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The multifactorial model was revised just over a decade later, prompted in part by the presentation of a new operational cyclical model by Gissane et al. (2001), alongside later suggestions (Bahr and Holme 2003; Bahr and Krosshaug 2005).

A multifactorial model was used to calculate a combined likelihood ratio [ 3, 4].

A second reason for favoring a multifactorial model is when a disorder is common.

The final multifactorial model is thus selected from the classification errors and prediction errors.

In terms of etiology, although the vitamin D deficiency hypothesis remains the most plausible mechanism for postoperative ePTH, other hypotheses including a multifactorial model are still possible given the interrelationship of these factors.

The major gene model was favoured, and the sporadic and multifactorial models were strongly rejected.

Contrary to that study, multifactorial models were finally used to predict the case-control status.

The multifactorial Risk Factor Model was then developed using odds ratios [ 10].

After construction of haplotypes for each gene, a multifactorial linear mixed model was performed to analyse the depression values over time.

External (to the case control data) epidemiological information on disease prevalence is required if the multifactorial threshold model is to be used to calculate locus-specific heritabilities.

The COX risk ratio model was used for multifactorial analysis on survival, where P < 0.05 had statistical significance.