Miracle-dz/UniFAR-FTUs huggingface dataset:
Empowerment and the architecture of rights based social policy

This article considers what the notions of empowerment, rights and citizenship imply in the way of structures and policies. It argues that a coherent model is emerging with recognizable elements. The article begins with a brief discussion of some background and theoretical questions. It then examines four elements: support for people to articulate their claims; support for people to identify, obtain and manage supports necessary to actualize their claims; providing control over resources; and governance. Examples will be drawn primarily from the UK and British Columbia, Canada to illustrate the elements. The article then looks at some of the issues related to successful implementation of a rights or empowerment based model of policy and structures for supporting people labelled as having a learning disability.
TRAIL/Apo2L Ligands Induce Apoptosis in Malignant Rhabdoid Tumor Cell Lines

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) is a potent inducer of apoptosis in various cancer cells, whereas normal cells are not sensitive to TRAIL-mediated apoptosis. Four TRAIL/Apo2L receptors (DR4, DR5, DcR1, and DcR2) have been identified. DR4 and DR5 have a death domain, whereas DcR1 and DcR2 are called decoy receptors because of their incomplete or lack of a death domain. Malignant rhabdoid tumor (MRT) is an aggressive neoplasm showing a poor prognosis because of its resistance to chemotherapeutic agents. In this study, we examined whether TRAIL could induce apoptotic cell death in MRT cell lines. We found that although half of the MRT cell lines examined were sensitive to TRAIL/Apo2L, Western blot analysis revealed that the expression of DcR2 was low in TRAIL-sensitive MRT cells. We examined the effect of doxorubicin on the expression levels of TRAIL receptors and its enhancement on the susceptibility of MRT cell lines to TRAIL. Western blot and flow cytometric analyses revealed that doxorubicin significantly increased the expression of DR5, and somewhat up-regulated the expression of DR4 and DcR2. Moreover, doxorubicin, NF-κB inhibitor (SN50), and PI3-kinase/Akt inhibitor (wortmannin, LY294002) enhanced the susceptibility of MRT cell lines to TRAIL/Apo2L-induced apoptosis. These results suggest that TRAIL/Apo2L may provide the basis for clinical trials of TRAIL-based treatment to improve the outcome of MRT patients.
Assessing Energy Security in a Low-Carbon Context: The Case of Electricity in the UK

As part of a growing body of research into potential ways of achieving a secure transition to a low-carbon energy system, this paper assesses the future security of the UK electricity system in a low-carbon context. A new mixed-method set of indicators for assessing security of both supply and demand has been developed and applied to a set of three transition pathways for the UK electricity system, all of which seek to reduce UK carbon emissions by 80% by 2050. This paper uses the results to highlight some of the key risks and trade-offs which may emerge under different routes to a low-carbon electricity transition. In particular, the results indicate that a major risk may be experienced by a lack of flexible, responsive supply capacity in low-carbon electricity pathways. A trade-off is also identified between ‘affordability’ and ‘environmental sustainability’ objectives. The paper finds that energy security is often conceptualised as the avoidance of causes of insecurity (such as insecure fuel imports), but that an equally important aspect of security lies in maximising responses to insecurity, for example by increasing the flexibility and responsiveness of both supply and demand.
Serotonin 5‐HT2 Receptor Stimulation of Dopamine Release in the Posterior but Not Anterior Nucleus Accumbens of the Rat

Abstract: The objective of the present study was to examine the involvement of serotonin 5‐HT2 receptors within the rat nucleus accumbens (Acc) in the regulation of dopamine (DA) release usingin vivo microdialysis. Perfusion with the 5‐HT2 agonist (+)‐1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI), at concentrations of 25‐250 μM, through microdialysis probes located in the posterior Acc increased extracellular DA levels to a maximum of 200% of baseline. DOI‐induced increases in the extracellular levels of DA were Ca2+ dependent and were inhibited by co‐perfusion with the 5‐HT2 antagonist LY‐53,857. DOI enhancement of the extracellular concentrations of DA was observed when probes were implanted in the Acc core and shell regions posterior to anteroposterior +1.2 mm from bregma, whereas a small reduction in the extracellular levels of DA was observed in the anterior Acc. There were no differences between core and shell subdivisions within either the anterior or the posterior Acc. These results suggest that activation of 5‐HT2 receptors within the posterior, but not anterior, Acc stimulates DA release, indicating rostral‐caudal differences in the interactions of 5‐HT with DA systems in the Acc.
Currents through single glutamate receptor channels in outside‐out patches from rat cerebellar granule cells.

1. Single‐channel currents evoked in outside‐out membrane patches from rat cerebellar granule cells by glutamate, aspartate, N‐methyl‐D‐aspartate (NMDA), kainate and quisqualate were studied. Each agonist produced openings to five discrete amplitude levels. At a membrane potential of ‐70 mV, these levels correspond to single‐channel conductances of about 8, 17, 30, 40 and 50 pS. NMDA, aspartate and glutamate evoked mainly 50 pS openings and also substantial numbers of 40 pS events. Kainate evoked primarily 8 and 17 pS openings. 2. The relative proportion of openings to each conductance level showed no dependence on membrane potential. At membrane potentials negative to ‐100 mV, current‐voltage plots for 30, 40 and 50 pS openings showed substantial inward rectification. 3. With NMDA, aspartate and glutamate, the most common type of direct transition was between the 50 pS open level and the shut level. Transitions between the 30, 40 and 50 pS levels were also relatively common. With few exceptions, 8 and 17 pS openings appeared to arise directly from, and return directly to, the shut level. The differences between granule cells and certain other central neurones, in the types of transitions associated with NMDA receptor channels, provide evidence for the existence of more than one type of NMDA receptor. 4. Four exponential components were identified consistently in the shut‐time distributions that were obtained with NMDA, aspartate and glutamate. Mean time constants for the briefest two components were 30 to 65 microseconds and 0.65 to 1.00 ms. The mean duration of these ‘gaps within bursts’ differed for different agonists, but did not vary with membrane potential. 5. Two exponential components were distinguished in most open‐time distributions for the 50 pS level (time constants, 0.9‐1.2 and 3.2‐3.9 ms at ‐100 mV), whereas open‐time distributions for 30 and 40 pS events were described adequately by single exponentials with time constants below 1.0 ms. The duration of 50 pS openings decreased with hyperpolarization. 6. Mean open times for 8 and 17 pS events produced by NMDA, aspartate and glutamate were 0.3 to 0.7 ms. The longest such openings were observed with quisqualate. 7. Three exponential components were present in distributions of burst length, and of total open time per burst, that were obtained with NMDA, aspartate and glutamate. The slowest two burst‐length components had mean time constants of 1.7‐2.4 and 10.6‐13.0 ms and originated from the kinetic behaviour of the 50 pS state. (ABSTRACT TRUNCATED AT 400 WORDS)
Effects of an individualised nutritional education and support programme on dietary habits, nutritional knowledge and nutritional status of older adults living alone

AIMS AND OBJECTIVES The effects of an individualised nutritional education and support programme on dietary habits, nutritional knowledge and nutritional status of 71 older adults living alone were examined. BACKGROUND Although a regular dietary meal plan is recommended for improving nutritional status of older adults living alone, little research is done in this field in Korea. DESIGN A pre- and post-test controlled quasi-experimental design was used at public health centres. METHODS The intervention group participated in an intensive nutritional education and support programme once a week for 8 weeks with dietary menus provided by home visiting nurses/dieticians; control group received usual care. Dietary habits and nutritional knowledge were assessed using structured questionnaires; nutritional intake status was analysed using Computer Aided Nutritional Analysis Program 5.0. RESULTS The mean age of participants was 77.6 years, and 81.7% of the participants were women. At 8 weeks, there were significant interactions of group by time for dietary habits, nutritional knowledge and selected nutritional status of protein, iron and vitamins of B2 and C. Changes over time in the mean score of dietary habits and nutritional knowledge were significantly improved in the intervention group compared to the control group. The percentages of normal nutrition intake of protein, iron and vitamins A and C in the intervention group were significantly higher than the control group at 8 weeks. CONCLUSIONS Nutritional education and support programme positively impacted dietary habits, nutritional knowledge and selected nutritional status in older adults living alone, and we highlight the need for community-based nutritional education and counselling programmes. RELEVANCE TO CLINICAL PRACTICE Older adults living alone in a community have relatively poor nutritional status and thus require tailored nutritional intervention according to objective nutritional analysis. It is necessary to link visiting nurses with dieticians in the community to manage effective nutritional programme continuously.
Well-Tuned Trust as an Intellectual Virtue

Are theists necessarily unreasonable (or unwarranted) in their religious beliefs? While this question is by no means new, it received renewed attention in the 1980s and 1990s, when new interest in externalist epistemological theories drew attention to defenses of justi&ed religious belief by philosophers such as Alvin Plantinga (1981, 2000), William Alston (1991), and Nicholas Wolterstor( (1983). Generalizing roughly, these philosophers promoted the broadening or shi*ing of conditions that can have justi&catory or warrant-conferring power, with the newly shi*ed conditions including some of the more typical grounds for religious belief—grounds that are broadly experiential or intuitive rather than involving reasoned argument. Today, however, some epistemologists are questioning the &eld’s focus on specifying necessary and su+cient conditions under which belief states count as warranted. ,ey favor instead the analysis of practices of belief formation and revision over time, calling excellence in these “intellectual virtue. ”1 If we grant that this is a productive and insightful broadening of focus, how might this change the opening question? How might we epistemically evaluate not only religious states of belief at particular moments in time, the justi&cation of which has received so much careful attention from both religious skeptics and optimistic champions of religious epistemology, but also the way that religious people form and revise those beliefs? Virtue epistemology o(ers a promising new way of framing the old question: can a person of faith be intellectually virtuous in the way she forms, maintains, and modi&es religious beliefs? We &nd this question fascinating—and much too large a topic for one essay. Our aim will be to take a chip at it by focusing &rst, not on faith, but on interpersonal trust. We
Dual Functional Effects of Interleukin-1β on Purine Nucleotides and Insulin Secretion in Rat Islets and INS-1 Cells

Interleukin-1β (IL-1β) has been shown to inhibit glucose-induced insulin secretion from rat islets and purified β-cells, primarily through the generation of nitric oxide (NO). However, the mechanisms by which NO exerts its effects remain unclear. To examine the role of purine nucleotides, we cultured intact rat islets or INS-1 (glucose-responsive transformed rat) β-cells for 18 h in the presence or absence of IL-1β. In islets, the exposure to IL-1β (100 pmol/l) inhibited subsequent glucose-induced insulin secretion by 91% with no significant effect on insulin content or basal insulin release. IL-1β also diminished insulin secretion induced by pure mitochondrial fuels, 40 mmol/l K+, or a phorbol ester. Concomitantly, IL-1β significantly decreased islet ATP (–45%), GTP (–33%), ATP/ADP (–54%), and GTP/GDP (–46%). These effects were totally reversed by provision of Nω-nitro-L-arginine methyl ester (NAME) in arginine-free media that inhibited NO production. In contrast, in INS-1 cells, IL-1β (10 or 100 pmol/l) reduced both basal and glucose-induced insulin secretion by 50%, but insulin content was also reduced by 35%. Therefore, the INS-1 cells were still able to respond to glucose stimulation with a 1.8–2.0–fold increase in insulin release in either the presence or absence of IL-1β. Concomitantly, in INS-1 cells, IL-1β had no effect on ATP/ADP or GTP/GDP ratios, although it modestly decreased ATP (–25%) and GTP (–22%). As in islets, all effects of IL-1β in INS-1 cells were prevented by NAME. Thus, in rat islets, IL-1β (via the generation of NO) abolishes insulin exocytosis in association with large decreases in the ATP/ADP (and GTP/GDP) ratio, implying the impairment of mitochondrial function. Furthermore, IL-1β inhibits cytosolic synthesis of new purine nucleotides (via the salvage pathway), as assessed by a decrease in their specific activity after labeling with [3H]hypoxanthine. In contrast, in INS-1 cells, IL-1β appears to impair cytosolic synthesis of purine nucleotides and insulin biosynthesis selectively (both possibly reflecting decreased glycolysis) with little direct effect on insulin exocytosis itself.
Investigating the neurodevelopmental mediators of aggression in children with a history of child maltreatment:An exploratory field study

ABSTRACT Maltreatment of children is a chronic community problem that increases the risk of future aggression. Despite several decades of research highlighting this relationship, few studies have explored the potential neuropsychological deficits that are likely to mediate it. This exploratory study aimed to examine how child maltreatment may be associated with aggression via impairment in the developing prefrontal-limbic-autonomic pathways that are implicated in neuropsychological models of aggression. Furthermore, it aimed to investigate the relationship between child maltreatment and both reactive and proactive aggression subtypes. To investigate this non-invasively in an at-risk population, children with a documented protective care history (n = 20) and a community control group (n = 30), aged between 6 and 12 years, were compared on measures of cardiovascular functioning, affect regulation and cognitive functioning aligned with this neuropsychological model. Whilst no group differences were found on cardiovascular functioning (i.e., resting heart rate, heart rate reactivity, heart rate variability), the protective care group performed significantly worse on measures of affect regulation and cognitive functioning (i.e., global intelligence, executive functioning, smell identification and social cognition). The relationship between child maltreatment and aggression was mediated by executive dysfunction and affect dysregulation but not global IQ, social cognition or olfactory identification. The results suggest that interventions targeting aggression in maltreated children will benefit from clinical assessment and psychological strategies that address the executive dysfunction and affect dysregulation that has been associated with this clinical outcome.
Clearance of Pseudomonas aeruginosa from a Healthy Ocular Surface Involves Surfactant Protein D and Is Compromised by Bacterial Elastase in a Murine Null-Infection Model

ABSTRACT Our previous studies showed that surfactant protein D (SP-D) is present in human tear fluid and that it can protect corneal epithelial cells against bacterial invasion. Here we developed a novel null-infection model to test the hypothesis that SP-D contributes to the clearance of viable Pseudomonas aeruginosa from the healthy ocular surface in vivo. Healthy corneas of Black Swiss mice were inoculated with 107 or 109 CFU of invasive (PAO1) or cytotoxic (6206) P. aeruginosa. Viable counts were performed on tear fluid collected at time points ranging from 3 to 14 h postinoculation. Healthy ocular surfaces cleared both P. aeruginosa strains efficiently, even when 109 CFU was used: e.g., <0.01% of the original inoculum was recoverable after 3 h. Preexposure of eyes to bacteria did not enhance clearance. Clearance of strain 6206 (low protease producer), but not strain PAO1 (high protease producer), was delayed in SP-D gene-targeted (SP-D−/−) knockout mice. A protease mutant of PAO1 (PAO1 lasAlasBaprA) was cleared more efficiently than wild-type PAO1, but this difference was negligible in SP-D−/− mice, which were less able to clear the protease mutant. Experiments to study mechanisms for these differences revealed that purified elastase could degrade tear fluid SP-D in vivo. Together, these data show that SP-D can contribute to the clearance of P. aeruginosa from the healthy ocular surface and that proteases can compromise that clearance. The data also suggest that SP-D degradation in vivo is a mechanism by which P. aeruginosa proteases could contribute to virulence.
Researching law enforcement and public health

ABSTRACT Academic and practitioner attention to law enforcement and public health/LEPH is relatively new. Its seemingly fresh promise can convey a picture of smart, joined-up and reflective inter-agency cooperation to assist the vulnerable and to support victims. But arriving at and establishing cooperation between the two worlds has been a prolonged and even vacillating process, while continuity may now be endangered. This Special Edition interrogates LEPH in detail; how has it developed, what are its current trajectories, and can its promise adapt and even survive in these tough times? The contributors pay special attention to the conceptual and research foundations that must underpin effective and just engagement between LEPH.
Broadband Circularly Polarized Slot Antenna Array Using Sequentially Rotated Technique for  $C$-Band Applications

This letter presents the investigation results on a novel circularly polarized square-slot antenna (CPSSA) array designed to operate at a frequency of 5.5 GHz. In order to realize the proposed antenna array, four miniature circular polarized square-slot antennas are used with L-shape grounded strips located at the slots' opposite corners to reduce cross polarization. The antenna is fed by symmetric coplanar waveguide. The CPSSA element achieves a bandwidth of 16.6% for an axial ratio <formula formulatype="inline"><tex Notation="TeX">$\leq 3~$</tex></formula>dB. The CPSSA's performance is further enhanced with the construction of a novel 2<formula formulatype="inline"><tex Notation="TeX">$\,\times\,$</tex> </formula>2 antenna array that is designed using sequentially rotated feed technique. The 3-dB axial ratio of the array extends to approximately 2 GHz with an impedance bandwidth of 31%. The CPSSA array was designed to operate over the frequency range between 4 and 6.825 GHz corresponding to an impedance bandwidth of 52% for <formula formulatype="inline"><tex Notation="TeX">${\rm VSWR}< 2$</tex></formula> (1.71:1). Acceptable agreement between the simulation and measured results validates the proposed design.
Elucidating the Early Signal Transduction Pathways Leading to Fetal Brain Injury in Preterm Birth

Adverse neurologic outcome, including cerebral palsy, is a significant contributor to long-term morbidity in preterm neonates. However, the mechanisms leading to brain injury in the setting of a preterm birth are poorly understood. In the last decade, there has been a growing body of evidence correlating infection or inflammation with preterm birth. The presence of intrauterine inflammation significantly increases the risk for adverse neurologic outcome in the neonate. These studies were performed to elucidate the early signal transduction pathways activated in the fetal brain that may result in long-term neurologic injury. Using our mouse model of localized intrauterine inflammation, the activation of TH1/TH2 pathways in the placenta, fetus corpus, fetal liver, and fetal brain was investigated. Additional studies determined whether activation of TH1/TH2 pathways could promote cell death and alter glial development. Real-time PCR studies demonstrated that a robust TH1/TH2 response occurs rapidly in the fetal brain after exposure to intrauterine inflammation. The cytokine response in the fetus and placenta was not significantly correlated with the response in the fetal brain. Along with an immune response, cell death pathways were activated early in the fetal brain in response to intrauterine LPS. Implicating TH1/TH2 and cell death pathways in permanent brain injury are our findings of an increase in GFAP mRNA and protein as well as a loss of pro-oligodendrocytes. With increased understanding of the mechanisms by which inflammation promotes brain injury in the preterm neonate, identification of potential targets to limit adverse neonatal outcomes becomes possible.
How effective is self‐guided learning of clinical technical skills? It’s all about process

Objectives Mounting evidence suggests that trainees acquire psychomotor skills better when they are allowed self‐guided access to instructional material and when they set goals that are related to performance processes rather than performance outcomes. The present study assessed whether self‐guided access to instruction and the setting of process goals lead to better acquisition of clinical technical skills.
The Effectiveness of a Fiscal Transfer Mechanism in a Monetary Union: A DSGE Model for the Euro Area

In this paper, we incorporate a transfer mechanism into a DSGE model with a rich fiscal sector to assess the effectiveness of fiscal transfers for a monetary union, in particular for the Economic and Monetary Union. Using a heterogeneous setup, the model is estimated for the North and the South of Europe using Bayesian methods. The results show that the transfer mechanism is effective in stabilizing the economy of the southern block of countries during the financial crisis, although the total welfare effect for the EMU is negative, though small. Ex ante, a transfer mechanism would be beneficial for both the North and the South in terms of welfare and stabilization purposes.