Forensic interviewing of mentally disordered suspects: The impact of interview style on investigation outcomes.

The investigative interviewing of a vulnerable suspect is a complex and difficult task. Current best practice advocates for the use of open questions in order to elicit a free recall. However, those with mental health conditions have limited cognitive abilities that relate to free recall and episodic memory, and there is emerging evidence that suggests open questions may not always be most suitable for the vulnerable interviewee. As such, the present study examined the impact of two different interview models (best practice v modified interview) on the amount and accuracy of investigation relevant information obtained within an experimental vulnerable ‘suspect’ sample. Participants engaged in two tasks; a minor transgression and a matched non-transgression. Each participant was then subject to either a best practice (containing largely open questions) or a modified interview (containing largely closed questions). Vulnerable participants provided a significantly higher and more accurate amount of investigation relevant information during the modified interview rather than the best practice interview. In addition, participants that have mental health conditions sought more clarifications during the best practice interviews. The type of interview did not impact upon the level of vulnerability displayed. Our findings challenge current best practice in that vulnerable participants performed worse in interviews containing more open questions than closed questions. These findings add to the emerging evidence base that vulnerable individuals may require an alternative method of questioning, including the use of closed questions as ‘scaffolding’ during an investigative interview

Police Strategies and Suspect Responses in Real-Life Serious Crime Interviews

This research focuses exclusively on real-life taped interviews with serious crime suspects and examines the strategies used and types of questions asked by police, and suspects’ responses to these. The information source was audio-tape-recorded interviews with 56 suspects. These recordings were obtained from 11 police services across England and Wales and were analysed using a specially designed coding frame. It was found that interviewers employed a range of strategies with presentation of evidence and challenge the most frequently observed. Closed questions were by far the most frequently used, and open questions, although less frequent, were found to occur more during the opening phases of the interviews. The frequency of ineffective question types (e.g. negative, repetitive, multiple) was low. A number of significant associations were observed between interviewer strategies and suspect responses. Rapport/empathy and open-type questions were associated with an increased likelihood of suspects admitting the offence whilst describing trauma, and negative questions were associated with a decreased likelihood

Vulnerable suspects in police interviews: exploring current practice in England and Wales

Mentally disordered individuals are increasingly coming into contact with the police. The current study explored investigative interview practice with mentally disordered suspects to examine how they respond, and the impact this has on the level of information obtained. Transcripts of interviews conducted with vulnerable and non-vulnerable suspects (N = 66) were analysed using a specially designed coding framework. Results highlighted that best practice is generally not being adhered to regarding questioning techniques (for example, the use of open questions). Furthermore, while police officers altered their communication to suit the needs of the vulnerable suspect, they were also more likely to use minimisation tactics. Mentally disordered suspects sought more clarification for open questions and provided more information to closed questions. They also demonstrated higher levels of vulnerability (suggestibility and compliance) when compared to their non-vulnerable counterparts. Implications regarding interviewing methods for this vulnerable group are discussed

Dissolved noble gases and stable isotopes as tracers of preferential fluid flow along faults in the Lower Rhine Embayment, Germany

Groundwater in shallow unconsolidated sedimentary aquifers close to the Bornheim fault in the Lower Rhine Embayment (LRE), Germany, has relatively low δ2H and δ18O values in comparison to regional modern groundwater recharge, and 4He concentrations up to 1.7 × 10−4 cm3 (STP) g–1 ± 2.2 % which is approximately four orders of magnitude higher than expected due to solubility equilibrium with the atmosphere. Groundwater age dating based on estimated in situ production and terrigenic flux of helium provides a groundwater residence time of ∼107 years. Although fluid exchange between the deep basal aquifer system and the upper aquifer layers is generally impeded by confining clay layers and lignite, this study’s geochemical data suggest, for the first time, that deep circulating fluids penetrate shallow aquifers in the locality of fault zones, implying  that sub-vertical fluid flow occurs along faults in the LRE. However, large hydraulic-head gradients observed across many faults suggest that they act as barriers to lateral groundwater flow. Therefore, the geochemical data reported here also substantiate a conduit-barrier model of fault-zone hydrogeology in unconsolidated sedimentary deposits, as well as corroborating the concept that faults in unconsolidated aquifer systems can act as loci for hydraulic connectivity between deep and shallow aquifers. The implications of fluid flow along faults in sedimentary basins worldwide are far reaching and of particular concern for carbon capture and storage (CCS) programmes, impacts of deep shale gas recovery for shallow groundwater aquifers, and nuclear waste storage sites where fault zones could act as potential leakage pathways for hazardous fluids

Bone Morphogenetic Protein (BMP)-7 expression is decreased in human hypertensive nephrosclerosis

Background: Bone Morphogenetic Protein (BMP)-7 is protective in different animal models of acute and chronic kidney disease. Its role in human kidneys, and in particular hypertensive nephrosclerosis, has thus far not been described. Methods: BMP-7 mRNA was quantified using real-time PCR and localised by immunostaining in tissue samples from normal and nephrosclerotic human kidneys. The impact of angiotensin (AT)-II and the AT-II receptor antagonist telmisartan on BMP-7 mRNA levels and phosphorylated Smad 1/5/8 (pSmad 1/5/8) expression was quantified in proximal tubular cells (HK-2). Functional characteristics of BMP-7 were evaluated by testing its influence on TGF-b induced epithelial-to-mesenchymal transition (EMT), expression of TGF-b receptor type I (TGF-bRI) and phosphorylated Smad 2 (pSmad 2) as well as on TNF-a induced apoptosis of proximal tubular cells. Results: BMP-7 was predominantly found in the epithelia of the distal tubule and the collecting duct and was less abundant in proximal tubular cells. In sclerotic kidneys, BMP-7 was significantly decreased as demonstrated by real-time PCR and immunostaining. AT-II stimulation in HK-2 cells led to a significant decrease of BMP-7 and pSmad 1/5/8, which was partially ameliorated upon co-incubation with telmisartan. Only high concentrations of BMP-7 (100 ng/ml) were able to reverse TNF-a-induced apoptosis and TGF-b-induced EMT in human proximal tubule cells possibly due to a decreased expression of TGF-bRI. In addition, BMP-7 was able to reverse TGF-b-induced phosphorylation of Smad 2. Conclusions: The findings suggest a protective role for BMP-7 by counteracting the TGF-b and TNF-a-induced negative effects. The reduced expression of BMP-7 in patients with hypertensive nephrosclerosis may imply loss of protection and regenerative potential necessary to counter the disease

Transgenic Expression of Nonclassically Secreted FGF Suppresses Kidney Repair

FGF1 is a signal peptide-less nonclassically released growth factor that is involved in angiogenesis, tissue repair, inflammation, and carcinogenesis. The effects of nonclassical FGF export in vivo are not sufficiently studied. We produced transgenic mice expressing FGF1 in endothelial cells (EC), which allowed the detection of FGF1 export to the vasculature, and studied the efficiency of postischemic kidney repair in these animals. Although FGF1 transgenic mice had a normal phenotype with unperturbed kidney structure, they showed a severely inhibited kidney repair after unilateral ischemia/reperfusion. This was manifested by a strong decrease of postischemic kidney size and weight, whereas the undamaged contralateral kidney exhibited an enhanced compensatory size increase. In addition, the postischemic kidneys of transgenic mice were characterized by hyperplasia of interstitial cells, paucity of epithelial tubular structures, increase of the areas occupied by connective tissue, and neutrophil and macrophage infiltration. The continuous treatment of transgenic mice with the cell membrane stabilizer, taurine, inhibited nonclassical FGF1 export and significantly rescued postischemic kidney repair. It was also found that similar to EC, the transgenic expression of FGF1 in monocytes and macrophages suppresses kidney repair. We suggest that nonclassical export may be used as a target for the treatment of pathologies involving signal peptide-less FGFs

Inelastic Black Hole Scattering from Charged Scalar Amplitudes

We explain how the lowest-order classical gravitational radiation produced during the inelastic scattering of two Schwarzschild black holes in General Relativity can be obtained from a tree scattering amplitude in gauge theory coupled to scalar fields. The gauge calculation is related to gravity through the double copy. We remove unwanted scalar forces which can occur in the double copy by introducing a massless scalar in the gauge theory, which is treated as a ghost in the link to gravity. We hope these methods are a step towards a direct application of the double copy at higher orders in classical perturbation theory, with the potential to greatly streamline gravity calculations for phenomenological applications.Comment: 28 pages, 6 figure

Bmp7 Functions via a Polarity Mechanism to Promote Cloacal Septation

During normal development in human and other placental mammals, the embryonic cloacal cavity separates along the axial longitudinal plane to give rise to the urethral system, ventrally, and the rectum, dorsally. Defects in cloacal development are very common and present clinically as a rectourethral fistula in about 1 in 5,000 live human births. Yet, the cellular mechanisms of cloacal septation remain poorly understood.We previously detected Bone morphogenetic protein 7 (Bmp7) expression in the urorectal mesenchyme (URM), and have shown that loss of Bmp7 function results in the arrest of cloacal septation. Here, we present evidence that cloacal partitioning is driven by Bmp7 signaling in the cloacal endoderm. We performed TUNEL and immunofluorescent analysis on cloacal sections from Bmp7 null and control littermate embryos. We found that loss of Bmp7 results in a dramatic decrease in the endoderm survival and a delay in differentiation. We used immunological methods to show that Bmp7 functions by activating the c-Jun N-terminal kinase (JNK) pathway. We carried out confocal and 3D imaging analysis of mitotic chromosome bundles to show that during normal septation cells in the cloacal endoderm divide predominantly in the apical-basal direction. Loss of Bmp7/JNK signaling results in randomization of mitotic angles in the cloacal endoderm. We also conducted immunohistochemical analysis of human fetal sections to show that BMP/phospho-SMAD and JNK pathways function in the human cloacal region similar as in the mouse.Our results strongly indicate that Bmp7/JNK signaling regulates remodeling of the cloacal endoderm resulting in a topological separation of the urinary and digestive systems. Our study points to the importance of Bmp and JNK signaling in cloacal development and rectourethral malformations

The Weyl double copy from twistor space

The Weyl double copy is a procedure for relating exact solutions in biadjoint scalar, gauge and gravity theories, and relates fields in spacetime directly. Where this procedure comes from, and how general it is, have until recently remained mysterious. In this paper, we show how the current form and scope of the Weyl double copy can be derived from a certain procedure in twistor space. The new formalism shows that the Weyl double copy is more general than previously thought, applying in particular to gravity solutions with arbitrary Petrov types. We comment on how to obtain anti-self-dual as well as self-dual fields, and clarify some conceptual issues in the twistor approach

A Small Peptide Modeled after the NRAGE Repeat Domain Inhibits XIAP-TAB1-TAK1 Signaling for NF-κB Activation and Apoptosis in P19 Cells

In normal growth and development, apoptosis is necessary to shape the central nervous system and to eliminate excess neurons which are not required for innervation. In some diseases, however, apoptosis can be either overactive as in some neurodegenerative disorders or severely attenuated as in the spread of certain cancers. Bone morphogenetic proteins (BMPs) transmit signals for regulating cell growth, differentiation, and apoptosis. Responding to BMP receptors stimulated from BMP ligands, neurotrophin receptor-mediated MAGE homolog (NRAGE) binds and functions with the XIAP-TAK1-TAB1 complex to activate p38MAPK and induces apoptosis in cortical neural progenitors. NRAGE contains a unique repeat domain that is only found in human, mouse, and rat homologs that we theorize is pivotal in its BMP MAPK role. Previously, we showed that deletion of the repeat domain inhibits apoptosis, p38MAPK phosphorylation, and caspase-3 cleavage in P19 neural progenitor cells. We also showed that the XIAP-TAB1-TAK1 complex is dependent on NRAGE for IKK-α/β phosphorylation and NF-κB activation. XIAP is a major inhibitor of caspases, the main executioners of apoptosis. Although it has been shown previously that NRAGE binds to the RING domain of XIAP, it has not been determined which NRAGE domain binds to XIAP. Here, we used fluorescence resonance energy transfer (FRET) to determine that there is a strong likelihood of a direct interaction between NRAGE and XIAP occurring at NRAGE's unique repeat domain which we also attribute to be the domain responsible for downstream signaling of NF-κB and activating IKK subunits. From these results, we designed a small peptide modeled after the NRAGE repeat domain which we have determined inhibits NF-κB activation and apoptosis in P19 cells. These intriguing results illustrate that the paradigm of the NRAGE repeat domain may hold promising therapeutic strategies in developing pharmaceutical solutions for combating harmful diseases involving excessive downstream BMP signaling, including apoptosis