Entrepreneurial cognition of the business model construct:A mixed methods study of stem and non-stem entrepreneurs

Applying the theory of socially situated cognition, we study how entrepreneurs cognitively process the business model construct during the early stages of launching technology-based new ventures. Through an abductive reasoning procedure, we aggregate four underlying socially situated cognitive functions of the business model and describe how these functions facilitate opportunity development. We examine if the entrepreneur’s educational background (STEM vs non-STEM) influences their cognitive processing of the construct. We discuss the contribution of our study to the literature on managerial cognition, business models, and to practice in detail

"Yes and. . ., but wait. . ., heck no!":A socially situated cognitive approach towards understanding how startup entrepreneurs process critical feedback

We examine sensebreaking, a meaning void, that entrepreneurs experience due to critical feedback from early stakeholders using the socially situated cognition perspective. We show that sensebreaking aids novel sensemaking via three mechanisms-redirecting, reframing, and questioning-through longitudinal analysis of weekly diary reports that we collected from 30 entrepreneurs for one year. We describe the cognitive changes due to novel sensemaking. We derive a process model that illustrates how sensebreaking-sensemaking iterations over time effect changes to the shared cognition between entrepreneurs and their stakeholders while driving opportunity development. We advance the opportunity coconstruction literature by adding microlevel understanding of stakeholder interactions and explicating their effects on entrepreneurial cognition

Entrepreneurial cognition of the business model construct:A mixed methods study of stem and non-stem entrepreneurs

Applying the theory of socially situated cognition, we study how entrepreneurs cognitively process the business model construct during the early stages of launching technology-based new ventures. Through an abductive reasoning procedure, we aggregate four underlying socially situated cognitive functions of the business model and describe how these functions facilitate opportunity development. We examine if the entrepreneur’s educational background (STEM vs non-STEM) influences their cognitive processing of the construct. We discuss the contribution of our study to the literature on managerial cognition, business models, and to practice in detail

Entrepreneurial cognition of the business model construct:A mixed methods study of stem and non-stem entrepreneurs

Applying the theory of socially situated cognition, we study how entrepreneurs cognitively process the business model construct during the early stages of launching technology-based new ventures. Through an abductive reasoning procedure, we aggregate four underlying socially situated cognitive functions of the business model and describe how these functions facilitate opportunity development. We examine if the entrepreneur’s educational background (STEM vs non-STEM) influences their cognitive processing of the construct. We discuss the contribution of our study to the literature on managerial cognition, business models, and to practice in detail

Embedding massive flavor in ABJM

We add massive fundamental matter to the ABJM model by adding D6-branes wrapped asymptotically over RP3. We find two types of solutions at finite temperature, one that enters the black hole and one that ends before the black hole. We analyze the behavior of the free energy as a function of temperature, and find that the system exhibits a phase transition between the two types of solutions, similar to what happens in the D3-D7 system. We also analyze the meson spectrum in the model and find several massive scalar modes, again, quite like the D3-D7 system. We end with a calculation of the conductivities in the two phases.Comment: 26 pages, 6 figures; version published in JHE

Tumour growth in mice resistant to diet-induced obesity

Obesity is a chronic disease with associated increases in the incidence, and a reduction in survival, of many cancer types. Obesity results from an imbalance in calorie intake and calorie requirement. This study aimed to investigate the separate effects of high-fat diet and obesity on cancer in an animal model resistant to diet-induced obesity. Male BALB/c mice fed long-term on a high-fat, Western-style diet were implanted with syngeneic CT26 colon adenocarcinoma cells and compared to mice fed normal diet. BALB/c mice on high-fat diet were 10% heavier than mice fed normal diet, with no difference in tumour growth rates or tumour cell proliferation. Subgroups of mice that became obese on high-fat diet, however, showed increased tumour growth rates compared to mice fed normal diet, whereas mice that remained slim showed no difference in tumour growth. Protein arrays identified several adipokines that were expressed at different levels, including serum Tissue Inhibitors of Metallo-Proteinases (TIMP-1) and tumour C-Reactive Protein (CRP). In conclusion, tumour growth was enhanced in mice unable to resist obesity, and adipokine profiles were affected by the animals’ ability to resist obesity

In vivo aging of rat skeletal muscle sarcoplasmic reticulum Ca-ATPase. Chemical analysis and quantitative simulation by exposure to low levels of peroxyl radicals

AbstractSarcoplasmic reticulum (SR) Ca-ATPase of young adult (5 months) and aged (28 months) Fischer 344 male rat skeletal muscle was analyzed for posttranslational modifications as a result of biological aging and their potential functional consequences. The significant differences in the amino acid composition were a 6.8% lower content of sulfhydryl groups and a ca. 4% lower content of Arg residues of the Ca-ATPase from old as compared to young rats. Based on a total of 24 Cys residues the difference in protein thiols corresponds to a loss of 1.5 mol Cys/mol Ca-ATPase as a result of in vivo aging. The loss of Cys residues was not accompanied by a loss of enzyme activity though the `aged' Ca-ATPase was more sensitive to heat inactivation, aggregation, and tryptic digestion. A comparison of the total sulfhydryl content of all SR proteins present revealed a 13% lower amount for SR vesicles isolated from aged rats. Compared to the alterations of Cys and Arg, there was only a slight and probably physiologically insignificant increase of protein carbonyls with aging, i.e. from 0.32 to 0.46 mol carbonyl groups per mol of Ca-ATPase. When SR vesicles from young rats were exposed to AAPH-derived peroxyl radicals, there was a loss of ca. 1.38×10−4 M total SR sulfhydryl groups per 4 mg SR protein/ml (corresponding to ca. 25%) and a loss of 9.6×10−5 M Ca-ATPase sulfhydryl groups (corresponding to ca. 31%) per 1.6×10−5 M initiating peroxyl radicals, indicating that the stoichiometry of sulfhydryl oxidation was ≥6 oxidized thiols per initiating AAPH-derived peroxyl radical. Besides Cys, the exposure to AAPH-derived radicals caused a slight loss of Ca-ATPase Arg, Met, and Ser residues. Most importantly, the SR Ca-ATPase exposed to this low concentration of peroxyl radicals displayed physical and functional properties quantitatively comparable to those of SR Ca-ATPase isolated from aged rats, i.e. no immediate loss of activity, increased susceptibility to heat inactivation, aggregation, and tryptic digestion. Moreover, a comparison of kinetically early tryptic fragments by HPLC-electrospray MS and N-terminal sequencing revealed that similar peptide fragments were produced from `aged' and AAPH-oxidized Ca-ATPase which were not (or kinetically significantly later) generated from the `young' Ca-ATPase, suggesting some conformational changes of the Ca-ATPase as a result of aging and AAPH-exposure. All except one of these peptides originated from locations remote from the nucleotide-binding and calcium-binding sites. The latter results suggest that aging and AAPH-exposure may target similar Cys residues, mainly at locations remote from the nucleotide-binding and calcium-binding sites, rationalizing the fact that Cys oxidation did not immediately cause inactivation of the Ca-ATPase. Our results provide a quantitative estimate of a net concentration of reactive oxygen species, here peroxyl radicals, which induces physical and chemical alterations of the SR Ca-ATPase quantitatively comparable to those induced by in vivo aging