Search

Introduction: This study aimed to examine the validity and accuracy of wrist accelerometers for classifying sedentary behavior (SB) in children., Methods: Fifty-seven children (5-8 and 9-12 yr) completed an ~170-min protocol, including 15 semistructured activities and transitions. Nine ActiGraph (GT3X+) and two GENEActiv wrist cut points were evaluated. Direct observation was the criterion measure. The accuracy of wrist cut points was compared with that achieved by the ActiGraph hip cut point (≤25 counts per 15 s) and the thigh-mounted activPAL3. Analyses included equivalence testing, Bland-Altman procedures, and area under the receiver operating curve (ROC-AUC)., Results: The most accurate ActiGraph wrist cut points (Kim; vector magnitude, ≤3958 counts per 60 s; vertical axis, ≤1756 counts per 60 s) demonstrated good classification accuracy (ROC-AUC = 0.85-0.86) and accurately estimated SB time in 5-8 yr (equivalence P = 0.02; mean bias = 4.1%, limits of agreement = -20.1% to 28.4%) and 9-12 yr (equivalence P < 0.01; -2.5%, -27.9% to 22.9%). The mean bias of SB time estimates from Kim were smaller than ActiGraph hip (5-8 yr: 15.8%, -5.7% to 37.2%; 9-12 yr: 17.8%, -3.9% to 39.5%) and similar to or smaller than activPAL3 (5-8 yr: 12.6%, -39.8% to 14.7%; 9-12 yr: -1.4%, -13.9% to 11.0%), although classification accuracy was similar to ActiGraph hip (ROC-AUC = 0.85) but lower than activPAL3 (ROC-AUC = 0.92-0.97). Mean bias (5-8 yr: 6.5%, -16.1% to 29.1%; 9-12 yr: 10.5%, -13.6% to 34.6%) for the most accurate GENEActiv wrist cut point (Schaefer: ≤0.19 g) was smaller than ActiGraph hip, and activPAL3 in 5-8 yr, but larger than activPAL3 in 9-12 yr. However, SB time estimates from Schaefer were not equivalent to direct observation (equivalence P > 0.05) and classification accuracy (ROC-AUC = 0.79-0.80) was lower than for ActiGraph hip and activPAL3., Conclusion: The most accurate SB ActiGraph (Kim) and GENEActiv (Schaefer) wrist cut points can be applied in children with similar confidence as the ActiGraph hip cut point (≤25 counts per 15 s), although activPAL3 was generally more accurate.

Few studies have explored the relationship between exposure to adverse race-related events and posttraumatic stress disorder (PTSD). This study examined whether adverse race-related events can give rise to symptoms that meet the criteria for a PTSD diagnosis as specified in the DSM-IV. Three hundred Asian American Vietnam veterans were administered a Mississippi Scale and a questionnaire that assessed exposure to adverse race-related events in the military and associated PTSD symptoms. A subsample was administered the Clinician-Administered PTSD Scale. A majority of the participants (77%) reported exposure to adverse race-related events. Depending on the number of events to which they were exposed, between 13% and 36% reported symptoms consistent with meeting full criteria for PTSD. Mississippi Scale scores increased significantly as a function of frequency of exposure to adverse race-related events. These results converge with the Clinician-Administered PTSD Scale findings to demonstrate that adverse race-related events can be traumatic and associated with PTSD. These findings support the construct and convergent validity of race-related PTSD.

Cannabinoid receptor (CB1) agonists strongly inhibit behavioral responses to acute noxious stimuli, but their effects on behavioral responses in persistent pain states are less clear. Here, we examined the effects of intrathecal (i.t.) administration of a CB1 agonist, WIN55,212-2, on mechanical allodynia (decreased withdrawal threshold) produced by injections of complete Freund's adjuvant (CFA) in the plantar surface of the rat hindpaw. We measured mechanical thresholds with calibrated von Frey filaments before and after CFA and used Fos expression as a marker of the activity of spinal cord neurons during inflammation and in response to a CB1 antagonist. One day post CFA-induced injury, mechanical sensitivity was significantly increased in the hindpaw ipsilateral to the CFA injection, as was the number of neurons that express Fos. Intrathecal injection of WIN55,212-2, significantly, reversed the allodynia at doses that had no effect on the mechanical threshold of the contralateral paw of CFA-treated or the withdrawal thresholds in naive animals. This effect was blocked by coadministration of the CB1 antagonist, SR141716A, with WIN55212-2. By itself, SR141716A, had no effect on mechanical thresholds in normal animals. In inflamed animals, SR141716A did not further reduce mechanical thresholds in the inflamed paw, but it significantly enhanced mechanical sensitivity 'contralateral' to the inflammation. Furthermore, i.t. injection of SR141716A increased Fos expression in both normal and inflamed animals, to a different extent in different laminae. In normal animals, the increase was primarily in laminae V-VI and in the ventral horn; in animals with persistent inflammation SR141716A increased the number of Fos neurons in laminae I-II and V-VI. These results demonstrate that WIN55212-2 reverses inflammation-induced allodynia at doses that do not produce analgesia and that SR141716A differentially affects the pattern of Fos expression in the spinal cord, depending on the presence or absence of inflammation. Taken together, these results suggest that the CB1 receptor system is tonically active in the spinal cord under normal conditions and that its activity is increased in response to injury.

Although many pharmacological studies indicate that bulbospinal noradrenergic projections contribute to antinociception, lesions of the major brainstem noradrenergic cell groups have provided conflicting evidence. Here we used a new immunotoxin, anti-dopamine beta-hydroxylase-saporin, to re-examine the contribution of noradrenergic pathways to nociception and to morphine analgesia. We treated rats intrathecally by lumbar puncture with the immunotoxin and examined dopamine beta-hydroxylase (DbetaH) immunoreactivity seven and 14 days after treatment. There was no change in DbetaH staining at 7 days; however, 14 days after treatment we demonstrated significant destruction of noradrenergic neurons in the locus coeruleus and in the A5 and A7 cell groups. There was a concomitant loss of noradrenergic axons in the dorsal and ventral horns of the lumbosacral and cervical cord. Consistent with the lack of anatomical changes, we found no difference in nociceptive responses in the hot-plate, tail-flick or formalin tests one week post-toxin. On day 14 we examined the behavioral response to injection of formalin into the hindpaw and found that responses during the second phase of pain behavior were significantly reduced. There was no change during the first phase. Formalin-evoked fos expression in the spinal cord was also reduced. We also evaluated morphine analgesia in the formalin test and found that toxin-treated animals exhibited enhanced morphine analgesia. These results establish the utility of using this immunotoxin to selectively destroy subpopulations of noradrenergic cell groups and provide evidence that acute and persistent nociception are differentially regulated by descending noradrenergic pathways.