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Dive into the research topics where Thornton B.A. Mason is active.

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Featured researches published by Thornton B.A. Mason.


Journal of Sleep Research | 2010

Shortened sleep duration does not predict obesity in adolescents

Christina J. Calamaro; Sunhee Park; Thornton B.A. Mason; Carole L. Marcus; Terri E. Weaver; Allan I. Pack; Sarah J. Ratcliffe

Obesity continues to be a major public health issue. In adolescents, there are limited studies on the relationship between obesity and sleep duration. We found hypothesized that an average sleep duration of <6 h in adolescents was associated with obesity. Data were from the National Longitudinal Study of Adolescent Health (ADD Health); a survey of 90 000 youths, aged 12–18 years; surveyed in several waves. The sample population for our study was 13 568. Weighted multiple logistic regression was used to identify the relationship between obesity at Wave II and sleep duration, having adjusted for skipping breakfast ≥ 2/week; race, gender, parental income, TV ≥ 2 h per day, depression, and obesity at Wave I. At Wave I, the mean age was 15.96 ± 0.11 years; mean sleep hours were 7.91 ± 0.04. At Waves I and II, respectively, 10.6 and 11.2% of adolescents were obese. Adjusted analyses suggest that the effect of shortened sleep duration in Wave I was not significantly predictive of obesity in Wave II (P < 0.218). Longitudinally, depression and TV ≥ 2  h per day at Wave I was associated with a higher risk of obesity at Wave II in adjusted analyses. Depressed adolescents were almost twice as likely to be obese (OR = 1.84, 95% CI = 1.25–2.72); adolescents who watched TV ≥ 2 h per day were 37% more likely to be obese (OR = 1.37, 95% CI = 1.09–1.72). Environmental factors including TV ≥ 2 h per day and depression were significantly associated with obesity; shortened sleep duration was not. Future longitudinal studies in adolescents are needed to determine whether timing of television watching directly influences sleep patterns and, ultimately, obesity.


Journal of Developmental and Behavioral Pediatrics | 2011

The Effects of Napping on Cognitive Function in Preschoolers

Janet Lam; E. Mark Mahone; Thornton B.A. Mason; Steven M. Scharf

Objective: To determine the relationship between napping and cognitive function in preschool-aged children. Methods: Daytime napping, nighttime sleep, and cognitive function were assessed in 59 typically developing children aged 3 to 5 years, who were enrolled in full-time childcare. Participants wore an actigraphy watch for 7 days to measure sleep and napping patterns and completed neuropsychological testing emphasizing attention, response control, and vocabulary. Parents of participants completed behavior ratings and sleep logs during the study. Sleep/wake cycles were scored with the Sadeh algorithm. Results: Children who napped more on weekdays were also more likely to nap during weekends. Weekday napping and nighttime sleep were inversely correlated, such that those who napped more slept less at night, although total weekday sleep remained relatively constant. Weekday napping was significantly (negatively) correlated with vocabulary and auditory attention span, and weekday nighttime sleep was positively correlated with vocabulary. Nighttime sleep was also significantly negatively correlated with performance, such that those who slept less at night made more impulsive errors on a computerized go/no-go test. Conclusions: Daytime napping is actually negatively correlated with neurocognitive function in preschoolers. Nighttime sleep seems to be more critical for development of cognitive performance. Cessation of napping may serve as a developmental milestone of brain maturation. Children who nap less do not appear to be sleep deprived, especially if they compensate with increased nighttime sleep. An alternative explanation is that children who sleep less at night are sleep deprived and require a nap. A randomized trial of nap restriction would be the next step in understanding the relationship between napping and neurocognitive performance.


Chest | 2012

Upper airway lymphoid tissue size in children with sickle cell disease.

Temima Strauss; Sanghun Sin; Carole L. Marcus; Thornton B.A. Mason; Joseph M. McDonough; Julian L. Allen; Jason B. Caboot; Cheryl Y. Bowdre; Abbas F. Jawad; Kim Smith-Whitley; Kwaku Ohene-Frempong; Allan I. Pack; Raanan Arens

BACKGROUND The prevalence of obstructive sleep apnea syndrome (OSAS) is higher in children with sickle cell disease (SCD) as compared with the general pediatric population. It has been speculated that overgrowth of the adenoid and tonsils is an important contributor. METHODS The current study used MRI to evaluate such an association. We studied 36 subjects with SCD (aged 6.9 ± 4.3 years) and 36 control subjects (aged 6.6 ± 3.4 years). RESULTS Compared with control subjects, children with SCD had a significantly smaller upper airway (2.8 ± 1.2 cm(3) vs 3.7 ± 1.6 cm(3), P < .01), and significantly larger adenoid (8.4 ± 4.1 cm(3) vs 6.0 ± 2.2 cm(3), P < .01), tonsils (7.0 ± 4.3 cm(3) vs 5.1 ± 1.9 cm(3), P < .01), retropharyngeal nodes (3.0 ± 1.9 cm(3) vs 2.2 ± 0.9 cm(3), P < .05), and deep cervical nodes (15.7 ± 5.7 cm(3) vs 12.7 ± 4.0 cm(3), P < .05). Polysomnography showed that 19.4% (seven of 36) of children with SCD had OSAS compared with 0% (zero of 20) of control subjects (P < .05) and that in children with SCD the apnea-hypopnea index correlated positively with upper airway lymphoid tissues size (r = 0.57, P < 001). In addition, children with SCD had lower arterial oxygen saturation nadir (84.3% ± 12.3% vs 91.2% ± 4.2%, P < .05), increased peak end-tidal CO(2) (53.4 ± 8.5 mm Hg vs 42.3 ± 5.3 mm Hg, P < .001), and increased arousals (13.7 ± 4.7 events/h vs 10.8 ± 3.8 events/h, P < .05). CONCLUSIONS Children with SCD have reduced upper airway size due to overgrowth of the surrounding lymphoid tissues, which may explain their predisposition to OSAS.


American Journal of Medical Genetics Part A | 2012

Subtelomeric deletion of chromosome 10p15.3: clinical findings and molecular cytogenetic characterization.

Cheryl DeScipio; Laura K. Conlin; Jill A. Rosenfeld; James Tepperberg; Romela Pasion; Ankita Patel; Marie McDonald; Swaroop Aradhya; Darlene Ho; Jennifer L. Goldstein; Marianne McGuire; Surabhi Mulchandani; Livija Medne; Rosemarie Rupps; Alvaro H. Serrano; Erik C. Thorland; Anne C.-H. Tsai; Yvonne Hilhorst-Hofstee; Claudia Ruivenkamp; Hilde Van Esch; Marie Claude Addor; Danielle Martinet; Thornton B.A. Mason; Dinah Clark; Nancy B. Spinner; Ian D. Krantz

We describe 19 unrelated individuals with submicroscopic deletions involving 10p15.3 characterized by chromosomal microarray (CMA). Interestingly, to our knowledge, only two individuals with isolated, submicroscopic 10p15.3 deletion have been reported to date; however, only limited clinical information is available for these probands and the deleted region has not been molecularly mapped. Comprehensive clinical history was obtained for 12 of the 19 individuals described in this study. Common features among these 12 individuals include: cognitive/behavioral/developmental differences (11/11), speech delay/language disorder (10/10), motor delay (10/10), craniofacial dysmorphism (9/12), hypotonia (7/11), brain anomalies (4/6) and seizures (3/7). Parental studies were performed for nine of the 19 individuals; the 10p15.3 deletion was de novo in seven of the probands, not maternally inherited in one proband and inherited from an apparently affected mother in one proband. Molecular mapping of the 19 individuals reported in this study has identified two genes, ZMYND11 (OMIM 608668) and DIP2C (OMIM 611380; UCSC Genome Browser), mapping within 10p15.3 which are most commonly deleted. Although no single gene has been identified which is deleted in all 19 individuals studied, the deleted region in all but one individual includes ZMYND11 and the deleted region in all but one other individual includes DIP2C. There is not a clearly identifiable phenotypic difference between these two individuals and the size of the deleted region does not generally predict clinical features. Little is currently known about these genes complicating a direct genotype/phenotype correlation at this time. These data however, suggest that ZMYND11 and/or DIP2C haploinsufficiency contributes to the clinical features associated with 10p15 deletions in probands described in this study.


Pediatric Pulmonology | 2012

Non-Invasive Measurements of Carboxyhemoglobin and Methemoglobin in Children with Sickle Cell Disease

Jason B. Caboot; Abbas F. Jawad; Joseph M. McDonough; Cheryl Y. Bowdre; Raanan Arens; Carole L. Marcus; Thornton B.A. Mason; Kim Smith-Whitley; Kwaku Ohene-Frempong; Julian L. Allen

Assessment of oxyhemoglobin saturation in patients with sickle cell disease (SCD) is vital for prompt recognition of hypoxemia. The accuracy of pulse oximeter measurements of blood oxygenation in SCD patients is variable, partially due to carboxyhemoglobin (COHb) and methemoglobin (MetHb), which decrease the oxygen content of blood. This study evaluated the accuracy and reliability of a non‐invasive pulse co‐oximeter in measuring COHb and MetHb percentages (SpCO and SpMet) in children with SCD. We hypothesized that measurements of COHb and MetHb by non‐invasive pulse co‐oximetry agree within acceptable clinical accuracy with those made by invasive whole blood co‐oximetry. Fifty children with SCD‐SS underwent pulse co‐oximetry and blood co‐oximetry while breathing room air. Non‐invasive COHb and MetHb readings were compared to the corresponding blood measurements. The pulse co‐oximeter bias was 0.1% for COHb and −0.22% for MetHb. The precision of the measured SpCO was ±2.1% within a COHb range of 0.4–6.1%, and the precision of the measured SpMet was ±0.33% within a MetHb range of 0.1–1.1%. Non‐invasive pulse co‐oximetry was useful in measuring COHb and MetHb levels in children with SCD. Although the non‐invasive technique slightly overestimated the invasive COHb measurements and slightly underestimated the invasive MetHb measurements, there was close agreement between the two methods. Pediatr Pulmonol. 2012. 47:808–815.


Nursing Clinics of North America | 2002

Sleep disorders in children

Teresa Ward; Thornton B.A. Mason

Sleep disorders are common in childhood, and may affect multiple aspects of a childs life and the lives of other family members. A sleep disorder assessment should begin with detailed sleep history and a review of interrelated health issues. Factors contributing to disturbed sleep may be discovered or confirmed by a thorough physical examination. Thereafter, appropriate ancillary testing can provide support for a specific clinical diagnosis. The spectrum of childhood sleep disorders includes OSA, narcolepsy, RLS/PLMD, sleep onset association disorder, and parasomnias. Diagnosing sleep disorders in children remains a challenge; however, a multidisciplinary approach may provide an opportunity for productive collaboration and, thereby, more effective patient management. Centers treating pediatric sleep disorders may include providers from a variety of disciplines in pediatric healthcare, such as child psychology, pulmonology, neurology, psychiatry, nursing, and otolaryngology. Over the last decade, research in pediatric sleep disorders has expanded greatly, paralleled by an increased awareness of the importance of adequate, restorative sleep in childhood.


Pediatric Neurology | 2008

Rapid Eye Movement Latency in Children and Adolescents

Thornton B.A. Mason; Laurel Teoh; Kristen Calabro; Joel Traylor; Laurie Karamessinis; Brian Schultz; John Samuel; Paul R. Gallagher; Carole L. Marcus

Rapid eye movement sleep distribution changes during development, but little is known about rapid eye movement latency variation in childhood by age, sex, or pathologic sleep states. We hypothesized that: (1) rapid eye movement latency would differ in normal children by age, with a younger cohort (1-10 years) demonstrating shorter rapid eye movement latency than an older group (>10-18 years); (2) rapid eye movement latency in children would differ from typical adult rapid eye movement latency; and (3) intrinsic sleep disorders (narcolepsy, pediatric obstructive sleep apnea syndrome) would disrupt normal developmental patterns of rapid eye movement latency. A retrospective chart review included data from clinic visits and of rapid eye movement latency and other parameters measured by overnight polysomnography. Participants included 98 control children, 90 children with obstructive sleep apnea syndrome, and 13 children with narcolepsy. There were no statistically significant main effects of age category or sex on rapid eye movement latency. Rapid eye movement latency, however, exhibited a significant inverse correlation with age within the older control children. Healthy children exhibited rapid eye movement latencies significantly longer than adults. Normal control patients demonstrated significantly longer rapid eye movement latency than obstructive sleep apnea syndrome and narcolepsy patients.


Sleep | 2014

Prevalence of Periodic Limb Movements during Sleep in Normal Children

Carole L. Marcus; Joel Traylor; Paul R. Gallagher; Lee J. Brooks; Jingtao Huang; Dorit Koren; Lorraine E. Levitt Katz; Thornton B.A. Mason; Ignacio E. Tapia

STUDY OBJECTIVES Although the American Academy of Sleep Medicine (AASM) mandates that periodic limb movements during sleep (PLMS) be scored on every polysomnogram, and considers a periodic limb movement index (PLMI) > 5/h abnormal in children, there is a lack of community-derived data regarding the prevalence of PLMS in children, and no data to support this cutoff value. Therefore, the aim of this study was to determine the prevalence of PLMS in a sample of normal children. DESIGN Retrospective study. PARTICIPANTS 195 healthy, non-snoring children aged 5-17 years, recruited from the community, who underwent polysomnography for research purposes. METHODS PLMS were scored using the AASM 2007 criteria. MEASUREMENTS AND RESULTS The group age (median [IQR]) was 12.9 [10-15] years, and 58% were male. Sleep architecture was normal, and the obstructive apnea hypopnea index was 0.1 [0-0.3]/h. The median PLMI was 0/h, ranging from 0 to 35.5/h. Fifteen (7.7%) subjects had a PLMI > 5/h, and only 3 (1.5%) met the adult pathologic criterion of more than 15/h. Use of the 95th percentile PLMI cutoff of 7.2/h produced little difference in categorization between groups. Children with a PLMI > 5/h had a higher arousal index than those with a lower PLMI (11.6 [8.8-14.6] vs 8.1 [6.1-9.9]/h, respectively, P = 0.003). CONCLUSIONS This study provides normative data to the field and supports the clinical periodic limb movement index cutoff of > 5/h based on both prevalence and the correlate of increased sleep fragmentation. Periodic limb movements during sleep are infrequent in normal children recruited from the community. CITATION Marcus CL, Traylor J, Gallagher PR, Brooks LJ, Huang J, Koren D, Katz L, Mason TB, Tapia IE. Prevalence of periodic limb movements during sleep in normal children.


Behavioral Sleep Medicine | 2011

Defining the Roles of Actigraphy and Parent Logs for Assessing Sleep Variables in Preschool Children

Janet Lam; E. Mark Mahone; Thornton B.A. Mason; Steven M. Scharf

Actigraphy provides a non-invasive objective means to assess sleep–wake cycles. In young children, parent logs can also be useful for obtaining sleep–wake information. The authors hypothesized that actigraphy and parent logs were both equally valid instruments in healthy preschool-aged children. The authors studied 59 children aged 3 to 5 years in full-time day care. Each child was screened for medical problems and developmental delays before being fitted with an actigraphy watch, which was worn for 1 week. Parents maintained logs of sleep and wakefulness during the same period, with input from day care workers. In general, parents overestimated the amount of nighttime sleep measured by actigraphy by 13% to 22% (all significant). Although there was no difference in sleep onset times, parents reported later rise times on the weekend and fewer nighttime awakenings. There was no significant difference between parent logs and actigraphy with regard to daytime napping. The authors conclude that parent logs are best utilized in assessing daytime sleep and sleep onset, whereas actigraphy should be used to assess nighttime sleep and sleep offset time.


British Journal of Haematology | 2013

Respiratory muscle force and lung volume changes in a population of children with sickle cell disease

Bruce A. Ong; Jason B. Caboot; Abbas F. Jawad; Joseph M. McDonough; Tannoa Jackson; Raanan Arens; Carole L. Marcus; Kim Smith-Whitley; Thornton B.A. Mason; Kwaku Ohene-Frempong; Julian L. Allen

Sickle cell disease (SCD) is a disorder known to impact the respiratory system. We sought to identify respiratory muscle force and lung volume relationships in a paediatric SCD population. Thirty‐four SCD‐SS subjects underwent pulmonary function testing. Height, weight, age, and gender‐adjusted percent predicted maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) values were compared to spirometry and lung volumes. Statistical analyses were performed using Pearsons correlation coefficient and paired two‐tailed t‐test. The mean ± standard deviation (SD) MIP and MEP was 69·6 ± 31·6 cm H2O and 66·9 ± 22·9 cm H2O, respectively, and mean ± SD percent predicted MIP (101·3 ± 45·9) exceeded MEP (72·1 ± 26·0) (P = 0·002). MIP correlated with forced vital capacity (FVC; r = 0·51, P = 0·001) and TLC (r = 0·54, P < 0·0001). MEP also correlated with FVC (r = 0·43, P = 0·011) and total lung capacity (TLC; r = 0·42, P = 0·013). Pearsons correlation coefficient testing yielded relationships between MIP and MEP (r = 0·64, P < 0·0001). SCD‐SS patients showed correlations between respiratory muscle force and lung volume, and reduced percent predicted expiratory muscle force compared to inspiratory muscle force. Respiratory muscle strength may affect lung volumes in these patients, and expiratory muscles may be more susceptible than the diaphragm to SCD‐induced vaso‐occlusive damage.

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Carole L. Marcus

Children's Hospital of Philadelphia

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Raanan Arens

Albert Einstein College of Medicine

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Kwaku Ohene-Frempong

Children's Hospital of Philadelphia

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Abbas F. Jawad

University of Pennsylvania

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Julian L. Allen

University of Pennsylvania

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Kim Smith-Whitley

Children's Hospital of Philadelphia

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Allan I. Pack

University of Pennsylvania

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Paul R. Gallagher

Children's Hospital of Philadelphia

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Brian Schultz

Children's Hospital of Philadelphia

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Cheryl Y. Bowdre

University of Pennsylvania

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