An instinct for detection: psychological perspectives on CCTV surveillance

The aim of this article is to inform and stimulate a proactive, multidisciplinary approach to research and development in surveillance-based detective work. In this article we review some of the key psychological issues and phenomena that practitioners should be aware of. We look at how human performance can be explained with reference to our biological and evolutionary legacy. We show how critical viewing conditions can be in determining whether observers detect or overlook criminal activity in video material. We examine situations where performance can be surprisingly poor, and cover situations where, even once confronted with evidence of these detection deficits, observers still underestimate their susceptibility to them. Finally we explain why the emergence of these relatively recent research themes presents an opportunity for police and law enforcement agencies to set a new, multidisciplinary research agenda focused on relevant and pressing issues of national and international importance

Detect the unexpected: a science for surveillance

Purpose – The purpose of this paper is to outline a strategy for research development focused on addressing the neglected role of visual perception in real life tasks such as policing surveillance and command and control settings. Approach – The scale of surveillance task in modern control room is expanding as technology increases input capacity at an accelerating rate. The authors review recent literature highlighting the difficulties that apply to modern surveillance and give examples of how poor detection of the unexpected can be, and how surprising this deficit can be. Perceptual phenomena such as change blindness are linked to the perceptual processes undertaken by law-enforcement personnel. Findings – A scientific programme is outlined for how detection deficits can best be addressed in the context of a multidisciplinary collaborative agenda between researchers and practitioners. The development of a cognitive research field specifically examining the occurrence of perceptual “failures” provides an opportunity for policing agencies to relate laboratory findings in psychology to their own fields of day-to-day enquiry. Originality/value – The paper shows, with examples, where interdisciplinary research may best be focussed on evaluating practical solutions and on generating useable guidelines on procedure and practice. It also argues that these processes should be investigated in real and simulated context-specific studies to confirm the validity of the findings in these new applied scenarios

Gamma Protocadherin Expression in the Embryonic Chick Nervous System

Protocadherin γ (pcdh-γ) family expression was examined in the embryonic chick central nervous system by in situ hybridization. Transcripts were visualized in discrete regions of fore-, mid-, and hindbrain at stages 23 and 25 and in spinal cord and optic lobe at stages 27 and 43, respectively. Results suggest that pcdh-γ may function cooperatively with other cell adhesion molecules in neuronal differentiation and establishment of neural networks in several areas of the developing brain, particularly regions involved in visual processing

Expansion of the Parkinson disease-associated SNCA-Rep1 allele upregulates human alpha-synuclein in transgenic mouse brain.

Alpha-synuclein (SNCA) gene has been implicated in the development of rare forms of familial Parkinson disease (PD). Recently, it was shown that an increase in SNCA copy numbers leads to elevated levels of wild-type SNCA-mRNA and protein and is sufficient to cause early-onset, familial PD. A critical question concerning the molecular pathogenesis of PD is what contributory role, if any, is played by the SNCA gene in sporadic PD. The expansion of SNCA-Rep1, an upstream, polymorphic microsatellite of the SNCA gene, is associated with elevated risk for sporadic PD. However, whether SNCA-Rep1 is the causal variant and the underlying mechanism with which its effect is mediated by remained elusive. We report here the effects of three distinct SNCA-Rep1 variants in the brains of 72 mice transgenic for the entire human SNCA locus. Human SNCA-mRNA and protein levels were increased 1.7- and 1.25-fold, respectively, in homozygotes for the expanded, PD risk-conferring allele compared with homozygotes for the shorter, protective allele. When adjusting for the total SNCA-protein concentration (endogenous mouse and transgenic human) expressed in each brain, the expanded risk allele contributed 2.6-fold more to the SNCA steady-state than the shorter allele. Furthermore, targeted deletion of Rep1 resulted in the lowest human SNCA-mRNA and protein concentrations in murine brain. In contrast, the Rep1 effect was not observed in blood lysates from the same mice. These results demonstrate that Rep1 regulates human SNCA expression by enhancing its transcription in the adult nervous system and suggest that homozygosity for the expanded Rep1 allele may mimic locus multiplication, thereby elevating PD risk

Study of the q^2-Dependence of B --> pi ell nu and B --> rho(omega)ell nu Decay and Extraction of |V_ub|

We report on determinations of |Vub| resulting from studies of the branching fraction and q^2 distributions in exclusive semileptonic B decays that proceed via the b->u transition. Our data set consists of the 9.7x10^6 BBbar meson pairs collected at the Y(4S) resonance with the CLEO II detector. We measure B(B0 -> pi- l+ nu) = (1.33 +- 0.18 +- 0.11 +- 0.01 +- 0.07)x10^{-4} and B(B0 -> rho- l+ nu) = (2.17 +- 0.34 +0.47/-0.54 +- 0.41 +- 0.01)x10^{-4}, where the errors are statistical, experimental systematic, systematic due to residual form-factor uncertainties in the signal, and systematic due to residual form-factor uncertainties in the cross-feed modes, respectively. We also find B(B+ -> eta l+ nu) = (0.84 +- 0.31 +- 0.16 +- 0.09)x10^{-4}, consistent with what is expected from the B -> pi l nu mode and quark model symmetries. We extract |Vub| using Light-Cone Sum Rules (LCSR) for 0<= q^2<16 GeV^2 and Lattice QCD (LQCD) for 16 GeV^2 <= q^2 < q^2_max. Combining both intervals yields |Vub| = (3.24 +- 0.22 +- 0.13 +0.55/-0.39 +- 0.09)x10^{-3}$ for pi l nu, and |Vub| = (3.00 +- 0.21 +0.29/-0.35 +0.49/-0.38 +-0.28)x10^{-3} for rho l nu, where the errors are statistical, experimental systematic, theoretical, and signal form-factor shape, respectively. Our combined value from both decay modes is |Vub| = (3.17 +- 0.17 +0.16/-0.17 +0.53/-0.39 +-0.03)x10^{-3}.Comment: 45 pages postscript, also available through http://w4.lns.cornell.edu/public/CLNS, submitted to PR

Search for CP Violation in D^0--> K_S^0 pi^+pi^-

We report on a search for CP violation in the decay of D0 and D0B to Kshort pi+pi-. The data come from an integrated luminosity of 9.0 1/fb of e+e- collisions at sqrt(s) ~ 10 GeV recorded with the CLEO II.V detector. The resonance substructure of this decay is well described by ten quasi-two-body decay channels (K*-pi+, K*0(1430)-pi+, K*2(1430)-pi+, K*(1680)-pi+, Kshort rho, Kshort omega, Kshort f0(980), Kshort f2(1270), Kshort f0(1370), and the ``wrong sign'' K*+ pi-) plus a small non-resonant component. We observe no evidence for CP violation in the amplitudes and phases that describe the decay D0 to K_S^0 pi+pi-.Comment: 10 pages, 3 figures, also available at http://w4.lns.cornell.edu/public/CLNS/, submitted to PR

Measurement of the Charge Asymmetry in B→K∗(892)±π∓B\to K^* (892)^{\pm}\pi^{\mp}

We report on a search for a CP-violating asymmetry in the charmless hadronic decay B -> K*(892)+- pi-+, using 9.12 fb^-1 of integrated luminosity produced at \sqrt{s}=10.58 GeV and collected with the CLEO detector. We find A_{CP}(B -> K*(892)+- pi-+) = 0.26+0.33-0.34(stat.)+0.10-0.08(syst.), giving an allowed interval of [-0.31,0.78] at the 90% confidence level.Comment: 7 pages postscript, also available through http://w4.lns.cornell.edu/public/CLNS, submitted to PR

Inter-hemispheric EEG coherence analysis in Parkinson's disease : Assessing brain activity during emotion processing

Parkinson’s disease (PD) is not only characterized by its prominent motor symptoms but also associated with disturbances in cognitive and emotional functioning. The objective of the present study was to investigate the influence of emotion processing on inter-hemispheric electroencephalography (EEG) coherence in PD. Multimodal emotional stimuli (happiness, sadness, fear, anger, surprise, and disgust) were presented to 20 PD patients and 30 age-, education level-, and gender-matched healthy controls (HC) while EEG was recorded. Inter-hemispheric coherence was computed from seven homologous EEG electrode pairs (AF3–AF4, F7–F8, F3–F4, FC5–FC6, T7–T8, P7–P8, and O1–O2) for delta, theta, alpha, beta, and gamma frequency bands. In addition, subjective ratings were obtained for a representative of emotional stimuli. Interhemispherically, PD patients showed significantly lower coherence in theta, alpha, beta, and gamma frequency bands than HC during emotion processing. No significant changes were found in the delta frequency band coherence. We also found that PD patients were more impaired in recognizing negative emotions (sadness, fear, anger, and disgust) than relatively positive emotions (happiness and surprise). Behaviorally, PD patients did not show impairment in emotion recognition as measured by subjective ratings. These findings suggest that PD patients may have an impairment of inter-hemispheric functional connectivity (i.e., a decline in cortical connectivity) during emotion processing. This study may increase the awareness of EEG emotional response studies in clinical practice to uncover potential neurophysiologic abnormalities

Measurement of Lepton Momentum Moments in the Decay bar{B} \to X \ell \bar{\nu} and Determination of Heavy Quark Expansion Parameters and |V_cb|

We measure the primary lepton momentum spectrum in B-bar to X l nu decays, for p_l > 1.5 GeV/c in the B rest frame. From this, we calculate various moments of the spectrum. In particular, we find R_0 = [int(E_l>1.7) (dGam/dE_sl)*dE_l] / [int(E_l>1.5) (dGam/dE_sl)*dE_l] = 0.6187 +/- 0.0014_stat +/- 0.0016_sys and R_1 = [int(E_l>1.5) E_l(dGam/dE_sl)*dE_l] / [int(E_l>1.5) (dGam/dE_sl)*dE_l] = (1.7810 +/- 0.0007_stat +/- 0.0009_sys) GeV. We use these moments to determine non-perturbative parameters governing the semileptonic width. In particular, we extract the Heavy Quark Expansion parameters Lambda-bar = (0.39 +/- 0.03_stat +/- 0.06_sys +/- 0.12_th) GeV and lambda_1 = (-0.25 +/- 0.02_stat +/- 0.05_sys +/- 0.14_th) GeV^2. The theoretical constraints used are evaluated through order 1/M_B^3 in the non-perturbative expansion and beta_0*alpha__s^2 in the perturbative expansion. We use these parameters to extract |V_cb| from the world average of the semileptonic width and find |V_cb| = (40.8 +/- 0.5_Gam-sl +/- 0.4_(lambda_1,Lambda-bar)-exp +/- 0.9_th) x 10^-3. In addition, we extract the short range b-quark mass m_b^1S = (4.82 +/- 0.07_exp +/- 0.11_th) GeV/c^2. Finally, we discuss the implications of our measurements for the theoretical understanding of inclusive semileptonic processes.Comment: 21 pages postscript, also available through http://w4.lns.cornell.edu/public/CLNS, submitted to PR

Tissue-Specific Genetic Control of Splicing: Implications for the Study of Complex Traits

Numerous genome-wide screens for polymorphisms that influence gene expression have provided key insights into the genetic control of transcription. Despite this work, the relevance of specific polymorphisms to in vivo expression and splicing remains unclear. We carried out the first genome-wide screen, to our knowledge, for SNPs that associate with alternative splicing and gene expression in human primary cells, evaluating 93 autopsy-collected cortical brain tissue samples with no defined neuropsychiatric condition and 80 peripheral blood mononucleated cell samples collected from living healthy donors. We identified 23 high confidence associations with total expression and 80 with alternative splicing as reflected by expression levels of specific exons. Fewer than 50% of the implicated SNPs however show effects in both tissue types, reflecting strong evidence for distinct genetic control of splicing and expression in the two tissue types. The data generated here also suggest the possibility that splicing effects may be responsible for up to 13 out of 84 reported genome-wide significant associations with human traits. These results emphasize the importance of establishing a database of polymorphisms affecting splicing and expression in primary tissue types and suggest that splicing effects may be of more phenotypic significance than overall gene expression changes