Improving Breastfeeding Environments and Feeding Practices in Family Child Care Homes with the Go NAP SACC Program

Maternal and Child Health Journal - Breastfeeding and responsive feeding are important practices that support the health of infants and women. In the United States, breastfeeding continuation rates...     

选择恰当的利益相关者开展更有效的继续医学教育活动

美国宾尼法尼亚州有全美数量最多的军队部署,调查发现当地为军人提供初级保健和精神健康保健的医务人员有大量继续医学教育需求.因此,美国宾尼法尼亚州医学院与当地红十字会决定针对当地的初级保健和精神健康医师举办继续医学教育活动,以提高他们的疾病筛查和转诊技术,从而更好地为退役军人提供医疗服务.     

Morphology of the uvula in obstructive sleep apnea

Alterations in pharyngeal structure and function are considered fundamental in the pathogenesis of obstructive sleep apnea (OSA). However, little is known about morphologic features of the pharynx in patients with OSA. We therefore studied the tissue composition of the uvula (midsagittal section) in patients with OSA, using a quantitative, morphometric point-counting technique. Uvula tissue was obtained by uvulopalatopharyngoplasty (UPPP) in 33 patients (mean number of apneas per hour of sleep = 32.7 +/- 5.2) and by autopsy in 22 normal subjects not known to have OSA. All statistical comparisons were controlled for differences caused by age and body mass index. Patients with OSA had a significantly greater percentage of muscle in the uvula (18.1 +/- 1.9% versus 9.3 +/- 2.1%, p = 0.02) than did normal subjects. A significant difference in fat content was also found (9.5 +/- 1.4% in patients versus 4.0 +/- 1.0% in normal subjects, p less than 0.02). These differences between patients with OSA and control subjects could not be accounted for by anthropometric or sex differences. The percentage of uvula fat tissue was significantly related to the frequency of apneas and hypopneas in sleep (r = 0.43, p less than 0.01). Uvula morphology in 6 nonapneic snorers undergoing UPPP was similar to that of patients with OSA. We conclude that the uvula in patients with OSA contains more muscle and fat than the uvula in control subjects, possibly contributing to pharyngeal narrowing in OSA.     

Insomnia and incident depression: role of objective sleep duration and natural history

Longitudinal studies that have examined the association of insomnia with incident depression using objective sleep measures are very limited. The aim of this study was to examine the predictive role of the severity of insomnia for incident depression in a general population sample using psychometric and polysomnographic data. From a random, general population sample of 1741 individuals of the Penn State Adult Cohort, 1137 adults without depression were followed up with a structured telephone interview after 7.5 years. All subjects completed a full medical evaluation, 1‐night polysomnogram and Multiphasic Minnesota Personality Inventory at baseline. The incidence of depression was 15%. Poor sleep (odds ratio = 1.5, P = 0.001) and insomnia (odds ratio = 1.9, P = 0.031) were significantly associated with incident depression. The odds of incident depression were highest (odds ratio = 2.2, P = 0.019) in insomnia with objective short sleep duration and independent of Multiphasic Minnesota Personality Inventory Ego Strength scores, an index of poor coping resources. The persistence of insomnia and worsening of poor sleep into insomnia significantly increased the odds of incident depression (odds ratios ranged from 1.8 to 6.3), whereas their full remission did not (odds ratio ranged from 1.2 to 1.8). Insomnia with short sleep duration is associated with incident depression independent of poor coping resources, whereas the association of insomnia with normal sleep duration with incident depression was mediated by poor coping resources. Persistence and worsening of poor sleep or insomnia, but not their full remission, are significant predictors of incident depression. These data suggest that there is a significant relationship between the severity of insomnia and incident depression.     

Marked decrease in sleepiness in patients with sleep apnea by etanercept, a tumor necrosis factor-alpha antagonist

The proinflammatory cytokines, TNFalpha and IL-6, are elevated in obstructive sleep apnea (OSA) and have been proposed as mediators of excessive daytime sleepiness in humans. We tested the effects of etanercept, a medication that neutralizes TNFalpha and is approved by the FDA for the treatment of rheumatoid arthritis, in eight obese male apneics. These patients participated in a pilot, placebo-controlled, double-blind study during which nighttime polysomnography, multiple sleep latency test, and fasting blood glucose and plasma levels of IL-6, C-reactive protein, insulin, and adiponectin were obtained. There was a significant and marked decrease in sleepiness by etanercept, which increased sleep latency during the multiple sleep latency test by 3.1 +/- 1.0 min (P < 0.05) compared with placebo. Also, the number of apneas/hypopneas per hour was reduced significantly by the drug compared with placebo (52.8 +/- 9.1 vs. 44.3 +/- 10.3; adjusted difference, -8.4 +/- 2.3; P < 0.05). Furthermore, IL-6 levels were significantly decreased after etanercept administration compared with placebo (3.8 +/- 0.9 vs. 1.9 +/- 0.4 pg/ml; adjusted difference, -1.9 +/- 0.5; P < 0.01). However, no differences were observed in etanercept vs. placebo in the levels of fasting blood glucose and plasma C-reactive protein, insulin, and adiponectin. We conclude that neutralizing TNFalpha activity is associated with a significant reduction of objective sleepiness in obese patients with OSA. This effect, which is about 3-fold higher than the reported effects of continuous positive airway pressure on objective sleepiness in patients with OSA (0.9 vs. 3.1 min), suggests that proinflammatory cytokines contribute to the pathogenesis of OSA/sleepiness.     

Rho guanine nucleotide exchange factor is an NFL mRNA destabilizing factor that forms cytoplasmic inclusions in amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is an adult-onset progressive disorder of unknown etiology characterized by the selective degeneration of motor neurons. Recent evidence supports the hypothesis that alterations in RNA metabolism in motor neurons can explain the development of protein inclusions, including neurofilamentous aggregates, observed in this pathology. In mice, p190RhoGEF, a guanine nucleotide exchange factor, is involved in neurofilament protein aggregation in an RNA-triggered transgenic model of motor neuron disease. Here, we observed that rho guanine nucleotide exchange factor (RGNEF), the human homologue of p190RhoGEF, binds low molecular weight neurofilament mRNA and affects its stability via 3′ untranslated region destabilization. We observed that the overexpression of RGNEF in a stable cell line significantly decreased the level of low molecular weight neurofilament protein. Furthermore, we observed RGNEF cytoplasmic inclusions in ALS spinal motor neurons that colocalized with ubiquitin, p62/sequestosome-1, and TAR (trans-active regulatory) DNA-binding protein 43 (TDP-43). Our results provide further evidence that RNA metabolism pathways are integral to ALS pathology. This is also the first described link between ALS and an RNA binding protein with aggregate formation that is also a central cell signaling pathway molecule.     

Insomnia with objective short sleep duration is associated with cognitive impairment: a first look at cardiometabolic contributors to brain health

Study ObjectivesInsomnia with objective short sleep duration has been previously associated with adverse cardiometabolic health outcomes as well as poorer cognitive performance in otherwise noncognitively impaired adults. However, studies demonstrating an increased prevalence of cognitive impairment (CI) in this insomnia phenotype are lacking.MethodsWe analyzed data from Penn State Adult Cohort (N = 1,524; 48.9 ± 13.4 years; 53.4% women). Self-reported sleep difficulty was defined as normal sleep (n = 899), poor sleep (n = 453), and chronic insomnia (n = 172). Objective short sleep duration was defined as less than 6-h of sleep, based on in-lab, 8-h polysomnography. CI (n = 155) and possible vascular cognitive impairment (pVCI, n = 122) were ascertained using a comprehensive neuropsychological battery. Analyses adjusted for age, sex, race, education, body mass index, apnea/hypopnea index, smoking, alcohol, psychoactive medication, and mental and physical health problems.ResultsParticipants who reported poor sleep or chronic insomnia and slept objectively less than 6 hours were associated with a 2-fold increased odds of CI (OR = 2.06, 95% confidence limits [CL] = 1.15–3.66 and OR = 2.18, 95% CL = 1.07–4.47, respectively) and of pVCI (OR = 1.94, 95% CL = 1.01–3.75 and OR = 2.33, 95% CL = 1.07–5.06, respectively). Participants who reported poor sleep or chronic insomnia and slept objectively more than 6 hours were not associated with increased odds of either CI (OR = 0.72, 95% CL = 0.30–1.76 and OR = 0.75, 95% CL = 0.21–2.71, respectively) or pVCI (OR = 1.08, 95% CL = 0.42–2.74 and OR = 0.76, 95% CL = 0.16–3.57, respectively).ConclusionsInsomnia with objective short sleep duration is associated with an increased prevalence of CI, particularly as it relates to cardiometabolic health (i.e. pVCI). These data further support that this insomnia phenotype may be a more biologically severe form of the disorder associated with cardiovascular, cerebrovascular, and neurocognitive morbidity.     

Insomnia with objective short sleep duration and incident hypertension: the penn state cohort

Insomnia with objective short sleep duration appears to be a biologically more severe phenotype of the disorder. No longitudinal study to date has examined the association of this type of insomnia with incident hypertension using polysomnography. From a random, general population sample of 1741 adults of the Penn State Cohort, 1395 were followed-up after 7.5 years, and 786 did not have hypertension at baseline. Hypertension was determined by a self-report of receiving treatment for high blood pressure. Chronic insomnia was defined as a complaint of insomnia lasting ≥1 year, whereas poor sleep was defined as moderate-to-severe sleep difficulties. All of the subjects underwent 8-hour polysomnography. Sleep-disordered breathing (SDB) was defined as an obstructive apnea/hypopnea index ≥5. We used the median polysomnographic percentage of sleep time to define short sleep duration (ie, <6 hours). We controlled for sex, race, age, caffeine, cigarettes and alcohol consumption, depression, sleep-disordered breathing, diabetes mellitus, obesity, and blood pressure in our analyses. Compared with normal sleepers who slept ≥6 hours, the highest risk for incident hypertension was in chronic insomniacs with short sleep duration (odds ratio, 3.8 [95% CI, 1.6-9.0]). The risk for incident hypertension in poor sleepers with short sleep duration was significantly increased but became marginally significant after controlling for obesity (odds ratio, 1.6 [95% CI, 0.9-2.8]). Chronic insomnia with short sleep duration is associated with an increased risk for incident hypertension in a degree comparable to sleep-disordered breathing. Objective short sleep duration in insomnia may serve as a useful predictor of the biological severity of the disorder.