Help or hindrance? Supplier involvement and causal ambiguity within inter-organisational NPD teams

Suppliers are increasingly involved in buyer firms’ interorganizational new product development (NPD) teams. Yet the transfer of knowledge within this context may be subject to varying degrees of causal ambiguity, potentially limiting the effect of supplier involvement on performance. We develop a theoretical model exploring the effect of supplier involvement practices on the level of causal ambiguity within interorganizational NPD teams, and the subsequent impact on competitor imitation, new product advantage, and project performance. Our model also serves as a test of the paradox that causal ambiguity both inhibits imitation by competitors, but also adversely affects organisational outcomes. Results from an empirical study of 119 R&D intensive manufacturing firms in the United Kingdom largely support these hypotheses. Results from structural equation modeling show that supplier involvement orientation and long-term commitment lower causal ambiguity within interorganizational NPD teams. In turn, this lower causal ambiguity generates a new product advantage and increases project performance for the buyer firm, but has no significant effect on competitor imitation. Instead, competitor imitation is delayed by the extent to which the firm develops a new product advantage within the market. These results shed light on the causal ambiguity paradox showing that lower causal ambiguity during interorganizational new product development increases both product and project performance, but without reducing barriers to imitation. Product development managers are encouraged to utilize supplier involvement practices to minimise ambiguity in the NPD project, and to target their supplier involvement efforts on solving causally ambiguous technological problems to sustain a competitive advantage.

Test stimulus characteristics determine the perceived speed of the dynamic motion aftereffect

Using a speed-matching task, we measured the speed tuning of the dynamic motion aftereVect (MAE). The results of our Wrst experiment, in which we co-varied dot speed in the adaptation and test stimuli, revealed a speed tuning function. We sought to tease apart what contribution, if any, the test stimulus makes towards the observed speed tuning. This was examined by independently manipulating dot speed in the adaptation and test stimuli, and measuring the eVect this had on the perceived speed of the dynamic MAE. The results revealed that the speed tuning of the dynamic MAE is determined, not by the speed of the adaptation stimulus, but by the local motion characteristics of the dynamic test stimulus. The role of the test stimulus in determining the perceived speed of the dynamic MAE was conWrmed by showing that, if one uses a test stimulus containing two sources of local speed information, observers report seeing a transparent MAE; this is despite the fact that adaptation is induced using a single-speed stimulus. Thus while the adaptation stimulus necessarily determines perceived direction of the dynamic MAE, its perceived speed is determined by the test stimulus. This dissociation of speed and direction supports the notion that the processing of these two visual attributes may be partially independent.

A novel diagnostic test detects a low frequency of the hemicentin Gln5345Arg variant among Northern Irish age related macular degeneration patients.

Purpose: Age related macular degeneration (AMD) is a common cause of severe vision loss. Identification of genes involved in AMD will facilitate early detection and ultimately help to identify pathways for treatment for this disorder. The A16,263G mutation in the HEMICENTIN-1 gene produces a non-conservative substitution of arginine for glutamine at codon 5345 which has been implicated in familial AMD. The aim of this study is to develop a rapid diagnostic assay for the detection of this mutation and to evaluate its frequency in a sample of AMD patients. Methods: A primer probe set was designed from exon 104 of the HEMICENTIN-1 gene to differentiate between mutant and wild type alleles. A region spanning the mutation was amplified by PCR using a LightCycler (Roche Diagnostic). The mutation was then detected by melt curve analysis of the hybrid formed between the PCR product and a specific fluorescent probe. The frequency of the mutation within the Northern Ireland population was evaluated by assaying 508 affected AMD patients, 25 possibly affected and 163 controls. Results: This assay clearly discriminates between the A16,263G mutant and wild type HEMICENTIN-1 alleles. The wild type sequence has a single base mismatch with the probe which decreases the stability of the hybrid, resulting in a lower TM (TM=51.27 °C) than that observed for the perfectly matched mutant allele (TM=59.9 °C). The mutant allele was detected in only one of the 696 subjects, an affected AMD patient. Conclusions: We describe a rapid assay for the genotyping of the Gln5345Arg mutation using real-time fluorescence PCR to facilitate rapid processing of samples through combined amplification and detection steps. These characteristics are suitable for a clinical setting where high throughput diagnostic procedures are required. The frequency of this mutation within the Northern Ireland population has been estimated at 0.2%, concurring with previous findings that this mutation is a rare variant associated with AMD. A rapid diagnostic assay will facilitate a reliable and convenient evaluation of the frequency of the Gln5345Arg mutation and its association with AMD within other populations.