Persuading Patients Using Rhetoric to Improve Artificial Intelligence Adoption: Experimental Study.

BACKGROUND: Artificial intelligence (AI) can transform health care processes with its increasing ability to translate complex structured and unstructured data into actionable clinical decisions. Although it has been established that AI is much more efficient than a clinician, the adoption rate has been slower in health care. Prior studies have pointed out that the lack of trust in AI, privacy concerns, degrees of customer innovativeness, and perceived novelty value influence AI adoption. With the promotion of AI products to patients, the role of rhetoric in influencing these factors has received scant attention. OBJECTIVE: The main objective of this study was to examine whether communication strategies (ethos, pathos, and logos) are more successful in overcoming factors that hinder AI product adoption among patients. METHODS: We conducted experiments in which we manipulated the communication strategy (ethos, pathos, and logos) in promotional ads for an AI product. We collected responses from 150 participants using Amazon Mechanical Turk. Participants were randomly exposed to a specific rhetoric-based advertisement during the experiments. RESULTS: Our results indicate that using communication strategies to promote an AI product affects users' trust, customer innovativeness, and perceived novelty value, leading to improved product adoption. Pathos-laden promotions improve AI product adoption by nudging users' trust (n=52; ß=.532; P<.001) and perceived novelty value of the product (n=52; ß=.517; P=.001). Similarly, ethos-laden promotions improve AI product adoption by nudging customer innovativeness (n=50; ß=.465; P<.001). In addition, logos-laden promotions improve AI product adoption by alleviating trust issues (n=48; ß=.657; P<.001). CONCLUSIONS: Promoting AI products to patients using rhetoric-based advertisements can help overcome factors that hinder AI adoption by assuaging user concerns about using a new AI agent in their care process.

Benefits of Blockchain Initiatives for Value-Based Care: Proposed Framework.

BACKGROUND: The potential of blockchain technology to achieve strategic goals, such as value-based care, is increasingly being recognized by both researchers and practitioners. However, current research and practices lack comprehensive approaches for evaluating the benefits of blockchain applications. OBJECTIVE: The goal of this study was to develop a framework for holistically assessing the performance of blockchain initiatives in providing value-based care by extending the existing balanced scorecard (BSC) evaluation framework. METHODS: Based on a review of the literature on value-based health care, blockchain technology, and methods for evaluating initiatives in disruptive technologies, we propose an extended BSC method for holistically evaluating blockchain applications in the provision of value-based health care. The proposed method extends the BSC framework, which has been extensively used to measure both financial and nonfinancial performance of organizations. The usefulness of our proposed framework is further demonstrated via a case study. RESULTS: We describe the extended BSC framework, which includes five perspectives (both financial and nonfinancial) from which to assess the appropriateness and performance of blockchain initiatives in the health care domain. CONCLUSIONS: The proposed framework moves us toward a holistic evaluation of both the financial and nonfinancial benefits of blockchain initiatives in the context of value-based care and its provision.

Time-dependent effects of CX3CR1 in a mouse model of mild traumatic brain injury.

BACKGROUND: Neuroinflammation is an important secondary mechanism that is a key mediator of the long-term consequences of neuronal injury that occur in traumatic brain injury (TBI). Microglia are highly plastic cells with dual roles in neuronal injury and recovery. Recent studies suggest that the chemokine fractalkine (CX3CL1, FKN) mediates neural/microglial interactions via its sole receptor CX3CR1. CX3CL1/CX3CR1 signaling modulates microglia activation, and depending upon the type and time of injury, either protects or exacerbates neurological diseases. METHODS: In this study, mice deficient in CX3CR1 were subjected to mild controlled cortical impact injury (CCI), a model of TBI. We evaluated the effects of genetic deletion of CX3CR1 on histopathology, cell death/survival, microglia activation, and cognitive function for 30 days post-injury. RESULTS: During the acute post-injury period (24 h-15 days), motor deficits, cell death, and neuronal cell loss were more profound in injured wild-type than in CX3CR1(-/-) mice. In contrast, during the chronic period of 30 days post-TBI, injured CX3CR1(-/-) mice exhibited greater cognitive dysfunction and increased neuronal death than wild-type mice. The protective and deleterious effects of CX3CR1 were associated with changes in microglia phenotypes; during the acute phase CX3CR1(-/-) mice showed a predominant anti-inflammatory M2 microglial response, with increased expression of Ym1, CD206, and TGFß. In contrast, increased M1 phenotypic microglia markers, Marco, and CD68 were predominant at 30 days post-TBI. CONCLUSION: Collectively, these novel data demonstrate a time-dependent role for CX3CL1/CX3CR1 signaling after TBI and suggest that the acute and chronic responses to mild TBI are modulated in part by distinct microglia phenotypes.

Sleep fragmentation and sepsis differentially impact blood-brain barrier integrity and transport of tumor necrosis factor-α in aging.

The factors by which aging predisposes to critical illness are varied, complex, and not well understood. Sepsis is considered a quintessential disease of old age because the incidence and mortality of severe sepsis increases in old and the oldest old individuals. Aging is associated with dramatic changes in sleep quality and quantity and sleep increasingly becomes fragmented with age. In healthy adults, sleep disruption induces inflammation. Multiple aspects of aging and of sleep dysregulation interact via neuroimmune mechanisms. Tumor necrosis factor-α (TNF), a cytokine involved in sleep regulation and neuroimmune processes, exerts some of its effects on the CNS by crossing the blood-brain barrier (BBB). In this study we examined the impact of sepsis, sleep fragmentation, and aging on BBB disruption and TNF transport into brain. We used the cecal ligation and puncture (CLP) model of sepsis in young and aged mice that were either undisturbed or had their sleep disrupted. There was a dichotomous effect of sepsis and sleep disruption with age: sepsis disrupted the BBB and increased TNF transport in young mice but not in aged mice, whereas sleep fragmentation disrupted the BBB and increased TNF transport in aged mice, but not in young mice. Combining sleep fragmentation and CLP did not produce a greater effect on either of these BBB parameters than did either of these manipulations alone. These results suggest that the mechanisms by which sleep fragmentation and sepsis alter BBB functions are fundamentally different from one another and that a major change in the organism's responses to those insults occurs with aging.

Effects of housing condition and cage change on characteristics of sleep in mice.

Although human subjects are widely used to study sleep and sleep disorders, animals have been invaluable in developing our understanding of the physiology of sleep and underlying mechanisms of sleep disorders. Environmental stimuli are likely to modify sleep in both animals and people, suggesting that environmental stability must be controlled carefully by both husbandry and research staff to allow collection of valid results with minimal numbers of animals. However, few studies have measured the effects of cage condition on sleep parameters in mice. Current guidelines recommend social housing and environmental enrichment for standard rodent housing. Environmental factors such as these create potential confounds in studies for which facets of sleep are outcome measures. We therefore sought to determine whether cage changes, group housing, or single housing with a shelter altered measures of sleep in C57BL/6J mice. The resulting data indicate that 1) cage changing disrupts sleep for approximately 3 h; 2) group housing is associated with shorter bouts of rapid-eye-movement sleep (REMS) and less slow-wave sleep (SWS) during the light phase and with more REMS during the dark phase; and 3) mice housed with a shelter spend less time awake and more time in SWS, with longer bouts of SWS during the dark phase. In additional, both group housing and housing with a shelter were associated with less locomotor activity than occurred in individually housed mice without a shelter. These findings provide evidence for long-held beliefs that housing conditions must be controlled carefully in studies that require assessment of sleep.

Prolonged sleep fragmentation of mice exacerbates febrile responses to lipopolysaccharide.

BACKGROUND: Sleep disruption is a frequent occurrence in modern society. Whereas many studies have focused on the consequences of total sleep deprivation, few have investigated the condition of sleep disruption. NEW METHOD: We disrupted sleep of mice during the light period for 9 consecutive days using an intermittently rotating disc. RESULTS: Electroencephalogram (EEG) data demonstrated that non-rapid eye movement (NREM) sleep was severely fragmented and REM sleep was essentially abolished during the 12h light period. During the dark period, when sleep was not disrupted, neither NREM sleep nor REM sleep times differed from control values. Analysis of the EEG revealed a trend for increased power in the peak frequency of the NREM EEG spectra during the dark period. The fragmentation protocol was not overly stressful as body weights and water consumption remained unchanged, and plasma corticosterone did not differ between mice subjected to 3 or 9 days of sleep disruption and home cage controls. However, mice subjected to 9 days of sleep disruption by this method responded to lipopolysaccharide with an exacerbated febrile response. COMPARISON WITH EXISTING METHODS: Existing methods to disrupt sleep of laboratory rodents often subject the animal to excessive locomotion, vibration, or sudden movements. This method does not suffer from any of these confounds. CONCLUSIONS: This study demonstrates that prolonged sleep disruption of mice exacerbates febrile responses to lipopolysaccharide. This device provides a method to determine mechanisms by which chronic insufficient sleep contributes to the etiology of many pathologies, particularly those with an inflammatory component.