[Increasing the Rate of Completion of the Therapeutic Hypothermia Procedure in the NICU].

BACKGROUND & PROBLEMS: The most effective treatment currently available for perinatal asphyxia-induced hypoxic-ischemic encephalopathy is therapeutic hypothermia, which reduces the mortality rate and neurological disorders in newborns. The earlier this therapy is performed, the better the protective effects on the nerves of the patient. In our neonatal intensive care unit (NICU), we discovered that nurses lack experience caring for patients undergoing hypothermia therapy due to the limited number of cases. In addition, outdated guidelines, the disorganized placement of equipment, and the paucity of hands-on simulations exacerbate the unfamiliarity of the nurses with this therapy. PURPOSE: To expand the knowledge of nurses regarding therapeutic hypothermia in the NICU and to increase the rate of completion of the therapeutic hypothermia procedure. RESOLUTIONS: 1. Regular care training programs and scenario-based simulations were conducted to help nurses obtain related knowledge and become more familiar with therapeutic hypothermia. 2. In order to reduce the preparation time, a specific preparation kit and an instruction folder for therapeutic hypothermia was developed that included a material placement checklist. 3. The procedure guidance booklet for therapeutic hypothermia was revised and a monitoring system was established. RESULTS: The accuracy of nurses' knowledge regarding therapeutic hypothermia in the NICU improved from 82.0% to 94.5%. The completion rate for the therapeutic hypothermia procedure rose from 75.6% to 100.0%. CONCLUSIONS: This project successfully enhanced the accuracy of nurses' knowledge regarding therapeutic hypothermia and increased the rate of completion for this care procedure, resulting in a safer and more-standardized procedure for neonates undergoing therapeutic hypothermia.

Induction of tubulin by docetaxel is associated with p53 status in human non small cell lung cancer cell lines.

Docetaxel (DOC), a member of the taxane family of anticancer drugs, binds to tubulin and produces unnaturally stable microtubules that induce cell death. DOC is used clinically alone or in combination with other compounds to treat advanced stages of cancer. We have treated the human lung cancer cell lines A549 and H1299 and human cervical cancer HeLa cells with low concentrations of DOC to characterize the response of beta-tubulin isotypes and p53 genes. The relationship between p53 function and DOC, acting through a microtubule-based mechanism, was examined. We found that after 18-hr treatment with DOC, beta-tubulin gene transcription was enhanced in p53-null H1299 cells but not in A549 cells. Also, p53 RNA was strongly induced in the A549 cells. In addition, beta-tubulin levels also increased in the H1299 cells after the DOC treatment. Further demonstrating an association of DOC treatment with p53 and beta-tubulin, inhibition of p53 expression by interference RNA in A549 cells showed increasing beta-tubulin gene expression with DOC treatment. We also selected a clone from the H1299 cells that stably expressed p53, examined the beta-tubulin expression after DOC treatment and found an inhibition of beta-tubulin induction in these p53-expressing cells. Our data suggest that the initial response of cells to DOC treatment involves p53; alternatively, in the absence of p53, tubulins may be transactivated. Selection of the DOC-resistant A549 cells showed beta-tubulin expression was increased, in contrast to the initial response to the DOC treatment. From the initial and selection responses of beta-tubulin in cancer cells, it appears that there is a p53-associated beta-tubulin expression as a result of the DOC treatment.