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Additional file 5. Detailed description of SEM analysis for the primary care and patient loyalty.

Additional file 3. Developed Questionnaire (in Japanese).

Additional file 2. Developed Questionnaire (in English) and correlations with patient satisfaction/loyalty.

Additional file 4. Detailed description of SEM analysis.

Additional file 1. Comparison between reference population and respondents.

Inter-scale correlations matrix. Reliability coefficients and inter-scale correlations. (DOCX 14 kb)

Distribution of each item of GPAQ-J. Item descriptive statistics. (DOCX 17 kb)

Distribution of each item of JPCAT. Item descriptive statistics. (DOCX 15 kb)

Contents of GPAQ-J. Question items â Japanese. (DOCX 15 kb)

Results of expert review and pilot test of GPAQ-J. Description of the development process. (DOCX 17 kb)

We performed a retrospective study using 161 colorectal surgical patients to explore the additional medical costs due to postoperative infections. Patients were divided into two groups based on antimicrobial drug use duration: the control group included 112 patients with standard antimicrobial prophylaxis use, and the case group included 49 patients with additional antimicrobial drug use （indicating postoperative infection）. The case group had additional medical costs of US$7,993 （95% CI: 5,481-10,506）and hospital stay of 24.8 days （95% CI: 17.5-32.2）. Factors significantly associated with postoperative infections were preoperative physical status scores of 3 or higher （OR: 3.447, 95%CI: 1.127-10.546）, preoperative ileus （OR 6.618, 95%CI: 2.491-17.579）, hypertension （OR: 2.140, 95%CI: 1.082-4.232）, contaminated surgery （OR: 11.784, 95%CI: 3.151-44.066）, open surgery （OR: 2.111, 95%CI: 1.065-4.187）, and operative duration exceeding 400 minutes （OR: 2.465, 95%CI: 1.111- 5.471）. These findings suggest that hospital administrators should take appropriate measures to prevent postoperative infections in surgical inpatients.

It is well established that c-myc expression is down-regulated during induction of differentiation in various leukemia cell lines including HL-60 human myeloid leukemia cells. Previously we have shown that c-myc protein expression was specifically down-regulated in G0/G1 phase of the cell cycle during induction of granulocytic differentiation with dimetylsulfoxide (DMSO) in HL-60 cells. In the present study, we examined whether c-myc protein expression is also down-regulated in G0/G1 phase during monocytic differentiation of HL-60 cells. HL-60 cells can be induced to differentiate along monocytic lineage by treatment with 1,25 dihydroxyvitamin D3 (D3). C-myc protein expression was down-regulated after 72h of treatment with D3 in HL-60 cells. Simultaneous analysis of protein level and cell cycle using a two-color flow cytometry showed that the down-regulation of c-myc protein expression occurred specifically in G0/G1 phase. Down-regulation of c-myc protein expression in G0/G1 phase was more clearly shown by using synchronized cell population that was arrested at G0/G1 phase by serum starvation. Furthermore, G0/G1-synchronized cells showed a higher susceptibility to differentiation in response to D3. These results suggest that c-myc protein is down-regulated in G0/G1-specific phase during not only granulocytic differentiation but also monocytic differentiation, and down-regulation of c-myc protein expression in G0/G1 phase is involved in the program of differentiation of HL-60 cells.

To study the stability of lineage commitment of acute promyelocytic leukemia (APL) cells, we treated freshly isolated leukemic cells from the patients with APL with various differentiation-inducers. APL cells showed granulocytic differentiation when treated with all-trans retinoic acid as previously reported. We showed here that freshly isolated APL cells could be also induced to differentiation to monocytic/macrophagic lineage with inducers such as 1,25 dihydroxyvitamin D3,12-O-tetradecanoylphorbol-13-acetate or tumor necrosis factor-α. These results suggest that APL cells have the capacity to differentiate toward not only granulocytic lineage but also monocytic/macrophagic macrophagic lineage. It is not clear that these results indicate the lineage promiscuity of normal promyelocytes or lineage infidelity of APL cells. However, these data provide an important clinical implication, because a possible therapeutic efficacy of using differentiation-inducing agents toward monocytic/macrophagic lineage in the remission induction therapy for the patient with APL or salvage therapy for the resistant APL cases to all-trans retinoic acid therapy is suggested.