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A process was proposed to hydrogenate methyl acetate to ethanol using methanol as an in-situ hydrogen donor over a Cu/SiO2catalyst. The catalyst was characterized by XRD, H2-TPR, XPS, and FT-IR, and the structure information of the catalyst was obtained. The effects of CH3OH, H2and mixed hydrogen source on the hydrogenation of methyl acetate on the same catalyst surface were compared, and it was concluded that methanol was an efficient hydrogen source. Furthermore, the influences of process conditions such as temperature and alcohol/ester ratio on methanol conversion, methyl ester conversion, and ethanol selectivity were investigated. The coupling mechanism was analyzed, that methanol decomposition to obtain in-situ hydrogen for methyl ester hydrogenation on a copper-based catalyst. The results showed that methanol as an in-situ hydrogen source could promote not only the efficient hydrogenation of methyl acetate but also inhibit the transesterification side reaction. At a lower alcohol/ester ratio, 90.9% ethanol selectivity and 82.8% methyl acetate conversion could be obtained using only the unmodified catalyst.

Metabolic reprogramming plays a critical role in many diseases. A recent study revealed that aerobic glycolysis in lung tissue is closely related to pulmonary fibrosis, and also occurs during lipopolysaccharide (LPS)-induced sepsis. However, whether LPS induces aerobic glycolysis in lung fibroblasts remains unknown. The present study demonstrated that LPS promotes collagen synthesis in the lung fibroblasts through aerobic glycolysis via the activation of the PI3K-Akt-mTOR/PFKFB3 pathway. Challenging the human lung fibroblast MRC-5 cell line with LPS activated the PI3K-Akt-mTOR pathway, significantly upregulated the expression of 6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 3 (PFKFB3), enhanced the aerobic glycolysis, and promoted collagen synthesis. These phenomena could be reversed by the PI3K-Akt inhibitor LY294002, mTOR inhibitor rapamycin, PFKFB3 inhibitor 3PO, or PFKFB3 silencing by specific shRNA, or aerobic glycolysis inhibitor 2-DG. In addition, PFKFB3 expression and aerobic glycolysis were also detected in the mouse model of LPS-induced pulmonary fibrosis, which could be reversed by the intraperitoneal injection of PFKFB3 inhibitor 3PO. Taken together, this study revealed that in LPS-induced pulmonary fibrosis, LPS might mediate lung fibroblast aerobic glycolysis through the activation of the PI3K-Akt-mTOR/PFKFB3 pathway.

Multinational enterprises in emerging economies (EMNEs) increasingly leverage cross-border mergers and acquisitions (M&As) to acquire strategic complementary assets to construct their innovation ecosystems. However, how will the EMNEs utilise the interactions between essential actors in their innovation ecosystems (i.e., EMNEs themselves, government, and national innovation systems) to conduct post-acquisition green innovation stays unclear. Based on the data of cross-border M&As completed by Chinese listed manufacturing firms during 2009-2015, this study finds that EMNEs' environmental, social, and governance (ESG) practices positively affect their post-acquisition green innovation. However, the knowledge distance between China and the host countries weakens the relationship. Meanwhile, Chinese governmental control over the economy promotes EMNEs' green innovation, and environmental subsidies strengthen the impacts. This study contributes to the innovation ecosystem and international business literature by shedding light on the construction of the innovation ecosystem of technology laggards and synergistically considering the influence of different actors involved and their interactions on EMNEs' post-acquisition green innovation.

The amino acid-based formulae were extensively added to diet of children for the treatment of Henoch-Schonlein purpura (HSP), and the nutrition and growth situation of children were evaluated after giving new dietary intervention. Patients were randomly divided into restricted diet group (n=30) and dietary guidance group (n=30). Besides, 30 cases with bronchiolitis who had normal diet were selected as the control group. The dietary questionnaire was designed to record the types and intakes of various foods taken by children every day, and the intake levels of nutrients were analyzed. Physical examination, biochemical analysis of blood and urine routine were carried out to evaluate the effect of dietary guidance on their growth and development. The results showed that restricted diet group had lower levels of nutrient intake and the actual/recommended percentage. However, overall nutrient intake level of the dietary guidance group was higher, basically equal to the recommended intake level. Besides, the actual intake and actual/recommended percentage of nutrients of dietary guidance group were significantly higher than those of restricted diet group (p<0.05). Dietary guidance can improve nutrients and protein intake of children with HSP, and reduce the relapse of rash and incidence of complications.

The upstart of a business may be motivated by a pull of an opportunity in the market or by a push of necessity to make a living. The business may be governed by family or by a non-family group. The question is whether motive and governance are coupled. Drawing on the resource-based view, we hypothesise that families especially often are motivated by opportunity. Representative samples of family and non-family businesses in Egypt, Madagascar, Morocco and Turkey reported on motives for the Global Entrepreneurship Monitor survey. Motive and governance are found to be coupled, in that family businesses, more than non-family businesses, tend to be motivated by opportunity. Moreover, this coupling is found in all four societies, and to be of similar strength in all four, suggesting that the coupling may be globally universal for similar contexts. Finding this coupling contributes to the theory of family business and practice for policymakers.

The amino acid-based formulae were extensively added to diet of children for the treatment of Henoch-Schonlein purpura (HSP), and the nutrition and growth situation of children were evaluated after giving new dietary intervention. Patients were randomly divided into restricted diet group (n=30) and dietary guidance group (n=30). Besides, 30 cases with bronchiolitis who had normal diet were selected as the control group. The dietary questionnaire was designed to record the types and intakes of various foods taken by children every day, and the intake levels of nutrients were analyzed. Physical examination, biochemical analysis of blood and urine routine were carried out to evaluate the effect of dietary guidance on their growth and development. The results showed that restricted diet group had lower levels of nutrient intake and the actual/recommended percentage. However, overall nutrient intake level of the dietary guidance group was higher, basically equal to the recommended intake level. Besides, the actual intake and actual/recommended percentage of nutrients of dietary guidance group were significantly higher than those of restricted diet group (p<0.05). Dietary guidance can improve nutrients and protein intake of children with HSP, and reduce the relapse of rash and incidence of complications.

Metabolic reprogramming plays a critical role in many diseases. A recent study revealed that aerobic glycolysis in lung tissue is closely related to pulmonary fibrosis, and also occurs during lipopolysaccharide (LPS)-induced sepsis. However, whether LPS induces aerobic glycolysis in lung fibroblasts remains unknown. The present study demonstrated that LPS promotes collagen synthesis in the lung fibroblasts through aerobic glycolysis via the activation of the PI3K-Akt-mTOR/PFKFB3 pathway. Challenging the human lung fibroblast MRC-5 cell line with LPS activated the PI3K-Akt-mTOR pathway, significantly upregulated the expression of 6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 3 (PFKFB3), enhanced the aerobic glycolysis, and promoted collagen synthesis. These phenomena could be reversed by the PI3K-Akt inhibitor LY294002, mTOR inhibitor rapamycin, PFKFB3 inhibitor 3PO, or PFKFB3 silencing by specific shRNA, or aerobic glycolysis inhibitor 2-DG. In addition, PFKFB3 expression and aerobic glycolysis were also detected in the mouse model of LPS-induced pulmonary fibrosis, which could be reversed by the intraperitoneal injection of PFKFB3 inhibitor 3PO. Taken together, this study revealed that in LPS-induced pulmonary fibrosis, LPS might mediate lung fibroblast aerobic glycolysis through the activation of the PI3K-Akt-mTOR/PFKFB3 pathway.

Lipopolysaccharide (LPS)-induced autophagy inhibition in lung fibroblasts is closely associated with the activation of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K-Akt-mTOR) pathway. However, the underlying mechanism remains unknown. In this study, we demonstrated that LPS activated the PI3K-Akt-mTOR pathway and inhibited lung fibroblast autophagy by depleting thymocyte differentiation antigen-1 (Thy-1) and upregulating integrin β3 (Itgb3). Challenge of the human lung fibroblast MRC-5 cell line with LPS resulted in significant upregulation of integrin β3, activation of the PI3K-Akt-mTOR pathway and inhibition of autophagy, which could be abolished by integrin β3 silencing by specific shRNA or treatment with the integrin β3 inhibitor cilengitide. Meanwhile, LPS could inhibit Thy-1 expression accompanied with PI3K-Akt-mTOR pathway activation and lung fibroblast autophagy inhibition; these effects could be prevented by Thy-1 overexpression. Meanwhile, Thy-1 downregulation with Thy-1 shRNA could mimic the effects of LPS, inducing the activation of PI3K-Akt-mTOR pathway and inhibiting lung fibroblast autophagy. Furthermore, protein immunoprecipitation analysis demonstrated that LPS reduced the binding of Thy-1 to integrin β3. Thy-1 downregulation, integrin β3 upregulation and autophagy inhibition were also detected in a mouse model of LPS-induced pulmonary fibrosis, which could be prohibited by intratracheal injection of Thy-1 overexpressing adeno-associated virus (AAV) or intraperitoneal injection of the integrin β3 inhibitor cilengitide. In conclusion, this study demonstrated that Thy-1 depletion and integrin β3 upregulation are involved in LPS-induced pulmonary fibrosis, and may serve as potential therapeutic targets for pulmonary fibrosis.

Lipopolysaccharide (LPS)-induced autophagy inhibition in lung fibroblasts is closely associated with the activation of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K-Akt-mTOR) pathway. However, the underlying mechanism remains unknown. In this study, we demonstrated that LPS activated the PI3K-Akt-mTOR pathway and inhibited lung fibroblast autophagy by depleting thymocyte differentiation antigen-1 (Thy-1) and upregulating integrin β3 (Itgb3). Challenge of the human lung fibroblast MRC-5 cell line with LPS resulted in significant upregulation of integrin β3, activation of the PI3K-Akt-mTOR pathway and inhibition of autophagy, which could be abolished by integrin β3 silencing by specific shRNA or treatment with the integrin β3 inhibitor cilengitide. Meanwhile, LPS could inhibit Thy-1 expression accompanied with PI3K-Akt-mTOR pathway activation and lung fibroblast autophagy inhibition; these effects could be prevented by Thy-1 overexpression. Meanwhile, Thy-1 downregulation with Thy-1 shRNA could mimic the effects of LPS, inducing the activation of PI3K-Akt-mTOR pathway and inhibiting lung fibroblast autophagy. Furthermore, protein immunoprecipitation analysis demonstrated that LPS reduced the binding of Thy-1 to integrin β3. Thy-1 downregulation, integrin β3 upregulation and autophagy inhibition were also detected in a mouse model of LPS-induced pulmonary fibrosis, which could be prohibited by intratracheal injection of Thy-1 overexpressing adeno-associated virus (AAV) or intraperitoneal injection of the integrin β3 inhibitor cilengitide. In conclusion, this study demonstrated that Thy-1 depletion and integrin β3 upregulation are involved in LPS-induced pulmonary fibrosis, and may serve as potential therapeutic targets for pulmonary fibrosis.