572 research outputs found
Cyber security fear appeals:unexpectedly complicated
Cyber security researchers are starting to experiment with fear appeals, with a wide variety of designs and reported efficaciousness. This makes it hard to derive recommendations for designing and deploying these interventions. We thus reviewed the wider fear appeal literature to arrive at a set of guidelines to assist cyber security researchers. Our review revealed a degree of dissent about whether or not fear appeals are indeed helpful and advisable. Our review also revealed a wide range of fear appeal experimental designs, in both cyber and other domains, which confirms the need for some standardized guidelines to inform practice in this respect. We propose a protocol for carrying out fear appeal experiments, and we review a sample of cyber security fear appeal studies, via this lens, to provide a snapshot of the current state of play. We hope the proposed experimental protocol will prove helpful to those who wish to engage in future cyber security fear appeal research
Acute symptomatic hypoglycaemia mimicking ischaemic stroke on imaging:a systemic review
<p>Abstract</p> <p>Background</p> <p>Acute symptomatic hypoglycaemia is a differential diagnosis in patients presenting with stroke-like neurological impairment, but few textbooks describe the full brain imaging appearances. We systematically reviewed the literature to identify how often hypoglycaemia may mimic ischaemic stroke on imaging, common patterns and relationships with hypoglycaemia severity, duration, clinical outcome and add two new cases.</p> <p>Methods</p> <p>We searched EMBASE and Medline databases for papers reporting imaging in adults with symptomatic hypoglycaemia. We analysed the clinical presentation, outcome, brain imaging findings, duration and severity of hypoglycaemia, time course of lesion appearance, including two new cases.</p> <p>Results</p> <p>We found 42 papers describing computed tomography or magnetic resonance imaging in 65 patients, plus our two cases with symptomatic hypoglycaemia. Imaging abnormalities on computed tomography and magnetic resonance were uni or bilateral, cortical or sub-cortical. Thirteen (20%) mimicked cortical or lacunar stroke. Acute lesions had restricted diffusion on magnetic resonance or low attenuation on computed tomography, plus swelling; older lesions showed focal atrophy or disappeared, as with ischaemic stroke. The association between the depth or duration of hypoglycaemia, the severity or extent of neurological deficit, and the imaging abnormalities, was weak.</p> <p>Conclusion</p> <p>Imaging abnormalities in patients with hypoglycaemia are uncommon but very variable, weakly associated with neurological deficit, and about a fifth mimic acute ischaemic stroke. Blood glucose testing should be routine in all patients with acute neurological impairment and hypoglycaemia should be included in the differential diagnosis of imaging appearances in patients presenting with acute stroke.</p
Pseudocoarctation of the Aorta Associated with the Anomalous Origin of the Left Vertebral Artery: a Case Report
Pseudocoarctation of the aorta is a rare congenital anomaly of the aortic arch, and it has been described as an elongation of the aortic arch with "kinking" at the level of the ligamentum arteriosum without a pressure gradient across the lesion. The treatment for this condition is controversial. We report here on an unusual case of pseudocoarctation of the aorta associated with the anomalous origin of the left vertebral artery and we include a review of the medical literature
Diagnosis and treatment of spontaneous intracranial hypotension due to cerebrospinal fluid leakage
Designing challenge questions for location‐based authentication systems: a real‐life study
AbstractOnline service providers often use challenge questions (a.k.a. knowledge‐based authentication) to facilitate resetting of passwords or to provide an extra layer of security for authentication. While prior schemes explored both static and dynamic challenge questions to improve security, they do not systematically investigate the problem of designing challenge questions and its effect on user recall performance. Interestingly, as answering different styles of questions may require different amount of cognitive effort and evoke different reactions among users, we argue that the style of challenge questions itself can have a significant effect on user recall performance and usability of such systems. To address this void and investigate the effect of question types on user performance, this paper explores location‐based challenge question generation schemes where different types of questions are generated based on users’ locations tracked by smartphones and presented to users. For evaluation, we deployed our location tracking application on users’ smartphones and conducted two real‐life studies using four different kinds of challenge questions. Each study was approximately 30 days long and had 14 and 15 users respectively. Our findings suggest that the question type can have a significant effect on user performance. Finally, as individual users may vary in terms of performance and recall rate, we investigate and present a Bayesian classifier based authentication algorithm that can authenticate legitimate users with high accuracy by leveraging individual response patterns while reducing the success rate of adversaries.</jats:p
Cannabinoid 1 Receptor Signaling on Hippocampal GABAergic Neurons Influences Microglial Activity
Microglia, the resident immune cells of the brain, play important roles in defending the brain against pathogens and supporting neuronal circuit plasticity. Chronic or excessive pro-inflammatory responses of microglia damage neurons, therefore their activity is tightly regulated. Pharmacological and genetic studies revealed that cannabinoid type 1 (CB1) receptor activity influences microglial activity, although microglial CB1 receptor expression is very low and activity-dependent. The CB1 receptor is mainly expressed on neurons in the central nervous system (CNS)—with an especially high level on GABAergic interneurons. Here, we determined whether CB1 signaling on this neuronal cell type plays a role in regulating microglial activity. We compared microglia density, morphology and cytokine expression in wild-type (WT) and GABAergic neuron-specific CB1 knockout mice (GABA/CB1−/−) under control conditions (saline-treatment) and after 3 h, 24 h or repeated lipopolysaccharide (LPS)-treatment. Our results revealed that hippocampal microglia from saline-treated GABA/CB1−/− mice resembled those of LPS-treated WT mice: enhanced density and larger cell bodies, while the size and complexity of their processes was reduced. No further reduction in the size or complexity of microglia branching was detected after LPS-treatment in GABA/CB1−/− mice, suggesting that microglia in naïve GABA/CB1−/− mice were already in an activated state. This result was further supported by correlating the level of microglial tumor necrosis factor α (TNFα) with their size. Acute LPS-treatment elicited in both genotypes similar changes in the expression of pro-inflammatory cytokines (TNFα, interleukin-6 (IL-6) and interleukin 1β (IL-1β)). However, TNFα expression was still significantly elevated after repeated LPS-treatment in WT, but not in GABA/CB1−/− mice, indicating a faster development of tolerance to LPS. We also tested the possibility that the altered microglia activity in GABA/CB1−/− mice was due to an altered expression of neuron-glia interaction proteins. Indeed, the level of fractalkine (CX3CL1), a neuronal protein involved in the regulation of microglia, was reduced in hippocampal GABAergic neurons in GABA/CB1−/− mice, suggesting a disturbed neuronal control of microglial activity. Our result suggests that CB1 receptor agonists can modulate microglial activity indirectly, through CB1 receptors on GABAergic neurons. Altogether, we demonstrated that GABAergic neurons, despite their relatively low density in the hippocampus, have a specific role in the regulation of microglial activity and cannabinoid signaling plays an important role in this arrangement
Cis P-tau is induced in clinical and preclinical brain injury and contributes to post-injury sequelae
Traumatic brain injury (TBI) is characterized by acute neurological dysfunction and asso- ciated with the development of chronic traumatic encephalopathy (CTE) and Alzheimer’s disease. We previously showed that cis phosphorylated tau (cis P-tau), but not the trans form, contributes to tau pathology and functional impairment in an animal model of severe TBI. Here we found that in human samples obtained post TBI due to a variety of causes, cis P-tau is induced in cortical axons and cerebrospinal fluid and positively correlates with axonal injury and clinical outcome. Using mouse models of severe or repetitive TBI, we showed that cis P-tau elimination with a specific neutralizing antibody administered immediately or at delayed time points after injury, attenuates the development of neuropathology and brain dysfunction during acute and chronic phases including CTE-like pathology and dysfunction after repetitive TBI. Thus, cis P-tau contributes to short-term and long-term sequelae after TBI, but is effectively neutralized by cis antibody treatment
Cerebrospinal fluid flow dynamics in patients with multiple sclerosis: a phase contrast magnetic resonance study
Cerebrospinal fluid (CSF) flow dynamics, which supposedly
have a strong relationship with chronic cerebrospinal
venous insufficiency (CCSVI), might be expected to be affected in multiple sclerosis (MS) patients.
In this study, CSF flow at the level of the cerebral aqueduct was evaluated quantitatively by phase contrast
magnetic resonance imaging (PC-MRI) to determine whether CSF flow dynamics are affected in MS patients.
We studied 40 MS patients and 40 healthy controls using PC-MRI. We found significantly higher caudocranial(p=0.010) and craniocaudal CSF flow volumes(p=0.015) and stroke volume (p=0.010) in the MS patients compared with the controls. These findings may support the venous occlusion theory, but may also be explained by atrophy-dependent ventricular dilatation independent of the venous theory in MS patients
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