What do We Know About Entrepreneurial Finance and its Relationship with Growth?

This article explores what we do (and do not) know about entrepreneurial finance and its relationship with growth. Broadly, there is a need for research to go beyond traditional supply side/market failure issues to better understand the role of entrepreneurial cognition, objectives, ownership types and firm life-cycle stages in financing/investment decisions. We show that little is known about the pivotal relationship between access to external finance and growth due to limitations in current approaches to testing financial constraints. Instead, we propose that the relationship between funding gaps and business performance as a direct and nuanced approach to identifying financial constraints in different entrepreneurial finance markets requires scrutiny. There is also a necessity for research to disentangle cognitive from financial constraints and to better understand the role of financiers in enabling growth. In particular, there is a need to explore the relationship between non-bank sources of finance and growth, shorn of inherent survival and selection bias. We outline an agenda for future research to address gaps in our understanding

CMOS implementation of hysteretic controller fo a DC-to-DC buck converter using 0.35um library

Hsyteretic comparators employ positive feedback mechanism which would enable the system to constantly check whether the output exceeds the lower and upper threshold voltages. By applying this system to a DC to DC buck converter, the use of pulse width modulated (PWM) signals would not be necessary anymore. In this research, a 3.3V input was stepped down to a 1.5 output with a minimum current of 10mA. A start-up circuit using XOR and XNOR gates were used to provide initial pulses from 0us to 100us in order to ensure that the buck converter can initially charge up and provide a change in the negative input of the comparator. An op-amp based reference bandgap voltage was also included in the design and was placed at the positive input terminal of the comparator. Testing was done on all process corner libraries and the output showed consistency, having only minimal deviations. Temperature sweep from 25°C to 80°C, line regulation from 2.9V to 3.3V, and load regulation from 100 to 500 were also checked and gave positive results. The output for load regulation ranged from 1.5038V to 1.5903V for a 100 load, and a 1.5239V to 1.6204V for a 500 load. The output voltage of the buck converter ranged from 1.2V to 2V thereby producing an average of around 1.5V. Among the process corner libraries, slow-slow (SS) produce the highest output voltage whihc was 1.55V. The overall circuit was implemented using tanner, and the pre-layout and post-layout designs had a maximum percent difference of 3.5% for both the voltage and the current. The final layout has a size of 1499.05um x 1056.1 um

Regulatory Focus and Information Cues in a Crowdfunding Context

It is well understood that information cues associated with an investment opportunity generally impact one\u27s willingness to participate in that opportunity. What is less well understood, however, is how different types of information cues affect individuals differently, and whether this effect is contingent on the decision maker\u27s individual attributes. Through a three-study experimental design involving a simulated crowdfunding portal, this research examined the effects of venture quality information and social information on participants’ willingness to invest in a new venture. We hypothesised that participants’ responsiveness to these information cues was contingent on their regulatory focus. Our results were generally supported, although some counterintuitive findings emerged regarding prevention-focused individuals. From a practical standpoint, our results suggest potential concerns regarding the general enthusiasm for crowdfunding, as well as some mitigating factors

Expression of insulin-like peptide 3 in the postnatal rat Leydig cell lineage: timing and effects of triiodothyronine-treatment

Copyright © 2007 Society for Reproduction and FertilityFetal (FLC) and adult Leydig cells (ALC) secrete insulin-like peptide 3 (INSL3), which is linked to cryptorchidism in the newborn rat. Its gene regulation appears to be independent of that for most steroidogenic enzymes, and may thus be a marker for other aspects of ALC differentiation. Our study examined the following on INSL3 peptide expression in ALC lineage (i) timing, (ii) which cell stage, and (iii) effects of triiodothyronine (T3). Male Sprague-Dawley (SD) rats of postnatal days (pd) 1, 5, 7-21, 28, 40, 60, and 90 were used for the objectives (i) and (ii). For the objective (iii), control and T3-treated (daily T3 SC, 50 mug/kg bw) SD rats of pd7-16 and 21 were used. INSL3 was immunolocalized in Bouin's-fixed testes. FLC were positive and mesenchymal and Leydig progenitor cells were negative for INSL3 at tested ages. INSL3 in ALC lineage was first detected in newly formed ALC on pd16, although they were present from pd10. The intensity of INSL3 label was greater in ALC of pd40-90. ALC were present in T3-treated testes at pd9, but INSL3 first detected in them was on pd12. While INSL3 in FLC regulates testicular descent, INSL3 in ALC still has no well-defined function. However, its pattern of expression correlates temporally with the development of steroidogenic function and spermatogenesis. Thus, the delay between ALC differentiation and INSL3 expression in them implies that INSL3 in ALC is associated with maturation. The advancement of INSL3 expression in the ALC of T3-treated rats implies that this function is established earlier with T3-treatment.S M L C Mendis-Handagama, H B S Ariyaratne, L Mrkonjich and R Ivel

Functional repair assay for the diagnosis of constitutional mismatch repair deficiency from non-neoplastic tissue

Purpose: Constitutional mismatch repair deficiency (CMMRD) is a highly penetrant cancer predisposition syndrome caused by biallelic mutations in mismatch repair (MMR) genes. As several cancer syndromes are clinically similar, accurate diagnosis is critical to cancer screening and treatment. As genetic diagnosis is confounded by 15 or more pseudogenes and variants of uncertain significance, a robust diagnostic assay is urgently needed. We sought to determine whether an assay that directly measures MMR activity could accurately diagnose CMMRD.Patients and Methods: In vitro MMR activity was quantified using a 3\u27-nicked G-T mismatched DNA substrate, which requires MSH2-MSH6 and MLH1-PMS2 for repair. We quantified MMR activity from 20 Epstein-Barr virus-transformed lymphoblastoid cell lines from patients with confirmed CMMRD. We also tested 20 lymphoblastoid cell lines from patients who were suspected for CMMRD. We also characterized MMR activity from patients with neurofibromatosis type 1, Li-Fraumeni syndrome, polymerase proofreading-associated cancer syndrome, and Lynch syndrome.Results: All CMMRD cell lines had low MMR activity (n = 20; mean, 4.14 ± 1.56%) relative to controls (n = 6; mean, 44.00 ± 8.65%; P \u3c .001). Repair was restored by complementation with the missing protein, which confirmed MMR deficiency. All cases of patients with suspected CMMRD were accurately diagnosed. Individuals with Lynch syndrome (n = 28), neurofibromatosis type 1 (n = 5), Li-Fraumeni syndrome (n = 5), and polymerase proofreading-associated cancer syndrome (n = 3) had MMR activity that was comparable to controls. To accelerate testing, we measured MMR activity directly from fresh lymphocytes, which yielded results in 8 days.Conclusion: On the basis of the current data set, the in vitro G-T repair assay was able to diagnose CMMRD with 100% specificity and sensitivity. Rapid diagnosis before surgery in non-neoplastic tissues could speed proper therapeutic management