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Hye-Yeon Choi

Publications and source records attributed to Hye-Yeon Choi.

2 recordsLinked to original sources

Improved time intervals by implementation of computerized physician order entry-based stroke team approach.

BACKGROUND: The need for rapid evaluation and treatment of acute stroke patients has been well documented. A computerized physician order entry (CPOE) system can improve communication and provide immediate access to information, which may be useful for an effective team approach program targeted to reduce in-hospital time delays. METHODS: To reduce the time from a patient's arrival at the emergency department to thrombolysis, a team approach program using CPOE was developed, and its efficacy was investigated by comparing time intervals from arrival to evaluation and intravenous tissue-type plasminogen activator (tPA) treatment before and after the implementation of the program. RESULTS: Among 379 consecutive patients who were screened as potential candidates for thrombolysis, 25 patients (6.6%) received tPA during a 1-year period after initiation of the program. Fourteen patients were treated with tPA in the previous year. After program implementation, time from arrival to computed tomography scan was reduced from 34 to 19 min (p = 0.01). Time to report of complete blood count was also shortened from 52 to 33 min (p < 0.01). Finally, time from arrival to tPA treatment was reduced by 23 min (from 79 to 56 min; p < 0.01). Onset-to-door time tended to be longer after the program implementation (from 41 to 60 min; p = 0.14). CONCLUSIONS: Implementation of the CPOE-based team approach program significantly reduced time from emergency department arrival to evaluations and treatment.

Acute Disease↗

Interplay between PI3K/Akt and MAPK signaling pathways in DNA-damaging drug-induced apoptosis.

In order to elucidate the role of the mitogen-activated protein kinases, including JNK, p38 MAPK and ERK, as well as the survival-associated PI3K/Akt signaling pathway, in the response to chemotherapy, we have conducted a comparative study regarding the effects of doxorubicin on these pathways. Doxorubicin was determined to elicit the apoptosis of NIH3T3 cells in a dose-dependent manner. Prior to cell death, both Akt and p38 MAPK were transiently activated, and subsequently inactivated almost wholly, whereas ERK and JNK evidenced sustained activations in response to the drug treatment. The inhibition of PI3K/Akt and p38 MAPK both accelerated and enhanced doxorubicin-induced apoptosis and ERK inhibition apparently exerted negative effect on apoptosis. The modulation of PI3K/Akt activation by treatment of LY294002 or expression of Akt mutants such as Akt-DN or Myr-Akt exerted a significant effect on the activation of ERK1/2. We also observed that PI3K/Akt and sustained ERK activation were associated intimately with the etoposide-induced apoptosis. Taken together, our results clearly suggest that the differential regulation of the PI3K/Akt, ERK1/2, and p38 MAPK signaling pathways are crucial in the context of DNA-damaging drug-induced apoptosis, and this has compelled us to propose that the sustained activation of ERK1/2 pathway may be generally involved in the apoptosis induced by anticancer DNA-damaging drugs, including doxorubicin and etoposide.

Animals↗