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Employee behaviors remain at the center of the cybersecurity of workplaces, despite the challenges they face in doing so. Time pressures and competing demands mean that users tend to rely on habitual behaviors that often run counter to good cybersecurity practice. One possible solution may be to encourage positive habit formation. Designing such interventions, however, relies on knowledge of the perception and experience of habit formation in the context of cybersecurity. To this end, a qualitative survey containing open-ended questions was completed by 195 participants (mean age = 35.51, 53 percent female) recruited via an online participant panel. Participants were asked what cybersecurity behaviors they perform at work and how they believe any habits were prompted, formed, and maintained. Thematic analysis identified three over-arching themes: (a) forming habits unavoidably or unconsciously (some were mandated, or formed without conscious awareness), (b) consciously cultivating habits (including the roles of intrinsic motivation and external prompts), and (c) social and organizational influences (including the influence of occupational culture, social modeling, previous experiences, and information gathering practices). Based on these findings, we present guidelines for supporting workplace cybersecurity habit formation reflecting these subjective experiences, namely introducing automatic solutions, facilitating external cues, fostering interest in cybersecurity issues among employees, creating a positive cybersecurity occupational culture and highlighting positive behavior, and providing access to accessible cybersecurity information to employees. These results constitute a first step in identifying how habits can be exploited for positive cybersecurity behavior change in a way that accounts for the reliance on habitual behaviors in busy, time-pressured workplaces.

ImportancePlasma biomarkers of Alzheimer disease may be useful as minimally invasive pharmacodynamic measures of treatment outcomes.ObjectiveTo analyze the association of donanemab treatment with plasma biomarkers associated with Alzheimer disease.Design, Setting, and ParticipantsTRAILBLAZER-ALZ was a randomized, double-blind, placebo-controlled clinical trial conducted from December 18, 2017, to December 4, 2020, across 56 sites in the US and Canada. Exploratory biomarkers were prespecified with the post hoc addition of plasma glial fibrillary acidic protein and amyloid-β. Men and women aged 60 to 85 years with gradual and progressive change in memory function for at least 6 months were included. A total of 1955 participants were assessed for eligibility. Key eligibility criteria include Mini-Mental State Examination scores of 20 to 28 and elevated amyloid and intermediate tau levels.InterventionsRandomized participants received donanemab or placebo every 4 weeks for up to 72 weeks. The first 3 doses of donanemab were given at 700 mg and then increased to 1400 mg with blinded dose reductions as specified based on amyloid reduction.Main Outcomes and MeasuresChange in plasma biomarker levels after donanemab treatment.ResultsIn TRAILBLAZER-ALZ, 272 participants (mean [SD] age, 75.2 [5.5] years; 145 [53.3%] female) were randomized. Plasma levels of phosphorylated tau217 (pTau217) and glial fibrillary acidic protein were significantly lower with donanemab treatment compared with placebo as early as 12 weeks after the start of treatment (least square mean change difference vs placebo, –0.04 [95% CI, –0.07 to –0.02]; P = .002 and –0.04 [95% CI, –0.07 to –0.01]; P = .01, respectively). No significant differences in plasma levels of amyloid-β 42/40 and neurofilament light chain were observed between treatment arms at the end of treatment. Changes in plasma pTau217 and glial fibrillary acidic protein were significantly correlated with the Centiloid percent change in amyloid (Spearman rank correlation coefficient [R] = 0.484 [95% CI, 0.359-0.592]; P R = 0.453 [95% CI, 0.306-0.579]; P 217 and glial fibrillary acidic protein were significantly correlated at baseline and following treatment (R = 0.399 [95% CI, 0.278-0.508], P R = 0.393 [95% CI, 0.254-0.517]; P Conclusions and RelevanceSignificant reductions in plasma biomarkers pTau217 and glial fibrillary acidic protein compared with placebo were observed following donanemab treatment in patients with early symptomatic Alzheimer disease. These easily accessible plasma biomarkers might provide additional evidence of Alzheimer disease pathology change through anti-amyloid therapy. Usefulness in assessing treatment response will require further evaluation.Trial RegistrationClinicalTrials.gov Identifier: NCT03367403

The term ‘cyber security’ is increasingly commonplace in everyday life, and is something that users of all ages will encounter in some form. However, there are varying interpretations about what it actually means, and because of this, people have similarly varying assumptions about the extent to which it applies to them or might affect them.

Galcanezumab, a humanized monoclonal antibody targeting calcitonin gene-related peptide, was recently approved for migraine prophylaxis. The pharmacokinetic/pharmacodynamic (PK/PD) relationship between galcanezumab concentration and inhibition of capsaicin-induced dermal blood flow (CIDBF) was evaluated using first-in-human data following 6 single subcutaneous doses (1 to 600 mg) or multiple (4) 150-mg doses every 2 weeks in 7 cohorts (7 actively treated subjects and 2 placebo-treated healthy subjects). Galcanezumab pharmacokinetics were best described by a 1-compartment model with delayed first-order absorption/linear elimination. Apparent estimates (between-subject variability) of clearance, volume of distribution, absorption rate constant, and lag time were 0.0106 L/h (27%CV), 11.2 L (21%CV), 0.0192 h-1 (89%CV), and 0.202 hours, respectively. Estimated elimination half-life was about 30 days. An effect compartment link model described the concentration-effect relationship; estimated maximum inhibitory effect was 70.5%, and 50% maximum inhibitory effect concentration (IC50 ) was 1060 ng/mL. Galcanezumab showed dose- and concentration-dependent potent and durable inhibition of CIDBF. Simulated effect compartment concentrations were maintained above IC50 after 12 weeks of dosing. Near-maximal CIDBF inhibition occurred with 150 mg biweekly for 12 weeks lasting ≥24 weeks or with ≥30 mg every 2 weeks or 195 mg every 13 weeks. Quantitative modeling of galcanezumab PK/PD supported dose selection for the phase 2 proof-of-concept study.

Clinical investigations have established that vascular-associated medical conditions are significant risk factors for various kinds of dementia. And yet, we are unable to associate certain types of vascular deficiencies with specific cognitive impairments. The reasons for this are many, not the least of which are that most vascular disorders are multi-factorial and the development of vascular dementia in humans is often a multi-year or multi-decade progression. To better study vascular disease and its underlying causes, the National Heart, Lung, and Blood Institute of the National Institutes of Health has invested considerable resources in the development of animal models that recapitulate various aspects of human vascular disease. Many of these models, mainly in the mouse, are based on genetic mutations, frequently using single-gene mutations to examine the role of specific proteins in vascular function. These models could serve as useful tools for understanding the association of specific vascular signaling pathways with specific neurological and cognitive impairments related to dementia. To advance the state of the vascular dementia field and improve the information sharing between the vascular biology and neurobehavioral research communities, National Heart, Lung, and Blood Institute convened a workshop to bring in scientists from these knowledge domains to discuss the potential utility of establishing a comprehensive phenotypic cognitive assessment of a selected set of existing mouse models, representative of the spectrum of vascular disorders, with particular attention focused on age, sex, and rigor and reproducibility. The workshop highlighted the potential of associating well-characterized vascular disease models, with validated cognitive outcomes, that can be used to link specific vascular signaling pathways with specific cognitive and neurobehavioral deficits.

This paper proposes a novel telemanipulation system that enables a human operator to control a dual-arm robot. The operation provides kinesthetic teaching via a digital twin of the robot which the operator cyber-physically guides to perform a task. Its key enabler is the concept of a virtual reality interactive marker, which serves as a simplified end effector of the digital twin robot. In virtual reality, the operator can interact with the marker using bare hands, which are sensed by the Leap Motion on top of a virtual reality headset. Then, the status (e.g. position/orientation) of the marker is transformed to the corresponding joint space command to the remote robot so that its end effector can follow the marker. We provide the details of the system architecture, and implement the system based on commercial robots/devices (i.e. UR5, Robotiq gripper, Leap Motion), virtual reality, ROS, and Unity3D. Moreover, the paper discusses the technical challenges that we had to address, and the system’s potential benefits from a human-robot interaction perspective.

COVID-19 has radically changed society as we know it. To reduce the spread of the virus, millions across the globe have been forced to work remotely, often in make-shift home offices, and using a plethora of new, unfamiliar digital technologies. In this article, we critically analyse cyber security and privacy concerns arising due to remote working during the coronavirus pandemic. Through our work, we discover a series of security risks emerging because of the realities of this period. For instance, lack of remote-working security training, heightened stress and anxiety, rushed technology deployment, and the presence of untrusted individuals in a remote-working environment (e.g., in flatshares), can result in new cyber-risk. Simultaneously, we find that as organisations look to manage these and other risks posed by their remote workforces, employee's privacy (including personal information and activities) is often compromised. This is apparent in the significant adoption of remote workplace monitoring, management and surveillance technologies. Such technologies raise several privacy and ethical questions, and further highlight the tension between security and privacy going forward., HCI International 2021 (HCII 2021)

Alzheimer’s Disease (AD) tau pathology originates in the brainstem and subsequently spreads to the entorhinal cortex, hippocampus and finally to temporal, parietal and prefrontal association cortices in a relatively stereotyped progression. Current evidence attributes this orderly progression to trans-neuronal spread of misfolded tau protein along the projection pathways of affected neurons. The aggregation of tau is being increasingly recognized as a trustworthy biomarker preceding the appearance of Alzheimer’s disease (AD) symptoms. One major goals of disease modifying therapies has been to stop or slow down the tau aggregation process. In order to evaluate drug efficacy, it would be desirable to have an accurate model predictive of a patient’s future tau burden, against which the tau measurements from drug-receiving cohorts could be compared. Here we report the development of such a model, evaluated in a cohort of 88 subjects clinically diagnosed as Mild Cognitively Impaired (MCI = 60) or Alzheimer’s disease (AD = 28) and tracked over a period of 18 months. Our approach combined data-driven and model-based methodologies, with the goal of predicting changes in tau within suitably specified target regions. We show that traditional statistical methods, allied to a network diffusion model for tau propagation in the brain, provide a remarkable prediction of the magnitude of incremental tau deposited in particular cortical areas of the brain over this period (MCI: R2 = 0.65±0.16; AD: R2 = 0.71±0.11) from baseline data. Our work has the potential to greatly strengthen the repertoire of analysis tools used in AD clinical trials, opening the door to future interventional trials with far fewer sample sizes than currently required.

Strategic word mimicry during negotiations facilitates better outcomes. We explore mimicry of specific word categories and perceptions of rapport, trust, and liking as underlying mechanisms. Dyads took part in an online negotiation exercise in which word mimicry was manipulated: Participants were instructed to mimic each other’s words (both‐mimic), one participant mimicked the other (half‐mimic), or neither participant mimicked (neither‐mimic). When given a simple instruction to mimic their partner, participants mimicked both the style (personal pronouns, adverbs, linguistic style, interrogative terms) and the content (affiliation terms, power terms, and assents) of their partner’s messages. Mimicry was associated with greater joint and individual points gain and perceptions of rapport from the mimicked partner. Further, mimicry of interrogative terms (e.g., how, why) mediated positive effects of mimicry upon negotiation outcomes, suggesting the coordination of question asking between negotiators is an important strategy to create beneficial interactions and add value in negotiations.