Managing entrepreneurial tensions in franchise systems

This is a draft chapter / article. The final version is available in handbook of Research on Franchising, edited by Frank Hoy, Rozenn Perrigot and Andrew Terry, published in 2017, Edward Elgar Publishing Ltd., http://dx.doi.org/10.4337/9781785364181. Under embargo until 27 April 2018. The material cannot be used for any other purpose without further permission of the publisher, and is for private use only.The role of entrepreneurship in franchise systems has been a complex issue. This Chapter aims to provide a better understanding on this issue by focusing on the entrepreneurial tensions that exist in franchise systems and the associated coping mechanisms for minimizing these tensions. It draws on a range of classic and emergent theoretical explanations, which are substantiated with empirical evidence. The Chapter highlights notable contributions in this research area and offers directions to guide future studies in order to provide clarity on the entrepreneurial paradoxes in franchising.Peer reviewe

Late-Onset Erythropoietic Porphyria Caused by a Chromosome 18q Deletion in Erythroid Cells

The erythropoietic porphyrias, erythropoietic protoporphyria and congenital erythropoietic porphyria, result from germline mutations in the ferrochelatase gene and uroporphyrinogen III synthase gene, respectively. Both conditions normally present in childhood but rare cases with onset past the age of 40 y have been reported. Here we show that late-onset erythropoietic protoporphyria can be caused by deletion of the ferrochelatase gene in hematopoietic cells with clonal expansion as part of the myelodysplastic process. This is the first direct demonstration of porphyria produced by an acquired molecular defect restricted to one tissue. Some other cases of late-onset erythropoietic porphyria may be explained by a similar mechanism

High rates of albuminuria but not of low eGFR in Urban Indigenous Australians: the DRUID Study

<p>Abstract</p> <p>Background</p> <p>Indigenous Australians have an incidence of end stage kidney disease 8-10 times higher than non-Indigenous Australians. The majority of research studies concerning Indigenous Australians have been performed in rural or remote regions, whilst the majority of Indigenous Australians actually live in urban settings. We studied prevalence and factors associated with markers of kidney disease in an urban Indigenous Australian cohort, and compared results with those for the general Australian population.</p> <p>Methods</p> <p>860 Indigenous adult participants of the Darwin Region Urban Indigenous Diabetes (DRUID) Study were assessed for albuminuria (urine albumin-creatinine ratio≥2.5 mg/mmol males, ≥3.5 mg/mmol females) and low eGFR (estimated glomular filtration rate < 60 mls/min/1.73 m²). Associations between risk factors and kidney disease markers were explored. Comparison was made with the AusDiab cohort (n = 8,936 aged 25-64 years), representative of the general Australian adult population.</p> <p>Results</p> <p>A high prevalence of albuminuria (14.8%) was found in DRUID, whilst prevalence of low eGFR was 2.4%. Older age, higher HbA1c, hypertension, higher C-reactive protein and current smoking were independently associated with albuminuria on multiple regression. Low eGFR was independently associated with older age, hypertension, albuminuria and higher triglycerides. Compared to AusDiab participants, DRUID participants had a 3-fold higher adjusted risk of albuminuria but not of low eGFR.</p> <p>Conclusions</p> <p>Given the significant excess of ESKD observed in Indigenous versus non-Indigenous Australians, these findings could suggest either: albuminuria may be a better prognostic marker of kidney disease than low eGFR; that eGFR equations may be inaccurate in the Indigenous population; a less marked differential between Indigenous and non-Indigenous Australians for ESKD rates in urban compared to remote regions; or that differences in the pathophysiology of chronic kidney disease exist between Indigenous and non-Indigenous populations.</p

Exploring assessment of medical students\u27 competencies in pain medicine - A review

Introduction: Considering the continuing high prevalence and public health burden of pain, it is critical that medical students are equipped with competencies in the field of pain medicine. Robust assessment of student expertise is integral for effective implementation of competency-based medical education. Objective: The aim of this review was to describe the literature regarding methods for assessing pain medicine competencies in medical students. Method: PubMed, Medline, EMBASE, ERIC, and Google Scholar, and BEME data bases were searched for empirical studies primarily focusing on assessment of any domain of pain medicine competencies in medical students published between January 1997 and December 2016. Results: A total of 41 studies met the inclusion criteria. Most assessments were performed for low-stakes summative purposes and did not reflect contemporary theories of assessment. Assessments were predominantly undertaken using written tests or clinical simulation methods. The most common pain medicine education topics assessed were pain pharmacology and the management of cancer and low-back pain. Most studies focussed on assessment of cognitive levels of learning as opposed to more challenging domains of demonstrating skills and attitudes or developing and implementing pain management plans. Conclusion: This review highlights the need for more robust assessment tools that effectively measure the abilities of medical students to integrate pain-related competencies into clinical practice. A Pain Medicine Assessment Framework has been developed to encourage systematic planning of pain medicine assessment at medical schools internationally and to promote continuous multidimensional assessments in a variety of clinical contexts based on well-defined pain medicine competencies

Pervasiveness of Parasites in Pollinators

Many pollinator populations are declining, with large economic and ecological implications. Parasites are known to be an important factor in the some of the population declines of honey bees and bumblebees, but little is known about the parasites afflicting most other pollinators, or the extent of interspecific transmission or vectoring of parasites. Here we carry out a preliminary screening of pollinators (honey bees, five species of bumblebee, three species of wasp, four species of hoverfly and three genera of other bees) in the UK for parasites. We used molecular methods to screen for six honey bee viruses, Ascosphaera fungi, Microsporidia, and Wolbachia intracellular bacteria. We aimed simply to detect the presence of the parasites, encompassing vectoring as well as actual infections. Many pollinators of all types were positive for Ascosphaera fungi, while Microsporidia were rarer, being most frequently found in bumblebees. We also detected that most pollinators were positive for Wolbachia, most probably indicating infection with this intracellular symbiont, and raising the possibility that it may be an important factor in influencing host sex ratios or fitness in a diversity of pollinators. Importantly, we found that about a third of bumblebees (Bombus pascuorum and Bombus terrestris) and a third of wasps (Vespula vulgaris), as well as all honey bees, were positive for deformed wing virus, but that this virus was not present in other pollinators. Deformed wing virus therefore does not appear to be a general parasite of pollinators, but does interact significantly with at least three species of bumblebee and wasp. Further work is needed to establish the identity of some of the parasites, their spatiotemporal variation, and whether they are infecting the various pollinator species or being vectored. However, these results provide a first insight into the diversity, and potential exchange, of parasites in pollinator communities

Handbook of Research on Franchising

In Memoriam by Patrick KaufmannForeward by Francine LafontaineInternational audienceFranchising is one of the major engines of business expansion and job creation globally. The Handbook of Research on Franchising contains original work by leading franchise scholars from around the world who offer new insights into entrepreneurial behavior, organizational forms, regulation, internationalization and other contemporary issues relating to this dynamic business strategy.The book will provide readers with a base of knowledge about the entrepreneurial opportunities and behaviors of franchisors and franchisees as well as explore the forms that franchise organizations may take, the regulation of franchise companies, how franchisors and franchisees relate to one another, the development of the franchise model, franchising in emerging markets, social franchising and more. It introduces theory and sets the agenda for future research and adds to education and practice.Practitioners will benefit from the high quality scientific research, and scholars will find exciting opportunities for contributing to the body of knowledge on a subject that has not received sufficient attention. The research contained in this book will also be of value to franchisors, franchisees, service providers and government regulators

GCSF augments post-progenitor proliferation in serum-free cultures of myelodysplastic marrow while ATRA enhances maturation

All-trans retinoic acid (ATRA) and granulocyte colony stimulating factor (GCSF) are potential inducers of myeloid progenitor cell growth and neutrophil differentiation in myelodysplasia (MDS). We have compared the effects of ATRA and GCSF on the colony growth of 10 MDS marrows, in semi-solid and liquid serum-free mononuclear cell (MNC) cultures, supplemented with a mixture of stem cell factor (SCF), interleukin 3 (IL-3) and granulocyte-monocyte colony stimulating factor (GmCSF) (SIGm mix), which is fully-supportive for myeloid and erythroid (with erythropoietin (EPO)) colony formation in normal marrow. Only 1/10 MDS patients produced normal granulocyte-macrophage colony-forming cell (GmCFC) numbers, under SIGm conditions and erythroid colonies (ECFC) were subnormal in all patients. ATRA (10(-7) M) increased GmCFC numbers (P=0.05) in semi-solid cultures of normal, but not MDS marrow MNC and decreased erythroid colonies in cultures of marrow from either source (P=0.008 and P=0.0001 for normal and MDS, respectively). ATRA enhanced neutrophilic maturation in liquid cultures of both normal and myelodysplastic CD34 + ve cells, as detected by conventional morphology and acquisition of CD15. In contrast to ATRA, GCSF increased Gm colony size but not numbers in semi-solid cultures of normal marrow MNC, which suggests the cytokine augments post-progenitor amplification. This would explain why GCSF increased cell yields in liquid cultures of normal and MDS MNC while GmCFC accumulation remained unchanged. GCSF, though, increased Gm colony numbers in semi-solid cultures of MDS marrow MNC (P=0.014) so that 4/10 patients now grew colonies within the normal range. This was again probably due to increasing clone size, so that some clusters, the numbers of which may be elevated in MDS, were now scored as colonies. Overall, these data indicate that ATRA can enhance the maturation of the progeny of MDS GmCFC whilst GCSF can augment their amplification