Dataset Information

Intensity Thresholds on Raw Acceleration Data: Euclidean Norm Minus One (ENMO) and Mean Amplitude Deviation (MAD) Approaches.

ABSTRACT:

Objectives

(1) To develop and internally-validate Euclidean Norm Minus One (ENMO) and Mean Amplitude Deviation (MAD) thresholds for separating sedentary behaviours from common light-intensity physical activities using raw acceleration data collected from both hip- and wrist-worn tri-axial accelerometers; and (2) to compare and evaluate the performances between the ENMO and MAD metrics.

Methods

Thirty-three adults [mean age (standard deviation (SD)) = 27.4 (5.9) years; mean BMI (SD) = 23.9 (3.7) kg/m2; 20 females (60.6%)] wore four accelerometers; an ActiGraph GT3X+ and a GENEActiv on the right hip; and an ActiGraph GT3X+ and a GENEActiv on the non-dominant wrist. Under laboratory-conditions, participants performed 16 different activities (11 sedentary behaviours and 5 light-intensity physical activities) for 5 minutes each. ENMO and MAD were computed from the raw acceleration data, and logistic regression and receiver-operating-characteristic (ROC) analyses were implemented to derive thresholds for activity discrimination. Areas under ROC curves (AUROC) were calculated to summarise performances and thresholds were assessed via executing leave-one-out-cross-validations.

Results

For both hip and wrist monitor placements, in comparison to the ActiGraph GT3X+ monitors, the ENMO and MAD values derived from the GENEActiv devices were observed to be slightly higher, particularly for the lower-intensity activities. Monitor-specific hip and wrist ENMO and MAD thresholds showed excellent ability for separating sedentary behaviours from motion-based light-intensity physical activities (in general, AUROCs >0.95), with validation indicating robustness. However, poor classification was experienced when attempting to isolate standing still from sedentary behaviours (in general, AUROCs <0.65). The ENMO and MAD metrics tended to perform similarly across activities and accelerometer brands.

Conclusions

Researchers can utilise these robust monitor-specific hip and wrist ENMO and MAD thresholds, in order to accurately separate sedentary behaviours from common motion-based light-intensity physical activities. However, caution should be taken if isolating sedentary behaviours from standing is of particular interest.

SUBMITTER: Bakrania K

PROVIDER: S-EPMC5051724 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Intensity Thresholds on Raw Acceleration Data: Euclidean Norm Minus One (ENMO) and Mean Amplitude Deviation (MAD) Approaches.

Bakrania Kishan K Yates Thomas T Rowlands Alex V AV Esliger Dale W DW Bunnewell Sarah S Sanders James J Davies Melanie M Khunti Kamlesh K Edwardson Charlotte L CL

PloS one 20161005 10

<h4>Objectives</h4>(1) To develop and internally-validate Euclidean Norm Minus One (ENMO) and Mean Amplitude Deviation (MAD) thresholds for separating sedentary behaviours from common light-intensity physical activities using raw acceleration data collected from both hip- and wrist-worn tri-axial accelerometers; and (2) to compare and evaluate the performances between the ENMO and MAD metrics.<h4>Methods</h4>Thirty-three adults [mean age (standard deviation (SD)) = 27.4 (5.9) years; mean BMI (SD ...[more]

PMID: 27706241

Similar Datasets

Project description:The trimethoprim and sulfamethoxazole combination, co-trimoxazole, plays a vital role in the treatment of Burkholderia pseudomallei infections. Previous studies demonstrated that the B. pseudomallei BpeEF-OprC efflux pump confers widespread trimethoprim resistance in clinical and environmental isolates, but this is not accompanied by significant resistance to co-trimoxazole. Using the excluded select-agent strain B. pseudomallei Bp82, we now show that in vitro acquired trimethoprim versus co-trimoxazole resistance is mainly mediated by constitutive BpeEF-OprC expression due to bpeT mutations or by BpeEF-OprC overexpression due to bpeS mutations. Mutations in bpeT affect the carboxy-terminal effector-binding domain of the BpeT LysR-type activator protein. Trimethoprim resistance can also be mediated by dihydrofolate reductase (FolA) target mutations, but this occurs rarely unless BpeEF-OprC is absent. BpeS is a transcriptional regulator that is 62% identical to BpeT. Mutations affecting the BpeS DNA-binding or carboxy-terminal effector-binding domains result in constitutive BpeEF-OprC overexpression, leading to trimethoprim and sulfamethoxazole efflux and thus to co-trimoxazole resistance. The majority of laboratory-selected co-trimoxazole-resistant mutants often also contain mutations in folM, encoding a pterin reductase. Genetic analyses of these mutants established that both bpeS mutations and folM mutations contribute to co-trimoxazole resistance, although the exact role of folM remains to be determined. Mutations affecting bpeT, bpeS, and folM are common in co-trimoxazole-resistant clinical isolates, indicating that mutations affecting these genes are clinically significant. Co-trimoxazole resistance in B. pseudomallei is a complex phenomenon, which may explain why resistance to this drug is rare in this bacterium.IMPORTANCEBurkholderia pseudomallei causes melioidosis, a tropical disease that is difficult to treat. The bacterium's resistance to antibiotics limits therapeutic options. The paucity of orally available drugs further complicates therapy. The oral drug of choice is co-trimoxazole, a combination of trimethoprim and sulfamethoxazole. These antibiotics target two distinct enzymes, FolA (dihydrofolate reductase) and FolP (dihydropteroate synthase), in the bacterial tetrahydrofolate biosynthetic pathway. Although co-trimoxazole resistance is minimized due to two-target inhibition, bacterial resistance due to folA and folP mutations does occur. Co-trimoxazole resistance in B. pseudomallei is rare and has not yet been studied. Co-trimoxazole resistance in this bacterium employs a novel strategy involving differential regulation of BpeEF-OprC efflux pump expression that determines the drug resistance profile. Contributing are mutations affecting folA, but not folP, and folM, a folate pathway-associated gene whose function is not yet well understood and which has not been previously implicated in folate inhibitor resistance in clinical isolates.

Dataset Information

Intensity Thresholds on Raw Acceleration Data: Euclidean Norm Minus One (ENMO) and Mean Amplitude Deviation (MAD) Approaches.

Objectives

Methods

Results

Conclusions

Publications

Intensity Thresholds on Raw Acceleration Data: Euclidean Norm Minus One (ENMO) and Mean Amplitude Deviation (MAD) Approaches.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets