Even within a hospital, the prognosis after a cardiac arrest is extremely poor if intervention starts only after the event; thus, early recognition and intervention is crucial to reduce inhospital cardiac arrests. This paper aims to assess the results of in-clinic surveys conducted for the implementation of the Rapid Response System (RRS) at our hospital and changes in awareness after awareness initiatives. Excluding the neonatal intensive care unit, all wards were targeted for implementation, with the creation of criteria for requesting the RRS and hospital-wide awareness initiatives. Four items were defined for the request criteria—namely, (1) respiration, (2) circulation, (3) state of consciousness, and (4) others (any concerns)—with a request being warranted if any one of these criteria was met. A pre-awareness survey revealed that respiratory rates were recorded only 6.9% of the time on average, indicating inadequate observation of respiratory rates across all wards. In response to this issue, we announced that respiratory status should be observed at least once a day, which resulted in the recording rate improving to 68.2% after 2 months. Survey results before and after the awareness initiatives among doctors and nurses showed a significant increase in RRS awareness. The percentage of nurses who answered “well aware” or “somewhat aware” increased from 34.8% to 77.6%, and from 63.4% to 88.0% among doctors. However, while the introduction of the RRS was relatively well-received by nurses struggling with on-site responses, some doctors questioned the necessity of the RRS. Upon implementation, it is important to make it known that it is a hospital-wide effort. Simplifying and thoroughly utilizing the request criteria can lead to early recognition of abnormalities. Since it is not easy to gain doctors’ understanding, it is necessary to listen to the needs and requests of each department and patiently continue awareness activities before implementation

Objective: Signal transducer and activator of transcription 3 (STAT3) plays key roles in regulating cancer cell proliferation, survival, and metastasis. We aimed to determine the effects of YHO-1701, an oral STAT3 inhibitor, in ovarian cancer (OC). Methods: We evaluated the impact of YHO-1701 on cell growth in patient-derived cells (PDCs) and OC cell lines using standard cell proliferation assays. Spheroid models derived from PDCs were assessed using three-dimensional (3D) cell viability assays. Antitumor activity was performed in SKOV3 xenograft mice treated orally administrated YHO-1701 with 20 mg/kg.Changes in STAT3 signaling were analyzed by western blotting. The molecular mechanisms of STAT3 inhibition were investigated by sequencing RNA and analyzing pathways in the SKOV3 using a small interfering RNA targeting STAT3 (STAT3 siRNA) and YHO-1701. Results: YHO-1701 inhibited the growth of OC cell lines by preventing STAT3 dimerization and decreasing the expression of its downstream signaling molecule, survivin. The growth of PDCs and spheroids obtained from patients with primary and recurrent OCs was significantly inhibited. Antitumor effect was observed in the SKOV3 xenograft mice with YHO-1701. YHO-1701 induced apoptosis in OC cells. Additionally, p53 and/or MAPK signaling pathways were upregulated in SKOV3 cells incubated with YHO-1701 and in those with STAT3 siRNA. Conclusion Our results showed that YHO-1701 suppressed cell growth in PDCs of OC, accompanied by survivin inhibition, and a decrease in the number of peritoneal metastasis in the mice by YHO-1701, compared with those treated with control. Therefore, YHO-1701 could be a promising candidate agent for treating OC