Who Is Influencing Whom? Latino Parent-Child Request Interactions and Product Purchases in Food Retail Environments.

This study examines Latino parent-child interactions about foods and beverages requested in food retail environments in San Diego, CA. It seeks to extend our understanding of parent-child request interactions and purchases by studying how the number of product request interactions and purchases differ based on four factors that have been understudied in previous parent-child interaction research: parent gender, child gender, product healthfulness, and who initiated the request interaction (parent or child). By unobtrusively observing Latino parent-child dyads for the duration of a brief shopping trip, we found that parent and child gender are related to the number of request interactions initiated by parents and children. For gender-specific child-initiated request interactions, sons initiated more request interactions with fathers while daughters initiated more request interactions with mothers. Most request interactions were for products that were categorized as calorie dense, and a higher percentage of these products were purchased as a result of parent-initiated (vs. child-initiated) request interactions. The results provide important considerations for practitioners and researchers working on improving nutrition and reducing obesity. Assumptions about who is influencing whom in food store request interactions are challenged, requiring more research.

What Happens When Parents and Children Go Grocery Shopping? An Observational Study of Latino Dyads in Southern California, USA.

The objective of this study was to observe parent-child interactions in tiendas, limited assortment food stores catering to Latinos in the United States, and to examine the extent to which child involvement influenced these interactions and their purchase outcomes. Two confederates, one posing as a tienda employee and one posing as a customer, observed the entire shopping trip of 100 Latino parent-child (mean age = 8 years) dyads and coded the following: number and type of parent- and child-initiated request interactions, types of purchase influence attempts used by children and how parents responded, and whether the product was purchased. Level of child involvement was examined as a potential influencing factor on purchasing. The observations were relatively short (mean duration of 10 minutes), reflecting the "quick trip" nature of the observed shopping trips. From the 100 parent-child dyads, 144 request interactions were observed, and among dyads with at least 1 request interaction during the shopping trip, the average number of request interactions per dyad was 2. Children initiated most of the request interactions by asking for a product or simply placing it in the basket; parents initiated 24% of the request interactions. Child involvement in shopping and checkout were associated with spending and purchase outcomes. These results indicate that children and parents influence each other during grocery shopping, and children who are more involved have greater influence over purchases. Furthermore, this study identified a number of targets for future family/parent and consumer food environment interventions.

Actigraphy for the assessment of sleep measures in Parkinson's disease.

OBJECTIVES: To assess the usefulness of actigraphy for assessment of nighttime sleep measures in patients with Parkinson's disease (PD). DESIGN: Participants underwent overnight sleep assessment simultaneously by polysomnography (PSG) and actigraphy. SETTING: Overnight sleep study in academic sleep research laboratory. PARTICIPANTS: Sixty-one patients (mean age 67.74 ± 8.88 y) with mild to moderate PD. MEASUREMENTS: Sleep measures including total sleep time (TST), sleep efficiency (SE), wake after sleep onset (WASO), and sleep onset latency (SOL) were calculated independently from data derived from PSG and from actigraphy. Different actigraphy scoring settings were compared. RESULTS: No single tested actigraphy scoring setting was optimal for all sleep measures. A customized setting of an activity threshold of 10, with five consecutive immobile minutes for sleep onset, yielded the combination of mean TST, SE, and WASO values that best approximated mean values determined by PSG with differences of 6.05 ± 85.67 min for TST, 1.1 ± 0.641% for SE, and 4.35 ± 59.56 min for WASO. There were significant but moderate correlations between actigraphy and PSG measurements (rs = 0.496, P < 0.001 for TST, rs = 0.384, P = 0.002 for SE, and rs = 0.400, P = 0.001 for WASO) using these settings. Greater disease stage was associated with greater differences between TST (R(2) = 0.099, beta = 0.315, P = 0.018), SE (R(2) = 0.107, beta = 0.327, P = 0.014), and WASO (R(2) = 0.094, beta = 0.307, P = 0.021) values derived by actigraphy and PSG explaining some of the variability. Using a setting of 10 immobile min for sleep onset yielded a mean SOL that was within 1 min of that estimated by PSG. However SOL values determined by actigraphy and PSG were not significantly correlated at any tested setting. CONCLUSIONS: Our results suggest that actigraphy may be useful for measurement of mean TST, SE, and WASO values in groups of patients with mild to moderate Parkinson's disease. However, there is a significant degree of variability in accuracy among individual patients. The importance of determining optimal scoring parameters for each population studied is underscored.

Block of neuronal Na+ channels by antidepressant duloxetine in a state-dependent manner.

BACKGROUND: Duloxetine is a mixed serotonin-norepinephrine reuptake inhibitor used for major depressive disorder. Duloxetine is also beneficial for patients with diabetic peripheral neuropathy and with fibromyalgia, but how it works remains unclear. METHODS: We used the whole cell, patch clamp technique to test whether duloxetine interacts with the neuronal Nav1.7 Na+ channel as a potential target. Resting and inactivated Nav1.7 Na+ channel block by duloxetine were measured by conventional pulse protocols in transfected human embryonic kidney cells. The open-channel block was determined directly using inactivation-deficient mutant Nav1.7 Na+ channels. RESULTS: The 50% inhibitory concentration (IC50) of duloxetine for the resting and inactivated wild-type hNav1.7 Na+ channel were 22.1+/-0.4 and 1.79+/-0.10 microM, respectively (mean+/-SE, n=5). The IC50 for the open Na+ channel was 0.25+/-0.02 microM (n=5), as determined by the block of persistent late Nav1.7 Na+ currents. Similar open-channel block by duloxetine was found in the muscle Nav1.4 isoform (IC50=0.51+/-0.05 microM; n=5). Block by duloxetine appeared via the conserved local anesthetic receptor as determined by site-directed mutagenesis. Finally, duloxetine elicited strong use-dependent block of neuronal transient Nav1.7 Na+ currents during repetitive stimulations. CONCLUSIONS: Duloxetine blocks persistent late Nav1.7 Na+ currents preferentially, which may in part account for its analgesic action.

State-dependent block of Na+ channels by articaine via the local anesthetic receptor.

Articaine is widely used as a local anesthetic (LA) in dentistry, but little is known regarding its blocking actions on Na+ channels. We therefore examined the state-dependent block of articaine first in rat skeletal muscle rNav1.4 Na+ channels expressed in Hek293t cells. Articaine exhibited a weak block of resting rNav1.4 Na+ channels at -140 mV with a 50% inhibitory concentration (IC(50)) of 378 +/- 26 microM (n = 5). The affinity was higher for inactivated Na+ channels measured at -70 mV with an IC50 value of 40.6 +/- 2.7 microM (n = 5). The open-channel block by articaine was measured using inactivation-deficient rNav1.4 Na+ channels with an IC50 value of 15.8 +/- 1.5 microM (n = 5). Receptor mapping demonstrated that articaine interacted strongly with a D4S6 phenylalanine residue, which is known to form a part of the LA receptor. Thus the block of rNav1.4 Na+ channels by articaine is via the conserved LA receptor in a highly state-dependent manner, with a ranking order of open (23.9x) > inactivated (9.3x) > resting (1x) state. Finally, the open-channel block by articaine was likewise measured in inactivation-deficient hNav1.7 and rNav1.8 Na+ channels, with IC(50) values of 8.8 +/- 0.1 and 22.0 +/- 0.5 microM, respectively (n = 5), indicating that the high-affinity open-channel block by articaine is indeed preserved in neuronal Na+ channel isoforms.

State- and use-dependent block of muscle Nav1.4 and neuronal Nav1.7 voltage-gated Na+ channel isoforms by ranolazine.

Ranolazine is an antianginal agent that targets a number of ion channels in the heart, including cardiac voltage-gated Na(+) channels. However, ranolazine block of muscle and neuronal Na(+) channel isoforms has not been examined. We compared the state- and use-dependent ranolazine block of Na(+) currents carried by muscle Nav1.4, cardiac Nav1.5, and neuronal Nav1.7 isoforms expressed in human embryonic kidney 293T cells. Resting and inactivated block of Na(+) channels by ranolazine were generally weak, with a 50% inhibitory concentration (IC(50)) >/= 60 microM. Use-dependent block of Na(+) channel isoforms by ranolazine during repetitive pulses (+50 mV/10 ms at 5 Hz) was strong at 100 microM, up to 77% peak current reduction for Nav1.4, 67% for Nav1.5, and 83% for Nav1.7. In addition, we found conspicuous time-dependent block of inactivation-deficient Nav1.4, Nav1.5, and Nav1.7 Na(+) currents by ranolazine with estimated IC(50) values of 2.4, 6.2, and 1.7 microM, respectively. On- and off-rates of ranolazine were 8.2 microM(-1) s(-1) and 22 s(-1), respectively, for Nav1.4 open channels and 7.1 microM(-1) s(-1) and 14 s(-1), respectively, for Nav1.7 counterparts. A F1579K mutation at the local anesthetic receptor of inactivation-deficient Nav1.4 Na(+) channels reduced the potency of ranolazine approximately 17-fold. We conclude that: 1) both muscle and neuronal Na(+) channels are as sensitive to ranolazine block as their cardiac counterparts; 2) at its therapeutic plasma concentrations, ranolazine interacts predominantly with the open but not resting or inactivated Na(+) channels; and 3) ranolazine block of open Na(+) channels is via the conserved local anesthetic receptor albeit with a relatively slow on-rate.