Communication between physicians, patients, their companions and other healthcare professionals in home medical care in Japan.

OBJECTIVE: To examine communication in home medical care. METHODS: Conversations that happened during home medical care involving physicians at nine clinics were recorded and analyzed using the Roter Interaction Analysis System (RIAS). Additional categories were developed to code aspects of home medical care. RESULTS: Overall, 55 conversations were analyzed. The mean age of the patients was 82.9 ± 10.1 years old. The most common triad was physician, patient, and patient's companion. Information about home medical care professionals who were not present during the conversation was provided by the physician in 21 cases (38.2%), the patient in nine cases (16.4%), and companions in 21 (39.6%) cases. CONCLUSION: In home medical care, the participants mentioned home medical care professions who were not present at the time, suggesting that these conversations may have facilitated interprofessional collaboration. PRACTICE IMPLICATIONS: Physicians should be aware that during home medical care, the presence of multiple attendants and other medical professionals contributing to communicate with the patient.

ASK1 and ASK2 differentially regulate the counteracting roles of apoptosis and inflammation in tumorigenesis.

Apoptosis and inflammation generally exert opposite effects on tumorigenesis: apoptosis serves as a barrier to tumour initiation, whereas inflammation promotes tumorigenesis. Although both events are induced by various common stressors, relatively little is known about the stress-induced signalling pathways regulating these events in tumorigenesis. Here, we show that stress-activated MAP3Ks, ASK1 and ASK2, which are involved in cellular responses to various stressors such as reactive oxygen species, differentially regulate the initiation and promotion of tumorigenesis. ASK2 in cooperation with ASK1 functioned as a tumour suppressor by exerting proapoptotic activity in epithelial cells, which was consistent with the reduction in ASK2 expression in human cancer cells and tissues. In contrast, ASK1-dependent cytokine production in inflammatory cells promoted tumorigenesis. Our findings suggest that ASK1 and ASK2 are critically involved in tumorigenesis by differentially regulating apoptosis and inflammation.

ASK1 promotes the contact hypersensitivity response through IL-17 production.

Contact hypersensitivity (CHS) is a form of delayed-type hypersensitivity triggered by the response to reactive haptens (sensitization) and subsequent challenge (elicitation). Here, we show that ASK1 promotes CHS and that suppression of ASK1 during the elicitation phase is sufficient to attenuate CHS. ASK1 knockout (KO) mice exhibited impaired 2,4-dinitrofluorobenzene (DNFB)-induced CHS. The suppression of ASK1 activity during the elicitation phase through a chemical genetic approach or a specific inhibitory compound significantly reduced the CHS response to a level similar to that observed in ASK1 KO mice. The reduced response was concomitant with the strong inhibition of production of IL-17, a cytokine that plays an important role in CHS and other inflammatory diseases, from sensitized lymph node cells. These results suggest that ASK1 is relevant to the overall CHS response during the elicitation phase and that ASK1 may be a promising therapeutic target for allergic contact dermatitis and other IL-17-related inflammatory diseases.