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IntroductionFaults or errors during use of closed-circuit rebreathers (CCRs) can cause hypoxia. Military aviators face a similar risk of hypoxia and undergo awareness training to determine their 'hypoxia signature', a personalised, reproducible set of symptoms. We aimed to establish a hypoxia signature among divers, and to investigate their ability to detect hypoxia and self-rescue while cognitively overloaded.MethodsEight CCR divers and 12 scuba divers underwent an initial unblinded hypoxia exposure followed by three trials; a second hypoxic trial and two normoxic trials in randomised order. Hypoxia was induced by breathing on a CCR with no oxygen supply. Subjects pedalled on a cycle ergometer while playing a neurocognitive computer game to simulate real world task loading. Subjects identified hypoxia symptoms by pointing to a board listing common hypoxia symptoms, and were instructed to perform a 'bailout' procedure to mimic self-rescue if they perceived hypoxia. Divers were prompted to bailout if peripheral oxygen saturation fell to 75%, or after six minutes during normoxic trials. Subsequently we interviewed subjects to determine their ability to distinguish hypoxia from normoxia.ResultsNinety-five percent of subjects (19/20) showed agreement between unblinded and blinded hypoxia symptoms. Subjects correctly identified the gas mixture in 85% of the trials. During unblinded hypoxia, only 25% (5/20) of subjects performed unprompted bailout. Fifty-five percent of subjects (11/20) correctly performed the bailout but only when prompted, while 15% (3/20) were unable to bailout despite prompting. During blinded hypoxia 45% of subjects (9/20) performed the bailout unprompted while 15% (3/20) remained unable to bailout despite prompting.ConclusionsAlthough our data support a normobaric hypoxia signature among both CCR and scuba divers under experimental conditions, most subjects were unable to recognise hypoxia in real time and perform a self-rescue unprompted, although

IntroductionArtisanal diving fishermen in Yucatán, Mexico have high rates of decompression sickness as a result of frequently unsafe diving practices with surface supplied compressed air. In this study, we investigated the prevalence of dysbaric osteonecrosis (DON), a type of avascular necrosis, in the most susceptible joints in a cohort of these fishermen.MethodsWe performed radiographs of bilateral shoulders, hips, and knees of 39 fishermen in Mexico and surveyed them about their medical and diving histories. We performed pairwise correlations to examine if the fishermen's diving behaviours affected the numbers of joints with DON.ResultsThe radiographs revealed Grade II or higher DON in 30/39 (76.9%) of the fishermen. Twenty-two of 39 fishermen (56.4%) had at least two affected joints. The number of joints with DON positively correlates with the lifetime maximum diving depth and average bottom time.ConclusionsThese findings represent among the highest prevalence rates of DON in divers and reflect the wide-spread scale of decompression sickness among these fishermen. Through this work, we hope to further educate the fishermen on the sequelae of their diving with the aim of improving their diving safety.

Introduction: The novel coronavirus disease 2019 (COVID-19) created challenges with access to care including increased burden on healthcare systems and potential exposure risks for vulnerable patients. To address these needs, Rush University Medical Center created a virtual, urgent care program specifically designed to address these challenges during the COVID-19 pandemic. Methods: This was a retrospective study analyzing adult patients with COVID-19-related telemedicine visits performed between March 1–June 30, 2020. COVID-19-related telemedicine visits refer to those who used the “Concern for Coronavirus” module. We assessed the total number of telemedicine visits using this module, percentage with a subsequent emergency department (ED) visit within seven days, and outcomes (ie, hospitalization status, intubation, and death) of patients who presented to the ED for evaluation. Data are presented using descriptive statistics. Results: A total of 2,974 adult patients accessed the program via the COVID-19 module over the four-month period. Of those, 142 patients (4.8%) had an ED visit within seven days. Only 14 patients (0.5%) required admission. One patient was intubated, and there were no deaths among the telemedicine population. Conclusion: The data suggests that telemedicine may be a safe and effective way to screen and treat patients with possible COVID-19, while reducing potential burdens on EDs.

Introduction: The novel coronavirus disease 2019 (COVID-19) created challenges with access to care including increased burden on healthcare systems and potential exposure risks for vulnerable patients. To address these needs, Rush University Medical Center created a virtual, urgent care program specifically designed to address these challenges during the COVID-19 pandemic. Methods: This was a retrospective study analyzing adult patients with COVID-19-related telemedicine visits performed between March 1–June 30, 2020. COVID-19-related telemedicine visits refer to those who used the “Concern for Coronavirus” module. We assessed the total number of telemedicine visits using this module, percentage with a subsequent emergency department (ED) visit within seven days, and outcomes (ie, hospitalization status, intubation, and death) of patients who presented to the ED for evaluation. Data are presented using descriptive statistics. Results: A total of 2,974 adult patients accessed the program via the COVID-19 module over the four-month period. Of those, 142 patients (4.8%) had an ED visit within seven days. Only 14 patients (0.5%) required admission. One patient was intubated, and there were no deaths among the telemedicine population. Conclusion: The data suggests that telemedicine may be a safe and effective way to screen and treat patients with possible COVID-19, while reducing potential burdens on EDs.

Q switching (QS) and mode locking (ML) are the two main techniques enabling generation of ultrashort pulses. Here, we report the first observation of pulse evolution and dynamics in the QS-ML transition stage, where the ML soliton formation evolves from the QS pulses instead of relaxation oscillations (or quasicontinuous-wave oscillations) reported in previous studies. We discover a new way of soliton buildup in an ultrafast laser, passing through four stages: initial spontaneous noise, QS, beating dynamics, and ML. We reveal that multiple subnanosecond pulses coexist within the laser cavity during the QS, with one dominant pulse transforming into a soliton when reaching the ML stage. We propose a theoretical model to simulate the spectrotemporal beating dynamics (a critical process of QS-ML transition) and the Kelly sidebands of the as-formed solitons. Numerical results show that beating dynamics is induced by the interference between a dominant pulse and multiple subordinate pulses with varying temporal delays, in agreement with experimental observations. Our results allow a better understanding of soliton formation in ultrafast lasers, which have widespread applications in science and technology.

Ventilatory acclimatization to hypoxia (VAH) is a time dependent increase in ventilation that develops after hypoxic exposures of hours to days. VAH consists of both a change in chemosensitivity to hypoxemia in the carotid body and a change in the central nervous system sensitivity to afferent carotid body signals (Nielsen et al., 1988; Dwinell &Powell, 1999). My dissertation tests the hypotheses that inflammation and reactive oxygen species (ROS) each plays an essential role in the respiratory control centers of the medulla during VAH. Inflammatory cytokines have recently been established as important in the increased O₂-sensitivity of the carotid body during VAH using ibuprofen to block this increased sensitivity (Liu et al., 2009). Using a similar experimental design to Liu et al. (2009), we examined the effect of systemic ibuprofen administration on the hypoxic ventilatory response and cytokine expression in the dorsal medulla, which contains respiratory control centers. Ibuprofen blocked VAH in rats breathing 10%O₂ and further analysis showed this result cannot be explained simply by the published effect of ibuprofen on the carotid body effect but it must involve the central nervous system as well. Measurements of cytokines in the dorsal medulla indicate that, inflammatory signals are increased with chronic hypoxia and this increase is blocked by ibuprofen, supporting our hypothesis of the signaling role inflammation plays in VAH. In a second set of experiments, we tested the hypothesis that ROS decrease in CNS respiratory centers with hypoxic exposure and these changes in ROS contribute to VAH in mice. To test this, we measured ROS in normoxia, acute hypoxia, chronic sustained hypoxia, and acute intermittent hypoxia under control conditions and under chronic anti-oxidant treatment. Results show a trend for decreased ROS in acute hypoxia and a return toward normoxic levels with chronic hypoxia. Chronic anti-oxidant treatment tended to decrease ROS more in n

Ventilatory acclimatization to hypoxia (VAH) is a time dependent increase in ventilation that develops after hypoxic exposures of hours to days. VAH consists of both a change in chemosensitivity to hypoxemia in the carotid body and a change in the central nervous system sensitivity to afferent carotid body signals (Nielsen et al., 1988; Dwinell &Powell, 1999). My dissertation tests the hypotheses that inflammation and reactive oxygen species (ROS) each plays an essential role in the respiratory control centers of the medulla during VAH. Inflammatory cytokines have recently been established as important in the increased O₂-sensitivity of the carotid body during VAH using ibuprofen to block this increased sensitivity (Liu et al., 2009). Using a similar experimental design to Liu et al. (2009), we examined the effect of systemic ibuprofen administration on the hypoxic ventilatory response and cytokine expression in the dorsal medulla, which contains respiratory control centers. Ibuprofen blocked VAH in rats breathing 10%O₂ and further analysis showed this result cannot be explained simply by the published effect of ibuprofen on the carotid body effect but it must involve the central nervous system as well. Measurements of cytokines in the dorsal medulla indicate that, inflammatory signals are increased with chronic hypoxia and this increase is blocked by ibuprofen, supporting our hypothesis of the signaling role inflammation plays in VAH. In a second set of experiments, we tested the hypothesis that ROS decrease in CNS respiratory centers with hypoxic exposure and these changes in ROS contribute to VAH in mice. To test this, we measured ROS in normoxia, acute hypoxia, chronic sustained hypoxia, and acute intermittent hypoxia under control conditions and under chronic anti-oxidant treatment. Results show a trend for decreased ROS in acute hypoxia and a return toward normoxic levels with chronic hypoxia. Chronic anti-oxidant treatment tended to decrease ROS more in n