Validity of a Global Positioning System-Based Algorithm and Consumer Wearables for Classifying Active Trips in Children and Adults

Accepted author manuscript version reprinted, by permission, from [Journal for the Measurement of Physical Behaviour, 2021, Volume 4: Issue 4: pp. 321–332, https://doi.org/10.1123/jmpb.2021-0019. © Human Kinetics, Inc.Objective: To investigate the convergent validity of a global positioning system (GPS)-based and two consumer-based measures with trip logs for classifying pedestrian, cycling, and vehicle trips in children and adults. Methods: Participants (N = 34) wore a Qstarz GPS tracker, Fitbit Alta, and Garmin vivosmart 3 on multiple days and logged their outdoor pedestrian, cycling, and vehicle trips. Logged trips were compared with device-measured trips using the Personal Activity Location Measurement System (PALMS) GPS-based algorithms, Fitbit’s SmartTrack, and Garmin’s Move IQ. Trip- and day-level agreement were tested. Results: The PALMS identified and correctly classified the mode of 75.6%, 94.5%, and 96.9% of pedestrian, cycling, and vehicle trips (84.5% of active trips, F1 = 0.84 and 0.87) as compared with the log. Fitbit and Garmin identified and correctly classified the mode of 26.8% and 17.8% (22.6% of active trips, F1 = 0.40 and 0.30) and 46.3% and 43.8% (45.2% of active trips, F1 = 0.58 and 0.59) of pedestrian and cycling trips. Garmin was more prone to false positives (false trips not logged). Day-level agreement for PALMS and Garmin versus logs was favorable across trip modes, though PALMS performed best. Fitbit significantly underestimated daily cycling. Results were similar but slightly less favorable for children than adults. Conclusions: The PALMS showed good convergent validity in children and adults and were about 50% and 27% more accurate than Fitbit and Garmin (based on F1). Empirically-based recommendations for improving PALMS’ pedestrian classification are provided. Since the consumer devices capture both indoor and outdoor walking/running and cycling, they are less appropriate for trip-based research

Floristic inventory and floristic quality assessment of the LSL tract, Straits of Mackinac, Emmet County, Michigan.

Field Biology of PlantsThe 55 ha Emmet County LSL tract was obtained in 1990 by Emmet County as an addition to their adjacent Cecil Bay Park. The perimeter of the preserve consists of disturbed roadside and a two-track clearing to the north and a power line in the southwest corner. Though the LSL tract is surrounded by paved road and residential properties, the central core of the site remains fairly untouched. The majority of the site consists of a Thuja forest (37 ha) that surrounds relict beach pools and their surrounding marshes (12 ha). Our objective was to conduct a botanical inventory and floristic quality assessment (FQA) of the LSL Tract to establish a baseline of botanical knowledge that may inform future management of the site. We surveyed the property on four separate occasions in June and July of 2013. We collected every new species we encountered within focal habitats. The inventory consisted of 199 species, 165 of which (83%) were native. Coefficients of conservatism and wetness were calculated for every species identified. The entire tract had an FQA of 66.6, the roadsides 24.0, the power line 14.9, the two-track 34.7, the Thuja forest 37.6, and the beach pool marshes 44.1. The majority of the native plants with high conservation value were located in the beach pool marshes. However, two federally threatened, Great Lakes endemic species (Iris lacustris and Solidago houghtonii) were found in the two-track clearing at the northern end of the property. Some invasive species found in the site that may be able to colonize inner parts of the preserve if trails are established. Of these, Cirsium palustre (swamp thistle) and Fallopia japonica (Japanese knotweed) need to be carefully monitored. Here, we provide suggestions for the protection of the valuable native flora of the LSL Tract, a property that is a noteworthy representation of a Straits of Mackinac native forest and wetland complex.http://deepblue.lib.umich.edu/bitstream/2027.42/106397/1/Gingerich_Heyman_Kuesel_Pethan_Steel_2013.pd

PPARα-independent effects of nitrate supplementation on skeletal muscle metabolism in hypoxia

Hypoxia is a feature of many disease states where convective oxygen delivery is impaired, and is known to suppress oxidative metabolism. Acclimation to hypoxia thus requires metabolic remodelling, however hypoxia tolerance may be aided by dietary nitrate supplementation. Nitrate improves tissue oxygenation and has been shown to modulate skeletal muscle tissue metabolism via transcriptional changes, including through the activation of peroxisome proliferator- activated receptor alpha (PPARα), a master regulator of fat metabolism. Here we investigated whether nitrate supplementation protects skeletal muscle mitochondrial function in hypoxia and whether PPARα is required for this effect. Wild-type and PPARα knockout (PPARα-/-) mice were supplemented with sodium nitrate via the drinking water or sodium chloride as control, and exposed to environmental hypoxia (10% O2) or normoxia for 4 weeks. Hypoxia suppressed mitochondrial respiratory function in mouse soleus, an effect partially alleviated through nitrate supplementation, but occurring independently of PPARα. Specifically, hypoxia resulted in 26% lower mass specific fatty acid-supported LEAK respiration and 23% lower pyruvate-supported oxidative phosphorylation capacity. Hypoxia also resulted in 24% lower citrate synthase activity in mouse soleus, possibly indicating a loss of mitochondrial content. These changes were not seen, however, in hypoxic mice when supplemented with dietary nitrate, indicating a nitrate dependent preservation of mitochondrial function. Moreover, this was observed in both wild-type and PPARα-/- mice. Our results support the notion that nitrate supplementation can aid hypoxia tolerance and indicate that nitrate can exert effects independently of PPARα.This work was supported by King’s College London, the Biotechnology and Biological Sciences Research Councils [grant number: BB/F016581/1] and the Research Councils UK [grant number: EP/E500552/1]

Inorganic nitrate, hypoxia, and the regulation of cardiac mitochondrial respiration-probing the role of PPARα.

Dietary inorganic nitrate prevents aspects of cardiac mitochondrial dysfunction induced by hypoxia, although the mechanism is not completely understood. In both heart and skeletal muscle, nitrate increases fatty acid oxidation capacity, and in the latter case, this involves up-regulation of peroxisome proliferator-activated receptor (PPAR)α expression. Here, we investigated whether dietary nitrate modifies mitochondrial function in the hypoxic heart in a PPARα-dependent manner. Wild-type (WT) mice and mice without PPARα (Ppara-/-) were given water containing 0.7 mM NaCl (control) or 0.7 mM NaNO3 for 35 d. After 7 d, mice were exposed to normoxia or hypoxia (10% O2) for the remainder of the study. Mitochondrial respiratory function and metabolism were assessed in saponin-permeabilized cardiac muscle fibers. Environmental hypoxia suppressed mass-specific mitochondrial respiration and additionally lowered the proportion of respiration supported by fatty acid oxidation by 18% (P < 0.001). This switch away from fatty acid oxidation was reversed by nitrate treatment in hypoxic WT but not Ppara-/- mice, indicating a PPARα-dependent effect. Hypoxia increased hexokinase activity by 33% in all mice, whereas lactate dehydrogenase activity increased by 71% in hypoxic WT but not Ppara-/- mice. Our findings indicate that PPARα plays a key role in mediating cardiac metabolic remodeling in response to both hypoxia and dietary nitrate supplementation.-Horscroft, J. A., O'Brien, K. A., Clark, A. D., Lindsay, R. T., Steel, A. S., Procter, N. E. K., Devaux, J., Frenneaux, M., Harridge, S. D. R., Murray, A. J. Inorganic nitrate, hypoxia, and the regulation of cardiac mitochondrial respiration-probing the role of PPARα

An occupational therapy intervention for residents with stroke related disabilities in UK care homes (OTCH): cluster randomised controlled trial

Objective To evaluate the clinical efficacy of an established programme of occupational therapy in maintaining functional activity and reducing further health risks from inactivity in care home residents living with stroke sequelae. Design Pragmatic, parallel group, cluster randomised controlled trial. Setting 228 care homes (>10 beds each), both with and without the provision of nursing care, local to 11 trial administrative centres across the United Kingdom. Participants 1042 care home residents with a history of stroke or transient ischaemic attack, including those with language and cognitive impairments, not receiving end of life care. 114 homes (n=568 residents, 64% from homes providing nursing care) were allocated to the intervention arm and 114 homes (n=474 residents, 65% from homes providing nursing care) to standard care (control arm). Participating care homes were randomised between May 2010 and March 2012. Intervention Targeted three month programme of occupational therapy, delivered by qualified occupational therapists and assistants, involving patient centred goal setting, education of care home staff, and adaptations to the environment. Main outcome measures Primary outcome at the participant level: scores on the Barthel index of activities of daily living at three months post-randomisation. Secondary outcome measures at the participant level: Barthel index scores at six and 12 months post-randomisation, and scores on the Rivermead mobility index, geriatric depression scale-15, and EuroQol EQ-5D-3L questionnaire, at all time points. Results 64% of the participants were women and 93% were white, with a mean age of 82.9 years. Baseline characteristics were similar between groups for all measures, personal characteristics, and diagnostic tests. Overall, 2538 occupational therapy visits were made to 498 participants in the intervention arm (mean 5.1 visits per participant). No adverse events attributable to the intervention were recorded. 162 (11%) died before the primary outcome time point, and 313 (30%) died over the 12 months of the trial. The primary outcome measure did not differ significantly between the treatment arms. The adjusted mean difference in Barthel index score at three months was 0.19 points higher in the intervention arm (95% confidence interval −0.33 to 0.70, P=0.48). Secondary outcome measures also showed no significant differences at all time points. Conclusions This large phase III study provided no evidence of benefit for the provision of a routine occupational therapy service, including staff training, for care home residents living with stroke related disabilities. The established three month individualised course of occupational therapy targeting stroke related disabilities did not have an impact on measures of functional activity, mobility, mood, or health related quality of life, at all observational time points. Providing and targeting ameliorative care in this clinically complex population requires alternative strategies

The timing of auditory sensory deficits in Norrie disease has implications for therapeutic intervention

Norrie disease is caused by mutation of the NDP gene, presenting as congenital blindness followed by later onset of hearing loss. Protecting patients from hearing loss is critical for maintaining their quality of life. This study aimed to understand the onset of pathology in cochlear structure and function. By investigating patients and juvenile Ndp-mutant mice, we elucidated the sequence of onset of physiological changes (in auditory brainstem responses, distortion product otoacoustic emissions, endocochlear potential, blood-labyrinth barrier integrity) and determined the cellular, histological, and ultrastructural events leading to hearing loss. We found that cochlear vascular pathology occurs earlier than previously reported and precedes sensorineural hearing loss. The work defines a disease mechanism whereby early malformation of the cochlear microvasculature precedes loss of vessel integrity and decline of endocochlear potential, leading to hearing loss and hair cell death while sparing spiral ganglion cells. This provides essential information on events defining the optimal therapeutic window and indicates that early intervention is needed. In an era of advancing gene therapy and small-molecule technologies, this study establishes Ndp-mutant mice as a platform to test such interventions and has important implications for understanding the progression of hearing loss in Norrie disease

Associations with photoreceptor thickness measures in the UK Biobank.

Spectral-domain OCT (SD-OCT) provides high resolution images enabling identification of individual retinal layers. We included 32,923 participants aged 40-69 years old from UK Biobank. Questionnaires, physical examination, and eye examination including SD-OCT imaging were performed. SD OCT measured photoreceptor layer thickness includes photoreceptor layer thickness: inner nuclear layer-retinal pigment epithelium (INL-RPE) and the specific sublayers of the photoreceptor: inner nuclear layer-external limiting membrane (INL-ELM); external limiting membrane-inner segment outer segment (ELM-ISOS); and inner segment outer segment-retinal pigment epithelium (ISOS-RPE). In multivariate regression models, the total average INL-RPE was observed to be thinner in older aged, females, Black ethnicity, smokers, participants with higher systolic blood pressure, more negative refractive error, lower IOPcc and lower corneal hysteresis. The overall INL-ELM, ELM-ISOS and ISOS-RPE thickness was significantly associated with sex and race. Total average of INL-ELM thickness was additionally associated with age and refractive error, while ELM-ISOS was additionally associated with age, smoking status, SBP and refractive error; and ISOS-RPE was additionally associated with smoking status, IOPcc and corneal hysteresis. Hence, we found novel associations of ethnicity, smoking, systolic blood pressure, refraction, IOPcc and corneal hysteresis with photoreceptor thickness