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  • 1
    Online Resource
    Online Resource
    Correlation of neuronal cell death, functional image and electrical activity after a focal cerebral ischemia in the mouse
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Stroke Vol. 32, No. suppl_1 ( 2001-01), p. 351-351
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. suppl_1 ( 2001-01), p. 351-351
    Abstract: P70 Functional loss and recovery are critical issues after an ischemic insult. The focal ischemia in the cerebral barrel cortex is an ideal model for studying short- and long-term functional alterations of sensory cortex. We extend the “mini-stroke” model from rat to mouse by studying the correlation between neuronal injury and functional activities, intrinsic optical signals (IOS) and evoked potentials in response to whisker stimulation in the ischemic barrel cortex of the mouse. Methods. Adult mice were anesthetized and multiple branches of the middle cerebral artery (MCA) that supply the right side of the barrel cortex were permanently ligated. IOS were used for identifying the barrel cortex; a recording electrode was placed in multiple sites of the barrel cortex in and around the ischemic region. Local cerebral blood flow (LCBF) was measured by Laser Doppler and quantitative autoradiography. Cell injury was determined by immunohistochemistry after the ischemia. Results. Immediately after MCA ligations LCBF was markedly reduced to 10% of control levels followed by simultaneous losses of IOS and evoked potentials in the ischemic side of the cortex. IOS responses and evoked potential were closely matched in all cases. TUNEL positive and/or CM-1 positive cell death and lack of cytochrome oxidase staining in the ischemic core were found 2 days after ischemia and continued for up to 10 days later. With the exception of ischemic injury, IOS image and evoked potential were partially recovered 30 days after the ischemia. Conclusion. The small focal stroke in the mouse barrel cortex shows high reliability for functional assays and their correlation to LCBF. Apoptosis may contribute to the ischemic barrel injury. The functional recovery 30 days after ischemia implies a neurovascular plasticity that is beneficial for long-term rehabilitation after a focal ischemic stroke. Supported by grants from NIH (NS37372) and AHA (IBN-9817151).
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/str.32.suppl_1.351-d
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 1467823-8
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  • 2
    Online Resource
    Online Resource
    Necrosis, apoptosis and hybrid death in the cortex and thalamus after barrel cortex ischemia in rats
    Elsevier BV ; 2004
    In:  Brain Research Vol. 1022, No. 1-2 ( 2004-10), p. 54-61
    Details
    In: Brain Research, Elsevier BV, Vol. 1022, No. 1-2 ( 2004-10), p. 54-61
    Type of Medium: Online Resource
    ISSN: 0006-8993
    URL: Article
    DOI: 10.1016/j.brainres.2004.06.080
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 1462674-3
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Potassium Channel Blockers Attenuate Hypoxia- and Ischemia-Induced Neuronal Death In Vitro and In Vivo
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Stroke Vol. 34, No. 5 ( 2003-05), p. 1281-1286
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 34, No. 5 ( 2003-05), p. 1281-1286
    Abstract: Background and Purpose— In light of recent evidence suggesting that an upregulation of K + efflux mediated by outward delayed rectifier ( I K ) channels promotes central neuronal apoptosis, we sought to test the possibility that blockers of I K channels might be neuroprotective against hypoxia/ischemia-induced neuronal death. Methods— Membrane currents were recorded with the use of patch clamp recordings in cultured murine cortical neurons. Protective effects of K + channel blockers were examined in rats subjected to transient middle cerebral artery occlusion followed by 14-day reperfusion. Results— The K + channel blocker tetraethylammonium (TEA) (5 mmol/L) selectively blocked I K without affecting N -methyl- d -aspartate receptor–mediated current or voltage-gated Ca 2+ currents. Both TEA and a lipophilic K + channel blocker, clofilium, attenuated neuronal apoptosis induced by hypoxia in vitro and infarct volume induced by ischemia in vivo. Conclusions— These data are consistent with the idea that K + channel–mediated K + efflux may contribute to ischemia-triggered apoptosis and suggest that preventing excessive K + efflux through K + channels may constitute a therapeutic approach for the treatment of stroke.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/01.STR.0000065828.18661.FE
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1467823-8
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    Autosomal Dominant Avascular Necrosis of Femoral Head in Two Taiwanese Pedigrees and Linkage to Chromosome 12q13
    Elsevier BV ; 2004
    In:  The American Journal of Human Genetics Vol. 75, No. 2 ( 2004-08), p. 310-317
    Details
    In: The American Journal of Human Genetics, Elsevier BV, Vol. 75, No. 2 ( 2004-08), p. 310-317
    Type of Medium: Online Resource
    ISSN: 0002-9297
    URL: Article
    DOI: 10.1086/422702
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 1473813-2
    SSG: 12
    Location Call Number Limitation Availability
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  • 5
    Online Resource
    Online Resource
    Clinicopathologic Correlation of Serum Tissue Polypeptide Specific Antigen in Hepatocellular Carcinoma
    S. Karger AG ; 2001
    In:  Oncology Vol. 61, No. 1 ( 2001), p. 64-70
    Details
    In: Oncology, S. Karger AG, Vol. 61, No. 1 ( 2001), p. 64-70
    Abstract: 〈 i 〉 Objective: 〈 /i 〉 Recently, tissue polypeptide specific antigen (TPS) has been introduced as a cell proliferation marker. Little is known about its clinical significance in hepatocellular carcinoma (HCC). This study aimed to clarify serum TPS levels and tumor invasiveness of HCC. 〈 i 〉 Methods: 〈 /i 〉 Serum TPS levels were determined with a monoclonal TPS IRMA assay in 69 patients with HCC. A correlation between serum TPS levels and clinical, biochemical, and pathological features was sought and compared with that of α-fetoprotein (AFP). In 57 healthy subjects, 56 patients with biopsy-proven chronic hepatitis and in 49 patients with liver cirrhosis, serum TPS levels were assayed and compared. 〈 i 〉 Results: 〈 /i 〉 Serum TPS levels were significantly correlated with glutamic oxalacetic transaminase (p 〈 0.0001), glutamic pyruvic transaminase (p 〈 0.001), and lactate dehydrogenase (p = 0.027). There tended to be a positive relationship between serum TPS levels and tumor size, histological differentiation, capsular invasion, portal invasion, and clinical staging, although it did not reach statistical significance. A significant correlation, however, was observed between AFP and tumor size (p = 0.01), number (p = 0.042), histological grading (p = 0.028), portal invasion (p = 0.009), and clinical staging (p = 0.03). Patients with HCC had significantly higher TPS than healthy subjects (p 〈 0.001). However, there was substantial overlap between patients with HCC, chronic hepatitis, and liver cirrhosis. 〈 i 〉 Conclusions: 〈 /i 〉 Our data suggest that serum TPS is not significantly related to tumor invasiveness in patients with HCC. Serum TPS levels are affected by the proliferative activity of the underlying chronic liver disease, which is frequently associated with HCC in Chinese patients. As a cell proliferation marker, serum TPS should be interpreted cautiously in the presence of chronic liver disease.
    Type of Medium: Online Resource
    ISSN: 0030-2414 , 1423-0232
    URL: Article
    DOI: 10.1159/000055355
    RVK:
    XH 3305
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2001
    detail.hit.zdb_id: 1483096-6
    detail.hit.zdb_id: 250101-6
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