bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accuracy of Activity Monitors in Assessing Sleep
Authors: Mitrzyk John , Swalve Natashia , Harfmann Brianna , Montoye Alexander HK. 
Published: June 2021

In addition to measuring steps and other physical activity metrics, body‐worn activity monitors are designed to measure sleep quantity and quality. However, little research has assessed activity monitors' sleep tracking accuracy or compared accuracy among different brands and models of monitors.PURPOSETo validate and compare several activity monitors for assessment of total sleep time and stages of sleep throughout a night.METHODSEleven participants, aged 18–31 years old, wore four activity monitors on their wrists. The Misfit Flash (MF) and Fitbit Charge (FC) were worn on the left wrist, while the Fitbit Flex (FF) and Jawbone UP 4 (JU) were worn on the right wrist. Three electroencephalogram (EEG) electrodes were attached to the head (one behind left ear, one on each side of the upper parietal portion of the skull), and the electrodes were connected via wires to a BIOPAC system and computer. The study took place overnight in a sleep laboratory, with participants going to bed and waking up as they would on a typical day. Total sleep, light sleep, deep sleep, REM sleep, and number of awakenings were recorded from the four activity monitors and compared to criterion‐measured values from the EEG. Repeated measures ANOVA tests were used to determine differences between predicted and measured values for each variable.RESULTSFor total sleep time, participants averaged 369.3±46.8 minutes/night. Compared to the EEG, the FC (p=0.005) and MF (p=0.002) significantly overestimated total sleep by 32.4–38.1 minutes, while the FF and JU were not significantly different from the EEG (p>0.05). For minutes of light sleep, the FC (p<0.001) and FF (p<0.001) underestimated by 176.5–191.2 minutes when compared to the EEG's time (206.0±58.0 minutes), while the MF and JU were not significantly different from the EEG (p>0.05). For deep sleep, all the monitors except the JU significantly overestimated time when compared to the EEG (163.3±39.0 minutes), by 72.8–214.4 minutes (p<0.01 for all). For REM sleep, the JU was not significantly different from the EEG (88.5±32.2 minutes), while the other monitors did not assess REM sleep. The number of times the participants woke up throughout the night averaged 3.1±2.2 times. Compared to the EEG, all monitors except the FF significantly underestimated by 1.3–2.0 times (p=0.001–0.036).CONCLUSIONOverall, the JU was the most accurate for all stages of sleep and total sleep time, but significantly underestimated the number of times awake. All other monitors had large differences from the EEG in at least one sleep variable. While reliability of these monitors still needs to be established, large inaccuracies seen by some of these activity monitors suggest that sleep data from the wearable activity monitors tested in this study should be interpreted cautiously.Support or Funding InformationAlma College CORE Research ProgramThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Reliability and Validity of NIRS Mitochondrial Capacity Protocol in Human Skeletal Muscle
Authors: La Mantia Anna M. , Neidert Leslie E. , Kluess Heidi A. 
Published: June 2021

To establish reliability of a near‐infrared spectroscopy (NIRS) mitochondrial capacity protocol and assess validity using heating and cooling interventions. We recruited 13 young, healthy participants (men=8, women=5), who were asked to attend four visits. Two of the visits consisted of a protocol which included a series of blood pressure occlusions proximal to the NIRS probe and electrical stimulation to the vastus lateralis (thigh), gastrocnemius (calf) and flexor carpi radialis (forearm), to establish reliability. Participants returned 24 hours after visit 2 to participate in one of two treatments, heating (40° Celsius) or cooling (15.6° Celsius) of the thigh, calf and forearm muscle also using the same protocol as above. The order of the visits was counterbalanced. The between day reliability coefficient of variation in the forearm (CV) was 3% and the time constants (TC) average was 42.5 ± 8.9 seconds (s). The within day CV in the forearm was 4.5%, calf 5.5% and thigh was 4.6% (n=13). The within day cold treatment testing CV for reliability in the forearm was 5.9%, calf 4.3% and thigh 4.4% and for the within day hot treatment testing CV in the forearm was 6.4%, calf 5.3% and thigh 4.6%. In the forearm (41.5 ± 2.4 s) and calf (51.6 ± 2.0 s), cold increased the mitochondrial capacity time constant however heat caused a decrease (p<0.05). Similarly, in the thigh (27.2 ± 1.2 s), heat decreased mitochondrial capacity (p<0.05), but cold was not different from control. These results suggest that the NIRS mitochondrial capacity has good within and between day reliability in all three muscles. Mitochondrial capacity time constants are increased by cold and decreased by heating in the forearm and calf, which suggests good construct validity. This study suggests the possibility of the involvement of NIRS in a clinical setting to monitor muscle health as well as utilize hot and cold treatment results to better understand the properties of the muscle's mitochondrial capacity.Support or Funding InformationThis work was supported and funded by The School of Kinesiology at Auburn University.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Do Graduated Compression Garments Enhance Whole‐body Heat Loss During an Extreme Heat Exposure in Older Adults?
Authors: D'Souza Andrew W. , Notely Sean R. , Meade Robert D. , Kenny Glen P. 
Published: June 2021

Graduated compression garments worn on the lower limbs are commonly used in clinical settings to enhance blood circulation and have been shown to elicit elevations in whole‐body heat loss relative to a control condition (no compression) in young men during post‐exercise recovery in the heat (Am J Physiol 2010;299:R119). To date, it remains unknown whether these garments can enhance heat dissipation in heat vulnerable older adults. Relative to their younger counterparts, older adults demonstrate an impaired ability to increase whole‐body heat loss during an extreme heat exposure. Consequently, these individuals store more heat, leading to potentially dangerous increases in body temperature (Temperature (Austin) 2017;4:79). The use of compression garments may help alleviate the level of thermal strain in these individuals. We therefore sought to determine whether lower limb graduated compression garments would enhance whole‐body heat dissipation and reduce body heat storage relative to a control condition (i.e., no compression) in older adults during passive heat exposure. To evaluate this possibility, we assessed changes in whole‐body heat exchange and heat storage in 6 older (mean ± SD: 69 ± 6 years) adults (4 men, 2 women) during a 2‐hour extreme heat exposure (40°C, ~10 %RH) on two separate occasions (separated by ≥48 h). In both trials, participants sat in a semi‐recumbent position wearing a graduated compression garment (SCD Express Sleeves; Kendall, Mansfield, MA) on each leg containing three bladders that either delivered intermittent graded compression (ankle: 45 mmHg, calf: 40 mmHg, thigh: 30 mmHg; Compression trial) or no compression (Control trial) throughout each exposure. Trials were administered in a balanced order. Wholebody heat loss and metabolic heat production were measured continuously by direct and indirect calorimetry, respectively. Body heat storage was quantified as the temporal summation of heat production and loss. Metabolic heat production (Compression: 98 ± 10 W vs. Control: 94 ± 13 W), evaporative heat loss (135 ± 20 W vs. 134 ± 23 W), dry heat exchange (−48 ± 19 W vs. −52 ± 12 W), and net (total) heat loss (89 ± 14 W vs. 82 ± 14 W), were similar between the Compression and Control trials (all P>0.05). Consequently, cumulative body heat storage did not differ between conditions (Compression: 85 ± 11 kJ; Control: 85 ± 24 kJ, P=0.98). Our preliminary findings suggest that graduated compression garments do not enhance whole‐body heat loss in older adults during exposure to hot ambient conditions.Support or Funding InformationThe Canadian Institutes of Health Research (funds held by Dr. Glen Kenny).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Acute Heat Exposure Results in an Appropriate Initial Decrease in Core Body Temperature in Subjects with Higher Levels of Spinal Cord Injury, but the Thermal Homeostatic Response to More Prolonged Heat Exposure is Insufficient
Authors: Kumar Nina S. , Graham Marin , Leung Patricia , Tittley Tishina D. , Tascione Oriana F. , Bauman William A. , Handrakis John P. 
Published: June 2021

Study ObjectiveTo determine the initial (30 minutes) and more prolonged (60 & 90 minutes) response to heat exposure in individuals with higher levels of spinal cord injury (Hi‐SCI; ≥thoracic level‐4).MethodsSixteen persons with Hi‐SCI (C4‐T4, AIS A‐B) and 16 age and body mass index‐matched AB controls were acclimated in a 27°C baseline (BL) room before being transitioned to a 35°C chamber for 90 minutes (Heat Challenge). Tcore (rectal temperature) was continuously measured throughout the Heat Challenge, and sweat rates of the upper extremities (SRUE) and lower extremities (SRLE) were measured at BL and then at 30‐minute intervals.ResultsAt BL, the average Tcore of the Hi‐SCI group was lower than that of the AB group (36.8±0.45°C vs. 37.35±0.27°C; p=0.0003, respectively). From BL to 30 minutes of Heat Challenge, in both Hi‐SCI and AB groups, a significant decrease (p<0.001) in Tcore (Hi‐SCI and AB: 36.57±0.47°C; 37.07±0.20°C, respectively) was accompanied by increases in SRUE for both Hi‐SCI and AB groups (63.77±83.15%; p=0.008 and 202.98±412.47%; p=0.068, respectively). SRLE also increased in the AB group from BL to 30 minutes (138.25±227.96%; p=0.028). From 30–60 minutes of Heat Challenge in the Hi‐SCI group, SRUE increased significantly (32.34±54.53%; p=0.031), but SRLE did not. From 60–90 minutes of Heat Challenge in the Hi‐SCI group, SRUE and SRLE failed to increase, which was associated with progressive increases in Tcore to BL values at 60 minutes (36.74±0.45°C) and above BL values at 90 minutes (37.01±0.45°C vs. 36.8±0.45°C; p=0.01). In the AB group, both SRUE and SRLE incrementally and significantly increased at each 30 minute interval of Heat Challenge, and Tcore remained lower than the BL value at 90 minutes (37.17±0.23 vs. 37.35±0.27°C; p=0.003).ConclusionsIn the Hi‐SCI group, we speculate that during the first 30 minutes of Heat Challenge, residual sympathetic sudomotor control allowed for increased SRUE, which resulted in a dip in Tcore that was similar to the dip observed in the AB group. However, because of limited sympathetic integrity in the upper and lower extremities, persons with Hi‐SCI were unable to mount a meaningful increase in SRUE from 60–90 minutes or in SRLE from BL to 90 minutes. The insufficient thermal homeostatic response to more prolonged Heat Challenge in the Hi‐SCI group resulted in a Tcore rise above BL values. Thus, prolonged exposure (>60 minutes) to elevated ambient temperatures poses a risk to persons with higher levels of SCI.Support or Funding Information: Department of Veterans Affairs Rehabilitation Research and Development Service (I21RX001734).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Identification of Novel mRNA Transcripts in the Sympathetic Stellate Ganglia using RNA Sequencing
Authors: Bardsley Emma N. , Davis Harvey , Ajijola Olujimi A. , Buckler Keith J. , Ardell Jeffrey , Shivkumar Kalyanam , Paterson David J. 
Published: June 2021

IntroductionSympathetic hyperactivity is a key feature of human hypertension as well as animal models of disease. In the spontaneously hypertensive rat (SHR), a genetic‐based model of hypertension, dysautonomia occurs prior to increases in blood pressure.AimIn this study, we aimed to establish the genetic changes in post‐ganglionic sympathetic neurons (PGSNs) obtained from SHR rats and to confirm the presence of these transcripts in stellate ganglia from human donor patients.MethodPGSNs were obtained from 16‐week normotensive Wistar rats and age‐matched hypertensive SHR with known sympathetic hyper‐responsiveness. RNA sequencing was used to investigate the transcriptomic changes within the cardiac sympathetic stellate ganglia in disease.ResultsRNAseq data were analysed using a Salmon‐DESeq2 pipeline1,2. We observed 768 differentially expressed mRNA transcripts in SHR compared with Wistar PGSNs, using the Benjamini‐Hochberg adjusted p<0.01 level. Gene ontology (GO) analysis of the rat dataset revealed extracellular ligand‐gated ion channels (GO:0005302) to be the most over‐represented ‘molecular function’ GO group. There were 15 differentially expressed genes in SHR stellate neurons within this group; including nicotinic, purinergic, glutamatergic, serotonergic, GABAergic and glycinergic receptor subunits. The presence of these transcripts was confirmed using qRT‐PCR in stellate ganglia obtained from human and rat.ConclusionRNAseq transcriptomics has revealed differential gene expression profiles in PGSNs obtained from SHR and normotensive Wistar rats. These key transcripts were also present in human stellate ganglia. Taken together, these genes require further investigation for their role in sympathetic hyperactivity and dysautonomias.Support or Funding InformationThis project was funded by the Wellcome Trust OXION initiative (105409/Z/14/Z), the British Heart Foundation, NIH SPARC (OT2OD023848) and new innovator (DP2HL142045) initiatives.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Bilirubin Induces the Burning of Fat via the Nuclear Receptor PPARα
Authors: Gordon Darren M. , John Kezia , Trabbic Christopher J. , Luniwal Amarjit , Hankins Michael W. , Baum Justin , Stec David E. , Hinds Terry D. 
Published: June 2021

Deposition fat in adipocytes has become key to understanding how obesity and insulin resistance impact morbidity and mortality. Several studies have shown a decreased amount of body fat in patients with increased plasma bilirubin, which was previously only thought to be a potent antioxidant. Increasing plasma bilirubin levels have been shown to play an integral role in weight loss and are preventive of diabetes as well as cardiovascular events. Our current studies reveal this phenomenon is potentially due to bilirubin binding to the fat burning nuclear receptor peroxisome proliferative‐activated receptor alpha (PPARα) to increase transcriptional activity. We have previously shown that wild‐type and PPARα knockout (KO) mice on a high‐fat diet that were treated with PPARα ligand fenofibrate or bilirubin, had lost the response in the KO mice. Also, the impact of bilirubin on glucose lowering ability as well as weight loss was reduced in the PPARα KO mice. To determine the mechanistic role of the bilirubin‐PPARα axis, we treated adipocytes with biliverdin, a precursor of bilirubin, and known PPARα agonist WY 14,643, and identified by chromatin immunoprecipitation (ChIP) that bilirubin‐PPARα activates the uncoupling protein UCP1 to induce the burning of fat. These all point to the importance and newfound role that bilirubin plays in the burning of fat in adipose to reduce accumulation via binding to PPARα.Support or Funding InformationSource of Funding: This research was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under Award Number K01HL125445 (T.D.H.).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
MafB Overexpression Enhances Functional Beta Cell Mass
Authors: Leifer Aaron H. , Tessem Jeffery Sivert 
Published: June 2021

Both Type 1 and Type 2 diabetes are characterized by loss of beta cell function and cell number. Therefore, any cure for diabetes will require increasing a patient's functional beta cell mass. Given that beta cell proliferation is extremely low after adolescence, we have sought to determine genetic mechanisms that can result in beta cell proliferation. Recent work has shown that the beta cell transcription factor Nkx6.1, which is essential for beta cell development, is sufficient to enhance glucose‐stimulated insulin secretion, improve beta cell survival and enhance beta cell proliferation. Additional studies have shown similar results for the transcription factor Pdx1. Given these results, we hypothesized that other transcription factors essential for beta cell development may have similar effects on enhancing functional beta cell mass. Here we present data that the transcription factor MafB, which is expressed in early stages of beta cell development, when overexpressed maintains glucose‐stimulated insulin secretion and cell survival, while enhancing beta cell proliferation. These data suggest that MafB may be useful in the process of expanding functional beta cell mass as a treatment for both major forms of diabetes.Support or Funding InformationThis research was funded by a BYU ORCA Grant to AHL.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
SGLT2 inhibition decreases oxygen consumption and increases oxygen tension in diabetic rats
Authors: Liu Zhizhao , Hall Elanore , Singh Prabhleen 
Published: June 2021

IntroductionDiabetes is a major cause of chronic kidney disease. Recent data reports that sodium‐glucose cotransporter 2 (SGLT2) inhibitor, empagliflozin (EMPA), slows down the progression of diabetic nephropathy in type 2 diabetes mellitus. Here we investigate the effects of empagliflozin on kidney function, renal oxygen tension and oxygen consumption in streptozotocin‐induced diabetic rats (type 1 diabetes mellitus) to understand the underlying protective mechanism of empagliflozin on kidney disease.MethodAge‐matched male Wistar rats were randomly divided into four groups: control, control+EMPA (30 mg/kg/day oral gavage), diabetes, and diabetes+EMPA. Two weeks later, GFR was estimated by clearance of 3H‐inulin. Total renal blood flow (RBF) was measured using an ultrasound probe placed around the left renal artery. Blood gas parameters and total oxygen consumption were analyzed on samples drawn from the left renal vein and femoral artery. In another set of experiments, intrarenal oxygen tension was measured in the renal cortex and medulla by oxygen microsensor.ResultsCompared with controls, diabetes displayed a slight higher RBF, decreased arterial oxygen saturation (85% VS. 92%) and decreased oxygen partial pressure (65 mmHg VS. 81 mmHg). Oxygen consumption increased in diabetes compared to controls (0.31 ml/min VS. 0.16 ml/min), and oxygen tension in renal cortex (39 mmHg VS. 54 mmHg) and medulla (35 mmHg VS. 40 mmHg) were lower in diabetes. Empagliflozin prevented the diabetes induced‐alterations in oxygen consumption (0.21 ml/min), and restored the decreased oxygen tension in renal cortex (45 mmHg), not in renal medulla (35 mmHg). Empagliflozin reduced 48% of the insulin requirement with 14% lower blood glucose level in diabetic groups.ConclusionEmpagliflozin prevents diabetes‐induced alteration in kidney oxygen metabolism by reducing proximal renal glucose reabsorption which reduced total renal oxygen consumption while increased renal cortex oxygen tension. Empagliflozin reduced blood glucose levels in a T1DM animal model. These improvements provide insights into the mechanisms by which empagliflozin reduces the rates of clinically relevant renal end points. Additional molecular mechanisms and mitochondrial function in response to SGLT2 inhibition in diabetes is being investigated.Support or Funding InformationAmerican Diabetes AssociationVA Merit Award
The β‐ and γ Epithelial Na+ Channel (ENaC) Subunits Modulate the Shear Force Activation
Authors: Baldin Jan‐Peter Markus , Fronius Martin 
Published: June 2021

The epithelial sodium channel (ENaC) is expressed in the kidney and vasculature and is important for blood pressure regulation. In the kidney and vasculature, ENaC is exposed to mechanical force such as shear force (SF) caused by the urine or blood flow. Canonical ENaC consists of three homologous subunits: α, β, γ and studies have shown that α‐ENaC plays an important role for the ability of the channel to respond to SF. Further evidence suggests that β‐and γ‐ENaC alone may be involved in mechanotransduction processes in arteries. Since little is known about the function of individual ENaC subunits and their regulation by SF, this project aims to characterize the role of β‐ and γ‐ENaC for SF sensation.Human ENaCs were expressed as homotrimers (α, β or γ alone) or heterotrimers (αβ, αγ or βγ) in Xenopus oocytes. Two‐electrode voltage‐clamp experiments were performed to measure ENaC activity in response to a fluid stream used for the application of SF. SF responses were normalized and expressed as percentage.Homotrimeric α‐ENaC showed an activation of 46 ± 7.4 (Mean ± SEM, p < 0.0001, n = 19) in response to SF, whereas homotrimeric β‐ or γ‐ENaCs did not respond to SF. In heterotrimeric αβ‐ENaC channels the activation by SF was 17 ± 3 (p < 0.0001, n = 19) and in heterotrimeric αγ‐ENaC 222 ± 35 (p < 0.0001, n = 17). Heterotrimeric βγ‐ENaC did not respond to SF.Homotrimeric α‐ENaC form a functional channel that responds to SF whereas β‐ and γ‐ENaC did not. Heterotrimeric αβ‐ENaC showed a lower SF responds, whereas αγ‐ENaC showed a higher responds to SF. This experiments identify a modulatory role of β‐ and γ‐ENaC for the activation in response to SF. Therefore, ENaC dysfunction is observed in hypertension may be due to changes in β‐ and γ‐ENaC expression that could influence its activity in response to SF caused by the urine or blood flow.Support or Funding InformationUniversity of Otago Doctoral ScholarshipDepartment of PhysiologyRoyal Society Te Aparangi ‐ Marsden FundThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.