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•We study experimentally consumers’ ability to coordinate on the Pareto-superior equilibrium in a network-good market.•The size of the critical mass is the decisive factor in whether the market converges to the inefficient or efficient equilibrium.•When the critical mass is sufficiently high, neither lower prices nor previous success at a lower critical mass can prevent rapid convergence to the inefficient equilibrium.•Yet, when the critical mass is lowered, the efficient equilibrium is quickly reached.

Two prevailing theories exist to explain why people engage in costly punishment in one-shot interactions when they cannot expect to gain from the punishment or to affect future behavior: to achieve balance or to send a message. In this paper we constructed new versions of the Dictator, Public Good, and Power-to-Take games, designed specifically to allow us to differentiate between these explanations. The results lend some support to each of the hypotheses; on the one hand, subjects punish even when the punisher knows that the offender will never learn that he was punished, and, on the other hand, there is more punishment when the punisher knows that the offender will be informed that he is being punished than when the punisher knows that the offender will remain oblivious to the punishment. Thus, punishers seek both "retributive justice" and to "send a message" to the offending party.

We report here the isolation ofTel-2, a novel member of the Ets transcription factor family, with high homology to Tel/ETV-6. Tel-2is the second mammalian member of the Tel Ets family subclass whose prototype Telis involved in various chromosomal translocations in human cancers. Six differentially expressed alternative splice products of Tel-2were characterized encoding different Tel-2 isoforms which either contain or lack the amino-terminal Pointed domain and also vary at the carboxyl terminus. In contrast to Tel, which is highly expressed in several different cell types and tissues, Tel-2is only weakly expressed in a variety of tissues and cell types, including placenta, prostate, spleen, liver, and lung. Tel-2 binds to functionally relevant Ets-binding sites of several genes and only the Tel-2 isoform containing the Pointed domain and the DNA-binding domain acts as a strong repressor of transcription. The retinoic acid receptorα and bone morphogenetic protein-6B(BMP-6) genes are specifically repressed by Tel-2 indicating a function for Tel-2 as an inhibitor of differentiation. Due to the important involvement of Telin human cancer and the location of Tel-2within the MHC cluster region,Tel-2might be involved in chromosomal translocations in human cancer as well.AF116509AF116510AF218235AF218365AF218366

Most cancers originate as a result of aberrant gene expression in mainly glandular epithelial tissues leading to defects in epithelial cell differentiation. The latter is governed by distinct sets of transcriptional regulators. Here we report the characterization of epithelium-specific Ets factor, family member 3 (ESE-3), a novel member of the ESE subfamily of Ets transcription factors. ESE-3 shows highest homology to two other epithelium restricted Ets factors, ESE-1 and ESE-2. ESE-3, like ESE-1 and ESE-2, is exclusively expressed in a subset of epithelial cells with highest expression in glandular epithelium such as prostate, pancreas, salivary gland, and trachea. A potential role in branching morphogenesis is suggested, since ESE-3 transactivates the c-MET promoter via three high affinity binding sites. Additionally, ESE-3 binding to DNA sequences in the promoters of several glandular epithelium-specific genes suggests a role for ESE-3 in later stages of glandular epithelium differentiation. Although ESE-3 and ESE-1 bind with similar affinity to various Ets binding sites, ESE-3 and ESE-1 differ significantly in their ability to transactivate the promoters containing these sites. Our results support the notion that ESE-1, ESE-2, and ESE-3 represent a unique epithelium-specific subfamily of Ets factors that have critical but distinct functions in epithelial cell differentiation and proliferation.

Prostate cancer, the most frequent solid cancer in older men, is a leading cause of cancer deaths. Although proliferation and differentiation of normal prostate epithelia and the initial growth of prostate cancer cells are androgen-dependent, prostate cancers ultimately become androgen-independent and refractory to hormone therapy. The prostate-specific antigen (PSA) gene has been widely used as a diagnostic indicator for androgen-dependent and -independent prostate cancer. Androgen-induced and prostate epithelium-specific PSA expression is regulated by a proximal promoter and an upstream enhancer via several androgen receptor binding sites. However, little progress has been made in identifying androgen-independent regulatory elements involved in PSA gene regulation. We report the isolation of a novel, prostate epithelium-specific Ets transcription factor, PDEF (prostate-derived Etsfactor), that among the Ets family uniquely prefers binding to a GGAT rather than a GGAA core. PDEF acts as an androgen-independent transcriptional activator of the PSA promoter. PDEF also directly interacts with the DNA binding domain of androgen receptor and enhances androgen-mediated activation of the PSA promoter. Our results, as well as the critical roles of other Ets factors in cellular differentiation and tumorigenesis, strongly suggest that PDEF is an important regulator of prostate gland and/or prostate cancer development.

The current research examined whether or not the interface of an extender attached to an assistive device should be identical to the interface of the assistive device. Given the profile of assistive devices such as wheelchairs and the need to extend them in special cases such when maneuvering over rough terrain or obstacles such as stairs and steep inclines, the interface design of these extenders (attached to existing assistive devices) should be evaluated. We have simulated a carrying platform for a wheelchair that is larger than the user’s regular wheelchair. We have examined whether participants used to handling their wheelchair, when asked to operate the carrying platform, handle the latter’s interface better or worse than their wheelchair’s interface. Participants (61) were assigned to one of two between-participants groups. Both groups were trained to navigate a wheelchair using the wheelchair’s interface and then operated the carrying platform. The Familiar Interface group navigated the carrying platform using the wheelchair’s interface, and the New Interface group navigated it with a new interface. The results demonstrated that the Familiar Interface group took longer to perform the task and collided more often with obstacles, compared to the New Interface group. The greater number of collisions can be linked directly to an erroneous mental model of the carrying platform’s size. The insights we reach can be linked to both extenders attached to an assistive device and other technological extenders.