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- Luke, Timothy J., et al.
(author)
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Training in the Strategic Use of Evidence technique: Improving deception detection accuracy of American law enforcement officers
- 2016
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In: Journal of Police and Criminal Psychology. - : Springer Science and Business Media LLC. - 0882-0783 .- 1936-6469. ; 31:4, s. 270-278
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Journal article (peer-reviewed)abstract
- © 2016, Society for Police and Criminal Psychology.The Strategic Use of Evidence (SUE) approach is a framework for planning and executing suspect interviews with the aim of facilitating judgments of truth and deception. US law enforcement officers (N = 59) either received training in the SUE approach or did not. Each officer interviewed a mock suspect (N = 59) who had either committed a simulated security breach or had completed a benign task. The officers who received SUE training interviewed in line with the training: They questioned the suspect systematically, withheld the evidence and critical case information until after questioning, and relied on statement-evidence inconsistency to detect deceit. Consequently, SUE-trained interviewers achieved a higher deception detection accuracy rate (65%) compared to untrained interviewers (43%).
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| 2. |
- Starker, Lee F., et al.
(author)
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Frequent germ-line mutations of the MEN1, CASR, and HRPT2/CDC73 genes in young patients with clinically non-familial primary hyperparathyroidism
- 2012
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In: Hormones & Cancer. - : Springer Science and Business Media LLC. - 1868-8497 .- 1868-8500. ; 3:1-2, s. 44-51
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Journal article (peer-reviewed)abstract
- Familial primary hyperparathyroidism (FPHPT) may occur due to an underlying germ-line mutation in the MEN1, CASR, or HRPT2/CDC73 genes. The disease may be undiagnosed in the absence of a history suggestive of FHPT. Young PHPT patients (≤45 years of age) are more likely to harbor occult FPHPT. A total of 1,161 (136 were ≤45 years of age) PHPT patients underwent parathyroidectomy from 2001 to 2009. Thirty-four patients declined participation. Sixteen patients were diagnosed in the clinical routine with FPHPT (11 MEN1, four MEN2A, and one HPT-JT) and were not included in the genetic analysis. Eighty-six young (≤45 years of age) patients with clinically non-syndromic PHPT underwent genetic analysis. Sanger sequencing of all coding regions of the MEN1, CASR, and the HRPT2/CDC73 genes was performed. Eight of 86 (9.3%) young patients with clinically non-familial PHPT displayed deleterious germ-line mutations in the susceptibility genes (4 MEN1, 3 CASR, and 1 HRPT2/CDC73). There was one insertion, one deletion, two nonsense, and four missense mutations, all predicted to be highly damaging to protein function and absent in 3,244 control chromosomes. Germ-line mutations in known susceptibility genes within young patients with PHPT, including those diagnosed in the clinical routine, was 24/102 (23.5%; 15 MEN1, four RET, three CASR, and two HRPT2/CDC73). We demonstrate that germ-line inactivating mutations in susceptibility genes are common in young patients with clinically non-familial PHPT. Thus, enhanced use of genetic analysis may be warranted in clinically non-familial young PHPT patients.
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