[Efforts of the dementia support care team at the cardiovascular institute].

OBJECTIVE: Evaluation the activities of the dementia support care team (D-CAST). METHOD: A total of 350 patients received intervention from the D-CAST from January 1, 2017, to December 31, 2017. At the beginning and end of the team intervention, the following items were evaluated: changes in the degree of life independence, period (days) from hospitalization to team intervention, request for team intervention, and duration of hospitalization. RESULTS: The average age of the 350 patients in this study was 81±9 years old. The major diseases causing hospitalization were heart failure in 94 patients (27%) and aortic valve disease for transcatheter aortic valve implantation (TAVI) in 45 patients (13%). The main reasons for requesting team intervention were cognitive impairment in 40% and delirium (prevention included) in 36%. Regarding the change in the degree of life independence, 29 people saw improvement (16%), 165 maintained their degree of independence (66%), and 46 experienced a decrease (18%). The team intervention was delayed as criteria for degree of independence of everyday life was lower for mild patients. CONCLUSION: We need to learn how to assess dementia patients with relatively mild life independence (potentially including mild cognitive impairment).

Skb5, an SH3 adaptor protein, regulates Pmk1 MAPK signaling by controlling the intracellular localization of the MAPKKK Mkh1.

The mitogen-activated protein kinase (MAPK) cascade is a highly conserved signaling module composed of MAPK kinase kinases (MAPKKKs), MAPK kinases (MAPKK) and MAPKs. The MAPKKK Mkh1 is an initiating kinase in Pmk1 MAPK signaling, which regulates cell integrity in fission yeast (Schizosaccharomyces pombe). Our genetic screen for regulators of Pmk1 signaling identified Shk1 kinase binding protein 5 (Skb5), an SH3-domain-containing adaptor protein. Here, we show that Skb5 serves as an inhibitor of Pmk1 MAPK signaling activation by downregulating Mkh1 localization to cell tips through its interaction with the SH3 domain. Consistent with this, the Mkh1(3PA) mutant protein, with impaired Skb5 binding, remained in the cell tips, even when Skb5 was overproduced. Intriguingly, Skb5 needs Mkh1 to localize to the growing ends as Mkh1 deletion and disruption of Mkh1 binding impairs Skb5 localization. Deletion of Pck2, an upstream activator of Mkh1, impaired the cell tip localization of Mkh1 and Skb5 as well as the Mkh1-Skb5 interaction. Interestingly, both Pck2 and Mkh1 localized to the cell tips at the G1/S phase, which coincided with Pmk1 MAPK activation. Taken together, Mkh1 localization to cell tips is important for transmitting upstream signaling to Pmk1, and Skb5 spatially regulates this process.