302 research outputs found

    From Acting What’s next to Speeding Trap: Co-Evolutionary Dynamics of an Emerging Technology-Leader

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    JEL Classifications: O33, O53, L63[[abstract]]How does technological innovation emerge and evolve? We approach such an inquiry by synthesizing the perspectives of dynamic capabilities and co-evolutionary dynamics to portray organizational routines and multi-phase strategic renewals of an emerging technology-leader. To untangle the emergence of technological innovation, we conducted a longitudinal case study on the first and the largest dedicated semiconductor foundry, TSMC, located in the emerging economy of Taiwan. The firm-case of TSMC illustrates two unique co-evolutionary paths, that is, transforming from industry-latecomer to technology-leader and from process innovation to product innovation. We found multi-motor co-evolutionary dynamics between TSMC and the semiconductor industry, where its co-evolutionary mechanism of managed selection in its creating phase of mature process-innovation (1987-1998) has migrated to hierarchical renewal in its extending phase of advanced process-innovation (1999-2001), and then to holistic renewal in its modifying phase of product-innovation (2002-2007). During such paths, our research discovered a unique type of organizational routines, acting what’s next because TSMC has proactively searched for potential problems sooner than its competitors. However, such routines, although driving technological innovation, also lead to a unique type of success-trap, that is, speeding trap. When an emerging technology-leader fundamentally changes the industrial structures to over-specs, the growth driven by technology speeding may trap such a leader in a loop of over-exploration.[[sponsorship]]The authors are grateful to the research grant from the National Science Council (NSC) in Taiwan. The earlier manuscript of this paper was presented at the 2009 Annual Meeting of Academy of International Business (AIB) in San Diego, USA.[[notice]]補正完畢[[journaltype]]國外[[ispeerreviewed]]Y[[booktype]]紙本[[booktype]]電子版[[countrycodes]]CA

    Looking the Part: Social Status Cues Shape Race Perception

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    It is commonly believed that race is perceived through another's facial features, such as skin color. In the present research, we demonstrate that cues to social status that often surround a face systematically change the perception of its race. Participants categorized the race of faces that varied along White–Black morph continua and that were presented with high-status or low-status attire. Low-status attire increased the likelihood of categorization as Black, whereas high-status attire increased the likelihood of categorization as White; and this influence grew stronger as race became more ambiguous (Experiment 1). When faces with high-status attire were categorized as Black or faces with low-status attire were categorized as White, participants' hand movements nevertheless revealed a simultaneous attraction to select the other race-category response (stereotypically tied to the status cue) before arriving at a final categorization. Further, this attraction effect grew as race became more ambiguous (Experiment 2). Computational simulations then demonstrated that these effects may be accounted for by a neurally plausible person categorization system, in which contextual cues come to trigger stereotypes that in turn influence race perception. Together, the findings show how stereotypes interact with physical cues to shape person categorization, and suggest that social and contextual factors guide the perception of race

    Increased costs reduce reciprocal helping behaviour of humans in a virtual evacuation experiment

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    Altruistic behaviour is widespread and highly developed in humans and can also be found in some animal species. It has been suggested that altruistic tendencies can depend on costs, benefits and context. Here, we investigate the changes in the occurrence of helping behaviour in a computer-based experiment that simulates an evacuation from a building exploring the effect of varying the cost to help. Our findings illuminate a number of key mechanistic aspects of human decision-making about whether to help or not. In a novel situation where it is difficult to assess the risks associated with higher costs, we reproduce the finding that increasing costs reduce helping and find that the reduction in the frequency of helping behaviour is gradual rather than a sudden transition for a threshold cost level. Interestingly, younger and male participants were more likely to help. We provide potential explanations for this result relating to the nature of our experiment. Finally, we find no evidence that participants in our experiment plan ahead over two consecutive, inter-dependent helping opportunities when conducting cost-benefit trade-offs in spontaneous decisions. We discuss potential applications of our findings to research into decision-making during evacuations

    NF-κB mediates proteolysis-inducing factor induced protein degradation and expression of the ubiquitin–proteasome system in skeletal muscle

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    Loss of skeletal muscle in cancer cachexia has a negative effect on both morbidity and mortality. The role of nuclear factor-κB (NF-κB) in regulating muscle protein degradation and expression of the ubiquitin–proteasome proteolytic pathway in response to a tumour cachectic factor, proteolysis-inducing factor (PIF), has been studied by creating stable, transdominant-negative, muscle cell lines. Murine C2C12 myoblasts were transfected with plasmids with a CMV promoter that had mutations at the serine phosphorylation sites required for degradation of I-κBα, an NF-κB inhibitory protein, and allowed to differentiate into myotubes. Proteolysis-inducing factor induced degradation of I-κBα, nuclear accumulation of NF-κB and an increase in luciferase reporter gene activity in myotubes containing wild-type, but not mutant, I-κBα proteins. Proteolysis-inducing factor also induced total protein degradation and loss of the myofibrillar protein myosin in myotubes containing wild-type, but not mutant, plasmids at the same concentrations as those causing activation of NF-κB. Proteolysis-inducing factor also induced increased expression of the ubiquitin–proteasome pathway, as determined by ‘chymotrypsin-like' enzyme activity, the predominant proteolytic activity of the β-subunits of the proteasome, protein expression of 20S α-subunits and the 19S subunits MSS1 and p42, as well as the ubiquitin conjugating enzyme, E214k, in cells containing wild-type, but not mutant, I-κBα. The ability of mutant I-κBα to inhibit PIF-induced protein degradation, as well as expression of the ubiquitin–proteasome pathway, confirms that both of these responses depend on initiation of transcription by NF-κB

    Novel Murine Infection Models Provide Deep Insights into the “Ménage à Trois” of Campylobacter jejuni, Microbiota and Host Innate Immunity

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    BACKGROUND: Although Campylobacter jejuni-infections have a high prevalence worldwide and represent a significant socioeconomic burden, it is still not well understood how C. jejuni causes intestinal inflammation. Detailed investigation of C. jejuni-mediated intestinal immunopathology is hampered by the lack of appropriate vertebrate models. In particular, mice display colonization resistance against this pathogen. METHODOLOGY/PRINCIPAL FINDINGS: To overcome these limitations we developed a novel C. jejuni-infection model using gnotobiotic mice in which the intestinal flora was eradicated by antibiotic treatment. These animals could then be permanently associated with a complete human (hfa) or murine (mfa) microbiota. After peroral infection C. jejuni colonized the gastrointestinal tract of gnotobiotic and hfa mice for six weeks, whereas mfa mice cleared the pathogen within two days. Strikingly, stable C. jejuni colonization was accompanied by a pro-inflammatory immune response indicated by increased numbers of T- and B-lymphocytes, regulatory T-cells, neutrophils and apoptotic cells, as well as increased concentrations of TNF-α, IL-6, and MCP-1 in the colon mucosa of hfa mice. Analysis of MyD88(-/-), TRIF(-/-), TLR4(-/-), and TLR9(-/-) mice revealed that TLR4- and TLR9-signaling was essential for immunopathology following C. jejuni-infection. Interestingly, C. jejuni-mutant strains deficient in formic acid metabolism and perception induced less intestinal immunopathology compared to the parental strain infection. In summary, the murine gut flora is essential for colonization resistance against C. jejuni and can be overcome by reconstitution of gnotobiotic mice with human flora. Detection of C. jejuni-LPS and -CpG-DNA by host TLR4 and TLR9, respectively, plays a key role in immunopathology. Finally, the host immune response is tightly coupled to bacterial formic acid metabolism and invasion fitness. CONCLUSION/SIGNIFICANCE: We conclude that gnotobiotic and "humanized" mice represent excellent novel C. jejuni-infection and -inflammation models and provide deep insights into the immunological and molecular interplays between C. jejuni, microbiota and innate immunity in human campylobacteriosis

    Acute hunger does not always undermine prosociality

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    This is the final version. Available on open access from Nature Research via the DOI in this recordData Availability: The data that support the findings of this paper are available on the OSF website (https://osf.io/zexd7/?view_only=480593713c904397a033e751a6da7a69).It has been argued that, when they are acutely hungry, people act in self-protective ways by keeping resources to themselves rather than sharing them. In four studies, using experimental, quasi-experimental, and correlational designs (total N = 795), we examine the effects of acute hunger on prosociality in a wide variety of non-interdependent tasks (e.g. dictator game) and interdependent tasks (e.g. public goods games). While our procedures successfully increase subjective hunger and decrease blood glucose, we do not find significant effects of hunger on prosociality. This is true for both decisions incentivized with money and with food. Metaanalysis across all tasks reveals a very small effect of hunger on prosociality in noninterdependent tasks (d = .108), and a non-significant effect in interdependent tasks (d = -0.076). In study five (N = 197), we show that, in stark contrast to our empirical findings, people hold strong lay theories that hunger undermines prosociality.Volkswagen Foundatio

    Single-channel properties of a stretch-sensitive chloride channel in the human mast cell line HMC-1

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    A stretch-activated (SA) Cl− channel in the plasma membrane of the human mast cell line HMC-1 was identified in outside-out patch-clamp experiments. SA currents, induced by pressure applied to the pipette, exhibited voltage dependence with strong outward rectification (55.1 pS at +100 mV and an about tenfold lower conductance at −100 mV). The probability of the SA channel being open (Po) also showed steep outward rectification and pressure dependence. The open-time distribution was fitted with three components with time constants of τ1o = 755.1 ms, τ2o = 166.4 ms, and τ3o = 16.5 ms at +60 mV. The closed-time distribution also required three components with time constants of τ1c = 661.6 ms, τ2c = 253.2 ms, and τ3c = 5.6 ms at +60 mV. Lowering extracellular Cl− concentration reduced the conductance, shifted the reversal potential toward chloride reversal potential, and decreased the Po at positive potentials. The SA Cl− currents were reversibly blocked by the chloride channel blocker 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS) but not by (Z)-1-(p-dimethylaminoethoxyphenyl)-1,2-diphenyl-1-butene (tamoxifen). Furthermore, in HMC-1 cells swelling due to osmotic stress, DIDS could inhibit the increase in intracellular [Ca2+] and degranulation. We conclude that in the HMC-1 cell line, the SA outward currents are mediated by Cl− influx. The SA Cl− channel might contribute to mast cell degranulation caused by mechanical stimuli or accelerate membrane fusion during the degranulation process
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