Prediction of obstructive sleep apnea using visual photographic analysis.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) has been historically underdiagnosed and may be associated with grave perioperative complications. The ASA and American Academy of Sleep Medicine recommend OSA screening prior to surgery; however, only a minority of patients are screened. The objective of this study was to determine the proficiency of anesthesiologists, otolaryngologists, and internists at predicting the presence of OSA by visual photographic analysis without the use of a computer program to assist, and determine if prediction accuracy varies by provider type. DESIGN: Prospective case series SETTING: Tertiary care hospital-based academic center PATIENTS: Fifty-six consecutive patients presenting to the sleep laboratory undergoing polysomnography had frontal and lateral photographs of the face and torso taken. INTERVENTIONS: Not applicable. MEASUREMENTS: Polysomnography outcomes and physician ratings. An obstructive apnea hypopnea index (oAHI) ≥15 was considered "positive." Twenty anesthesiologists, 10 otolaryngologists, and 11 internists viewed patient photographs and scored them as OSA "positive" or "negative" before and after being informed of patient comorbidities. MAIN RESULTS: Nineteen patients had an oAHI <15, 18 were ≥15 but <30, and 19 were ≥30. The mean oAHI was 28.7 ± 26.7 events/h (range, 0-125.7), and the mean body mass index was 34.1 ± 9.7 kg/m(2) (range, 17.4-63.7). Overall, providers predicted the correct answer with 61.8% accuracy without knowledge of comorbidities and 62.6% with knowledge (P < .0001). There was no difference between provider groups (P = .307). Prediction accuracy was unrelated to patient age (P = .067), gender (P = .306), or race (P = .087), but was related to body mass index (P = .0002). CONCLUSION: The ability to predict OSA based on visual inspection of frontal and lateral photographs is marginally superior to chance and did not differ by provider type. Knowledge of comorbidities did not improve prediction accuracy.

A Novel Population of Inner Cortical Cells in the Adrenal Gland That Displays Sexually Dimorphic Expression of Thyroid Hormone Receptor-ß1.

The development of the adrenal cortex involves the formation and then subsequent regression of immature or fetal inner cell layers as the mature steroidogenic outer layers expand. However, controls over this remodeling, especially in the immature inner layer, are incompletely understood. Here we identify an inner cortical cell population that expresses thyroid hormone receptor-ß1 (TRß1), one of two receptor isoforms encoded by the Thrb gene. Using mice with a Thrb(b1) reporter allele that expresses lacZ instead of TRß1, ß-galactosidase was detected in the inner cortex from early stages. Expression peaked at juvenile ages in an inner zone that included cells expressing 20-α-hydroxysteroid dehydrogenase, a marker of the transient, so-called X-zone in mice. The ß-galactosidase-positive zone displayed sexually dimorphic regression in males after approximately 4 weeks of age but persisted in females into adulthood in either nulliparous or parous states. T3 treatment promoted hypertrophy of inner cortical cells, induced some markers of mature cortical cells, and, in males, delayed the regression of the TRß1-positive zone, suggesting that TRß1 could partly divert the differentiation fate and counteract male-specific regression of inner zone cells. TRß1-deficient mice were resistant to these actions of T3, supporting a functional role for TRß1 in the inner cortex.

Rewarming from therapeutic hypothermia induces cortical neuron apoptosis in a swine model of neonatal hypoxic-ischemic encephalopathy.

The consequences of therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy are poorly understood. Adverse effects from suboptimal rewarming could diminish neuroprotection from hypothermia. Therefore, we tested whether rewarming is associated with apoptosis. Piglets underwent hypoxia-asphyxia followed by normothermic or hypothermic recovery at 2 hours. Hypothermic groups were divided into those with no rewarming, rewarming at 0.5 °C/hour, or rewarming at 4 °C/hour. Neurodegeneration at 29 hours was assessed by hematoxylin and eosin staining, TUNEL assay, and immunoblotting for cleaved caspase-3. Rewarmed piglets had more apoptosis in motor cortex than did those that remained hypothermic after hypoxia-asphyxia. Apoptosis in piriform cortex was greater in hypoxic-asphyxic, rewarmed piglets than in naive/sham piglets. Caspase-3 inhibitor suppressed apoptosis with rewarming. Rapidly rewarmed piglets had more caspase-3 cleavage in cerebral cortex than did piglets that remained hypothermic or piglets that were rewarmed slowly. We conclude that rewarming from therapeutic hypothermia can adversely affect the newborn brain by inducing apoptosis through caspase mechanisms.