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Heavy binge drinking in adolescence can cause long-term cognitive and behavioral dysfunctions. Recent experimental evidence indicates the participation of immune system activation in the effects of ethanol in the adolescent brain and suggests gender differences. The present study aims to assess plasma cytokine and chemokine levels in male and female adolescents and young adults during acute alcohol intoxication and to correlate these results with the toll-like receptor 4 (TLR4) response. The potential role of the TLR4 signaling response was also assessed in plasma and prefrontal cortex (PFC) of adolescent wild-type and TLR4-knockout male and female mice with binge ethanol treatment. The results showed that alcohol intoxication increased the plasma levels of several cytokine and chemokine [interferon-γ, interleukin (IL)-10, IL-17A, IL-1β, IL-2, IL-4, IL-6, IL-8, fractalkine, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein 1α (MIP-1α)] and the upregulation of TLR4 mRNA levels occurred in intoxicated females, while elevation of colony-stimulating factor was only observed in the plasma of males. In wild-type female adolescent mice, intermittent ethanol treatment increased the levels of several cytokines (IL-17A and IL-1β) and chemokines (MCP-1, MIP-1α and fractalkine) in PFC and in serum (IL-17A, MCP-1 and MIP-1α), but significant differences in the fractalkine levels in PFC were observed only in male mice. No changes in serum or prefrontal cortex cytokine and chemokine levels were noted in ethanol-treated male or female TLR4-knockout mice. Our findings revealed that females are more vulnerable than males to inflammatory effects of binge ethanol drinking and suggested that TLR4 is an important target of ethanol-induced inflammation and neuroinflammation in adolescence. [ABSTRACT FROM AUTHOR]

Adolescent development is accompanied by profound changes in the timing and amounts of sleep and wakefulness. Many aspects of these changes result from altered psychosocial and life-style circumstances that accompany adolescence. The maturation of biological processes regulating sleep/wake systems, however, may be strongly related to the sleep timing and amount during adolescence℄either as "compelling" or "permissive" factors. The two- process model of sleep regulation posits a fundamental sleep-wake homeostatic process (process S) working in concert with the circadian biological timing system (process C) as the primary intrinsic regulatory factors. How do these systems change during adolescence? We present data from adolescent participants examining EEG markers of sleep homeostasis to evaluate whether process S shows maturational changes permissive of altered sleep patterns across puberty. Our data indicate that certain aspects of the homeostatic system are unchanged from late childhood to young adulthood, while other features change in a manner that is permissive of later bedtimes in older adolescents. We also show alterations of the circadian timing system indicating a possible circadian substrate for later adolescent sleep timing. The circadian parameters we have assessed include phase, period, melatonin secretory pattern, light sensitivity, and phase relationships, all of which show evidence of changes during pubertal development with potential to alter sleep patterns substantially. However the changes are mediated—whether through process S, process C, or by a combination—many adolescents have too little sleep at the wrong circadian phase. This pattern is associated with increased risks for excessive sleepiness, difficulty with mood regulation, impaired academic performance, learning difficulties, school tardiness and absenteeism, and accidents and injuries. [ABSTRACT FROM AUTHOR]

To clarify the clinical usefulness of the second derivative of the waveform of the fingertip photoplethysmogram (SDPTG), we examined the relationship between the pattern of the SDPTG waveform and risk factors related to atherosclerosis in 1,495 boys and girls aged 9–17 years. The fingertip photoplethysmogram and its second derivative wave were automatically recorded from the second digit of the right hand with the subjects lying in a supine position. The SDPTG waveform consisted of a, b, c and d waves in systole and an e wave in diastole. The heights of the a and d waves were measured from the baseline, and the ratio of the height of the d wave to that of the a wave (d/a ratio) was calculated. The d/a ratio had a negative correlation with the systolic (SBP) and diastolic blood pressures (DBP), atherogenic index (AI) and immunoreactive insulin concentrations (IRI) after adjustment for age. Multiple linear regression analysis revealed that the d/a ratio was associated more with body height than the risk factors for atherosclerosis in boys and girls at the growth period. The effect of sex- and height-specific cutoff values of the 10th percentile for the d/a ratio was therefore tested. The results showed that subjects with d/a ratios lower than the 10th percentile had significantly higher SBP, DBP, AI and IRI values compared to those with higher d/a ratios. These findings suggest that differences in the length of the vascular system, which are related to increases in body height, may modify the SDPTG waveform pattern during adolescence. When the body height as well as age and sex is adequately allowed for, the d/a ratio may be useful for the evaluation of arterial distensibility and for identification of individuals at an increased risk of developing atherosclerosis. [ABSTRACT FROM AUTHOR]

The present study examines the relationship between femur length and stature in children between the ages of 8 and 18 years. In previous investigations, my colleagues and I reported the surprising finding that femur length bears a nearly constant relationship to stature in adult humans regardless of ethnicity or gender. This earlier study revealed that the femur/stature ratio averages 26.74% in adult humans, and that using the ratio to predict stature from femur length yields remarkably accurate estimates. The current study shows that femur/stature ratios of children between the ages of 8 and 11 differ significantly from their older counterparts. Between the ages of 12 and 18, there are no significant differences due to age in the femur/stature ratio; however, there are significant differences in this age group attributable to gender. This study also shows that the worldwide average adult femur/stature ratio does not adequately describe children in this age range. This study strongly documents the adolescent growth spurt in the femur/stature ratios of both males and females at the precise time one would expect to see the spurt occur (10-12 in females; 12-14 in males). This growth follows a nearly identical trajectory in both genders, with relative femur growth dominating before the peak years of the growth spurt, and relative stature growth dominating afterward. This accounts for the ratio's rise to maximum values just before peak growth, and its decline toward the adult ratio thereafter. These findings require us to use separate adolescent femur/stature ratios of 27.16 (females) and 27.44 (males) to estimate the stature of children between the ages of 12 and 18. Preliminary testing shows these ratios to be more accurate in estimating stature than the properly selected Trotter and Gleser adult regression equation. Use of the adolescent male ratio with the Homo erectus juvenile WT 15000 results in a lower stature estimate (157.4 cm) than previously reported. It is suggested that continued testing of the ratio occur, but that the values herein derived may be useful in routine forensic cases involving children in this age range, and with subadult paleontological specimens. [ABSTRACT FROM AUTHOR]

Current studies evidence the role of miRNAs in extracellular vesicles (EVs) as key regulators of pathological processes, including neuroinflammation and neurodegeneration. As EVs can cross the blood–brain barrier, and EV miRNAs are very stable in peripheral circulation, we evaluated the potential gender differences in inflammatory-regulated miRNAs levels in human and murine plasma EVs derived from alcohol-intoxicated female and male adolescents, and whether these miRNAs could be used as biomarkers of neuroinflammation. We demonstrated that while alcohol intoxication lowers anti-inflammatory miRNA (mir-146a-5p, mir-21-5p, mir-182-5p) levels in plasma EVs from human and mice female adolescents, these EV miRNAs increased in males. In mice brain cortices, ethanol treatment lowers mir-146a-5p and mir-21-5p levels, while triggering a higher expression of inflammatory target genes (Traf6, Stat3, and Camk2a) in adolescent female mice. These results indicate, for the first time, that female and male adolescents differ as regards the ethanol effects associated with the inflammatory-related plasma miRNAs EVs profile, and suggest that female adolescents are more vulnerable than males to the inflammatory effects of binge alcohol drinking. These findings also support the view that circulating miRNAs in EVs could be useful biomarkers for screening ethanol-induced neuroinflammation and brain damage in adolescence. [ABSTRACT FROM AUTHOR]