Treatment and advice on amoebic dysentery from case studies onboard H.M.H.S. Lanfranc, May 1916.

In order to expand global market share and enhance the benefits of economics of scale, Trans-National Media Corporations (TNMCs) exploits overseas markets actively. The Chinese region which contains more than one billion audience is regarded as an important target market by TNMCs. Taiwan TV industry which allows foreign investments is always the leading region of Chinese film industry and popular culture. On condition that analyzing the glocalization strategy of foreign satellite channels in Taiwan, we can construct the best operation strategy among Chinese regions. Therefore, we use case study method to investigate not only the business strategies of Star Ltd. Group¡¦s Channel[V] and Viacom¡¦s MTV Taiwan channel but also the synergy that parent company integrates from local resource. The research method for collecting data combines qualitative and quantitative method. Use literature analysis and in-depth interview for qualitative approach that acquire industrial data. And use questionnaire for quantitative that analyze the market response of audience to see whether they accept the positioning and strategy of Channel[V] and MTV or not. Finally, develop research conclusion and suggestion base on case study method. Regarding research framework, we apply I-R framework and Institutional Theory as our theoretical basis. And divide three strategic perspectives to compare the operation of Channel[V] and MTV. We find that they operate in different ways among glocalization strategy and programming production strategy. The differentiation of Channel positioning leads to competitive strength. Besides, monitoring advertisement sales, product placement, road shows, integration of channel resource, and cross-media marketing campaigns can promote firm¡¦s operational performance. We hope our research conclusion and will help the following researchers and industrial managers.

Background: Toll-like receptors (TLRs) have been implicated in myocardial ischemia/reperfusion (I/R) injury. The TLR9 ligand, CpG-ODN has been reported to improve cell survival. We examined effect of CpG-ODN on myocardial I/R injury. Methods: Male C57BL/6 mice were treated with either CpG-ODN, control-ODN, or inhibitory CpG-ODN (iCpG-ODN) 1. h prior to myocardial ischemia (60. min) followed by reperfusion. Untreated mice served as I/R control (n. =10/each group). Infarct size was determined by TTC straining. Cardiac function was examined by echocardiography before and after myocardial I/R up to 14. days. Results: CpG-ODN administration significantly decreased infarct size by 31.4% and improved cardiac function after myocardial I/R up to 14. days. Neither control-ODN nor iCpG-ODN altered I/R-induced myocardial infarction and cardiac dysfunction. CpG-ODN attenuated I/R-induced myocardial apoptosis and prevented I/R-induced decrease in Bcl2 and increase in Bax levels in the myocardium. CpG-ODN increased Akt and GSK-3β phosphorylation in the myocardium. In vitro data suggested that CpG-ODN treatment induced TLR9 tyrosine phosphorylation and promoted an association between TLR9 and the p85 subunit of PI3K. Importantly, PI3K/Akt inhibition and Akt kinase deficiency abolished CpG-ODN-induced cardioprotection. Conclusion: CpG-ODN, the TLR9 ligand, induces protection against myocardial I/R injury. The mechanisms involve activation of the PI3K/Akt signaling pathway.

Background: Toll-like receptors (TLRs) have been implicated in myocardial ischemia/reperfusion (I/R) injury. The TLR9 ligand, CpG-ODN has been reported to improve cell survival. We examined effect of CpG-ODN on myocardial I/R injury. Methods: Male C57BL/6 mice were treated with either CpG-ODN, control-ODN, or inhibitory CpG-ODN (iCpG-ODN) 1. h prior to myocardial ischemia (60. min) followed by reperfusion. Untreated mice served as I/R control (n. =10/each group). Infarct size was determined by TTC straining. Cardiac function was examined by echocardiography before and after myocardial I/R up to 14. days. Results: CpG-ODN administration significantly decreased infarct size by 31.4% and improved cardiac function after myocardial I/R up to 14. days. Neither control-ODN nor iCpG-ODN altered I/R-induced myocardial infarction and cardiac dysfunction. CpG-ODN attenuated I/R-induced myocardial apoptosis and prevented I/R-induced decrease in Bcl2 and increase in Bax levels in the myocardium. CpG-ODN increased Akt and GSK-3β phosphorylation in the myocardium. In vitro data suggested that CpG-ODN treatment induced TLR9 tyrosine phosphorylation and promoted an association between TLR9 and the p85 subunit of PI3K. Importantly, PI3K/Akt inhibition and Akt kinase deficiency abolished CpG-ODN-induced cardioprotection. Conclusion: CpG-ODN, the TLR9 ligand, induces protection against myocardial I/R injury. The mechanisms involve activation of the PI3K/Akt signaling pathway.

AimsThe present study examined the role of microRNA-125b (miR-125b) in myocardial ischaemia/reperfusion (I/R) injury. We constructed lentivirus-expressing miR-125b (LmiR-125b) and developed transgenic mice with overexpression of miR-125b.Methods and resultsLmiR-125b was transfected into mouse hearts through the right common carotid artery. Lentivirus vector (LmiR-Con) served as vector control. Untreated mice served as I/R control. Sham operation served as sham control. Seven days after transfection, the hearts were subjected to ischaemia (45 min) followed by reperfusion (4 h). Myocardial infarct size was analysed by 2,3,5-triphenyltetrazolium chloride staining. In separate experiments, hearts were subjected to ischaemia (45 min) followed by reperfusion for up to 7 days. Cardiac function was measured by echocardiography before, as well as 3 and 7 days after myocardial I/R. Increased expression of miR-125b significantly decreased I/R-induced myocardial infarct size by 60 and prevented I/R-induced decreases in ejection fraction (EF) and fractional shortening (FS). Transgenic mice with overexpression of miR-125b also showed the protection against myocardial I/R injury. Increased expression of miR-125b attenuated I/R-induced myocardial apoptosis and caspase-3/7 and-8 activities. Western blot showed that increased expression of miR-125b suppresses p53 and Bak1 expression in the myocardium. In addition, transfection of LmiR-125b decreased the levels of TNF receptor-associated factor 6 (TRAF6) and prevented I/R-induced NF-κB activation.ConclusionmiR-125 protects the myocardium from I/R injury by preventing p53-mediated apoptotic signalling and suppressing TRAF6-mediated NF-κB activation.

Innate immune and inflammatory responses mediated by Toll like receptors (TLRs) have been implicated in myocardial ischemia/reperfusion (I/R) injury. This study examined the role of TLR3 in myocardial injury induced by two models, namely, myocardial infarction (MI) and I/R. First, we examined the role of TLR3 in MI. TLR3 deficient (TLR3-/-) and wild type (WT) mice were subjected to MI induced by permanent ligation of the left anterior descending (LAD) coronary artery for 21days. Cardiac function was measured by echocardiography. Next, we examined whether TLR3 contributes to myocardial I/R injury. TLR3-/- and WT mice were subjected to myocardial ischemia (45min) followed by reperfusion for up to 3days. Cardiac function and myocardial infarct size were examined. We also examined the effect of TLR3 deficiency on I/R-induced myocardial apoptosis and inflammatory cytokine production. TLR3-/- mice showed significant attenuation of cardiac dysfunction after MI or I/R. Myocardial infarct size and myocardial apoptosis induced by I/R injury were significantly attenuated in TLR3-/- mice. TLR3 deficiency increases B-cell lymphoma 2 (BCL2) levels and attenuates I/R-increased Fas, Fas ligand or CD95L (FasL), Fas-Associated protein with Death Domain (FADD), Bax and Bak levels in the myocardium. TLR3 deficiency also attenuates I/R-induced myocardial nuclear factor KappaB (NF-κB) binding activity, Tumor necrosis factor alpha (TNF-α) and Interleukin-1 beta (IL-1β) production as well as I/R-induced infiltration of neutrophils and macrophages into the myocardium. TLR3 plays an important role in myocardial injury induced by MI or I/R. The mechanisms involve activation of apoptotic signaling and NF-κB binding activity. Modulation of TLR3 may be an effective approach for ameliorating heart injury in heart attack patients.

AimsInnate immune and inflammatory responses are involved in myocardial ischaemia/reperfusion (I/R) injury. The interleukin-1 receptor (IL-1R)-mediated, MyD88-dependent nuclear factor kappa B (NF-κB) activation pathway plays an important role in the induction of innate immunity and inflammation. However, the role of the IL-1R-MyD88 pathway in myocardial I/R injury has not been thoroughly investigated. We hypothesized that inhibition of the interaction of IL-1R with MyD88 will attenuate myocardial ischaemic injury through reducing inflammatory responses.Methods and resultsMale C57BL/6 mice were subjected to myocardial ischaemia (45 min) followed by reperfusion (4 h). In the treatment group, after mice were subjected to ischaemia (45 min), the TIR/BB-loop mimetic (AS-1), which inhibits the interaction of IL-1R with MyD88, was administered immediately before reperfusion. Hearts were harvested and cellular proteins were isolated for immunoprecipitation and immunoblotting. AS-1 administration significantly decreased infarct size by 32.92 compared with the untreated I/R group. Ejection fraction and fractional shortening in AS-1-treated mice were also significantly increased by 18.0 and 25.6, respectively, compared with the untreated I/R group. AS-1 administration significantly decreased the I/R-increased interaction between IL-1R and MyD88, attenuated the I/R-increased NF-κB binding activity, and reduced levels of inflammatory cytokines and adhesion molecules in the myocardium compared with the untreated I/R group. In addition, AS-1 administration significantly decreased myocardial myeloperoxidase activity by 23.6 and neutrophil infiltration in the myocardium compared with the untreated I/R group.ConclusionThe results demonstrated an important role for the IL-1R-mediated MyD88-dependent signalling pathway in myocardial I/R injury. The data suggest that modulation of the IL-1R/MyD88 interaction could be a strategy for reducing myocardial ischaemic injury.

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal.

Significant structural changes in the retail sector, due to retailer consolidation within and across countries as well as retailer internationalisation, lead to significant changes of the sales function within the FMCG industry. Whilst formally sales functions acted traditionally predominantly locally, manufacturers are recently pressured to act more integrated, i.e. centrally, regarding its sales function. From an IB perspective this study strives to investigate into the result of the competing forces for integration and responsiveness at the manufacturers side in the special context of Germany, being a pivotal market for this industry. Identifying the potential division of strategic sales activities between subsidiary and HQ, the study investigates into how such division impacts on the subsidiary market performance. Using the I/R framework as a starting point, network theory and the concept of subsidiary importance are utilized to understand the interrelationships a subsidiary is embedded in and its potential strategic importance to the wider MNE. The framework connects the antecedents of the division of strategic sales activities between HQ and subsidiary, to subsidiary market performance. The research follows a mixed-method approach using contextualising interviews and a quantitative survey. The data analysis has been conducted with PLS SEM reflecting both the more explorative character of the study and the relatively small sample size. Empirical evidence showed that most strategic sales decisions are still made at subsidiary level, pointing at a low level of division between HQ and subsidiary. The results show that strong customer relationships as well as the positive impact of a formalised sales strategy, which ideally follows a global strategic framework, seem to be the main contributors to subsidiary market performance. Unexpectedly, subsidiary importance, the visibility and relevance of sales capabilities to other subsidiaries, fails to be a driver for the subsidiary strategic role within the MNE, mainly due to the functional (sales competencies stay rather local) and country (sheer importance of the German market) context of the study. The key contributions of this study are related to the area of IB and the sales literature. This study adds to the extant IB literature from a downstream value chain perspective supporting existing findings regarding the network theory and subsidiary market performance. The irrelevance of the concept of subsidiary importance highlights the importance of the empirical context in IB research. Finally, the study sheds light on the sales function from a strategic perspective in the IB context and thus adds to the sparse literature regarding the sales strategy as well as it starts bridging both fields.

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal