Sooner or later, people develop a fairly stable set of ways for thinking, judging and responding; this is called one's habitual domain. Our habitual domains (HDs) grow and go wherever we go and have great impact on our behavior and decision making. When we are vital and growing our HDs are expanding and flexible; and when we find ourselves in ruts, not growing, it is because our HDs have become rigid and inflexible, as in death. This book discusses all aspects of habitual domains: their foundations, expansion, dynamics and applications to various nontrivial decision problems in our lives, including effective decision making, effective goal setting, cooperation, conflict resolution, negotiation and career management. Based on an integration of psychology, system science, management and common sense and wisdom, the book provides a simple but unified set of tools in terms of habitual domains and the behavior mechanism. The tools can be applied to expand and sharpen our capacity for knowing ourselves, our coworkers, our rivals, and our environments, and to form winning strategies for solving our problems. To make the book fun to read and the concepts introduced easy to understand and apply, the book is written in plain language with many lively and interesting examples as illustrations. The first half of the book focuses on general descriptions of the behavior mechanism and habitual domains, the second half on applications.
This book introduces a new paradigm called ‘Optimization in Changeable Spaces’ (OCS) as a useful tool for decision making and problem solving. It illustrates how OCS incorporates, searches, and constructively restructures the parameters, tangible and intangible, involved in the process of decision making. The book elaborates on OCS problems that can be modeled and solved effectively by using the concepts of competence set analysis, Habitual Domain (HD) and the mental operators called the 7-8-9 principles of deep knowledge of HD. In addition, new concepts of covering and discovering processes are proposed and formulated as mathematical tools to solve OCS problems. The book also includes reformulations of a number of illustrative real-life challenging problems that cannot be solved by traditional optimization techniques into OCS problems, and details how they can be addressed. Beyond that, it also includes perspectives related to innovation dynamics, management, artificial intelligence, artificial and e-economics, scientific discovery and knowledge extraction. This book will be of interest to managers of businesses and institutions, policy makers, and educators and students of decision making and behavior in DBA and/or MBA.
Autophagy, a conserved “self-eating” process aimed at maintaining cellular homeostasis, has diverse functions in host–pathogen interactions. Many viruses, including hepatitis C virus (HCV), have evolved strategies to subvert the host autophagic machinery and enhance their own replication. Nevertheless, the underlying mechanism for the role of autophagy in HCV replication and whether autophagy modulates the innate immunity in HCV infection are still poorly understood. In a recent study, we showed that infection of hepatoma Huh7 cells with cell culture-derived HCVcc perturbs the autophagy pathway, which proceeds to fusion of the autophagosome with a lysosome, through the unfolded protein response (UPR), to promote HCV RNA replication. Deregulation of the UPR and autophagy by gene silencing or interference with complete autolysosome formation with inhibitors such as chloroquine and Bafilomycin A1 impeded HCV RNA replication. Interruption of the UPR and autophagy concurred with upregulation of the HCV pathogen-associated molecular pattern (PAMP) RNA-mediated cytoplasmic retinoic acid-inducible gene-I signaling and interferon beta (IFN-β)-mediated antiviral responses. With the battery of UPR and autophagy inducers, we demonstrated that activated UPR–autophagy signaling downregulates HCV PAMP RNA-mediated innate immunity even in a context without HCV infection. Moreover, disruption of the autophagic flux by chloroquine or individual knockdown of lysosome-associated membrane protein 2 and RAS-related GTP-binding protein 7, which are critical for fusion of autophagosomes with lysosomes, mitigated UPR- and autophagy-mediated suppression of innate antiviral immunity. Our results manifest that the UPR and autophagy machinery acts as a negative regulator in innate immunity, thus stimulating HCV replication. Our study will also benefit the development of efficacious anti-HCV therapeutic and intervention approaches targeting and/or modifying the UPR and autophagy signaling pathway.
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