Driver Fatigue: Is Something Missing?

Drowsiness and fatigue are serious problems in all transportation systems. One persistent issue is the lack of an agreed definition of these respective energetic states. Here we review the theoretical approaches (cognitive versus physiological) framing the driver fatigue problem. Known contributing factors to drowsiness include sleep debt, circadian rhythm, and shift work. However, we also suggest that certain inherent physiological reactions engaged in responses to motion itself represent a previously unrecognized but significant source of fatigue. We confirm the impact of this factor through comparisons of studies that either have or have not included prolonged motion

Vibrotactile Stimuli Parameters on Detection Reaction Times

Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG geförderten) Allianz- bzw. Nationallizenz frei zugänglich.This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.Signaling system designers are leveraging the tactile modality to create alarms, alerts, and warnings. The purpose of this research was to map detection reaction times (RT) toward tactile stimuli with various parameter manipulations. We employed a 3 (wave form) × 3 (inter-pulse interval) × 3 (envelope) within subjects design. The dependent measure was detection RT. Twenty participants (15 female) responded to 270 tactile stimuli. ANOVAs indicated three two-way interactions. Generally, shorter inter-pulse intervals led to quicker RT and the fade-in envelope led to longer RT, when compared to envelopes starting at the maximum amplitude. Square and sinusoidal waves tended to prompt quicker RT than the noise wave. The strength of these relationships, however, depended upon the presence of the other parameters. Designers can use the results of this study to effectively and appropriately assign tactile parameter manipulations to signals that require varied levels of response urgencies

Matters of Ethics, Trust, and Potential Liability for Autonomous Systems

Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG geförderten) Allianz- bzw. Nationallizenz frei zugänglich.This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.The objective of this panel was to discuss issues related to the development and use of autonomous systems, with specific focus on the overriding themes of ethical considerations and potential liability for Human Factors and Ergonomics (HF/E) professionals who are involved in their development. Chris Brill provided opening remarks to frame the discussion and introduce the panelists. James Bliss discussed legal implications related to our collective penchant for developing conservative, false-alarm prone automation. Peter Hancock advocated for human-centered constraints on autonomous systems, as they may, one day, pose an existential threat to humanity. Dietrich Manzey discussed ethical considerations for autonomous systems, including how design can encourage ethical user behavior. Joachim Meyer argued that HF/E professionals have an obligation to help designers understand the ethical implications of poor design, particularly in the context of autonomous systems. Lastly, Alison Vredenburgh provided thoughts on potential liability for HF/E professionals, particularly in light of the relative newness of autonomous systems. The panel then turned to facilitated discussion with panelists and audience members. Specific themes included the boundaries of our responsibilities as HF/E professionals for ill-conceived or morally-objectionable systems, potential implications of manipulating user trust through design, cross-cultural perspectives on public acceptance and legal peril, and how concerns might differ by domain (e.g., medical vs. combat vs. manufacturing). The session concluded with panelists summarizing how ethics influence design and recommendations for how HF/E professionals can potentially protect themselves from legal liability for mishaps involving autonomous systems they helped develop

Adipose Tissue Serves as a Reservoir for Recrudescent Rickettsia prowazekii Infection in a Mouse Model

Brill-Zinsser disease, the relapsing form of epidemic typhus, typically occurs in a susceptible host years or decades after the primary infection; however, the mechanisms of reactivation and the cellular reservoir during latency are poorly understood. Herein we describe a murine model for Brill-Zinsser disease, and use PCR and cell culture to show transient rickettsemia in mice treated with dexamethasone >3 months after clinical recovery from the primary infection. Treatment of similarly infected mice with cyclosporine failed to produce recrudescent bacteremia. Therapy with doxycycline for the primary infection prevented recrudescent bacteremia in most of these mice following treatment with dexamethasone. Rickettsia prowazekii (the etiologic agent of epidemic typhus) was detected by PCR, cell culture, and immunostaining methods in murine adipose tissue, but not in liver, spleen, lung, or central nervous system tissues of mice 4 months after recovery from the primary infection. The lungs of dexamethasone-treated mice showed impaired expression of β-defensin transcripts that may be involved in the pathogenesis of pulmonary lesions. In vitro, R. prowazekii rickettsiae infected and replicated in the murine adipocyte cell line 3T3-L1. Collectively these data suggest a role for adipose tissue as a potential reservoir for dormant infections with R. prowazekii

The Receptor Tyrosine Kinase FGFR4 Negatively Regulates NF-kappaB Signaling

NFκB signaling is of paramount importance in the regulation of apoptosis, proliferation, and inflammatory responses during human development and homeostasis, as well as in many human cancers. Receptor Tyrosine Kinases (RTKs), including the Fibroblast Growth Factor Receptors (FGFRs) are also important in development and disease. However, a direct relationship between growth factor signaling pathways and NFκB activation has not been previously described, although FGFs have been known to antagonize TNFα-induced apoptosis. assays. FGF19 stimulation of endogenous FGFR4 in TNFα-treated DU145 prostate cancer cells also leads to a decrease in IKKβ activity, concomitant reduction in NFκB nuclear localization, and reduced apoptosis. Microarray analysis demonstrates that FGF19 + TNFα treatment of DU145 cells, in comparison with TNFα alone, favors proliferative genes while downregulating genes involved in apoptotic responses and NFκB signaling.These results identify a compelling link between FGFR4 signaling and the NFκB pathway, and reveal that FGFR4 activation leads to a negative effect on NFκB signaling including an inhibitory effect on proapoptotic signaling. We anticipate that this interaction between an RTK and a component of NFκB signaling will not be limited to FGFR4 alone

Neutrophil-Derived MMP-8 Drives AMPK-Dependent Matrix Destruction in Human Pulmonary Tuberculosis.

Pulmonary cavities, the hallmark of tuberculosis (TB), are characterized by high mycobacterial load and perpetuate the spread of M. tuberculosis. The mechanism of matrix destruction resulting in cavitation is not well defined. Neutrophils are emerging as key mediators of TB immunopathology and their influx are associated with poor outcomes. We investigated neutrophil-dependent mechanisms involved in TB-associated matrix destruction using a cellular model, a cohort of 108 patients, and in separate patient lung biopsies. Neutrophil-derived NF-kB-dependent matrix metalloproteinase-8 (MMP-8) secretion was up-regulated in TB and caused matrix destruction both in vitro and in respiratory samples of TB patients. Collagen destruction induced by TB infection was abolished by doxycycline, a licensed MMP inhibitor. Neutrophil extracellular traps (NETs) contain MMP-8 and are increased in samples from TB patients. Neutrophils lined the circumference of human pulmonary TB cavities and sputum MMP-8 concentrations reflected TB radiological and clinical disease severity. AMPK, a central regulator of catabolism, drove neutrophil MMP-8 secretion and neutrophils from AMPK-deficient patients secrete lower MMP-8 concentrations. AMPK-expressing neutrophils are present in human TB lung biopsies with phospho-AMPK detected in nuclei. These data demonstrate that neutrophil-derived MMP-8 has a key role in the immunopathology of TB and is a potential target for host-directed therapy in this infectious disease

Readout of a quantum processor with high dynamic range Josephson parametric amplifiers

We demonstrate a high dynamic range Josephson parametric amplifier (JPA) in which the active nonlinear element is implemented using an array of rf-SQUIDs. The device is matched to the 50 $\Omega$ environment with a Klopfenstein-taper impedance transformer and achieves a bandwidth of 250-300 MHz, with input saturation powers up to -95 dBm at 20 dB gain. A 54-qubit Sycamore processor was used to benchmark these devices, providing a calibration for readout power, an estimate of amplifier added noise, and a platform for comparison against standard impedance matched parametric amplifiers with a single dc-SQUID. We find that the high power rf-SQUID array design has no adverse effect on system noise, readout fidelity, or qubit dephasing, and we estimate an upper bound on amplifier added noise at 1.6 times the quantum limit. Lastly, amplifiers with this design show no degradation in readout fidelity due to gain compression, which can occur in multi-tone multiplexed readout with traditional JPAs.Comment: 9 pages, 8 figure

Measurement-Induced State Transitions in a Superconducting Qubit: Within the Rotating Wave Approximation

Superconducting qubits typically use a dispersive readout scheme, where a resonator is coupled to a qubit such that its frequency is qubit-state dependent. Measurement is performed by driving the resonator, where the transmitted resonator field yields information about the resonator frequency and thus the qubit state. Ideally, we could use arbitrarily strong resonator drives to achieve a target signal-to-noise ratio in the shortest possible time. However, experiments have shown that when the average resonator photon number exceeds a certain threshold, the qubit is excited out of its computational subspace, which we refer to as a measurement-induced state transition. These transitions degrade readout fidelity, and constitute leakage which precludes further operation of the qubit in, for example, error correction. Here we study these transitions using a transmon qubit by experimentally measuring their dependence on qubit frequency, average photon number, and qubit state, in the regime where the resonator frequency is lower than the qubit frequency. We observe signatures of resonant transitions between levels in the coupled qubit-resonator system that exhibit noisy behavior when measured repeatedly in time. We provide a semi-classical model of these transitions based on the rotating wave approximation and use it to predict the onset of state transitions in our experiments. Our results suggest the transmon is excited to levels near the top of its cosine potential following a state transition, where the charge dispersion of higher transmon levels explains the observed noisy behavior of state transitions. Moreover, occupation in these higher energy levels poses a major challenge for fast qubit reset

Overcoming leakage in scalable quantum error correction

Leakage of quantum information out of computational states into higher energy states represents a major challenge in the pursuit of quantum error correction (QEC). In a QEC circuit, leakage builds over time and spreads through multi-qubit interactions. This leads to correlated errors that degrade the exponential suppression of logical error with scale, challenging the feasibility of QEC as a path towards fault-tolerant quantum computation. Here, we demonstrate the execution of a distance-3 surface code and distance-21 bit-flip code on a Sycamore quantum processor where leakage is removed from all qubits in each cycle. This shortens the lifetime of leakage and curtails its ability to spread and induce correlated errors. We report a ten-fold reduction in steady-state leakage population on the data qubits encoding the logical state and an average leakage population of less than $1 \times 10^{-3}$ throughout the entire device. The leakage removal process itself efficiently returns leakage population back to the computational basis, and adding it to a code circuit prevents leakage from inducing correlated error across cycles, restoring a fundamental assumption of QEC. With this demonstration that leakage can be contained, we resolve a key challenge for practical QEC at scale.Comment: Main text: 7 pages, 5 figure