Lean Product Development in Early Stage Startups

Software startups are more popular than ever and growing innumbers. They operate under conditions of extreme uncertainty and face plentyof challenges, underlined by their high failure rate. Using Design ScienceResearch, these challenges were investigated. A literaturestudy showed that inrecent years, several authors have suggested ways to increase the odds ofsucceeding as a startup, such as customer focused development, fact baseddecision making, pivoting and agile/lean thinking. Interviews with industryprofessionals showed that few usedtheseLean Startup practices: many foundthem difficult to implement in practice. In response, we developed the EarlyStage Software Startup Development Model (ESSSDM) for managing earlystage software startups by applying Lean Startup principles. The modelis novelin that itsupports managing a portfolio of product ideas and provides clearcriteria for when to move forward with product ideas, when to abandon productideasas well asrecommends whatconcrete techniques that can be used andwhen, in order to achieve this. The process was instantiated and evaluated on astartup project in an incubator setting

Regularizations of residue currents

Under assumptions about complete intersection, we prove that Coleff-Herrera type currents satisfy a robust calculus in the sense that natural regularizations of such currents can be multiplied to yield regularizations of the Coleff-Herrera product of the currents

Regularizations of residue currents

Under assumptions about complete intersection, we prove that Coleff-Herrera type currents satisfy a robust calculus in the sense that natural regularizations of such currents can be multiplied to yield regularizations of the Coleff-Herrera product of the currents

Regularizations of Residue Currents

Under assumptions about complete intersection, we prove that Coleff-Herrera type currents satisfy a robust calculus in the sense that natural regularizations of such currents can be multiplied to yield regularizations of the Coleff-Herrera product of the currents

The Early Stage Software Startup Development Model: A Framework for Operationalizing Lean Principles in Software Startups

Software startups are more popular than ever and growing in numbers. They operate under conditions of extreme uncertainty and face many challenges. Often, agile development practices and lean principles are suggested as ways to increase the odds of succeeding as a startup, as they both advocate close customer collaboration and short feedback cycles focusing on delivering direct customer value. However, based on an interview study we see that despite guidance and support in terms of well-known and documented development methods, practitioners find it difficult to implement and apply these in practice. To explore this further, and to propose operational support for software startup companies, this study aims at investigating (1) what are the typical challenges when finding a product idea worth scaling, and (2) what solution would serve to address these challenges. To this end, we propose the ‘Early Stage Software Startup Development Model’ (ESSSDM). The model extends already existing lean principles, but offers novel support for practitioners for investigating multiple product ideas in parallel, for determining when to move forward with a product idea, and for deciding when to abandon a product idea. The model was evaluated in a software startup project, as well as with industry professionals within the software startup domain

GREM1 and POLE variants in hereditary colorectal cancer syndromes

Hereditary factors are thought to play a role in at least one third of patients with colorectal cancer (CRC) but only a limited proportion of these have mutations in known high-penetrant genes. In a relatively large part of patients with a few or multiple colorectal polyps the underlying genetic cause of the disease is still unknown. Using exome sequencing in combination with linkage analyses together with detection of copy-number variations (CNV), we have identified a duplication in the regulatory region of the GREM1 gene in a family with an attenuated/atypical polyposis syndrome. In addition, 107 patients with colorectal cancer and/or polyposis were analyzed for mutations in the candidate genes identified. We also performed screening of the exonuclease domain of the POLE gene in a subset of these patients. The duplication of 16 kb in the regulatory region of GREM1 was found to be disease-causing in the family. Functional analyses revealed a higher expression of the GREM1 gene in colorectal tissue in duplication carriers. Screening of the exonuclease domain of POLE in additional CRC patients identified a probable causative novel variant c.1274A>G, p.Lys425Arg. In conclusion a high penetrant duplication in the regulatory region of GREM1, predisposing to CRC, was identified in a family with attenuated/atypical polyposis. A POLE variant was identified in a patient with early onset CRC and a microsatellite stable (MSS) tumor. Mutations leading to increased expression of genes can constitute disease-causing mutations in hereditary CRC syndromes. \ua9 2015 The Authors. Genes, Chromosomes & Cancer Published by Wiley Periodicals, Inc

GREM1 and POLE variants in hereditary colorectal cancer syndromes

Hereditary factors are thought to play a role in at least one third of patients with colorectal cancer (CRC) but only a limited proportion of these have mutations in known high-penetrant genes. In a relatively large part of patients with a few or multiple colorectal polyps the underlying genetic cause of the disease is still unknown. Using exome sequencing in combination with linkage analyses together with detection of copy-number variations (CNV), we have identified a duplication in the regulatory region of the GREM1 gene in a family with an attenuated/atypical polyposis syndrome. In addition, 107 patients with colorectal cancer and/or polyposis were analyzed for mutations in the candidate genes identified. We also performed screening of the exonuclease domain of the POLE gene in a subset of these patients. The duplication of 16 kb in the regulatory region of GREM1 was found to be disease-causing in the family. Functional analyses revealed a higher expression of the GREM1 gene in colorectal tissue in duplication carriers. Screening of the exonuclease domain of POLE in additional CRC patients identified a probable causative novel variant c.1274A>G, p.Lys425Arg. In conclusion a high penetrant duplication in the regulatory region of GREM1, predisposing to CRC, was identified in a family with attenuated/atypical polyposis. A POLE variant was identified in a patient with early onset CRC and a microsatellite stable (MSS) tumor. Mutations leading to increased expression of genes can constitute disease-causing mutations in hereditary CRC syndromes. \ua9 2015 The Authors. Genes, Chromosomes & Cancer Published by Wiley Periodicals, Inc