Mechanisms influencing older adolescents' bedtimes during videogaming: the roles of game difficulty and flow.

A relationship between evening technology use and sleep has been established, and models suggest various mechanisms to explain this relationship. Recent updates to these models also suggest the influence of individual difference factors, such that the relationship between technology and sleep varies between young people. Flow is an experience of immersion and time distortion that could vary between adolescents when using technology. The aim of the present study was to investigate the effects of flow on the self-selected bedtimes of adolescents when videogaming. Seventeen older adolescent, experienced videogamers (age = 15.9 ± 0.83 years), played a new videogame on two school-night evenings in a sleep laboratory. Game difficulty was set to "hard" one evening (flow condition) and "easy" on the other evening (disrupted flow). Trait and state flow were measured, along with heart rate during videogaming, and bedtime measured objectively with real-time cameras. An interaction effect for heart rate indicated an elevated heart rate in the easy condition after 150 min of gaming (p < 0.02). No significant differences were found in bedtimes between the easy and hard conditions (p = 0.77). Adolescents high on trait flow played for longer and selected significantly later bedtimes than their low trait flow peers but only for the hard (flow) condition (12:22 AM vs. 10:53 PM, p = 0.004). Similarly, adolescents with high state flow went to bed significantly later than those low on state flow (12:24 PM vs. 10:52 PM, p = 0.001), again only in the hard condition. These findings suggest that individual and situational characteristics may amplify the effects of technology use on the "sleep" of adolescents and provides support for the displacement of bedtime hypothesis.

Intrinsic and extrinsic predictors of video-gaming behaviour and adolescent bedtimes: the relationship between flow states, self-perceived risk-taking, device accessibility, parental regulation of media and bedtime.

How computer games affect the time at which adolescents go to bed is of growing research interest; however, the intrinsic individual and extrinsic sociocultural factors mediating the relationship between gaming and sleep have received minimal attention. This paper investigates how gaming duration mediates the relationship between intrinsic factors (perception of risky events and flow) and extrinsic factors (parental regulation and media accessibility) and adolescent bedtime. Adolescents (N = 422; age = 16.3 ± 2.02 years, 41% M) from six metropolitan schools and the Flinders University completed a questionnaire battery. More flow states (r = .34, p < .01) and increased accessibility (r= .21, p < .01) significantly predicted longer gaming duration, whereas greater parental regulation (r = - .15, p < .01) predicted fewer hours spent playing video games. In addition, higher perception of the negative consequences of risk-taking (r = .14, p < .01) significantly predicted later bedtimes in adolescence. The relationship between flow and bedtime during adolescence was fully mediated by gaming duration (b = .142, p < .001), whereas the association between parental regulation and bedtime was independent of gaming duration. Flow and parental regulation of media were identified as the key points for clinical intervention to decrease the duration of gaming of adolescents, thus promoting earlier bedtimes.

Parental influences on adolescent video game play: a study of accessibility, rules, limit setting, monitoring, and cybersafety.

Adolescents' video gaming is increasing at a rapid rate. Yet, little is known about what factors contribute toward more hours of gaming per week, as well as what factors may limit or protect adolescents from excessive gaming. The aim of the present study was to examine associations between adolescents' accessibility to video gaming devices, the locations played (i.e., bedroom, shared rooms), parental regulation of technology use, and the amount of hours spent video gaming during the week (weekdays vs. weekends). Adolescents (N=422; age 16.3±2.0 years, 41% male) completed an online questionnaire battery, including demographics, video gaming behaviors (e.g., hours played weekdays/weekends, time of day played, devices owned, locations played, etc.), and a questionnaire measuring aspects of parents' regulation of game playing (e.g., rules, limit setting, co-gaming). Accessibility to the adolescents' own devices, but not shared devices or device portability, was predictive of hours gaming on weekdays and weekends. Location (i.e., bedroom) was associated with increased gaming across the week. Parents discussing cybersafety was predictive of lower hours of gaming (weekdays and weekends). However, limit setting, monitoring, and co-gaming showed no significant effects. Adolescents' access to their own gaming equipped devices, as well as gaming in their bedrooms, were linked to increased hours of gaming. The findings suggest that in order to curb the increase in hours gaming, parents are advised to delay the ownership of adolescents' devices, encourage use in shared rooms, and discuss aspects of cybersafety with their teenage children.

Serotonin in microdialysate from the mediobasal hypothalamus increases after progesterone administration to estrogen primed macaques.

Estrogen and progesterone act on gene and protein expression in serotonin neurons in a manner that suggests serotonin neurotransmission should increase. However, measurement of extracellular serotonin in macaques was lacking. Elevated prolactin secretion can be an indicator of increased serotonergic function and prolactin is increased by combined estrogen and progesterone treatment. We examined extracellular serotonin by microdialysis in a well-characterized macaque model of steroid-induced prolactin secretion. Monkeys were fitted with 2 guide tubes directed to the arcuate nucleus of the hypothalamus. Samples (75 microl/15-minute interval) were obtained via a tether-swivel device through sample lines into an adjoining room. Serotonin was measured with a modified commercial enzyme linked immunoassay (ELISA) kit. Fenfluramine infused through the probe (300 microM for 2 h; n=2 trials) or administered intravenously (2.5 mg/kg; n=2 trials) caused a marked increase in extracellular serotonin and verified the efficacy of the procedure. Three monkeys were maintained with an estrogen implant for 2 weeks. Each monkey was injected with 20 mg of progesterone s.c. in oil at 1500 h; microdialysis was initiated the next morning and samples were obtained for 24 h. There was a significant increase in serotonin between 40 and 43 h after the progesterone injection (P<0.001, ANOVA). Serotonin averaged 59+/-1 pg/sample from 18-30 h post-progesterone injection, and averaged 76+/-2 pg/sample from 30-48 h post-progesterone injection (P<0.0001; t-test). Since the increase in serotonin is delayed by approximately 40 h after progesterone-injection, we speculate that the action of progesterone may involve either nuclear progestin receptors or membrane progestin receptors.

Nuclear factor kappa B in the dorsal raphe of macaques: an anatomical link for steroids, cytokines and serotonin.

OBJECTIVE: Nuclear factor kappa B (NFkappaB) is a transcription factor that activates gene expression in response to proinflammatory cytokines, and elevated cytokines are associated with depression, which has a serotonergic component. We questioned (1) whether serotonin neurons contain NFkappaB, (2) whether NFkappaB detection with immunocytochemistry is changed in the dorsal raphe nucleus (DRN) by ovarian hormone treatment and (3) whether ovarian hormones regulate midbrain NFkappaB gene or protein expression. METHODS: Monkeys were spayed and treated with placebo, estrogen (E), progesterone (P) or E+P for 1 month (n = 4 animals/treatment group), and the midbrain was harvested for immunocytochemistry and stereology. An antibody that detects nuclear location-specific (NLS)-NFkappaB p65 was applied, and the numbers of NLS-NFkappaB-immunopositive cells were counted in 9 sections of the DRN. Additional monkeys were used for Western blot analysis and quantitative reverse transcription-polymerase chain reaction (RT-PCR) for NFkappaB p65. RESULTS: In placebo-treated macaques, neurons were double-immunostained for serotonin and nuclear NFkappaB p65 throughout the DRN. The mean total number of NFkappaB-positive cells equalled 2178 (and standard error of the mean [SEM] 129) in the placebo group, 1631 (SEM 221) in the E-treated group, 2314 (SEM 186) in the P-treated group and 1162 (SEM 100) in the E+P-treated group (analysis of variance p = 0.003). The E-treated and E+P-treated groups had a significantly lower density of cells stained positive for NFkappaB than the placebo or P-treated groups (post hoc). Unmasking of NLS-NFkappaB immunostaining in the DRN revealed dense immunostaining in the cytoplasm of large dorsal raphe neurons. There was no difference between treatment groups in the amount of NFkappaB p65 detected by Western blot or in the relative expression of NFkappaB p65 mRNA with quantitative RT-PCR. CONCLUSIONS: These observations are consistent with the notion that gene and protein expression of NFkappaB are constitutive but that ovarian hormones can decrease the nuclear location of NFkappaB in dorsal raphe neurons and, thereby, decrease the ability of NFkappaB to drive gene expression in response to cytokines.

Effects of ovarian steroids and raloxifene on proteins that synthesize, transport, and degrade serotonin in the raphe region of macaques.

In the monkey dorsal raphe, we reported that 1-month (mo) of estrogen replacement, with or without progesterone supplementation for 14 days, significantly increased tryptophan hydroxylase-1 (TPH-1) mRNA; decreased serotonin reuptake transporter (SERT) mRNA and decreased monoamine oxidase (MAO)-A mRNA, but had no effect on MAO-B mRNA. Here, we questioned what effect would 1 or 5 mo of ovarian hormones or the selective estrogen receptor modulator (SERM), raloxifene, have on TPH protein and phosphorylation, and on protein expression of SERT, MAO-A or MAO-B? Raloxifene antagonizes estrogen in breast or uterus, but estrogen-like activities in the brain have been reported. Cytoplasmic and membrane extracts of the dorsal raphe region were processed for Western blotting. TPH, phosphoserine, SERT, MAO-A, and MAO-B were detected with specific antibodies. The optical densities of the signals were measured with NIH image and analyzed by ANOVA. Both 1 and 5 mo of estrogen, with or without progesterone, and 5 mo of raloxifene significantly increased TPH protein. Administration for 5 mo of estrogen plus progesterone and raloxifene also increased TPH phosphorylation. Estrogen, with or without progesterone, for 1 mo had no effect on SERT protein. However, 5 mo of estrogen and 5 mo of raloxifene increased SERT protein. Estrogen alone or combined with progesterone for 1 mo caused a significant reduction in MAO-A. Yet, after 5 mo of the same treatments, MAO-A was not different from spayed controls. Estrogen alone had no effect on MAO-B. However, the addition of progesterone significantly increased MAO-B. Raloxifene for 5 mo had no effect on MAO-A or MAO-B. Thus, to various extents, estrogen, progesterone, and raloxifene may increase serotonin production and transport. The expression of the degradative enzymes suggests a complex combination of gene transcription, post-transcriptional processing, and substrate feedback mechanisms.

Ultrasound-assisted lipoplasty.

The use of ultrasound-assisted lipoplasty (UAL) to assist in the removal of subcutaneous fat has been practiced in Europe for nearly 15 years and over the last 7 years has gained popularity in the United States. Liposuction is now one of the most commonly performed cosmetic procedures by board-certified plastic surgeons. This article will review the UAL procedure, its history, regulatory issues, instrumentation and equipment needed. It will also review changes and recent updates, clinical protocol, complications, and future considerations.