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Brand M&A has long been an extremely common strategy for expanding the scale of an organization and entering new business areas, but various signs show that many brand mergers and acquisitions (M&As) do not add value. They often lose money and fail. This research explores the value, scarcity, and non-replicability of resources in corporate M&A, as well as organizational resource management, innovation resource management, and implementation of the combination of resource utilization and brand strategy that incorporate M&As. Taking 03 of China’s sporting shoe industry cases, this study uses the literature to collect, analyze, and organize the conversations of high-level managers to compare and integrate the motivations of corporate M&As to conduct confirmatory analysis. Using case studies and cross-border M&A related secondary data from 2014 to 2021 and supplemented by senior executives’ conversations, 1,836 articles were collected as analysis units. The research results show that Chinese companies’ cross-border M&A’s main corporate strategic motives have four key elements: accelerated expansion, integration of resources, brand integration, rapid entry into the international market, and obstacles to the construction of new entrants. The research results also show that integrating resources and brand execution strategies after M&As correlates to their success or failure. The purpose of the research was first to discuss brand M&As and corporate strategies in the Taiwanese context. Secondly, it discusses the issue of the use of resources by the acquired party in specific to emerging trends in consumer resistance to innovation and acceptance of technological innovativeness in the sports industry brands. Third, it analyzes the effectiveness of brand strategy integration and implementation. Finally, it provides a strategic reference for brand M&As in the industry.

Aim: To determine whether the anti-inflammatory effect of minocycline on postis-chemic brain injury is mediated by the inhibition of 5-lipoxygenase (5-LOX) expression and enzymatic activation in rats. Methods: Focal cerebral ischemia was induced for 30 min with middle cerebral artery occlusion, followed by reperfusion. The ischemic injuries, endogenous IgG exudation, the accumulation of neutrophils and macrophage/microglia, and 5-LOX mRNA expression were determined 72 h after reperfusion. 5-LOX metabolites (leukotriene B4 and cysteinyl leukotrienes) were measured 3 h after reperfusion. Results: Minocycline (22.5 and 45 mg/kg, ip, for 3 d) attenuated ischemic injuries, IgG exudation, and the accumulation of neutrophils and macrophage/microglia 72 h after reperfusion. It also inhibited 5-LOX expression 72 h after reperfusion and the production of leukotrienes 3 h after reperfusion. Conclusion: Minocycline inhibited postischemic brain inflammation, which might be partly mediated by the inhibition of 5-LOX expression and enzymatic activation. [ABSTRACT FROM AUTHOR]

Aim: To investigate the effects of caffeic acid on early and delayed injuries after focal cerebral ischemia in rats, and the possible relation to 5-lipoxygenase inhibition. Methods: Transient focal cerebral ischemia was induced by middle cerebral artery occlusion in Sprague-Dawley rats. Caffeic acid (10 and 50 mg/kg) was ip injected for 5 d after ischemia. The brain injuries were observed, and the levels of cysteinyl leukotrienes and leukotriene B4 in the brain tissue were measured. Results: Caffeic acid (50 mg/kg) ameliorated neurological dysfunction and neuron loss, and decreased infarct volume 24 h after ischemia; it attenuated brain atrophy, infarct volume, and particularly astrocyte proliferation 14 d after ischemia. In addition, it reduced the production of leukotrienes (5-lipoxygenase metabolites) in the ischemic hemispheres 3 h and 7 d after ischemia. Conclusion: Caffeic acid has protective effect on both early and delayed injuries after focal cerebral ischemia in rats; and this effect may partly relate to 5-lipoxygenase inhibition. [ABSTRACT FROM AUTHOR]

Aim: To determine whether pranlukast, a cysteinyl leukotriene receptor-1 antagonist, exerts an anti-inflammatory effect on focal cerebral ischemia in mice. Methods: Focal cerebral ischemia in mice was induced by permanent middle cerebral artery occlusion (MCAO). In addition to neurological deficits, infarct volume, degenerated neurons and endogenous IgG exudation, we detected accumulation of neutrophils and macrophage/microglia in the ischemic brain tissue 72 h after MCAO. Pranlukast was ip injected 30 min before and after MCAO. Results: Pranlukast significantly attenuated neurological deficits, infarct volume, neuron degeneration and IgG exudation. Importantly, pranlukast (0.01 and 0.1 mg/kg) inhibited myeloperoxidase-positive neutrophil, but not CD 11b-positive macrophage/microglial accumulation in the ischemic cortical tissue. Conclusion: Pranlukast exerts an anti-inflammatory effect on focal cerebral ischemia in the subacute phase that is limited to neutrophil recruitment through the disrupted blood-brain barrier. [ABSTRACT FROM AUTHOR]

Our previous studies showed that cysteinyl leukotriene receptor-1 (CysLT1) antagonist pranlukast has a neuroprotective effect on cerebral ischemia in rats and mice. However, whether the neuroprotective effect of pranlukast is its special action or a common action of CysLT1 receptor antagonists remains to be clarified. This study was performed to determine whether montelukast, another CysLT1 receptor antagonist, has the neuroprotective effect on focal cerebral ischemia in mice, and to observe its dose- and time-dependent properties. Permanent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). Montelukast was injected intraperitoneally either as multiple doses (once a day for 3 days and 30 min before MCAO) or as a single dose (at 30 min before, 30 min after, or 1 h after MCAO), respectively, and pranlukast and edaravone were used as controls. The neurological deficits, infarct volumes, brain edema, neuron density, and Evans blue extravasation in the brain were determined 24 h after MCAO. Pretreatments with multiple doses or a single dose of montelukast (0.1 and 1.0 mg/kg) before MCAO significantly attenuated all the ischemic insults. Post-treatment with a single dose of montelukast (0.1 and 1.0 mg/kg) at 30 min after MCAO also significantly decreased brain edema and infarct volume, but not neurological deficits. However, post-treatment with a single dose of montelukast at 1 h after MCAO had no significant effect. Pranlukast showed the same effects as montelukast, but edaravone attenuated the ischemic insults only with multiple doses before MCAO. Thus, montelukast has a dose- and time-dependent neuroprotective effect on permanent focal cerebral ischemia in mice, with an effective dose range of 0.1–1.0 mg/kg and a therapeutic window of 30 min. These findings further support the therapeutic potential of CysLT1 receptor antagonists in the treatment of cerebral ischemia at earlier phases. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]