Publications by authors named "P Menke"

Careless responding measures are important for several purposes, whether it's screening for careless responding or for research centered on careless responding as a substantive variable. One such approach for assessing carelessness in surveys is the use of an instructional manipulation check. Despite its apparent popularity, little is known about the construct validity of instructional manipulation checks as measures of careless responding.

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This paper presents two studies in which a peer-assisted learning condition was compared to an individual learning condition. The first study used the paired-associates learning task and the second study used an incrementally more complex task-the remote associate test. Participants in the peer-assisted learning condition worked in groups of four.

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Background: Amino acid production features of Corynebacterium glutamicum were extensively studied in the last two decades. Many metabolic pathways, regulatory and transport principles are known, but purely rational approaches often provide only limited progress in production optimization. We recently generated stable synthetic co-cultures, termed Communities of Niche-optimized Strains (CoNoS), that rely on cross-feeding of amino acids for growth.

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Current bioprocesses for production of value-added compounds are mainly based on pure cultures that are composed of rationally engineered strains of model organisms with versatile metabolic capacities. However, in the comparably well-defined environment of a bioreactor, metabolic flexibility provided by various highly abundant biosynthetic enzymes is much less required and results in suboptimal use of carbon and energy sources for compound production. In nature, non-model organisms have frequently evolved in communities where genome-reduced, auxotrophic strains cross-feed each other, suggesting that there must be a significant advantage compared to growth without cooperation.

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Checkpoint kinase 1 (CHK1) is critical for intrinsic cell cycle control and coordination of cell cycle progression in response to DNA damage. Despite its essential function, CHK1 has been identified as a target to kill cancer cells and studies using Chk1 haploinsufficient mice initially suggested a role as tumor suppressor. Here, we report on the key role of CHK1 in normal B-cell development, lymphomagenesis and cell survival.

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