Clean water from clean energy: removal of dissolved contaminants from brackish groundwater using wind energy powered electrodialysis

Around 770 million people lack access to improved drinking water sources (WHO 2013), urgently necessitating implementation of contaminant removal by e.g. desalination systems on a large scale. To improve water quality and enable use of brackish water sources for human consumption in remote arid areas, a directly coupled wind – electrodialysis system (Wind-ED) was developed. Modularity, sustainability and above all suitability for the practical use in off-grid locations were the main motivations and design objectives. The direct coupling of wind energy with membranes reduces the system costs as well as technical drawbacks associated with using intermediate energy storage systems. During this research, systematic experiments were performed using the Wind-ED system in order to determine desalination performance and clean water production, specific energy consumption (SEC) and current efficiency (ηc) under relevant conditions, such as varying: i) wind speed, ii) wind turbulence intensity, iii) oscillation periods, iv) varying NaCl concentrations and v) flow rates. Moreover, the competitive removal of four commonly available inorganic contaminants in brackish groundwater sources, nitrate (NO3-), fluoride (F-), sulphate (SO42-) and chloride (Cl-), were investigated. Firstly, to establish a systematic understanding of how and to what extent energy fluctuations influence the transport of the salt (i.e. NaCl) ions across the membranes, experiments were conducted using pulsed electric field assisted electrodialysis (pulsed-ED) over a wide range of frequencies (0.001 – 10 Hz) and duty cycles (20 – 80). The results showed that pulsation applied in the sub-limiting regime resulted in reduced water production, explained by the delays caused by the off-periods during the pulsed desalination process. At higher current densities, pulsation led to considerable improvements in current (e.g. up to 95%, for a feed solution of 500 mg/L and a pulse regime of 1 Hz at 50 V peak voltage) and significant reduction in water dissociation, explained by a reduction of concentration polarisation. Importantly, the pulsation had no significant effect on energy consumption or current efficiency suggesting that ED could be suitable for direct coupling to fluctuating energy sources such as wind energy. ED was consequently coupled to a wind turbine system and a series of desalination tests were performed over a wide range of wind speeds (2-10 m/s), turbulence intensities (TI of 0-0.6) and oscillation periods (0-180 s). Results showed that water production and SEC increased with wind speed. However, both the water production and SEC stopped increasing as the power output from the turbine levelled off at wind speeds above the rated value (vrated: 7.9 – 8.4 m/s). The impact of wind speed fluctuations on the system performance were insignificant up to a TI of 0.4. The desalination performance declined under high turbulence intensity fluctuations (TIs ≥ 0.5) and long periods of oscillation (> 40 s), as the wind-ED system periodically cycled off in response to operation below the cut-in wind speed of the wind turbine (vcut-in: ~ 2 m/s). The off-cycling of the system caused significant delays in the desalination process, and thus resulted in reduced water production. Further reduction in the water production resulted as the wind-ED system operated under intermittent wind speed conditions with off-wind periods longer than 10 s. It was concluded that the main challenge in direct coupling of ED to a wind resource was not the magnitude of the fluctuations but the impact of the power cycling off during long periods of oscillation and lengthy periods of no wind. Interestingly, the SEC of the process remained relatively unaffected by the fluctuations and intermittencies in the wind resource. The effect of energy fluctuations on the competitive transport of F-, Cl-, NO3- and SO42- from artificial brackish water (TDS ~4350 mg/L) was investigated using different sets of real wind data. The ion removal, independent of the wind regime tested, followed the order: NO3- ≥ Cl- > F- > SO42-. The competitive removal of the ions was linked to differences in physicochemical properties (i.e. hydration energy, ionic mobility and valence). The specific selectivity (e.g. preferential transport of NO3- over SO42- ions) was found to increase with concentration polarisation being either minimised (by lowering the mean wind speed) or disrupted (by fluctuations in the wind resource). The results from flow rate and feed concentration experiments, showed that power production of the wind turbine depended on not only the available wind energy but also the resistance of the load (i.e. the ED stack). Thus, increasing the feed concentration and the flow rate resulted in reduced resistance in the ED stack (Rstack), which inversely influenced the current induction counter torque force applied on the shaft of the wind turbine and caused the rotor to spin at a lower angular velocity. This led to increased sensitivity of the wind-ED system to wind speed fluctuations (e.g. system cycled off due to extreme fluctuations and intermittencies with low TDS feed concentration of 2400 mg/L) and hence a reduction of desalination performance. Impact of flow rate on the SEC was found to be negligible; this was attributed to the automatic voltage to current adjustments done by the wind turbine, in order to minimise the impacts of Rstack on the power production by the turbine at a given wind speed. Increased flow rate and resulting shrinkage of the boundary layer’s thickness, caused the concentration profiles at the solution-membrane interface to become steeper. This favoured the transport of ions with the highest diffusion coefficients in the mixture (i.e. Cl- and NO3-). Decreased flow rate favoured the transport of ions with larger valence numbers and higher electric mobility inside the electrolyte (i.e. SO42-); as the former property governed the faster migration of SO42- ions through the thick boundary layer and the latter property assisted with the improved affinity of the ion-exchange membrane to SO42- ions compared to the monovalent anions in the mixture. Increasing the feed concentration of Cl- from 500 to 2,550 mg/L led to reduced transport numbers for the other anions in the mixture and significantly reducing their removal rate. The results obtained from both the pulsed-ED and wind-ED experiments showed that, despite direct coupling to the fluctuating energy source the SEC of the process remained relatively unaffected by the energy fluctuations. Although the desalination process might require more time to be completed when operating under extreme wind speed fluctuations and intermittencies, the quality of the drinking water produced was always within the WHO standards. In conclusion, the findings from this research prove the wind-ED system to be an energetically robust and a reliable off-grid desalination technique suitable for the treatment of brackish groundwater in water stressed remote regions

Age-At-Injury Influences the Glial Response to Traumatic Brain Injury in the Cortex of Male Juvenile Rats

Few translational studies have examined how age-at-injury affects the glial response to traumatic brain injury (TBI). We hypothesized that rats injured at post-natal day (PND) 17 would exhibit a greater glial response, that would persist into early adulthood, compared to rats injured at PND35. PND17 and PND35 rats (n = 75) received a mild to moderate midline fluid percussion injury or sham surgery. In three cortical regions [peri-injury, primary somatosensory barrel field (S1BF), perirhinal], we investigated the glial response relative to age-at-injury (PND17 or PND35), time post-injury (2 hours, 1 day, 7 days, 25 days, or 43 days), and post-natal age, such that rats injured at PND17 or PND35 were compared at the same post-natal-age (e.g., PND17 + 25D post-injury = PND42; PND35 + 7D post-injury = PND42). We measured Iba1 positive microglia cells (area, perimeter) and quantified their activation status using skeletal analysis (branch length/cell, mean processes/cell, cell abundance). GFAP expression was examined using immunohistochemistry and pixel analysis. Data were analyzed using Bayesian multivariate multi-level models. Independent of age-at-injury, TBI activated microglia (shorter branches, fewer processes) in the S1BF and perirhinal cortex with more microglia in all regions compared to uninjured shams. TBI-induced microglial activation (shorter branches) was sustained in the S1BF into early adulthood (PND60). Overall, PND17 injured rats had more microglial activation in the perirhinal cortex than PND35 injured rats. Activation was not confounded by age-dependent cell size changes, and microglial cell body sizes were similar between PND17 and PND35 rats. There were no differences in astrocyte GFAP expression. Increased microglial activation in PND17 brain-injured rats suggests that TBI upregulates the glial response at discrete stages of development. Age-at-injury and aging with an injury are translationally important because experiencing a TBI at an early age may trigger an exaggerated glial response. </div

Epidemiology of Pediatric Traumatic Brain Injury and Hypothalamic-Pituitary Disorders in Arizona

Traumatic brain injury (TBI) in children can result in long-lasting social, cognitive, and neurological impairments. In adults, TBI can lead to endocrinopathies (endocrine system disorders), but this is infrequently reported in children. Untreated endocrinopathies can elevate risks of subsequent health issues, such that early detection in pediatric TBI survivors can initiate clinical interventions. To understand the risk of endocrinopathies following pediatric TBI, we identified patients who had experienced a TBI and subsequently developed a new-onset hypothalamic regulated endocrinopathy (n = 498). We hypothesized that pediatric patients who were diagnosed with a TBI were at higher risk of being diagnosed with a central endocrinopathy than those without a prior diagnosis of TBI. In our epidemiological assessment, we identified pediatric patients enrolled in the Arizona Health Care Cost Containment System (AHCCCS) from 2008 to 2014 who were diagnosed with one of 330 TBI International Classification of Diseases (ICD)-9 codes and subsequently diagnosed with one of 14 central endocrinopathy ICD-9 codes. Additionally, the ICD-9 code data from over 600,000 Arizona pediatric patients afforded an estimate of the incidence, prevalence, relative risk, odds ratio, and number needed to harm, regarding the development of a central endocrinopathy after sustaining a TBI in Arizona Medicaid pediatric patients. Children with a TBI diagnosis had 3.22 times the risk of a subsequent central endocrine diagnosis compared with the general population (±0.28). Pediatric AHCCCS patients with a central endocrine diagnosis had 3.2-fold higher odds of a history of a TBI diagnosis than those without an endocrine diagnosis (±0.29). Furthermore, the number of patients with a TBI diagnosis for one patient to receive a diagnosis of a central endocrine diagnosis was 151.2 (±6.12). Female subjects were more likely to present with a central endocrine diagnosis after a TBI diagnosis compared to male subjects (64.1 vs. 35.9%). These results are the first state-wide epidemiological study conducted to determine the risk of developing a hypothalamic-pituitary disorder after a TBI in the pediatric population. Our results contribute to a body of knowledge demonstrating a TBI etiology for idiopathic endocrine disorders, and thus advise physicians with regard to TBI follow-up care that includes preventive screening for endocrine disorders.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Traumatic Brain Injury Characteristics Predictive of Subsequent Sleep-Wake Disturbances in Pediatric Patients

Simple Summary Traumatic brain injury is a leading cause of death and disabilities in children and adolescents. Poor sleep after brain injury can slow recovery and worsen outcomes. We investigated clinical sleep problems following pediatric brain injury. We examined characteristics of the injury and details about the patients that may be risk factors for developing sleep problems. The number of patients that developed problems with their sleep after a brain injury was similar between genders. The probability of insomnia increased with increasing patient age. The probability of &lsquo;difficulty sleeping&rsquo; was highest in 7&ndash;9 year-old brain-injured patients. Older patients had a shorter time between brain injury and sleep problems compared to younger patients. Patients with severe brain injury had the shortest time between brain injury and development of sleep problems, whereas patients with mild or moderate brain injury had comparable times between brain injury and the onset of poor sleep. Multiple characteristics of brain injury and patient details were identified as risk factors for developing sleep problems following a brain injury in children. Untreated sleep problems after a brain injury can worsen symptoms, lengthen hospital stays, and delay return to school. Identifying risk factors could improve the diagnosis, management, and treatment of sleep problems in survivors of pediatric brain injury. Abstract The objective of this study was to determine the prevalence of sleep-wake disturbances (SWD) following pediatric traumatic brain injury (TBI), and to examine characteristics of TBI and patient demographics that might be predictive of subsequent SWD development. This single-institution retrospective study included patients diagnosed with a TBI during 2008&ndash;2019 who also had a subsequent diagnosis of an SWD. Data were collected using ICD-9/10 codes for 207 patients and included the following: age at initial TBI, gender, TBI severity, number of TBIs diagnosed prior to SWD diagnosis, type of SWD, and time from initial TBI to SWD diagnosis. Multinomial logit and negative-binomial models were fit to investigate whether the multiple types of SWD and the time to onset of SWD following TBI could be predicted by patient variables. Distributions of SWD diagnosed after TBI were similar between genders. The probability of insomnia increased with increasing patient age. The probability of &lsquo;difficulty sleeping&rsquo; was highest in 7&ndash;9 year-old TBI patients. Older TBI patients had shorter time to SWD onset than younger patients. Patients with severe TBI had the shortest time to SWD onset, whereas patients with mild or moderate TBI had comparable times to SWD onset. Multiple TBI characteristics and patient demographics were predictive of a subsequent SWD diagnosis in the pediatric population. This is an important step toward increasing education among providers, parents, and patients about the risk of developing SWD following TBI. &nbsp;</p

LSST: from Science Drivers to Reference Design and Anticipated Data Products

(Abridged) We describe here the most ambitious survey currently planned in the optical, the Large Synoptic Survey Telescope (LSST). A vast array of science will be enabled by a single wide-deep-fast sky survey, and LSST will have unique survey capability in the faint time domain. The LSST design is driven by four main science themes: probing dark energy and dark matter, taking an inventory of the Solar System, exploring the transient optical sky, and mapping the Milky Way. LSST will be a wide-field ground-based system sited at Cerro Pach\'{o}n in northern Chile. The telescope will have an 8.4 m (6.5 m effective) primary mirror, a 9.6 deg$^2$ field of view, and a 3.2 Gigapixel camera. The standard observing sequence will consist of pairs of 15-second exposures in a given field, with two such visits in each pointing in a given night. With these repeats, the LSST system is capable of imaging about 10,000 square degrees of sky in a single filter in three nights. The typical 5$\sigma$ point-source depth in a single visit in $r$ will be $\sim 24.5$ (AB). The project is in the construction phase and will begin regular survey operations by 2022. The survey area will be contained within 30,000 deg$^2$ with $\delta<+34.5^\circ$, and will be imaged multiple times in six bands, $ugrizy$, covering the wavelength range 320--1050 nm. About 90\% of the observing time will be devoted to a deep-wide-fast survey mode which will uniformly observe a 18,000 deg$^2$ region about 800 times (summed over all six bands) during the anticipated 10 years of operations, and yield a coadded map to $r\sim27.5$. The remaining 10\% of the observing time will be allocated to projects such as a Very Deep and Fast time domain survey. The goal is to make LSST data products, including a relational database of about 32 trillion observations of 40 billion objects, available to the public and scientists around the world.Comment: 57 pages, 32 color figures, version with high-resolution figures available from https://www.lsst.org/overvie

Registered Replication Report on Fischer, Castel, Dodd, and Pratt (2003)

The attentional spatial-numerical association of response codes (Att-SNARC) effect (Fischer, Castel, Dodd, & Pratt, 2003)—the finding that participants are quicker to detect left-side targets when the targets are preceded by small numbers and quicker to detect right-side targets when they are preceded by large numbers—has been used as evidence for embodied number representations and to support strong claims about the link between number and space (e.g., a mental number line). We attempted to replicate Experiment 2 of Fischer et al. by collecting data from 1,105 participants at 17 labs. Across all 1,105 participants and four interstimulus-interval conditions, the proportion of times the effect we observed was positive (i.e., directionally consistent with the original effect) was .50. Further, the effects we observed both within and across labs were minuscule and incompatible with those observed by Fischer et al. Given this, we conclude that we failed to replicate the effect reported by Fischer et al. In addition, our analysis of several participant-level moderators (finger-counting habits, reading and writing direction, handedness, and mathematics fluency and mathematics anxiety) revealed no substantial moderating effects. Our results indicate that the Att-SNARC effect cannot be used as evidence to support strong claims about the link between number and space

Registered replication report on Fischer, Castel, Dodd, and Pratt (2003)

The attentional spatial-numerical association of response codes (Att-SNARC) effect (Fischer, Castel, Dodd, & Pratt, 2003)—the finding that participants are quicker to detect left-side targets when the targets are preceded by small numbers and quicker to detect right-side targets when they are preceded by large numbers—has been used as evidence for embodied number representations and to support strong claims about the link between number and space (e.g., a mental number line). We attempted to replicate Experiment 2 of Fischer et al. by collecting data from 1,105 participants at 17 labs. Across all 1,105 participants and four interstimulus-interval conditions, the proportion of times the effect we observed was positive (i.e., directionally consistent with the original effect) was .50. Further, the effects we observed both within and across labs were minuscule and incompatible with those observed by Fischer et al. Given this, we conclude that we failed to replicate the effect reported by Fischer et al. In addition, our analysis of several participant-level moderators (finger-counting habits, reading and writing direction, handedness, and mathematics fluency and mathematics anxiety) revealed no substantial moderating effects. Our results indicate that the Att-SNARC effect cannot be used as evidence to support strong claims about the link between number and space

The Bidirectional Relationship Between Sleep and Inflammation Links Traumatic Brain Injury and Alzheimer's Disease

Traumatic brain injury (TBI) and Alzheimer’s disease (AD) are diseases during which the fine-tuned autoregulation of the brain is lost. Despite the stark contrast in their causal mechanisms, both TBI and AD are conditions which elicit a neuroinflammatory response that is coupled with physical, cognitive, and affective symptoms. One commonly reported symptom in both TBI and AD patients is disturbed sleep. Sleep is regulated by circadian and homeostatic processes such that pathological inflammation may disrupt the chemical signaling required to maintain a healthy sleep profile. In this way, immune system activation can influence sleep physiology. Conversely, sleep disturbances can exacerbate symptoms or increase the risk of inflammatory/neurodegenerative diseases. Both TBI and AD are worsened by a chronic pro-inflammatory microenvironment which exacerbates symptoms and worsens clinical outcome. Herein, a positive feedback loop of chronic inflammation and sleep disturbances is initiated. In thisreview, the bidirectional relationship between sleep disturbances and inflammation is discussed, where chronic inflammation associated with TBI and AD can lead to sleep disturbances and exacerbated neuropathology. The role of microglia and cytokines in sleep disturbances associated with these diseases is highlighted. The proposed sleep and inflammation-mediated link between TBI and AD presents an opportunity for a multifaceted approach to clinical intervention

The Bidirectional Relationship Between Sleep and Inflammation Links Traumatic Brain Injury and Alzheimer's Disease

Traumatic brain injury (TBI) and Alzheimer’s disease (AD) are diseases during which the fine-tuned autoregulation of the brain is lost. Despite the stark contrast in their causal mechanisms, both TBI and AD are conditions which elicit a neuroinflammatory response that is coupled with physical, cognitive, and affective symptoms. One commonly reported symptom in both TBI and AD patients is disturbed sleep. Sleep is regulated by circadian and homeostatic processes such that pathological inflammation may disrupt the chemical signaling required to maintain a healthy sleep profile. In this way, immune system activation can influence sleep physiology. Conversely, sleep disturbances can exacerbate symptoms or increase the risk of inflammatory/neurodegenerative diseases. Both TBI and AD are worsened by a chronic pro-inflammatory microenvironment which exacerbates symptoms and worsens clinical outcome. Herein, a positive feedback loop of chronic inflammation and sleep disturbances is initiated. In thisreview, the bidirectional relationship between sleep disturbances and inflammation is discussed, where chronic inflammation associated with TBI and AD can lead to sleep disturbances and exacerbated neuropathology. The role of microglia and cytokines in sleep disturbances associated with these diseases is highlighted. The proposed sleep and inflammation-mediated link between TBI and AD presents an opportunity for a multifaceted approach to clinical intervention

Microglia Are Necessary to Regulate Sleep after an Immune Challenge

Microglia play a critical role in the neuroimmune response, but little is known about the role of microglia in sleep following an inflammatory trigger. Nevertheless, decades of research have been predicated on the assumption that an inflammatory trigger increases sleep through microglial activation. We hypothesized that mice (n = 30) with depleted microglia using PLX5622 (PLX) would sleep less following the administration of lipopolysaccharide (LPS) to induce inflammation. Brains were collected and microglial morphology was assessed using quantitative skeletal analyses and physiological parameters were recorded using non-invasive piezoelectric cages. Mice fed PLX diet had a transient increase in sleep that dissipated by week 2. Subsequently, following a first LPS injection (0.4 mg/kg), mice with depleted microglia slept more than mice on the control diet. All mice were returned to normal rodent chow to repopulate microglia in the PLX group (10 days). Nominal differences in sleep existed during the microglia repopulation period. However, following a second LPS injection, mice with repopulated microglia slept similarly to control mice during the dark period but with longer bouts during the light period. Comparing sleep after the first LPS injection to sleep after the second LPS injection, controls exhibited temporal changes in sleep patterns but no change in cumulative minutes slept, whereas cumulative sleep in mice with repopulated microglia decreased during the dark period across all days. Repopulated microglia had a reactive morphology. We conclude that microglia are necessary to regulate sleep after an immune challenge