How strategic orientations influence the building of dynamic capability in emerging economies

Under the fierce pressures of the fast changing environments that characterize emerging economies, firms must develop dynamic capabilities to survive the competition. This study examines how strategic orientation helps build dynamic capability and its contingencies in China's emerging economy. A survey of 380 firms indicates strategic orientations are important drivers of adaptive capability, a key element of dynamic capabilities. The effectiveness of strategic orientations is contingent on market dynamics. In particular, when market demand becomes increasingly uncertain, customer orientation has a weaker impact, whereas technology orientation has a stronger effect on adaptive capability. As competition intensifies, both competitor and technology orientations build adaptive capability more effectively. © 2009 Elsevier Inc. All rights reserved.postprin

Unsupervised Domain Adaptation for 3D Keypoint Estimation via View Consistency

In this paper, we introduce a novel unsupervised domain adaptation technique for the task of 3D keypoint prediction from a single depth scan or image. Our key idea is to utilize the fact that predictions from different views of the same or similar objects should be consistent with each other. Such view consistency can provide effective regularization for keypoint prediction on unlabeled instances. In addition, we introduce a geometric alignment term to regularize predictions in the target domain. The resulting loss function can be effectively optimized via alternating minimization. We demonstrate the effectiveness of our approach on real datasets and present experimental results showing that our approach is superior to state-of-the-art general-purpose domain adaptation techniques.Comment: ECCV 201

Reasoning about goal-directed real-time teleo-reactive programs

The teleo-reactive programming model is a high-level approach to developing real-time systems that supports hierarchical composition and durative actions. The model is different from frameworks such as action systems, timed automata and TLA+, and allows programs to be more compact and descriptive of their intended behaviour. Teleo-reactive programs are particularly useful for implementing controllers for autonomous agents that must react robustly to their dynamically changing environments. In this paper, we develop a real-time logic that is based on Duration Calculus and use this logic to formalise the semantics of teleo-reactive programs. We develop rely/guarantee rules that facilitate reasoning about a program and its environment in a compositional manner. We present several theorems for simplifying proofs of teleo-reactive programs and present a partially mechanised method for proving progress properties of goal-directed agents. © 2013 British Computer Society

Rapid Processing of Both Reward Probability and Reward Uncertainty in the Human Anterior Cingulate Cortex

Reward probability and uncertainty are two fundamental parameters of decision making. Whereas reward probability indicates the prospect of winning, reward uncertainty, measured as the variance of probability, indicates the degree of risk. Several lines of evidence have suggested that the anterior cingulate cortex (ACC) plays an important role in reward processing. What is lacking is a quantitative analysis of the encoding of reward probability and uncertainty in the human ACC. In this study, we addressed this issue by analyzing the feedback-related negativity (FRN), an event-related potential (ERP) component that reflects the ACC activity, in a simple gambling task in which reward probability and uncertainty were parametrically manipulated through predicting cues. Results showed that at the outcome evaluation phase, while both win and loss-related FRN amplitudes increased as the probability of win or loss decreased, only the win-related FRN was modulated by reward uncertainty. This study demonstrates the rapid encoding of reward probability and uncertainty in the human ACC and offers new insights into the functions of the ACC

Regulation of aldosterone secretion by Ca(v)1.3

This work is supported by NIHR Senior Investigator grant NF-SI-0512-10052 awarded to M.J.B.; the Austin Doyle Award (Servier Australia) and the Tunku Abdul Rahman Centenary Fund (St Catharine's College, Cambridge, UK) awarded to E.A.B.A.; Gates Cambridge Scholarship awarded to C.B.X.; L.H.S., S.G. and C.M. are supported by the British Heart Foundation PhD studentship FS/11/35/28871, FS/14/75/31134 and FS/14/12/30540 respectively; J.Z. was supported by the Cambridge Overseas Trust Scholarship and the Sun Hung Kai Properties-Kwoks’ Foundation; A.E.D.T. is funded by the Agency for Science, Technology & Research (A*STAR) Singapore and Wellcome Trust Award 085686/Z/08/A; LHS, JZ and EABA were further supported by the NIHR Cambridge Biomedical Research Centre; the Human Research Tissue Bank is supported by the NIHR Cambridge Biomedical Research Centre. The Cav1.3 constructs were kindly gifted by Dr. Joerg Striessnig and Dr Petronel Tuluc

Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain.

INTRODUCTION: Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG. RESULTS: MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks. CONCLUSIONS: These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients

Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain.

INTRODUCTION: Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG. RESULTS: MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks. CONCLUSIONS: These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients

Predators reduce extinction risk in noisy metapopulations

Background Spatial structure across fragmented landscapes can enhance regional population persistence by promoting local “rescue effects.” In small, vulnerable populations, where chance or random events between individuals may have disproportionately large effects on species interactions, such local processes are particularly important. However, existing theory often only describes the dynamics of metapopulations at regional scales, neglecting the role of multispecies population dynamics within habitat patches. Findings By coupling analysis across spatial scales we quantified the interaction between local scale population regulation, regional dispersal and noise processes in the dynamics of experimental host-parasitoid metapopulations. We find that increasing community complexity increases negative correlation between local population dynamics. A potential mechanism underpinning this finding was explored using a simple population dynamic model. Conclusions Our results suggest a paradox: parasitism, whilst clearly damaging to hosts at the individual level, reduces extinction risk at the population level

Bias in trials comparing paired continuous tests can cause researchers to choose the wrong screening modality

<p>Abstract</p> <p>Background</p> <p>To compare the diagnostic accuracy of two continuous screening tests, a common approach is to test the difference between the areas under the receiver operating characteristic (ROC) curves. After study participants are screened with both screening tests, the disease status is determined as accurately as possible, either by an invasive, sensitive and specific secondary test, or by a less invasive, but less sensitive approach. For most participants, disease status is approximated through the less sensitive approach. The invasive test must be limited to the fraction of the participants whose results on either or both screening tests exceed a threshold of suspicion, or who develop signs and symptoms of the disease after the initial screening tests.</p> <p>The limitations of this study design lead to a bias in the ROC curves we call <it>paired screening trial bias</it>. This bias reflects the synergistic effects of inappropriate reference standard bias, differential verification bias, and partial verification bias. The absence of a gold reference standard leads to inappropriate reference standard bias. When different reference standards are used to ascertain disease status, it creates differential verification bias. When only suspicious screening test scores trigger a sensitive and specific secondary test, the result is a form of partial verification bias.</p> <p>Methods</p> <p>For paired screening tests with bivariate normally distributed scores, we give formulae and programs to quantify the effect of <it>paired screening trial bias </it>on a paired comparison of area under the curves. We fix the prevalence of disease, and the chance a diseased subject manifests signs and symptoms. We derive the formulas for true sensitivity and specificity, and those for the sensitivity and specificity observed by the study investigator.</p> <p>Results</p> <p>The observed area under the ROC curves is quite different from the true area under the ROC curves. The typical direction of the bias is a strong inflation in sensitivity, paired with a concomitant slight deflation of specificity.</p> <p>Conclusion</p> <p>In paired trials of screening tests, when area under the ROC curve is used as the metric, bias may lead researchers to make the wrong decision as to which screening test is better.</p