Saiseikai Yokohama-shi Nanbu Hospital has been charging an additional fee for enhanced collaboration for surgical patients concerning outpatient cancer drug chemotherapy since March 2022. In this survey, we compared the number of consultations and pharmacological interventions performed by pharmacists for target and non-target departments from September 2021 to February 2022 before the calculation began, and from March to August 2022 after the calculation started. In the target department, the number of consultations was 1.5±1.3 and 8.1±4.8 per day for before and after the calculation began, respectively, showing a significant increase (P<0.001). The number of pharmacological interventions increased from 35 preoperatively to 66 postoperatively. However, in the non-target departments, there was no change in the number of consultations and pharmacological interventions between before and after the calculation started. The results suggest that the additional fee for enhanced collaboration effectively enables pharmacists to continuously intervene in pharmacological problems.

Objective To assess the effect of D-JNKI1, an inhibitor of c-Jun N-terminal kinase (JNK), on delayed neuronal death (DND) in a gerbil model of transient global cerebral ischemia, so as to further study the roles of JNK activation in mediating neuronal cell death in brain ischemia. Methods Fifty-five Mongolian gerbils were randomly divided into 11 groups. Animals (n=35) assigned into 7 groups (n=5 per group) were subjected to 5-min occlusion of bilateral common carotid arteries (BCCAO);among the 7 groups, different doses of D-JNKI1 (0.00012, 0.0012, 0.012, 0.12, 1.2 μmol/L in 2 μL PBS,n=5 each) were administered stereotaxically into right lateral ventricles 3 h after reperfusion; the control group (n=5) received 2 μL PBS; and another group (n=5) received 1.2 μmol/L of D-JNKI1 in 0.5 mL PBS intraperitoneally. Sham-operated animals (n=5) only received the exposure of bilateral common carotid arteries without occlusion. Three groups (n=5 in each) were pretreated with D-JNKI1 (0.00012,0.0012 μmol/L in 2 μL PBS) or only 2 μL PBS 30 min before 2-min BCCAO, and subjected to 5-min BCCAO 48 h after the first ischemic insult. All animals were sacrificed 4 d after 5-min BCCAO and prepared for frozen section and Nissl staining. Results The treatment with D-JNKI 3 h after 5-min ischemia was neuroprotective with a maximum effect at a dose of 0.0012 μmol/L. Pretreatment with D-JNKI augmented ischemic tolerance induced by 2-min ischemia. Conclusion D-JNKI1 has a potential neuroprotective effect on DND in CA1 of hippocampus in gerbils with global cerebral ischemia-reperfusion injury.