Exploring Entrepreneurship (2nd edition)

We have written this book to help you to explore entrepreneurship in all its complexity and variety. Our approach is based on the view that some subjects, such as medicine, engineering, and entrepreneurship, are particularly well-suited to experience-based learning. The basic idea is that people can learn a lot more if they are able to connect the research evidence and the theory to some kind of direct personal experience. The nature of this ‘experience’ depends a great deal on what you are studying. For example, a medical student spends time working in different parts of a hospital, while an engineering student might design a new product or test some materials in a laboratory. Providing practical experience is more difficult for entrepreneurship students, but it is possible to re-create some aspects of a ‘real-life’ experience using new venture exercises, business plan competitions, and computer simulations. In this book, we provide support for all three types of activity. However, experience-based learning is about more than just having an experience. Some of the most important learning happens when practical activity is combined with well-structured reflection. With this in mind, we have designed the book around three related aims: 1. to help you gain essential practical skills and underpinning knowledge, and reflect on the challenges involved in creating an entrepreneurial venture, either individually or as part of a team; 2. to help you develop a deeper understanding of entrepreneurship, as you make connections between your experiences, relevant theoretical concepts, research findings, and the experiences of others; 3. to encourage you to take part in a broader debate about entrepreneurship in the twenty-first century, examining contrasting perspectives on entrepreneurship across a wide range of ventures. Exploring Entrepreneurship covers practical issues related to the creation of an entrepreneurial venture, together with reviews of related research evidence and more theoretical discussion about entrepreneurship. We also make considerable use of case-based examples, so that you can learn from the experiences of real entrepreneurs as they struggle to create and to develop their ventures. It is worth noting two distinctive features of this book. Firstly, it provides detailed coverage of many different types of entrepreneurship. You will find examples of commercial, primarily profit-oriented ventures and what are often termed ‘social’ enterprises, where the primary aim is to address a social or environmental challenge, rather than simply to secure a profit. In contrast to most other texts, it also addresses ‘anti-social’ forms of entrepreneurship, with examples that range from the unethical and environmentally destructive behaviour of legitimate firms to the shady world of organised crime. The argument behind these decisions is simple: entrepreneurial activity is clearly a very powerful force in the world. We think it is important for entrepreneurship students to consider seriously how that power is exercised. In summary, this book offers a fresh, wide-ranging, and up-to-date approach to entrepreneurship, combining practical relevance with critical reflection. We also hope that it will help you to experience something of the excitement, uncertainty, passion, and sheer hard work that is involved in creating a successful entrepreneurial venture

<i>CXCL5</i> expression is modulated by atorvastatin and IL-1β.

<p>(A) Gel electrophoresis of <i>CXCL5</i> and <i>GAPDH</i> PCR products; (B) Log₁₀ relative quantification of <i>CXCL5</i> modulated by atorvastatin, IL-1β, and their combination normalized to <i>GAPDH</i> (N = 2 experiments). *P<0.005, †P<0.0001. AT, atorvastatin.</p

Adjusted hazard ratio and 95% confidence intervals for all-cause mortality by genotype.

<p>Top panel is overall population (p = 0.017) and bottom panel is Caucasians only (p = 0.043). Models adjusted for age, race, sex, ACS type, revascularization strategy, history of diabetes, and history of heart failure.</p

Atorvastatin effects on ENA-78 are reversed by mevalonate and its downstream metabolites.

<p>Data are presented as mean±SEM of 10 experiments. *p<0.001 and †p = 0.05 compared to IL-1β stimulation alone. AT, atorvastatin; FPP, farnesyl pyrophosphate; GGPP, geranylgeranyl pyrophosphate; MEV, mevalonate.</p

Kaplan Meier estimates for all-cause mortality by <i>CXCL5</i> −156 G>C genotype.

<p>Panel A represents the overall population; panel B represents the Caucasians only.</p

Baseline Characteristics.

<p>*n = 603; ^†n = 594; ^‡n = 565; ^§n = 593; ACS = Acute coronary syndrome; MI = Myocardial infarction; LBB = Left bundle block; HTN = Hypertension; BMI = Body mass index; EF = Ejection fraction; SBP = Systolic blood pressure; DBP = Diastolic blood pressure; HDL = High density lipoprotein; LDL = Low density lipoprotein; PCI = Percutaneous coronary intervention; CABG = Coronary artery bypass graft.</p

Atorvastatin attenuates ENA-78 production over time.

<p>Levels are relative to baseline (0 hour) for each condition. Data are presented as mean±SEM of 4 experiments. *p≤0.01. —○—, IL-1β stimulation+atorvastatin 10 µM; —•—, IL-1β stimulation alone; AT, atorvastatin.</p

Atorvastatin attenuates IL-1β-induced ENA-78 production in a dose-dependent fashion.

<p>Data are presented as mean±SEM of 4 experiments. * p<0.0001 vs. IL-1β, †p = NS vs. control. AT, atorvastatin.</p

All-cause mortality rate by genotype among statin-treated and non-treated patients.

<p>*p = 0.0009., †p = 0.48; ‡p = 0.46.</p

Proportions of the ApoE4 allele carriers, mean age at the time of biospecimens collection, and the allele-specific proportions of deaths, CVD, cancer, and ND for the genotyped participants of the FHS, FHSO, and LLFS.

<p>FHS = the Framingham Heart Study (FHS) original cohort; FHSO = the FHS offspring cohort.</p><p>LLFS_P = long-living parental generation of the Long Life Family Study (LLFS) participants; LLFS_O = offspring of the LLFS long-living participants; LLFS_S = spouses of the LLFS long-living participants and their offspring.</p><p>CVD = cardiovascular diseases including diseases of heart and stroke; Cancer = all sites but skin; ND = dementia and Alzheimer disease combined; SD = standard deviation.</p>*<p>proportion of the ApoE4 allele carriers is in percentages;</p>**<p>maximal sample size; the number of individuals with non-missing information on ND is about 1% less in the FHS and about 3% less in the FHSO.</p>***<p>age at biospecimens collection at the 19^th FHS, 4^th FHSO and baseline LLFS examinations.</p><p>The ApoE4-allele-specific proportions of CVD, cancer, and ND are not given for the LLFS because this information was not used in this paper.</p