Impact of brand authenticity on word-of-mouth for tourism souvenirs

Although prior studies have shown that consumers who perceive brand authenticity are more likely to spread word-of-mouth (WOM) recommendations, the underlying explanatory mechanism in the context of souvenir products in tourism remains unclear. To fill this gap, this study presents a hypothetical framework that elucidates the mechanisms through which brand authenticity influences positive WOM and identifies the boundary condition that enhances its effects, drawing on consumer inference theory. Through a survey conducted on a fictitious food souvenir brand in Uji City, Kyoto Prefecture, a prominent tourist destination in Japan, we confirm that a company’s commitment to the brand’s roots, as inferred from brand authenticity, mediates the relationship between brand authenticity and positive WOM. Additionally, we show that this indirect effect is strengthened by consumers’ perceptions of the craftsman’s passion. These findings offer novel insights into marketing communication strategies aimed at amplifying positive WOM for future food souvenirs in a tourism context.</p

Early inflammatory reactions after receiving the marginal number of islets into the liver, beneath the kidney capsules, or into the spleen.

<p><b>(A–C)</b> Plasma MCP-1, G-CSF, and HMGB1 levels were measured 6 hours after islet transplantation into the portal vein (PV), beneath the kidney capsule (KC), or into the spleen (SP) (n = 7). Untreated naïve mice were used as a control (n = 7). Values are means±SD. *p<0.05. <b>(D)</b> Photomicrographs of islet cells after transplantation in the PV, KC, or SP. Sections were stained with anti-Gr-1 or F4/80 followed by staining with Haematoxylin. Scale bars: 100 μm.</p

Long-term effects of intra-splenic islet transplantation.

<p><b>(A)</b> Non-fasting blood glucose levels in STZ-induced diabetic mice (C57BL/6) transplanted with 25 syngeneic islets in the spleen (SP) and 100 syngeneic islets under the kidney capsule (KC). Individual lines represent glucose levels in each animal. <b>(B)</b> Photomicrographs of transplanted islet cells in the SP on day 290. Sections were stained with anti-insulin antibody followed by hematoxylin. Scale bars: 100 μm. <b>(C)</b> Insulin content was measured after islet transplantation on days 0 (n = 6) and 280 (n = 6). Values are means±SD. *p<0.0001.</p

Tlx1-related gene expression analysis.

<p><b>(A)</b> Tlx1 (Hox11)-related gene expression levels were significantly altered. A hierarchical clustering image reveals differences between Samples 1, 2, and 3. <b>(B)</b> Photomicrographs of transplanted islet cells in the spleen on days 0, 154, and 290. Sections were stained with anti-insulin antibody (green) and anti-Rrm2b antibody (red). Scale bars: 100 μm. The yellow boxed regions in the second column were enlarged, and the scale bars are 200 μm. <b>(C)</b> Photomicrographs of transplanted islet cells in the spleen on days 0, 154, and 290. Sections were stained with anti-insulin antibody (green) and anti-Pla2g2d antibody (red). Scale bars: 100 μm. The yellow boxed regions in the second column were enlarged, and the scale bars are 200 μm.</p

Additional file 1: Figure S1. of Cooperation of Sox4 with β-catenin/p300 complex in transcriptional regulation of the Slug gene during divergent sarcomatous differentiation in uterine carcinosarcoma

(A) Ishikawa (Ish) cells were transfected with Sox4, Sox7, and Sox9 reporter constructs, together with either Sox4, Sox7, or Sox9. Relative activity was determined based on arbitrary light units of luciferase activity normalized to pRL-TK activity. The activities of the reporter plus the effector relative to that of the reporter plus empty vector are shown as means ± SDs. The experiment was performed in duplicate. (B) Western blot analysis for the indicated proteins from Ishikawa, Hec251, and Hec6 cells cultured in STK2. (C) Western blot analysis for the indicated proteins from H6SL#8 and mock cells. (TIF 2816 kb

Additional file 3: Figure S3. of Cooperation of Sox4 with β-catenin/p300 complex in transcriptional regulation of the Slug gene during divergent sarcomatous differentiation in uterine carcinosarcoma

(A) Hec251 (left) and Hec6 cells (right) were transfected with Slug reporter constructs, together with β-cateninΔS45 (β-cat), Sox4, and p300. Relative activity was determined based on arbitrary light units of luciferase activity normalized to pRL-TK activity. The activities of the reporter plus the effector relative to that of the reporter plus empty vector are shown as means ± SDs. The experiment was performed in duplicate. (B) After transfection of HA-β-cateninΔS45 and GFP-Sox4, cells were stained with anti-HA antibody. Immunopositive cell is indicated by arrow. Nuclei were stained by DAPI. (C,D) Hec251 (C) and Hec6 (D) cells were transfected with pM-β-catenin (left) or pM-Sox4 (right), along with pGL5 luc, Sox4, Sox7, Sox9, and p300. The experiment was performed in duplicate. (TIF 2017 kb

Diffusion-weighted magnetic resonance imaging of parotid glands before and after abatacept therapy in patients with Sjögren’s syndrome associated with rheumatoid arthritis: Utility to evaluate and predict response to treatment

<p><b>Objective:</b> To compare parotid diffusion-weighted images (DWIs) taken before and after abatacept therapy in patients with Sjögren’s syndrome (SS) associated with rheumatoid arthritis (RA) and to examine the utility in evaluation and prediction of response to therapy.</p> <p><b>Methods:</b> DWIs of the parotid glands taken at baseline and 52 weeks after initiation of abatacept were analyzed in nine SS patients with RA using relative standard deviation (RSD) of the entire glands and signal intensity ratio (SIR) within the residual parenchyma. The correlation between changes in RSD and SIR and changes in salivary secretion based on Saxon’s test was examined. Furthermore, baseline characteristics were compared in patients with increased and decreased salivary secretion after treatment. The predictive power of the parameter at baseline was examined using receiver operating characteristic (ROC) analysis.</p> <p><b>Results:</b> Abatacept improved salivary secretion from 2076 ± 1535 at baseline to 2857 ± 1431 mg/2 min at 52 weeks (<i>n</i> = 9, <i>p</i> = .05). Increase of salivary secretion was significantly higher in patients with decreased RSD (<i>n</i> = 6) than increased RSD (<i>n</i> = 3) (1241 ± 713, –137 ± 142 mg/2 min, <i>p</i> = .02). The increase and decrease in RSD completely accorded with those of salivary secretion. Furthermore, SIR was the only parameter that was significantly different between patients with posttreatment increase and decrease in salivary secretion (<i>p</i> = .04). ROC analysis showed the sensitivity and specificity of SIR at baseline of ≥13.0 × 10⁻² for the prediction of the response to abatacept were 75.0% and 83.3%, respectively.</p> <p><b>Conclusions:</b> Parotid DWI seems to be useful for evaluating and predicting the response in salivary secretion to abatacept in SS patients with RA.</p

Phlorizin increased myocardial injury after ischemia-reperfusion.

<p>(A) CPK profiles in the effluent collected during the reperfusion period. (B) Area under the curve (AUC) was calculated from the CPK profile shown in (A). (phlorizin-perfused hearts, n = 11; control hearts, n = 10). (C) Micrograph showing representative TTC staining of cardiac sections obtained from the control (top row) and phlorizin-perfused hearts (bottom row). (D) Effects on quantitated cumulative infarct area size in the phlorizin-perfused hearts (n = 9) compared with that observed in the control group (n = 8). %MI, myocardial infarct area/ventricular area. *P<0.05 and **P<0.01 versus control.</p

SGLT1 is highly expressed in human hearts.

<p>(A) Results of the immunohistochemical analysis of the SGLT1 expression in the various parts of the myocardium (in each panel: left, HE staining; right, immunostaining with an SGLT1 antibody) obtained from the human autopsied hearts (x40). Representative data from five independent patients are shown. Bars: 20 μm. (B) Immunohistochemical analysis of the SGLT1 expression using the same antibody in the brush border membrane of the human small intestine (left panel, x10, bar: 100 μm) and proximal tubule straight segment in the deep cortex and medullary rays (Cortico-medullary junction) of human kidneys (mid panel, x10, bar: 100 μm; right panel, x2, bar: 1mm) obtained from intraoperative samples shown as positive controls. (C) Representative immunoblots of SGLT1 in the membrane fraction from the indicated regions in the human autopsied hearts from four independent patients are shown. Total lysates extracted from the human autopsied small intestine and kidneys were immunoblotted as positive controls. Immunoblots of Na⁺/K⁺ ATPase from the same membrane are shown as a loading control for the membrane fraction.</p

Phlorizin reduced tissue ATP content in the heart, associated with decreased glucose uptake and glycolytic flux during IRI.

<p>(A) Ischemic contracture was observed as a sigmoid increase in end-diastolic pressure, the onset and extent of which was recorded. The definitions of the individual parameters are shown. (B) The tissue ATP content in the hearts measured at the indicated time points (Ischemia 0 minutes: n = 4 each, Ischemia 5 minutes: n = 4 each, Ischemia 20 minutes: phlorizin-perfused; n = 4, control; n = 7, Reperfusion 10 minutes: phlorizin-perfused; n = 7, control; n = 8, Reperfusion 40 minutes: phlorizin-perfused; n = 7, control; n = 8). *P<0.05 versus control. (C) Glucose uptake in the hearts perfused with or without phlorizin under the pre-ischemic baseline condition (n = 6 each) and post-ischemic condition measured at 10-minute reperfusion following 20-minute global ischemia (phlorizin-perfused; n = 7, control; n = 6). **P<0.01 versus the control hearts at baseline; ^†P<0.01 versus the phlorizin-perfused hearts at baseline; ^$P<0.05 versus the control hearts at post-ischemia. (D) Glycogen content in the perfused hearts under the baseline condition prior to global ischemia (n = 4 each). (E) Lactate output profiles in the effluent collected during the reperfusion period (n = 10 each). *P<0.05 versus control. (F) AUC was calculated from the lactate output profiles shown in (E) (n = 10 each). *P<0.05 versus control.</p