104 research outputs found

    Internationalization propensity in family-controlled public firms in emerging markets: The effects of family ownership, governance, and top management team heterogeneity

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    Internationalization propensity is a growing issue faced by family firms. This study contributes to the family business literature by developing a conceptual framework that can identify the family and managerial determinants that affect the extensiveness of internationalization. Drawing on the socioemotional wealth and upper echelon perspectives, it empirically examines the association among family heterogeneity (i.e., family participation is heterogeneous in terms of ownership and governance oversight), top management team (TMT) heterogeneity (i.e., the TMT’s background is heterogeneous in terms of its overseas education and industry experience), and internationalization propensity in publicly traded enterprises. The analysis of data collected from 105 public firms in Taiwan shows that active family participation in ownership and governance oversight and TMT overseas industry experience heterogeneity are significantly and positively associated with internationalization propensity. However, family ownership is found to be significantly but negatively associated with internationalization propensity. We finally discuss the implications of the presented findings for practitioners and organizational theorists

    Effects of natto extract on endothelial injury in a rat model

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    Vascular endothelial damage has been found to be associated with thrombus formation, which is considered to be a risk factor for cardiovascular disease. A diet of natto leads to a low prevalence of cardiovascular disease. The aim of the present study was to investigate the effects of natto extract on vascular endothelia damage with exposure to laser irradiation. Endothelial damage both in vitro and in vivo was induced by irradiation of rose bengal using a DPSS green laser. Cell viability was determined by MTS assay, and the intimal thickening was verified by a histological approach. The antioxidant content of natto extract was determined for the free radical scavenging activity. Endothelial cells were injured in the presence of rose bengal irradiated in a dose-dependent manner. Natto extract exhibits high levels of antioxidant activity compared with purified natto kinase. Apoptosis of laser-injured endothelial cells was significantly reduced in the presence of natto extract. Both the natto extract and natto kinase suppressed intimal thickening in rats with endothelial injury. The present findings suggest that natto extract suppresses vessel thickening as a synergic effect attributed to its antioxidant and anti-apoptosis properties

    A Novel Surgical Technique: Single-Incision Transumbilical Laparoscopic Roux-en-Y Gastric Bypass

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    Conventional laparoscopic Roux-en-Y gastric bypass (LRYGB) is a gold standard for bariatric surgery, but the procedure requires five to seven incisions for placement of multiple trocars and thus may produce less-than-ideal cosmetic results. We have developed a new approach, single-incision transumbilical LRYGB (SITU-LRYGB) to treat morbid obesity. We compared the surgical results and patient satisfaction in a study of five-port LRYGB and SITU-LRYGB. Fifty morbidly obese patients (14 males, 36 females) underwent either Roux-en-Y gastric bypass with five-port LRYGB or the SITU-LRYGB approach. During the operation, we used a novel intraoperative liver traction method with a “liver suspension tape” that we specifically designed for SITU-LRYGB. Compared to five-port surgery with SITU-LRYGB, there were no intraoperative complications, wound healing was excellent, and there was no abdominal scarring. SITU surgical time was longer than that with five-port LRYGB (99.8 vs. 67.6 min, P < 0.001). Patients treated with the five-port method were more obese than those in the SITU group (127.9 vs. 112.4 kg, P = 0.016). After the bariatric surgery, no difference in comorbidity was found in both groups. Patient satisfaction was greater with SITU than with the five-port method (4.48 vs. 3.96, P = 0.006). Roux-en-Y gastric bypass can be successfully achieved via a single umbilical incision, a method that provides a short operative time and good recovery and eliminates abdominal scarring

    Elevated plasma level of visfatin/pre-b cell colony-enhancing factor in male oral squamous cell carcinoma patients

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    Objectives: Visfatin, also known as nicotiamide phosphoribosyltransferase or pre-B cell colony enhancing factor, is a pro-inflammatory cytokine whose serum level is increased in various cancers. In this study, we investigated whether plasma visfatin levels were altered in patients with oral squamous cell carcinoma (OSCC). The relation ship between plasma visfatin levels and the pretreatment hematologic profile was also explored. Study Design: Plasma visfatin concentrations were measured through ELISA in OSCC patients and control sub- D esign: Plasma visfatin concentrations were measured through ELISA in OSCC patients and control sub- esign: Plasma visfatin concentrations were measured through ELISA in OSCC patients and control sub jects. A total of 51 patients with OSCC and 57 age- and body mass index (BMI)-matched control subjects were studied. All study subjects were male. Results: Plasma visfatin was found to be elevated in patients with OSCC (7.0 ± 4.5 vs. 4.8 ± 1.9 ng/ml, p = 0.002). Multiple logistic regression analysis revealed visfatin as an independent association factor for OSCC, even after full adjustment of known biomarkers. Visfatin level was significantly correlated with white blood cell (WBC) count, neutrophil count, and hematocrit (all p < 0.05). In addition, WBC count, neutrophil count, and visfatin gradually increased with stage progression, and hematocrit gradually decreased with stage progression (all p < 0.05). Conclusion: Increased plasma visfatin levels were associated with OSCC, independent of risk factors, and were cor related with inflammatory biomarkers. These data suggest that visfatin may act through inflammatory reactions to play an important role in the pathogenesis of OSC

    Leukocyte Cell-Derived Chemotaxin 2 Retards Non-Small Cell Lung Cancer Progression Through Antagonizing MET and EGFR Activities

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    Background/Aims: Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) therapy is a clinical option for non-small cell lung cancer (NSCLC) harboring activating EGFR mutations or for cancer with wild-type (WT) EGFR when chemotherapy has failed. MET receptor activation or MET gene amplification was reported to be a major mechanism of acquired resistance to EGFR-TKI therapy in NSCLC cells. Leukocyte cell-derived chemotaxin 2 (LECT2) is a multifunctional cytokine that was shown to suppress metastasis of hepatocellular carcinoma via inhibiting MET activity. Until now, the biological function responsible for LECT2’s action in human NSCLC remains unclear. Methods: LECT2-knockout (KO) mice and NOD/SCID/IL2rgnull (NSG) mice were respectively used to investigate the effects of LECT2 on the tumorigenicity and metastasis of murine (Lewis lung carcinoma, LLC) and human (HCC827) lung cancer cells. The effect of LECT2 on in vitro cell proliferation was evaluated, using MTS and colony formation assays. The effect of LECT2 on cell motility was evaluated using transwell migration and invasion assays. An enzyme-linked immunosorbent assay was performed to detect secreted LECT2 in plasma and media. Co-immunoprecipitation and Western blot assays were used to investigate the underlying mechanisms of LECT2 in NSCLC cells. Results: Compared to WT mice, mice with LECT2 deletion exhibited enhanced growth and metastasis of LLC cells, and survival times decreased in LLC-implanted mice. Overexpression of LECT2 in orthotopic human HCC827 xenografts in NSG mice resulted in significant inhibition of tumor growth and metastasis. In vitro, overexpression of LECT2 or treatment with a recombinant LECT2 protein impaired the colony-forming ability and motility of NSCLC cells (HCC827 and PC9) harboring high levels of activated EGFR and MET. Mechanistic investigations found that LECT2 bound to MET and EGFR to antagonize their activation and further suppress their common downstream pathways: phosphatidylinositol 3-kinase/Akt and extracellular signal-regulated kinase. Conclusion: EGFR-MET signaling is critical for aggressive behaviors of NSCLC and is recognized as a therapeutic target for NSCLC especially for patients with acquired resistance to EGFR-TKI therapy. Our findings demonstrate, for the first time, that LECT2 functions as a suppressor of the progression of NSCLC by targeting EGFR-MET signaling
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