11 research outputs found

    Phosphodiesterase III inhibitor promotes drainage of cerebrovascular β-amyloid

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    The predominant action of cilostazol on Aβ metabolism is likely to facilitate Aβ clearance due to the sustained cerebrovascular function in vivo. Our findings mechanistically demonstrate that cilostazol is a promising therapeutic approach for AD and CAA

    Urinary Frequency as a Presentation of Bulky Malignant Lymphoma in the Pelvis

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    Malignant lymphomas may originate from any area of the body and cause a variety of symptoms. However, a malignant lymphoma causing urinary symptoms is uncommon. We report a unique case of a 77-year-old woman who presented with a persistent pollakiuria. Radiographic imaging showed a large pelvic mass ( cm) remarkably compressing and invading the bladder wall and accompanied with bilateral hydronephrosis. Urinary cytology revealed malignant lymphoma, and a final diagnosis of malignant lymphoma was made on the basis of transvaginal needle biopsy. Urinary cytology facilitated the definite diagnosis, following which we initiated a rapid and successful treatment with cyclophosphamide, doxorubicin, vincristine, and prednisone with rituximab

    Activation of NR2A receptors induces ischemic tolerance through CREB signaling

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    Previous exposure to a nonlethal ischemic insult protects the brain against subsequent harmful ischemia. N-methyl--aspartate (NMDA) receptors are a highly studied target of neuroprotection after ischemia. Recently, NMDA receptor subtypes were implicated in neuronal survival and death. We focused on the contribution of NR2A and cyclic-AMP response element (CRE)-binding protein (CREB) signaling to ischemic tolerance using primary cortical neurons. Ischemia in vitro was modeled by oxygen–glucose deprivation (OGD). Ischemic tolerance was induced by applying 45-mins OGD 24 h before 180-mins OGD. Sublethal OGD also induced cross-tolerance against lethal glutamate and hydrogen peroxide. After sublethal OGD, expression of phosphorylated CREB and CRE transcriptional activity were significantly increased. When CRE activity was inhibited by CREB-S133A, a mutant CREB, ischemic tolerance was abolished. Inhibiting NR2A using NVP-AAM077 attenuated preconditioning-induced neuroprotection and correlated with decreased CRE activity levels. Activating NR2A using bicuculline and 4-aminopiridine induced resistance to lethal ischemia accompanied by elevated CRE activity levels, and this effect was abolished by NVP-AAM077. Elevated brain-derived neurotrophic factor (BDNF) transcriptional activities were observed after sublethal OGD and administration of bicuculline and 4-aminopiridine. NR2A-containing NMDA receptors and CREB signaling have important functions in the induction of ischemic tolerance. This may provide potential novel therapeutic strategies to treat ischemic stroke
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