An investigation into the cause of the inner dark areas and outer lighter areas (ghosting) seen in dynamically-created two-dimensional bare footprints

Dynamic bare footprints differ from static bare footprints through the presence of additional, lighter markings around the rear of the heel print and apices of the toe print areas. These images can appropriately be described as inner dark and outer ghosting features. To date, the functional cause of both features has not been understood. To gain such an understanding could potentially allow the further development and use of these features in forensic identification. The aim of this project was to investigate the causes of the inner dark and outer ghosting features seen in dynamic bare footprints through an observational, practice-based action research approach within a gait laboratory. Volunteer male participants provided bare footprints on inkless paper taped to a Kistler force plate with video cameras situated either side. Ground reaction force data were collected as the footprints were formed and the event recorded using video cameras to allow these data to be correlated later. The findings suggest that the ghosting at the heel is the result of splaying of the fibro fatty pad, while that at the toes is the result of the distal ends of the toes coming into contact with the ground as the heel is lifted. Footprint, ground reaction force and video data comparisons showed that the inner dark area of the heel print corresponded with the main body of the heel contacting the ground. Outer ghosting corresponded with a backward splaying of the fat pad and the heel strike transient spike in vertical ground reaction force during increased loading. The inner dark area of the toes corresponded with a longer period of toe contact with the ground. Outer ghosting corresponded with the decreasing vertical ground reaction force and shorter contact time as the toes were leaving the ground towards the end of the contact phase of gait. Although the sample size was limited, these are new appreciations which could facilitate the use of the inner dark features in identification to provide additional points for comparison in cases involving dynamic bare footprints. Further work is now indicated to study these features in different populations and under varying conditions

Analysis of cross-correlations in electroencephalogram signals as an approach to proactive diagnosis of schizophrenia

We apply flicker-noise spectroscopy (FNS), a time series analysis method operating on structure functions and power spectrum estimates, to study the clinical electroencephalogram (EEG) signals recorded in children/adolescents (11 to 14 years of age) with diagnosed schizophrenia-spectrum symptoms at the National Center for Psychiatric Health (NCPH) of the Russian Academy of Medical Sciences. The EEG signals for these subjects were compared with the signals for a control sample of chronically depressed children/adolescents. The purpose of the study is to look for diagnostic signs of subjects' susceptibility to schizophrenia in the FNS parameters for specific electrodes and cross-correlations between the signals simultaneously measured at different points on the scalp. Our analysis of EEG signals from scalp-mounted electrodes at locations F3 and F4, which are symmetrically positioned in the left and right frontal areas of cerebral cortex, respectively, demonstrates an essential role of frequency-phase synchronization, a phenomenon representing specific correlations between the characteristic frequencies and phases of excitations in the brain. We introduce quantitative measures of frequency-phase synchronization and systematize the values of FNS parameters for the EEG data. The comparison of our results with the medical diagnoses for 84 subjects performed at NCPH makes it possible to group the EEG signals into 4 categories corresponding to different risk levels of subjects' susceptibility to schizophrenia. We suggest that the introduced quantitative characteristics and classification of cross-correlations may be used for the diagnosis of schizophrenia at the early stages of its development.Comment: 36 pages, 6 figures, 2 tables; to be published in "Physica A

An investigation into retrofitting the pre-1919 owner-occupied UK housing stock to reduce carbon emissions

In the UK, housing has been identified as a significant sector for contributing to the 80% reduction in emissions over the 1990 baseline by 2050, required by the Climate Change Act of 2008. However, pre-1919 housing stock is the least energy efficient and consequently poses challenges to meeting this target. Using a mixed methods approach, the current study demonstrates that, in actuality, there is a significant potential for reducing emissions among this sub-sector of housing, and that the major barriers to energy efficiency retrofits concern a lack of funding, the payback period for the investment, disruption to home life and finding a trustworthy and skilled installer. Moreover, this study finds that homeowners are motivated primarily by the desire to improve home comfort and aesthetics along with a reduction in energy bills rather than in reducing carbon emissions. The paper concludes with recommendations for improving the viability of retrofitting pre-1919 homes through enhanced financial resources, policy support and the promotion of social and economic benefits

Glutathione and glutamate in schizophrenia: a 7T MRS study

In schizophrenia, abnormal neural metabolite concentrations may arise from cortical damage following neuroinflammatory processes implicated in acute episodes. Inflammation is associated with increased glutamate, whereas the antioxidant glutathione may protect against inflammation-induced oxidative stress. We hypothesized that patients with stable schizophrenia would exhibit a reduction in glutathione, glutamate and/or glutamine in the cerebral cortex, consistent with a postinflammatory response, and that this reduction would be most marked in patients with residual schizophrenia an early stage with positive psychotic symptoms has progressed to a late stage characterised by long-term negative symptoms and impairments. We recruited 28 patients with stable schizophrenia and 45 healthy participants matched for age, gender and parental socio-economic status. We measured glutathione, glutamate and glutamine concentrations in the anterior cingulate cortex (ACC), left insula, and visual cortex using 7T proton Magnetic Resonance Spectroscopy (MRS). Glutathione and glutamate were significantly correlated in all three voxels. Glutamine concentrations across the three voxels were significantly correlated with each other. Principal Components Analysis (PCA) produced three clear components: an ACC glutathione-glutamate component; an insula-visual glutathione-glutamate component; and a glutamine component. Patients with stable schizophrenia had significantly lower scores on the ACC glutathione-glutamate component, an effect almost entirely leveraged by the sub-group of patients with residual schizophrenia. All three metabolite concentration values in the ACC were significantly reduced in this group. These findings are consistent with the hypothesis that excito-toxicity during the acute phase of illness leads to reduced glutathione and glutamate in the residual phase of the illness

Regional brain correlates of beta bursts in health and psychosis: A concurrent electroencephalography and functional magnetic resonance imaging study

ª 2020 Society of Biological Psychiatry. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).BACKGROUNDThere is emerging evidence for abnormal beta oscillations in psychosis. Beta oscillations are likely to play a key role in the coordination of sensorimotor information that is crucial to healthy mental function. Growing evidence suggests that beta oscillations typically manifest as transient beta bursts that increase in probability following a motor response, observable as post-movement beta rebound. Evidence indicates that post-movement beta rebound is attenuated in psychosis, with greater attenuation associated with greater symptom severity and impairment. Delineating the functional role of beta bursts therefore may be key to understanding the mechanisms underlying persistent psychotic illness.METHODSWe used concurrent electroencephalography and functional magnetic resonance imaging to identify blood oxygen level-dependent correlates of beta bursts during the n-back working memory task and intervening rest periods in healthy participants (n = 30) and patients with psychosis (n = 48).RESULTSDuring both task blocks and intervening rest periods, beta bursts phasically activated regions implicated in task-relevant content while suppressing currently tonically active regions. Patients showed attenuated post-movement beta rebound that was associated with persisting disorganization symptoms as well as impairments in cognition and role function. Patients also showed greater task-related reductions in overall beta burst rate and showed greater, more extensive, beta burst-related blood oxygen level-dependent activation.CONCLUSIONSOur evidence supports a model in which beta bursts reactivate latently maintained sensorimotor information and are dysregulated and inefficient in psychosis. We propose that abnormalities in the mechanisms by which beta bursts coordinate reactivation of contextually appropriate content can manifest as disorganization, working memory deficits, and inaccurate forward models and may underlie a core deficit associated with persisting symptoms and impairment.https://www.sciencedirect.com/science/article/pii/S2451902220303220?via%3Dihu

Regional Brain Correlates of Beta Bursts in Health and Psychosis: A Concurrent Electroencephalography and Functional Magnetic Resonance Imaging Study

Background: There is emerging evidence for abnormal beta oscillations in psychosis. Beta-oscillations are likely to play a key role in the coordination of sensorimotor information, crucial to healthy mental function. Growing evidence suggests that beta oscillations typically manifest as transient “beta-bursts” that increase in probability following a motor response, observable as Post-Movement Beta Rebound (PMBR). Evidence indicates that PMBR is attenuated in psychosis, with greater attenuation associated with greater symptom severity and impairment. Delineating the functional role of beta-bursts may therefore be key to understanding the mechanisms underlying persistent psychotic illness.Methods: We used concurrent EEG and fMRI to identify BOLD correlates of beta-bursts during the N-back working memory task and intervening rest periods in healthy participants (N = 30) and patients with psychosis (N = 48). Results: During both task-blocks and intervening rest periods, beta-bursts phasically activated regions implicated in task-relevant content, while suppressing currently tonically active regions. Patients showed attenuated PMBR that was associated with persisting Disorganisation symptoms, as well as impairments in cognition and role function. Patients also showed greater task-related reductions in overall beta-burst rate, and greater, more extensive, beta-burst-related BOLD activation.Conclusions: Our evidence supports a model in which beta-bursts reactivate latently maintained sensorimotor information and are dysregulated and inefficient in psychosis. We propose that abnormalities in the mechanisms by which beta-bursts coordinate reactivation of contextually appropriate content can manifest as Disorganisation, working memory deficits and inaccurate forward models, and may underlie a “core deficit” associated with persisting symptoms and impairment

Michigan Neural Distinctiveness (MiND) study protocol: investigating the scope, causes, and consequences of age-related neural dedifferentiation

Abstract Background Aging is often associated with behavioral impairments, but some people age more gracefully than others. Why? One factor that may play a role is individual differences in the distinctiveness of neural representations. Previous research has found that neural activation patterns in visual cortex in response to different visual stimuli are often more similar (i.e., less distinctive) in older vs. young participants, a phenomenon referred to as age-related neural dedifferentiation. Furthermore, older people whose neural representations are less distinctive tend to perform worse on a wide range of behavioral tasks. The Michigan Neural Distinctiveness (MiND) project aims to investigate the scope of neural dedifferentiation (e.g., does it also occur in auditory, motor, and somatosensory cortex?), one potential cause (age-related reductions in the inhibitory neurotransmitter gamma-aminobutyric acid (GABA)), and the behavioral consequences of neural dedifferentiation. This protocol paper describes the study rationale and methods being used in complete detail, but not the results (data collection is currently underway). Methods The MiND project consists of two studies: the main study and a drug study. In the main study, we are recruiting 60 young and 100 older adults to perform behavioral tasks that measure sensory and cognitive function. They also participate in functional MRI (fMRI), MR spectroscopy, and diffusion weighted imaging sessions, providing data on neural distinctiveness and GABA concentrations. In the drug study, we are recruiting 25 young and 25 older adults to compare neural distinctiveness, measured with fMRI, after participants take a placebo or a benzodiazepine (lorazepam) that should increase GABA activity. Discussion By collecting multimodal imaging measures along with extensive behavioral measures from the same subjects, we are linking individual differences in neurochemistry, neural representation, and behavioral performance, rather than focusing solely on group differences between young and old participants. Our findings have the potential to inform new interventions for age-related declines. Trial registration This study was retrospectively registered with the ISRCTN registry on March 4, 2019. The registration number is ISRCTN17266136 .https://deepblue.lib.umich.edu/bitstream/2027.42/148569/1/12883_2019_Article_1294.pd