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Additional file 1: Figure S1. Nilotinib does not alter LPS-mediated nuclear p-NF-kB levels in BV2 microglial cells. a Western blotting analysis of NF-kB in LPS-treated BV2 microglial cells post-treated with nilotinib as shown (n = 5/group). b Immunocytochemistry of CD11b and p-NF-kB in LPS-treated BV2 microglial cells post-treated with nilotinib as shown. The graph shows the quantification of the data in the left panel (C, n = 546; L, n = 263; L + Nil, n = 342). C: control, L: LPS, L + Nil: LPS + Nilotinib, ***p < 0.001, scale bar = 20 μm. Figure S2. Nilotinib does not affect LPS-induced NLRP3, NRF2, SOD1, and Sirt3 levels in BV2 microglial cells. a-b Real-time PCR analysis of NLRP3, NRF2, SOD1, and Sirt3 levels in LPS-treated BV2 microglial cells post-treated with nilotinib as shown (n = 6/group). C: control, L: LPS, L + Nil: LPS + Nilotinib, ***p < 0.001. Table S1. One-way ANOVA (Tukey’s test) and significance of the results of the in vitro experiments in this study. Table S2. t-Tests or one-way ANOVA (Tukey’s test) and significance of the results of the in vivo experiments in this study.

Additional file 1: Figure S1. Anti-inflammatory effects of dapagliflozin on immunohistochemistry analysis. A-C The expression of RAM11, RAGE and TNF-α in the myocardium was detected by immunostaining. Values are means ± SEM (n = 10 per group). Scale bar = 200 μm. ***p < 0.001 compared to Control group, ††p < 0.01, †††p < 0.001 compared to Diabetes group. Figure S2. Dapagliflozin significantly decreased inflammation markers in H9C2. A RT-PCR expression of TNF-α and IL-6. Comparisons of relative mRNA expression, normalized to expression of β-actin. B Western blot expression of pNF-kB, NF-kB, TNF-α and IL-6. Representative data showing protein expression, normalized to expression of GAPDH. Values are means ± SEM (n = 6). *p < 0.05, **p < 0.01, ***p < 0.001 compared to Control, †p < 0.05 compared to DMSO, §p < 0.05, §§p < 0.01 compared to HG. GAPDH, glyceraldehyde 3-phosphate dehydrogenase; IL-6, interlukin-6; NF-κB, Nuclear factor kappa-light-chain-enhancer of activated B cells; TNF-α, tumor necrosis factor-α. Figure S3. Schematic design of the study protocol. Animals were randomized to Control, Diabetes, Diabetes+Dapa groups. Diabetic condition was induced for animals in Diabetes and Diabetes+Dapa groups. Dapagliflozin (1mg/kg/day) treated depending on their group assignment, for 8 weeks. After follow up echocardiography, animals were subsequently sacrificed and tissue samples were collected for assessment of histological and molecular remodeling. Table S1. List of rabbit primers. Table S2. List of H9C2 primers.

Additional file 1.: Materials and methods.

Additional file 1: Figure 1. Histograms of maximum SUV (a), MTV (b), TLG (c), BM SUV (d), and BLR (e).

This table details the characteristics, measurement information, and results of individual patients participating in the study.

Figure S1. Treatment with 100 nM dasatinib significantly reduces LPS-induced proinflammatory cytokine COX-2 and IL-6 mRNA levels in BV2 microglial cells. Figure S2. Treatment with 250 nM dasatinib significantly reduces low-dose LPS-induced proinflammatory cytokine COX-2, IL-6, and TNF-Îą mRNA levels in BV2 microglial cells. Figure S3. Treatment with 250 nM dasatinib regulates anti-inflammatory cytokine Il4 and Il10 levels in BV2 microglial cells in the presence of LPS. Figure S4. Post-treatment with dasatinib significantly reduces LPS-induced proinflammatory cytokine COX-2 mRNA levels. Figure S5. Dasatinib does not alter LPS-induced p-P38 levels in BV2 microglial cells. Figure S6. Dasatinib significantly inhibits 200 ng/ml LPS-induced AKT/ERK phosphorylation. Figure S7. Treatment with dasatinib increases anti-inflammatory cytokine Il10 levels in mouse primary astrocytes in the presence of LPS. Figure S8. Dasatinib treatment does not reduce LPS-induced p-P38 levels in mouse primary astrocytes. (DOCX 1020 kb)

Purpose: The purpose of this study is to find out how much influence nursing students’ environmental consciousness and knowledge of medical waste have on their attitudes toward medical waste. Methods: The subjects were 211 nursing students recruited from 2 universities. Data were collected with a structured self-report questionnaire comprising measures of environmental consciousness, and knowledge of and attitude toward medical waste. Data analysis was conducted with the SPSS/WIN 25.0 program. Results: A total of 211 copies of the questionnaire were used for the final analysis, except for 9 untrusted responses out of 220 that included missing values. Those subjects’ environmental consciousness who received environmental education in middle and high schools was higher (t=3.15, p=.002). The higher their grades, the better their knowledge of medical waste (F=3.40, p=.035). Those subjects’ knowledge of medical waste who received medical waste education was relatively high (t=3.14, p=.002). Those subjects with clinical practice experience had more sensitive attitudes toward medical waste (t=2.06, p=.041). Those subjects’ attitudes toward Medical waste who received medical waste education at the universities were relatively high (t=2.04, p=.043). The subjects’ environmental consciousness was positively correlated with their attitudes toward medical waste (r=.44, p

Crude extract prepared from sweet potato possessed inhibitory activity toward mushroom tyrosinase. The inhibitory activity was dependent upon the addition amount of sweet potato extract. After heating the sweet potato extract at for 20 min, its inhibitory activity retained 37.3%. Its optimum activity was shown at pH ranges of 5.0-7.0. The tyrosinase inhibitory activity was disappeared by dialysis, which suggests the inhibitory activity of sweet potato extract is caused by some compounds of low molecular weight.