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  • Ovid Technologies (Wolters Kluwer Health)  (382)
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  • 1
    Online Resource
    Online Resource
    Methodological study on real-time three-dimensional echo cardiography and its application in the diagnosis of complex congenital heart disease
    Ovid Technologies (Wolters Kluwer Health) ; 2006
    In:  Chinese Medical Journal Vol. 119, No. 14 ( 2006-07), p. 1190-1194
    Details
    In: Chinese Medical Journal, Ovid Technologies (Wolters Kluwer Health), Vol. 119, No. 14 ( 2006-07), p. 1190-1194
    Type of Medium: Online Resource
    ISSN: 0366-6999
    URL: Article
    DOI: 10.1097/00029330-200607020-00009
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2006
    detail.hit.zdb_id: 2108782-9
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  • 2
    Online Resource
    Online Resource
    Association between ABCB1 (3435C〉T) polymorphism and susceptibility of colorectal cancer : A meta-analysis
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Medicine Vol. 99, No. 8 ( 2020-02), p. e19189-
    Details
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 99, No. 8 ( 2020-02), p. e19189-
    Abstract: Studies on the relationship between ABCB1 3435C 〉 T polymorphism (rs1045642) and colorectal cancer (CRC)susceptibility have yielded inconclusive results. To clarify this issue, we undertook a meta-analysis to investigate the relationship between rs1045642 and CRC risk. Three electronic scientific publication databases (Cochrane Library, Pubmed, Embase) were screened using specific search terms. Relevant literature was identified using literature traceability methods. Selected publications were evaluated according to the inclusion and exclusion criteria. Effect size information (odds ratio and the corresponding 95% confidence interval [CI]) was obtained following quality assessment and data extraction from the included publications, and a meta-analysis conducted. Statistical analysis was performed with the Stata sofz (Version 13.0) software. Overall, 17 case-control studies involving 7129 CRC patients and 7710 healthy control subjects satisfied the criteria for inclusion in the meta-analysis. There was no significant association between ABCB1 3435C 〉 T polymorphism and CRC risk in any of the genetic models. In the CC versus CT model ( I 2  = 20.9%, P heterogeneity  = .276), CC versus CT + TT model ( I 2  = 45.6%, P heterogeneity  = .102) and CT versus CC + TT model ( I 2  = 17.8%, P heterogeneity  = .298) analyses, between-study heterogeneities were detected as significant in Asian populations. In the CT versus TT model ( I 2  = 24%, P heterogeneity  = .254) and CC + CT versus TT model ( I 2  = 0, P heterogeneity  = .55), between-study heterogeneities were found to be significant in groups of different populations. The meta-analysis described here suggests that the ABCB1 3435C 〉 T polymorphism is not related to CRC susceptibility.
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    URL: Article
    DOI: 10.1097/MD.0000000000019189
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2049818-4
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  • 3
    Online Resource
    Online Resource
    Macrophage-Inducible C-Type Lectin/Spleen Tyrosine Kinase Signaling Pathway Contributes to Neuroinflammation After Subarachnoid Hemorrhage in Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Stroke Vol. 46, No. 8 ( 2015-08), p. 2277-2286
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 46, No. 8 ( 2015-08), p. 2277-2286
    Abstract: Macrophage-inducible C-type lectin (Mincle, CLEC4E) receptor is reported involved in neuroinflammation in cerebral ischemia and traumatic brain injury. This study was designed to investigate the role of Mincle and its downstream spleen tyrosine kinase (Syk) signal pathway in early brain injury after subarachnoid hemorrhage (SAH) in a rat model. Methods— Two hundred fifteen male Sprague-Dawley rats (280–320 g) were subjected to endovascular perforation model of SAH. SAH grade, neurological score, and brain water content were measured at 24 hours after SAH. Mincle/Syk, as well as CARD9 (a member of the caspase-associated recruitment domain [CARD], involved in innate immune response), interleukin-1β,and myeloperoxidase expressions were analyzed by Western blot at 24 hours after SAH. Specific cell types that expressed Mincle were detected with double immunofluorescence staining. Mincle small interfering RNA, recombinant SAP130, and a selective Syk phosphorylation inhibitor piceatannol were used for intervention. Results— Brain water content increased and neurological functions decreased in rats after SAH. The expression of SAP130, Mincle, Syk, and p-Syk increased at 12 hours and peaked at 24 hours after SAH. Mincle small interfering RNA reduced interleukin-1β and infiltration of myeloperoxidase positive cells, decreased brain water content, and improved neurological functions at 24 hours after SAH. Recombinant SAP130 upregulated the expression of p-Syk and CARD9 and increased the levels of interleukin-1β and myeloperoxidase, even though it did not increase brain water content nor it deteriorated neurological function at 24 hours after SAH. Syk inhibitor piceatannol reduced brain edema at 24 hours after SAH. Conclusion— Mincle/Syk is involved in early brain injury after SAH, and they may serve as new targets for therapeutic intervention.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.115.010088
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1467823-8
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  • 4
    Online Resource
    Online Resource
    Reader response: Sauna bathing reduces the risk of stroke in Finnish men and women: A prospective cohort study
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Neurology Vol. 92, No. 4 ( 2019-01-22), p. 204.2-204
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 4 ( 2019-01-22), p. 204.2-204
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000006807
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
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  • 5
    Online Resource
    Online Resource
    Changes in cerebral autoregulation and blood biomarkers after remote ischemic preconditioning
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Neurology Vol. 93, No. 1 ( 2019-07-02), p. e8-e19
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 93, No. 1 ( 2019-07-02), p. e8-e19
    Abstract: To determine the effect of remote ischemic preconditioning (RIPC) on dynamic cerebral autoregulation (dCA) and various blood biomarkers in healthy adults. Methods A self-controlled interventional study was conducted. Serial measurements of dCA were performed at 7 time points (7, 9, and 11 am; 2, 5, and 8 pm , and 8 am on the next day) without or with RIPC, carried out at 7:20 to 8 am . Venous blood samples were collected at baseline (7 am ) and 1 hour after RIPC, and blood biomarkers, including 5 neuroprotective factors and 25 inflammation-related biomarkers, were measured with a quantitative protein chip. Results Fifty participants were enrolled (age 34.54 ± 12.01 years, 22 men). Compared with the results on the day without RIPC, dCA was significantly increased at 6 hours after RIPC, and the increase was sustained for at least 24 hours. After RIPC, 2 neuroprotective factors (glial cell-derived neurotrophic factor and vascular endothelial growth factor-A) and 4 inflammation-related biomarkers (transforming growth factor-β1, leukemia inhibitory factor, matrix metallopeptidase-9, and tissue inhibitor of metalloproteinase-1) were significantly elevated compared with their baseline levels. Conversely, monocyte chemoattractant protein-1 was significantly lower compared with its baseline level. Conclusions RIPC induces a sustained increase of dCA from 6 to at least 24 hours after treatment in healthy adults. In addition, several neuroprotective and inflammation-related blood biomarkers were differentially regulated shortly after RIPC. The increased dCA and altered blood biomarkers may collectively contribute to the beneficial effects of RIPC on cerebrovascular function. ClinicalTrials.gov identifier: NCT02965547.
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000007732
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
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    Online Resource
  • 6
    Online Resource
    Online Resource
    Treatment of traumatic brain injury in rats with transplantation of human amniotic cells
    Ovid Technologies (Wolters Kluwer Health) ; 2006
    In:  Chinese Medical Journal Vol. 119, No. 21 ( 2006-11), p. 1843-1845
    Details
    In: Chinese Medical Journal, Ovid Technologies (Wolters Kluwer Health), Vol. 119, No. 21 ( 2006-11), p. 1843-1845
    Type of Medium: Online Resource
    ISSN: 0366-6999
    URL: Article
    DOI: 10.1097/00029330-200611010-00014
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2006
    detail.hit.zdb_id: 2108782-9
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  • 7
    Online Resource
    Online Resource
    Lipoxin A4 Reduces Inflammation Through Formyl Peptide Receptor 2/p38 MAPK Signaling Pathway in Subarachnoid Hemorrhage Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Stroke Vol. 47, No. 2 ( 2016-02), p. 490-497
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 47, No. 2 ( 2016-02), p. 490-497
    Abstract: Lipoxin A4 (LXA4) has been reported to reduce inflammation in several neurological injury models. We studied the effects of LXA4 on neuroinflammation after subarachnoid hemorrhage (SAH) in a rat model. Methods— Two hundred and thirty-eight Sprague–Dawley male rats, weight 280–320 g, were used. Exogenous LXA4 (0.3 and 1.0 nmol) were injected intracerebroventricularly at 1.5 hours after SAH. Neurological scores, brain water content, and blood–brain barrier were evaluated at 24 hours after SAH; Morris water maze and T-maze tests were examined at 21 days after SAH. The expression of endogenous LXA4 and its receptor formyl peptide receptor 2 (FPR2), as well as p38, interleukin-1β, and interleukin-6 were studied either by ELISA or by Western blots. Neutrophil infiltration was observed by myeloperoxidase staining. FPR2 siRNA was used to knock down LXA4 receptor. Results— The expression of endogenous LXA4 decreased, and the expression of FPR2 increased after SAH. Exogenous LXA4 decreased brain water content, reduced Evans blue extravasation, and improved neurological functions and improved the learning and memory ability after SAH. LXA4 reduced neutrophil infiltration and phosphorylation of p38, interleukin-1β, and interleukin-6. These effects of LXA4 were abolished by FPR2 siRNA. Conclusions— Exogenous LXA4 inhibited inflammation by activating FPR2 and inhibiting p38 after SAH. LXA4 may serve as an alternative treatment to relieve early brain injury after SAH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.115.011223
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467823-8
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  • 8
    Online Resource
    Online Resource
    Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD + /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Stroke Vol. 48, No. 6 ( 2017-06), p. 1655-1664
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 48, No. 6 ( 2017-06), p. 1655-1664
    Abstract: Energy depletion is a critical factor leading to cell death and brain dysfunction after ischemic stroke. In this study, we investigated whether energy depletion is involved in hyperglycemia-induced hemorrhagic transformation after ischemic stroke and determined the pathway underlying the beneficial effects of hyperbaric oxygen (HBO). Methods— After 2-hour middle cerebral artery occlusion, hyperglycemia was induced by injecting 50% dextrose (6 mL/kg) intraperitoneally at the onset of reperfusion. Immediately after it, rats were exposed to HBO at 2 atmospheres absolutes for 1 hour. ATP synthase inhibitor oligomycin A, nicotinamide phosphoribosyl transferase inhibitor FK866, or silent mating type information regulation 2 homolog 1 siRNA was administrated for interventions. Infarct volume, hemorrhagic volume, and neurobehavioral deficits were recorded; the level of blood glucose, ATP, and nicotinamide adenine dinucleotide and the activity of nicotinamide phosphoribosyl transferase were monitored; the expression of silent mating type information regulation 2 homolog 1, acetylated p53, acetylated nuclear factor-κB, and cleaved caspase 3 were detected by Western blots; and the activity of matrix metalloproteinase-9 was assayed by zymography. Results— Hyperglycemia deteriorated energy metabolism and reduced the level of ATP and nicotinamide adenine dinucleotide and exaggerated hemorrhagic transformation, blood–brain barrier disruption, and neurological deficits after middle cerebral artery occlusion. HBO treatment increased the levels of the ATP and nicotinamide adenine dinucleotide and consequently increased silent mating type information regulation 2 homolog 1, resulting in attenuation of hemorrhagic transformation, brain infarction, as well as improvement of neurological function in hyperglycemic middle cerebral artery occlusion rats. Conclusions— HBO induced activation of ATP/nicotinamide adenine dinucleotide/silent mating type information regulation 2 homolog 1 pathway and protected blood–brain barrier in hyperglycemic middle cerebral artery occlusion rats. HBO might be promising approach for treatment of acute ischemic stroke patients, especially patients with diabetes mellitus or treated with r-tPA (recombinant tissue-type plasminogen activator).
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.116.015753
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1467823-8
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  • 9
    Online Resource
    Online Resource
    Hyperbaric Oxygen Preconditioning Attenuates Hemorrhagic Transformation Through Reactive Oxygen Species/Thioredoxin-Interacting Protein/Nod-Like Receptor Protein 3 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Critical Care Medicine Vol. 44, No. 6 ( 2016-06), p. e403-e411
    Details
    In: Critical Care Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 44, No. 6 ( 2016-06), p. e403-e411
    Abstract: To clarify whether hyperbaric oxygen preconditioning can attenuate hyperglycemia-enhanced hemorrhagic transformation and to establish a role for Nod-like receptor protein 3 inflammasome in the pathophysiology of hemorrhagic transformation. Design: Controlled prospective animal study. Setting: University research laboratory. Subjects: Male Sprague-Dawley rats weighing 260–280 g. Interventions: Rats received 1-hour-long hyperbaric oxygen preconditioning for five consecutive days. Hyperglycemic middle cerebral artery occlusion model was induced at 24 hours after the last hyperbaric oxygen exposure. Reactive oxygen species scavenger (N-acetyl- l -cysteine), thioredoxin-interacting protein small interfering RNA, and Nod-like receptor protein 3 small interfering RNA were given in different groups separately to verify the possible pathway. Measurements and Main Results: Rats were randomly divided into sham, middle cerebral artery occlusion, middle cerebral artery occlusion + dextrose, middle cerebral artery occlusion + dextrose + normobaric oxygen preconditioning, middle cerebral artery occlusion + dextrose + hyperbaric oxygen, middle cerebral artery occlusion + dextrose + hyperbaric oxygen + N-acetyl- l -cysteine, middle cerebral artery occlusion + dextrose + hyperbaric oxygen + control small interfering RNA, middle cerebral artery occlusion + dextrose + hyperbaric oxygen + thioredoxin-interacting protein small interfering RNA, and middle cerebral artery occlusion + dextrose + hyperbaric oxygen + Nod-like receptor protein 3 small interfering RNA groups. Hyperglycemia was induced by administration of 50% dextrose (6 mL/kg) intraperitoneally 30 minutes before middle cerebral artery occlusion. Control small interfering RNA/thioredoxin-interacting protein small interfering RNA or Nod-like receptor protein 3 small interfering RNA (500 pmol/5 μL) were injected intracerebroventricularly 72 hours before middle cerebral artery occlusion for intervention. The neurologic scores, infarction and hemorrhage volumes, the expression of Nod-like receptor protein 3, and its downstream targets were analyzed. Hyperbaric oxygen preconditioning decreased both infarction and hemorrhage volumes and improved neurobehavioral function. In addition, hyperbaric oxygen preconditioning provided additional protective effects in hemorrhagic transformation, which was independent of infarction volume. The benefits of hyperbaric oxygen preconditioning on hyperglycemic middle cerebral artery occlusion rats were reversed after blocking the reactive oxygen species/thioredoxin-interacting protein/Nod-like receptor protein 3 pathway. Conclusions: Nod-like receptor protein 3 inflammasome played an important role in hyperglycemia-enhanced hemorrhagic transformation. Hyperbaric oxygen preconditioning attenuated hemorrhagic transformation through reactive oxygen species/thioredoxin-interacting protein/Nod-like receptor protein 3 pathway.
    Type of Medium: Online Resource
    ISSN: 0090-3493
    URL: Article
    DOI: 10.1097/CCM.0000000000001468
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2034247-0
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  • 10
    Online Resource
    Online Resource
    Transplantation of human amniotic epithelial cells improves hindlimb function in rats with spinal cord injury
    Ovid Technologies (Wolters Kluwer Health) ; 2006
    In:  Chinese Medical Journal Vol. 119, No. 24 ( 2006-12), p. 2101-2107
    Details
    In: Chinese Medical Journal, Ovid Technologies (Wolters Kluwer Health), Vol. 119, No. 24 ( 2006-12), p. 2101-2107
    Type of Medium: Online Resource
    ISSN: 0366-6999
    URL: Article
    DOI: 10.1097/00029330-200612020-00013
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2006
    detail.hit.zdb_id: 2108782-9
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