Estimates of the prices customers are willing to pay for new products or services using responses from survey questionnaires are notoriously biased on the high side. An approach to obtaining more realistic estimates is suggested here, called the exaggeration bias-corrected contingent valuation method (EBC-CVM). The method is an alternative to conventional contingent valuation methods (CVMs) that have been used in economics and, to a lesser extent, in marketing. Two experiments and one field study are presented to demonstrate the effectiveness of the method. In each case, the proposed method outperformed conventional CVMs in comparison with real choices or more realistic price estimates.willingness to pay, contingent valuation method, exaggeration bias, new product pricing

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The double-bounded contingent valuation method (DBCVM) has long been criticized as an inappropriate estimation method because of respondents' inconsistent behavior during a course of DBCVM survey. Many experimental studies have reported that two subsequent answers are not made independently, but the second answer depends upon the first. There are many kinds of hypotheses, each of which contends a different pattern of dependence of the answers. In this study, it will be tested which hypothesis is more appropriate in explaining the dependence of the answers. For the test, the DBCVM under uncertainty is newly developed here in which some uncertainties associated with the CVM are recognized and the risk premium plays a criterion for respondents to answer.

Measuring consumers' Willingness To Pay (WTP) without considering the level of uncertainty in valuation and the consequent risk premiums will result in estimates that are biased toward lower values. This research proposes a model and method for correctly assessing WTP in cases involving valuation uncertainty. The new method, called Risk Adjustment Mechanism (RAM), is presented theoretically and demonstrated empirically. It is shown that the RAM outperforms the traditional method for assessing WTP, especially in a context of a nonmarket good such as a totally new product.

Whole-genome sequencing (WGS) was used to determine the molecular mechanisms of multidrug resistance for 10 serial Candida glabrata bloodstream isolates obtained from a neutropenic patient during 82 days of amphotericin B (AMB) or echinocandin therapy. For WGS, a library was prepared and sequenced using a Nextera DNA Flex Kit (Illumina) and the MiseqDx (Illumina) instrument. All isolates harbored the same Msh2p substitution, V239L, associated with multilocus sequence type 7 and a Pdr1p substitution, L825P, that caused azole resistance. Of six isolates with increased AMB MICs (≥2 mg/L), three harboring the Erg6p A158fs mutation had AMB MICs ≥ 8 mg/L, and three harboring the Erg6p R314K, Erg3p G236D, or Erg3p F226fs mutation had AMB MICs of 2–3 mg/L. Four isolates harboring the Erg6p A158fs or R314K mutation had fluconazole MICs of 4–8 mg/L while the remaining six had fluconazole MICs ≥ 256 mg/L. Two isolates with micafungin MICs > 8 mg/L harbored Fks2p (I661_L662insF) and Fks1p (C499fs) mutations, while six isolates with micafungin MICs of 0.25–2 mg/L harbored an Fks2p K1357E substitution. Using WGS, we detected novel mechanisms of AMB and echinocandin resistance; we explored mechanisms that may explain the complex relationship between AMB and azole resistance.