Development of Hospital Nurses' Job Description based on DACUM Method: Focusing on General Ward and Intensive Care Unit / 간호행정학회지

PURPOSE: This study was done to clarify nurses' duties, tasks and task elements and to develop a job description for clinical nurses on general and intensive care units in tertiary-level hospitals, and dramatically reflect changing medical trends in Korea. METHODS: The job description was developed based on the Developing a Curriculum Method (DACUM). The questionnaire included frequency, importance, and difficulty of duties, tasks and task elements, measured on a 4-point scale. Results were analyzed using SPSS version 21.0. Data were collected from September 4 to 7, 2017, and analyzed using descriptive statistics and a scattered graph. RESULTS: The job description consisted of 10 duties, 38 tasks, and 51 elements. Of the 10 duties, the highest duty in order of importance was ‘Direct nursing care’ followed by ‘Infection control’. The highest duties according to frequency and difficulty were ‘Document and notify’ and ‘Research and quality improvement’. ‘Safety management’ and ‘Infection control’ were considered as relatively simple duties, however, these two duties were still included as important jobs for clinical nurses. CONCLUSION: The job descriptions for clinical nurses developed from this study contain nursing ethics and safety as well as infection control, to faithfully reflect clinical nurses' jobs.

Modulation of SOD1 Subcellular Localization by Transfection with Wild- or Mutant-type SOD1 in Primary Neuron and Astrocyte Cultures from ALS Mice

Amyotrophic lateral sclerosis (ALS) is a fatal neurological disorder characterized by selective degeneration of motor neurons. Mutant superoxide dismutase 1 (SOD1) is often found as aggregates in the cytoplasm in motor neurons of various mouse models and familial ALS patients. The interplay between motor neurons and astrocytes is crucial for disease outcome, but the mechanisms underlying this phenomenon remain unknown. In this study, we investigated whether transient transfection with wild-type and mutant-type SOD1 may lead to amplification of mutant SOD1-mediated toxicity in cortical neurons and astrocytes derived from wild-type and mutant-type (human G93A-SOD1) mice. In transgenic mice expressing either wild- or mutant-type SOD1, we found that green fluorescent protein (GFP)-wtSOD1 was present in the cytoplasm and nuclei of wild-type cortical neurons and astrocytes, whereas GFP-mutant SOD1 was mainly cytoplasmic in wild- and mutant-type cortical neurons and astrocytes. These findings indicate that intracellular propagation of misfolding of GFP-wt or mtSOD1 are possible mediators of toxic processes involved in initiating mislocalization and aggregation. Here, we provide evidence that cytoplasmic aggregates induce apoptosis in G93A-SOD1 mouse cortical neurons and astrocytes and that the toxicity of mutant SOD1 in astrocytes is similar to the pathological effects of ALS on neurons in vitro. Collectively, our results indicate that mtSOD1 probably interacts with wtSOD1 via an unknown mechanism to produce augmented toxicity and may influence aggregate formation and apoptosis.