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Journal of neurochemistry (1)
Journal of the National Medical Association (1)
Bosworth, Hayden B. (1)
Dominick, Kelli L. (1)
Gao, Xuwen (1)
Hsieh, Jason (1)
Hsieh, Jason B. (1)
Liao, Janette (1)
Moser, Barry K. (1)
Steinberg, Gary K. (1)
Takahashi, Tetsuya (1)
Zhang, Hanfeng (1)
Zhao, Heng (1)
Year of Publication
The Akt signaling pathway contributes to postconditioning’s protection against stroke; the protection is associated with the MAPK and PKC pathways
Steinberg, Gary K.
Journal of neurochemistry
We previously reported that ischemic postconditioning with a series of mechanical interruptions of reperfusion reduced infarct volume 2 days after focal ischemia in rats. Here, we extend this data by examining long-term protection and exploring underlying mechanisms involving the Akt, mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) signaling pathways. Post-conditioning reduced infarct and improved behavioral function assessed 30 days after stroke. Additionally, postconditioning increased levels of phosphorylated Akt (Ser473) as measured by western blot and Akt activity as measured by an in vitro kinase assay. Inhibiting Akt activity by a phosphoinositide 3-kinase inhibitor, LY294002, enlarged infarct in postconditioned rats. Postconditioning did not affect protein levels of phosphorylated-phosphatase and tensin homologue deleted on chromosome 10 or -phosphoinositide-dependent protein kinase-1 (molecules upstream of Akt) but did inhibit an increase in phosphorylated-glycogen synthase kinase 3β, an Akt effector. In addition, postconditioning blocked β-catenin phosphorylation subsequent to glycogen synthase kinase, but had no effect on total or non-phosphorylated active β-catenin protein levels. Furthermore, postconditioning inhibited increases in the amount of phosphorylated-c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2 in the MAPK pathway. Finally, postconditioning blocked death-promoting δPKC cleavage and attenuated reduction in phosphorylation of survival-promoting εPKC. In conclusion, our data suggest that postconditioning provides long-term protection against stroke in rats. Additionally, we found that Akt activity contributes to postconditioning’s protection; furthermore, increases in εPKC activity, a survival-promoting pathway, and reductions in MAPK and δPKC activity; two putative death-promoting pathways correlate with postconditioning’s protection.
Akt; cerebral ischemia; mitogen-activated protein kinase; postconditioning; protein kinase C; β-catenin
Racial differences in analgesic/anti-inflammatory medication use and perceptions of efficacy.
Dominick, Kelli L.
Bosworth, Hayden B.
Moser, Barry K.
Journal of the National Medical Association
BACKGROUND AND OBJECTIVE: Pharmacotherapy is a key component to osteoarthritis (OA) treatment. Research has shown important racial differences in pain thresholds and perceptions, but little is known about racial variations in responses to pain medications. The purpose of this study was to compare perceptions of efficacy of pain medications among African-American and Caucasian veterans with OA. METHODS: Participants (N = 202; 70% Caucasian, 30% African-American) were under care for OA within the VA healthcare system. Participants rated the helpfulness of current analgesic/anti-inflammatory medications (scale of 1--not at all helpful to 10--very helpful). RESULTS: The mean rating of medication helpfulness was 6.1. African-American participants reported significantly greater ratings of medication helpfulness than Caucasians (6.6 vs. 5.9), controlling for demographics, disease severity, total number of analgesic/anti-inflammatory medications being taken, and the class of the medication. CONCLUSION: African Americans had somewhat more favorable perceptions of medication helpfulness than Caucasians. However, overall ratings of medication helpfulness were relatively low. Further research is needed to examine whether modifiable factors (such as low dosing or patient nonadherence to prescription instructions) contribute to perceptions of poor efficacy.
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