ACE Research Vignette 042: Nascent ventures’ surprising resistance to macroeconomic crisis

This series of research vignettes is aimed at sharing current and interesting research findings from our team of international entrepreneurship researchers. This vignette, written by Professor Per Davidsson, reports findings on how the onset of the Global Financial Crisis affected “nascent ventures”, i.e., on-going business start-up efforts.

A preference-based semantics for CTD reasoning

In [8] the authors developed a logical system based on the definition of a new non-classical connective ⊗ capturing the notion of reparative obligation. The system proved to be appropriate for handling well-known contrary-to-duty paradoxes but no model-theoretic semantics was presented. In this paper we fill the gap and define a suitable possible-world semantics for the system for which we can prove soundness and completeness. The semantics is a preference-based non-normal one extending and generalizing semantics for classical modal logics.

Diário da Constituinte [gravação de vídeo] : [programa n. 042]

A Deputada Cristina Tavares defende a reserva de mercado para a informática. O Ministro da Educação defende verbas públicas para as escolas públicas. O Deputado Luiz Carlos Sigmaringa defende eleições diretas para o Distrito Federal, para Governador e Deputados Distritais. Equipe de médicos discute a situação do aborto no Brasil e são contra a utilização de métodos não naturais para a limitação da vida.

Nutrient Enhanced Coastal Ocean Productivity (NECOP). Data report: CTD and hydrographic data, R/V Pelican cruise, April 3-11, 1993

The Nutrient Enhanced Coastal Ocean Productivity (NECOP) Program is a component of NOAA's Coastal Ocean Program. The central hypothesis of this research is: Anthropogenic nutrient inputs have enhanced coastal ocean productivity with subsequent impacts on coastal ocean water quality, living resource yields, and the global marine carbon cycle. The initial study area for this program is the Mississippi/Atchafalaya River Outflow and adjacent Louisiana shelf region.

Yeast screens identify the RNA polymerase II CTD and SPT5 as relevant targets of BRCA1 interaction.

BRCA1 has been implicated in numerous DNA repair pathways that maintain genome integrity, however the function responsible for its tumor suppressor activity in breast cancer remains obscure. To identify the most highly conserved of the many BRCA1 functions, we screened the evolutionarily distant eukaryote Saccharomyces cerevisiae for mutants that suppressed the G1 checkpoint arrest and lethality induced following heterologous BRCA1 expression. A genome-wide screen in the diploid deletion collection combined with a screen of ionizing radiation sensitive gene deletions identified mutants that permit growth in the presence of BRCA1. These genes delineate a metabolic mRNA pathway that temporally links transcription elongation (SPT4, SPT5, CTK1, DEF1) to nucleopore-mediated mRNA export (ASM4, MLP1, MLP2, NUP2, NUP53, NUP120, NUP133, NUP170, NUP188, POM34) and cytoplasmic mRNA decay at P-bodies (CCR4, DHH1). Strikingly, BRCA1 interacted with the phosphorylated RNA polymerase II (RNAPII) carboxy terminal domain (P-CTD), phosphorylated in the pattern specified by the CTDK-I kinase, to induce DEF1-dependent cleavage and accumulation of a RNAPII fragment containing the P-CTD. Significantly, breast cancer associated BRCT domain defects in BRCA1 that suppressed P-CTD cleavage and lethality in yeast also suppressed the physical interaction of BRCA1 with human SPT5 in breast epithelial cells, thus confirming SPT5 as a relevant target of BRCA1 interaction. Furthermore, enhanced P-CTD cleavage was observed in both yeast and human breast cells following UV-irradiation indicating a conserved eukaryotic damage response. Moreover, P-CTD cleavage in breast epithelial cells was BRCA1-dependent since damage-induced P-CTD cleavage was only observed in the mutant BRCA1 cell line HCC1937 following ectopic expression of wild type BRCA1. Finally, BRCA1, SPT5 and hyperphosphorylated RPB1 form a complex that was rapidly degraded following MMS treatment in wild type but not BRCA1 mutant breast cells. These results extend the mechanistic links between BRCA1 and transcriptional consequences in response to DNA damage and suggest an important role for RNAPII P-CTD cleavage in BRCA1-mediated cancer suppression.