Resilience and distress among young adults with chronic health conditions: A longitudinal study.

OBJECTIVES: To test the beneficial associations of a resilient personality prototype among emerging adults with chronic health conditions (CHC) over an 8-year period. DESIGN: Longitudinal, prospective observation study. METHODS: Data obtained from emerging adults in the Add Health project with a CHC and completed study measures at two time points (286 men, 459 women) were examined. Cluster analysis was used to identify a resilient personality prototype at the first time point, as defined in the Block model of personality. Differences between those with a resilient and non-resilient prototype were examined. A structural equation model (SEM) tested the association of a resilience prototype with positive affect, perceived control and family relationships in predicting distress over time. RESULTS: A resilient personality profile was identified (n = 256). These individuals reported higher positive affect, greater perceived control and less distress at both measurement occasions than those without this profile (n = 489). Women reported more distress than men. SEM revealed the relationship of a resilient prototype to distress was explained by its beneficial association with positive affect and perceived control at the first assessment, and through its beneficial association with perceived control 8 years later. Gender independently predicted distress. CONCLUSIONS: A resilient personality prototype appears to operate through its beneficial association with perceived control to prospectively predict distress reported by emerging adults with CHC. The self-regulatory properties theoretically associated with a resilient personality prototype may function through perceptions of control which, in turn, prevent prolonged experiences of distress. Clinical implications are considered.

Temperature-dependent Development, Survival, and Oviposition of Laricobius osakensis (Coleoptera: Derodontidae): A Specialist Predator of Adelges tsugae (Hemiptera: Adelgidae).

A predator, Laricobius osakensis Montgomery and Shiyake (Coleoptera: Derodontidae), is being mass-produced and released for the biological control of the invasive hemlock woolly adelgid (HWA), Adelges tsugae Annand (Hemiptera: Adelgidae). To better understand and predict the seasonality of this predator in North America, the development and reproduction of L. osakensis were evaluated at constant temperatures ranging from 5 to 22°C. The predicted seasonal biology was compared with data from field collections. L. osakensis did not complete development from egg to adult at the two lowest temperatures tested, 5 and 8°C, but did so at the highest temperature of 22°C. The minimum development thresholds were estimated for eggs (4.2°C), first (1.8°C), second (5.5°C), third (4.6°C), and fourth instar (4.1°C), prepupa (3.6°C), and pupa (7.5°C). Oviposition rates were significantly greater at 5 and 10°C than at 20 and 25°C. Head capsule width significantly increased for each of the four larval instars with a mean of 0.19, 0.26, 0.35, and 0.44 mm, respectively. Laboratory and field data were used to develop a phenology forecasting model to predict the occurrence of all developmental stages of L. osakensis. This model will allow land managers to more accurately predict the optimal timing for L. osakensis larval sampling throughout its established range.

mTORC1 promotes denervation-induced muscle atrophy through a mechanism involving the activation of FoxO and E3 ubiquitin ligases.

Skeletal muscle mass and function are regulated by motor innervation, and denervation results in muscle atrophy. The activity of mammalian target of rapamycin complex 1 (mTORC1) is substantially increased in denervated muscle, but its regulatory role in denervation-induced atrophy remains unclear. At early stages after denervation of skeletal muscle, a pathway involving class II histone deacetylases and the transcription factor myogenin mediates denervation-induced muscle atrophy. We found that at later stages after denervation of fast-twitch muscle, activation of mTORC1 contributed to atrophy and that denervation-induced atrophy was mitigated by inhibition of mTORC1 with rapamycin. Activation of mTORC1 through genetic deletion of its inhibitor TSC1 (tuberous sclerosis complex 1) sensitized mice to denervation-induced muscle atrophy and suppressed the kinase activity of Akt, leading to activation of FoxO transcription factors and increasing the expression of genes encoding E3 ubiquitin ligases atrogin [also known as MAFbx (muscle atrophy F-box protein)] and MuRF1 (muscle-specific ring finger 1). Rapamycin treatment of mice restored Akt activity, suggesting that the denervation-induced increase in mTORC1 activity was producing feedback inhibition of Akt. Genetic deletion of the three FoxO isoforms in skeletal muscle induced muscle hypertrophy and abolished the late-stage induction of E3 ubiquitin ligases after denervation, thereby preventing denervation-induced atrophy. These data revealed that mTORC1, which is generally considered to be an important component of anabolism, is central to muscle catabolism and atrophy after denervation. This mTORC1-FoxO axis represents a potential therapeutic target in neurogenic muscle atrophy.

Diaphragm muscle atrophy in the mouse after long-term mechanical ventilation.

INTRODUCTION: Mechanical ventilation (MV) is a life-saving measure, but full ventilator support causes ventilator-induced diaphragm atrophy (VIDA). Previous studies of VIDA have relied on human biopsies or a rat model. If MV can induce diaphragm atrophy in mice, then mechanistic study of VIDA could be explored via genetic manipulation. RESULTS: We show that 18 hours of MV in mice results in a 15% loss of diaphragm weight and a 17% reduction in fiber cross-sectional area. Important catabolic cascades are activated in this mouse model: transcription of the ubiquitin ligases, atrogin and MuRF1, and the apoptotic marker, Bim, are increased; the marker of autophagy, LC3, is induced at the protein level and shows a punctate distribution in diaphragm muscle fibers. CONCLUSIONS: This mouse model recapitulates the key pathophysiological findings of other models of VIDA, and it will enable the genetic manipulation required to fully explore the mechanisms underlying this important process.

Bronchoscopy findings in children and young adults with tracheostomy due to congenital anomalies and neurological impairment.

The aim of this study was to examine bronchoscopy findings for children and young adults with long-term tracheostomies due to congenital anomalies and neurological impairment and identify characteristics associated with abnormal bronchoscopic findings. We conducted a retrospective study of 128 bronchoscopy cases (81 children) at a pediatric rehabilitation center. Thirty-eight cases (30%) had normal findings and 14 children (17% of all children) were decannulated following bronchoscopy. Ninety cases (70% of cases) had abnormal findings (e.g. granulomas, airway inflammation, fixed obstruction). An acute indication for bronchoscopy was the strongest predictor of an abnormal finding, while age (younger) and diagnosis (multiple congenital anomalies (MCA)) also were associated with abnormalities. For a subsample of children undergoing bronchoscopy for routine surveillance (n= 90), underlying diagnosis (MCA) was the strongest predictor of an abnormal finding, while younger age contributed slightly. These findings add to the limited literature describing bronchoscopic findings in children and youth with tracheostomies due to congenital anomalies or neurological impairment. These findings may be useful for rehabilitation clinicians in determining care needs for children with long-term tracheostomy.