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Effective access control techniques are in demand, as electronically assisted healthcare services require the patient’s sensitive health records. In emergency situations, where the patient’s well-being is jeopardized, different healthcare actors associated with emergency cases should be granted permission to access Electronic Health Records (EHRs) of patients. The research objective of our study is to develop machine learning techniques based on patients’ time sequential health metrics and integrate them with an Attribute Based Access Control (ABAC) mechanism. We propose an ABAC mechanism that can yield access to sensitive EHRs systems by applying prognostic context handlers where contextual information, is used to identify emergency conditions and permit access to medical records. Specifically, we use patients’ recent health history to predict the health metrics for the next two hours by leveraging Long Short Term Memory (LSTM) Neural Networks (NNs). These predicted health metrics values are evaluated by our personalized fuzzy context handlers, to predict the criticality of patients’ status. The developed access control method provides secure access for emergency clinicians to sensitive information and simultaneously safeguards the patient’s well-being. Integrating this predictive mechanism with personalized context handlers proved to be a robust tool to enhance the performance of the access control mechanism to modern EHRs System.

The COVID-19 pandemic has tremendously affected the whole of human society worldwide. Travel patterns have greatly changed due to the increased risk perception and the governmental interventions regarding COVID-19. This study aimed to identify contributing factors to the changes in public and private transportation mode choice behavior in China after COVID-19 based on an online questionnaire survey. In the survey, travel behaviors in three periods were studied: before the outbreak (before 27 December 2019), the peak (from 20 January to 17 March 2020), and after the peak (from 18 March to the date of the survey). A series of random-parameter bivariate Probit models was developed to quantify the relationship between individual characteristics and the changes in travel mode choice. The key findings indicated that individual sociodemographic characteristics (e.g., gender, age, ownership, occupation, residence) have significant effects on the changes in mode choice behavior. Other key findings included (1) a higher propensity to use a taxi after the peak compared to urban public transportation (i.e., bus and subway); (2) a significant impact of age on the switch from public transit to private car and two-wheelers; (3) more obvious changes in private car and public transportation modes in more developed cities. The findings from this study are expected to be useful for establishing partial and resilient policies and ensuring sustainable mobility and travel equality in the post-pandemic era.

Hepatic steatosis is a key initiating event in the pathogenesis of alcohol-associated liver disease (ALD), the most detrimental organ damage resulting from alcohol use disorder. However, the mechanisms by which alcohol induces steatosis remain incompletely understood. We have previously found that alcohol binging impairs brain insulin action, resulting in increased adipose tissue lipolysis by unrestraining sympathetic nervous system (SNS) outflow. Here, we examined whether an impaired brain-SNS-adipose tissue axis drives hepatic steatosis through unrestrained adipose tissue lipolysis and increased lipid flux to the liver.We examined the role of lipolysis, and the brain-SNS-adipose tissue axis and stress in alcohol induced hepatic triglyceride accumulation in a series of rodent models: pharmacological inhibition of the negative regulator of insulin signaling protein-tyrosine phosphatase 1β (PTP1b) in the rat brain, tyrosine hydroxylase (TH) knockout mice as a pharmacogenetic model of sympathectomy, adipocyte specific adipose triglyceride lipase (ATGL) knockout mice, wildtype (WT) mice treated with β3 adrenergic agonist or undergoing restraint stress.Intracerebral administration of a PTP1b inhibitor, inhibition of adipose tissue lipolysis and reduction of sympathetic outflow ameliorated alcohol induced steatosis. Conversely, induction of adipose tissue lipolysis through β3 adrenergic agonism or by restraint stress worsened alcohol induced steatosis.Brain insulin resistance through upregulation of PTP1b, increased sympathetic activity, and unrestrained adipose tissue lipolysis are key drivers of alcoholic steatosis. Targeting these drivers of steatosis may provide effective therapeutic strategies to ameliorate ALD.

Background:  We previously found that activation of the glial cell line‐derived neurotrophic factor (GDNF) pathway in the ventral tegmental area (VTA) reduces ethanol‐drinking behaviors. In this study, we set out to assess the contribution of endogenous GDNF or its receptor GFRα1 to the regulation of ethanol‐related behaviors.Methods:  GDNF and GFRα1 heterozygote mice (HET) and their wild‐type littermate controls (WT) were used for the studies. Ethanol‐induced hyperlocomotion, sensitization, and conditioned place preference (CPP), as well as ethanol consumption before and after a period of abstinence were evaluated. Blood ethanol concentration (BEC) was also measured.Results:  We observed no differences between the GDNF HET and WT mice in the level of locomotor activity or in sensitization to ethanol‐induced hyperlocomotion after systemic injection of a nonhypnotic dose of ethanol and in BEC. However, GDNF and GFRα1 mice exhibited increased place preference to ethanol as compared with their WT littermates. The levels of voluntary ethanol or quinine consumption were similar in the GDNF HET and WT mice, however, a small but significant increase in saccharin intake was observed in the GDNF HET mice. No changes were detected in voluntary ethanol, saccharin or quinine consumption of GFRα1 HET mice as compared with their WT littermates. Interestingly, however, both the GDNF and GFRα1 HET mice consumed much larger quantities of ethanol after a period of abstinence from ethanol as compared with their WT littermates. Furthermore, the increase in ethanol consumption after abstinence was found to be specific for ethanol as similar levels of saccharin intake were measured in the GDNF and GFRα1 HET and WT mice after abstinence.Conclusions:  Our results suggest that endogenous GDNF negatively regulates the rewarding effect of ethanol and ethanol‐drinking behaviors after a period of abstinence.

ABSTRACTPrenatal ethanol exposure causes a variety of cognitive deficits that have a persistent impact on quality of life, some of which may be explained by ethanol-induced alterations in interneuron function. Studies from several laboratories, including our own, have demonstrated that a single binge-like ethanol exposure during the equivalent to the third trimester of human pregnancy leads to acute apoptosis and long-term loss of interneurons in the rodent retrosplenial cortex (RSC). The RSC is interconnected with the hippocampus, thalamus, and other neocortical regions and plays distinct roles in visuospatial processing and storage, as well as retrieval of hippocampal-dependent episodic memories. Here we used slice electrophysiology to characterize the acute effects of ethanol on GABAergic neurotransmission in the RSC of neonatal mice, as well as the long-term effects of neonatal ethanol exposure on parvalbumin-interneuron mediated neurotransmission in adolescent mice. Mice were exposed to ethanol using vapor inhalation chambers. In postnatal day (P) 7 mouse pups, ethanol unexpectedly failed to potentiate GABAAreceptor-mediated synaptic transmission. Binge-like ethanol exposure of P7 mice expressing channel rhodopsin in parvalbumin-positive interneurons enhanced the peak amplitudes, asynchronous activity and total charge, while decreasing the rise-times of optically-evoked GABAAreceptor-mediated inhibitory postsynaptic currents in adolescent animals. These effects could partially explain the learning and memory deficits that have been documented in adolescent and young adult mice exposed to ethanol during the third trimester-equivalent developmental period.

Nearly three billion people in low- and middle-income countries (LMICs) rely on polluting fuels, resulting in millions of avoidable deaths annually. Polluting fuels also emit short-lived climate forcers and greenhouse gases (GHGs). Liquefied petroleum gas (LPG) and grid-based electricity are scalable alternatives to polluting fuels but have raised climate and health concerns. Here, we compare emissions and climate impacts of a business-as-usual household cooking fuel trajectory to four large-scale transitions to gas and/or grid electricity in 77 LMICs. We account for upstream and end-use emissions from gas and electric cooking, assuming electrical grids evolve according to the 2022 World Energy Outlook’s “Stated Policies” Scenario. We input the emissions into a reduced-complexity climate model to estimate radiative forcing and temperature changes associated with each scenario. We find full transitions to LPG and/or electricity decrease emissions from both well-mixed GHG and short-lived climate forcers, resulting in a roughly 5 millikelvin global temperature reduction by 2040. Transitions to LPG and/or electricity also reduce annual emissions of PM2.5 by over 6 Mt (99%) by 2040, which would substantially lower health risks from Household Air Pollution. Primary input data was collected from the following sources: Baseline household fuel choices - WHO household energy database (https://www.nature.com/articles/s41467-021-26036-x) End-use emissions - US EPA lifecycle assessment of household fuels (https://cfpub.epa.gov/si/si_public_record_report.cfm?dirEntryId=339679&Lab=NRMRL&simplesearch=0&showcriteria=2&sortby=pubDate&timstype=Published+Report&datebeginpublishedpresented) Upstream emissions - Argonne National Labs GREET Model (https://greet.es.anl.gov/index.php) Current and future population estimates - UNECA (http://data.un.org/Explorer.aspx?d=EDATA) Input data was processed by defining household fuel choice scenarios, estimating national household fuel consumption based on these scenarios, and applying fuel-specific emission factors to create country-specific emission pathways. These emission pathways were input into the FaIR model (https://zenodo.org/record/5513022#.Yt_jfHbMLb0) which generated additional data for each scenario including time series of pollution concentrations, radiative forcing, and temperature changes. All data is provided in CSV format. Nothing proprietary is required. 

{"references": ["Liu, Z., Ciais, P., Deng, Z., Lei, R., Davis, S. J., Feng, S., Zheng, B., Cui, D., Dou, X., Zhu, B., Guo, R., Ke, P., Sun, T., Lu, C., He, P., Wang, Y., Yue, X., Wang, Y., Lei, Y., Zhou, H., Cai, Z., Wu, Y., Guo, R., Han, T., Xue, J., Boucher, O., Boucher, E., Chevallier, F., Tanaka, K., Wei, Y., Zhong, H., Kang, C., Zhang, N., Chen, B., Xi, F., Liu, M., Br\u00e9on, F.-M., Lu, Y., Zhang, Q., Guan, D., Gong, P., Kammen, D. M., He, K. & Schellnhuber, H. J. (2020). Near-real-time monitoring of global CO2 emissions reveals the effects of the COVID-19 pandemic. Nature Communications 11, 5172 (2020). https://doi.org/10.1038/s41467-020-18922-7", "Meinshausen, M., Smith, S. J., Calvin, K., Daniel, J. S., Kainuma, M. L. T., Lamarque, J. F., Matsumoto, K., Montzka, S. A., Raper, S. C. B., Riahi, K., Thomson, A., Velders, G. J. M., & van Vuuren, D. P. (2011). The RCP greenhouse gas concentrations and their extensions from 1765 to 2300. Climatic Change, 109(1\u20132), 213\u2013241. https://doi.org/10.1007/s10584-011-0156-z", "Moss, R. H., Edmonds, J. A., Hibbard, K. A., Manning, M. R., Rose, S. K., van Vuuren, D. P., Carter, T. R., Emori, S., Kainuma, M., Kram, T., Meehl, G. A., Mitchell, J. F. B., Nakicenovic, N., Riahi, K., Smith, S. J., Stouffer, R. J., Thomson, A. M., Weyant, J. P. & Wilbanks, T. J. (2010). The next generation of scenarios for climate change research and assessment. Nature, 463(7282), 747\u2013756. https://doi.org/10.1038/nature08823", "Myhre, G., Highwood, E. J., Shine, K. P., & Stordal, F. (1998). New estimates of radiative forcing due to well mixed greenhouse gases. Geophysical Research Letters, 25(14), 2715\u20132718. https://doi.org/10.1029/98gl01908", "Strassmann, K. M. and Joos, F. (2018). The Bern Simple Climate Model (BernSCM) v1.0: an extensible and fully documented open-source re-implementation of the Bern reduced-form model for global carbon cycle\u2013climate simulations, Geosci. Model Dev., 11, 1887\u20131908, https://doi.org/10.5194/gmd-11-1887-2018", "Thomas, M. A., and Lin, T. (2018). A dual model for emulation of thermosteric and dynamic sea-level change. Climatic Change, 148(1\u20132), 311\u2013324. https://doi.org/10.1007/s10584-018-2198-y"]} Supplementary materials for Gonzalez, A. R., & Lin, T. (2022). Translated Emission Pathways (TEPs): Long-Term Simulations of COVID-19 CO2 Emissions and Thermosteric Sea Level Rise Projections. Earth's Future. In Press. Summary: This study introduces climate science to a broader audience by presenting an accessible research framework and environmental data related to the ongoing COVID-19 pandemic. A series of translated emission pathways (TEPs) were constructed based on the CO2 emission patterns from the various phases of COVID-19 response. In addition to resembling the forcing scenarios used within climate research, a thermosteric sea level rise analysis was incorporated to further emphasize the environmental benefits that can be obtained from long-term sustainability. As a promising start for including the general public in climate change discussion, this research promotes collective environmental action that mirrors the recommendations of the scientific community. We acknowledge the Carbon Monitor initiative (Liu et al., 2020) for providing the COVID-19 CO2 sectoral emission data used to construct the proposed TEPs. In addition, we acknowledge the developers of the BernSCM (Strassmann and Joos, 2018) that was utilized in this study to relate TEP CO2 emissions to their respective CO2 atmospheric concentrations. Furthermore, we thank the Texas Tech University McNair Scholars Program and the Multi-Hazard Sustainability (HazSus) research group for guidance and support throughout the course of this study. Analyses presented herein were performed using the RedRaider computing cluster at Texas Tech University. We thank the team at the High Performance Computing Center (HPCC) for their generous support. In addition, the equipment support from the Vice President for Research & Innovation for T.L.'s HazSus Research Group is gratefully acknowledged.

AbstractBackgroundBinge alcohol exposure during adolescence results in long‐lasting alterations in the brain and behavior. For example, adolescent intermittent ethanol (AIE) exposure in rodents results in long‐term loss of functional connectivity among prefrontal cortex (PFC) and striatal regions as well as a variety of neurochemical, molecular, and epigenetic alterations. Interneurons in the PFC and striatum play critical roles in behavioral flexibility and functional connectivity. For example, parvalbumin (PV) interneurons are known to contribute to neural synchrony and cholinergic interneurons contribute to strategy selection. Furthermore, extracellular perineuronal nets (PNNs) that surround some interneurons, particularly PV+ interneurons, further regulate cellular plasticity. The effect of AIE exposure on the expression of these markers within the PFC is not well understood.MethodsThe present study tested the hypothesis that AIE exposure reduces the expression of PV+ and choline acetyltransferase (ChAT)+ interneurons in the adult PFC and striatum and increases the related expression of PNNs (marked by binding of Wisteria floribunda agglutinin lectin) in adulthood. Male rats were exposed to AIE (5 g/kg/day, 2‐days‐on/2‐days‐off, i.e., P25 to P54) or water (CON), and brain tissue was harvested in adulthood (>P80). Immunohistochemistry and co‐immunofluorescence were used to assess the expression of ChAT, PV, and PNNs within the adult PFC and striatum following AIE exposure.ResultsChAT and PV interneuron densities in the striatum and PFC were unchanged after AIE exposure. However, PNN density in the PFC of AIE‐exposed rats was greater than in CON rats. Moreover, significantly more PV neurons were surrounded by PNNs in AIE‐exposed subjects than controls in both PFC subregions assessed: orbitofrontal cortex (CON = 34%; AIE = 40%) and medial PFC (CON = 10%; AIE = 14%).ConclusionsThese findings indicate that, following AIE exposure, PV interneuron expression in the adult PFC and striatum is unaltered, while PNNs surrounding these neurons are increased. This increase in PNNs may restrict the plasticity of the ensheathed neurons, thereby contributing to impaired microcircuitry in frontostriatal connectivity and related behavioral impairments.