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Dimo Dimov

Researcher at University of Bath

Publications -  137
Citations -  7275

Dimo Dimov is an academic researcher from University of Bath. The author has contributed to research in topics: Entrepreneurship & Venture capital. The author has an hindex of 33, co-authored 117 publications receiving 6158 citations. Previous affiliations of Dimo Dimov include University of Connecticut & IE University.

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Journal ArticleDOI

Action! Impulse Driven Logic & Entrepreneurial Opportunity Pursuit

TL;DR: This article explore the limits of this premise by considering less deliberate, more impulse decision-making, and consider less deliberate and more impulse-driven decision-makers, instead of evaluating opportunities before deciding to pursue them.
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Concepts as Mirrors and Torches: Rigor and Relevance as Scholarly Performativity

TL;DR: In this article , the authors argue that tensions arise due to an adherence to a rigor-as-correspondence perspective, which can be addressed through the advancement of a rigorspecificity perspective.
Book ChapterDOI

Cross-Functional Collaboration, Knowledge Transfer and Product Innovativeness: Contingency Effects of Social Context

TL;DR: In this paper, a contingency perspective is used to examine how social capital influences the relationship between cross-functional collaboration and product innovativeness, and it is found that the relationship is amplified at higher levels of the three social capital dimensions.
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A translational framework for entrepreneurship research

TL;DR: A new translational research framework for entrepreneurship is proposed in this article , which leverages translational knowledge from biomedical science and design science to lay the ground for a new research ecosystem of entrepreneurship.
Journal ArticleDOI

Single Nucletide Polymorphisms in Gene of IL-1Beta in Bronchial Asthma

TL;DR: It is suggested that the -511C>T promoter polymorphism and +3953C >T silent polymorphism in exon 5 of IL1B may influence the genetic predisposition of Bronchial asthma in Bulgarian population, as the carriers of alleles and haplotypes supposed to define higher IL-1β protein levels are more susceptible for this lung diseases.