetype Tregs migrated across the endothelial cell layer towards CCL3; CCR5 -/- Tregs, however, failed to migrate. CONCLUSIONS: In conclusion, Treg transplantation protected the ischemic brain against ICAM-1 experssion on endothelial cells and profoundly inhibited peripheral immune cell infiltration. A novel contributing mechanism was defined that CCR5 and CCL3 mediated recruitment of Tregs to inflamed endothelial cells and played an important role in the cell-cell interaction between Tregs and endothelial cells.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.44.suppl_1.AWP168
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
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  • 10
    Online Resource
    Online Resource
    Coming to the Rescue: Regulatory T Cells for Promoting Recovery After Ischemic Stroke
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Stroke Vol. 52, No. 12 ( 2021-12)
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 52, No. 12 ( 2021-12)
    Abstract: Immune cell infiltration to the injured brain is a key component of the neuroinflammatory response after ischemic stroke. In contrast to the large amount of proinflammatory immune cells, regulatory T cells, are an important subgroup of T cells that are involved in maintaining immune homeostasis and suppress an overshooting immune reaction after stroke. Numerous previous reports have consistently demonstrated the beneficial role of this immunosuppressive immune cell population during the acute phase after experimental stroke by limiting inflammatory lesion progression. Two recent studies expanded now this concept and demonstrate that regulatory T cells-mediated effects also promote chronic recovery after stroke by promoting a proregenerative tissue environment. These recent findings suggest that boosting regulatory T cells could be beneficial beyond modulating the immediate neuroinflammatory response and improve chronic functional recovery.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.121.036072
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1467823-8
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