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This report presents the following population-based measures: incidence rates, mortality rates, and relative survival rates (for more information on definitions of terms and Estimation of Expected Numbers of Brain and Other CNS Tumors in 2017 and 2018Estimated numbers of expected malignant and non-malignant brain and other CNS tumors were calculated for 2017 and 2018. To project estimates of newly diagnosed brain and other CNS tumors in 2017 and 2018, age-adjusted annual brain tumor incidence rates were generated for 2000-2014 for malignant tumors, and 2006-2014 for nonmalignant tumors. These were generated by state, age, and histologic type. Joinpoint 4.2.0.2 32 was used to fit regression models to these incidence rates, 33 which were used to predict numbers of cases in future years using the parameter from the selected models. Joinpoint regression allows for multiple lines to be fit to incidence data across time, rather than assuming a consistent trend across the whole period. The points where these lines intersect are called 'joinpoints'. The models allowed for a maximum of 2 joinpoints (1 for non-malignant tumors), a minimum of 3 observations from a joinpoint to either end of the data, and a minimum of 3 observations between joinpoints. 34 Modified Bayesian Information Criterion procedures included in Joinpoint were used to select the best fitting model. Overall total rates presented are based on total malignant and

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The CBTRUS Statistical Report: Alex's Lemonade Stand Foundation Infant and Childhood Primary Brain and Central Nervous System Tumors Diagnosed in the United States in 2007–2011 comprehensively describes the current population-based incidence of primary malignant and non-malignant brain and CNS tumors in children ages 0–14 years, collected and reported by central cancer registries covering approximately 99.8% of the United States population (for 2011 only, data were available for 50 out of 51 registries). Overall, brain and CNS tumors are the most common solid tumor, the most common cancer, and the most common cause of cancer death in infants and children 0–14 years. This report aims to serve as a useful resource for researchers, clinicians, patients, and families.

A lthough obstructive sleep apnea (OSA) is common, up to 82% of men and 92% of women with moderate-to-severe sleep apnea have not been diagnosed. The use of preoperative screening instruments may help identify these undiagnosed patients. The STOP-Bang questionnaire has 8 questions and is scored on the basis of yes/no answers. Scores range from a value of 0 to 8, with a score of 3 or greater having a high sensitivity for detecting OSA, 93% and 100% for moderate and severe OSA, respectively. Because the specificity is 47% and 37% for moderate and severe OSA, the false-positive rate of the questionnaire is high. This study was performed to evaluate the predictive probabilities for OSA at different scores on the STOP-Bang questionnaire.Patients older than 18 years undergoing elective procedures were included in the screening process and approached for consent for the preoperative polysomnography (PSG), either portable at home or in the laboratory. All patients were asked to complete the STOP questionnaire. Information on the patient_s body mass index, age, neck circumference, and sex were collected. Manual scoring of PSG was performed according to the Manual of the American Academy of Sleep Medicine. The PSG recordings were scored by a sleep physician. The sleep stages and apnea-hypopnea index (AHI) were scored. The diagnosis of OSA was based on an AHI greater than 5 with fragmented sleep and daytime sleepiness. The severity of OSA with laboratory and portable PSG was classified based on the AHI values: greater than 5 to 15 as mild OSA, greater than 15 to 30 as moderate OSA, and greater than 30 as severe OSA.Over 4 years, 6469 patients were approached, and 1312 consented. Of these, 930 completed PSG, and 746 patients with complete data on PSG and the STOP-Bang questionnaire were included in the final analysis. Their median age was 60 years, 49% were male, body mass index was 30 kg/m 2 , and neck circumference was 39 cm. Of the 746 patients, 510 (68.4%) had OSA, with 287 (38.5%) and 134 (18.0%), respectively, having moderate/severe OSA and severe OSA. Most patients had a STOP-Bang score of 3 and 4 (22.9% and 22.3%, respectively). The area under the receiver operating curves was 0.65, 0.67, and 0.71 for all OSA, moderate/severe OSA, and severe OSA, respectively. For STOP-Bang scores of 5 and 6, the odds ratios (ORs) for moderate/severe OSA were 4.8 and 6.3, respectively, and for severe OSA, 10.4 and 11.6, respectively. For STOPBang scores of 7 and 8, the ORs were 6.9 for moderate/severe OSA and 14.9 for severe OSA. As the STOP-Bang score increased from 3 to 8, sensitivity decreased from 68.4% to 0.4% for patients with moderate/severe OSA and from 94.8% to 0% for those with severe OSA. When the STOP-Bang score was 5, the specificity for moderate/severe and severe OSA was 56.1% and 74.2%, respectively. The probabilities of having OSA were greater and the STOP-Bang score increased, a trend that was the same for the groups of all OSA, moderate/severe OSA, and severe OSA. As the STOP-Bang score increased from 0 to 2 to 7 an...

We found that anaesthetists and surgeons failed to identify a significant number of patients with pre-existing OSA and symptomatic undiagnosed OSA, before operation. This study may provide an impetus for more diligent case finding of OSA before operation.

How mechanical signals are transmitted in the cardiac myocyte is poorly understood. In this study, we produced a tamoxifen-inducible mouse model in which β1 integrin could be reduced specifically in the adult cardiomyocyte, so that the function of this integrin could be assessed in the postnatal and mechanically stressed heart. The expression of β1 integrin was reduced to 35% of control levels, but function remained normal at baseline. With aortic constriction, the knockout mice survived but had a blunted hypertrophic response. Integrin knockout myocytes, in contrast to controls, showed reduced integrin-linked kinase expression both at baseline and after hemodynamic stress; focal adhesion kinase expression was reduced after stress. Alterations in multiple signaling pathways were detected in the integrin knockout group after acute and chronic hemodynamic stress. Most remarkably, when we challenged the knockout mice with short-term loading, the robust responses of several kinases (extracellular signal-regulated kinase 1/2, p38, and Akt) evident in control mice were essentially abolished in the knockout mice. We also found that reduction of myocyte β1 integrin expression modified adrenergic-mediated signaling through extracellular signal-regulated kinase, p38, and Akt. Reduction of β1 integrin expression in the mature cardiac myocyte leads to a varied response compared with when this protein is reduced during either the embryonic or perinatal period. These results show that β1 integrin expression is required for proper mechanotransductive and adrenergic responses of the adult heart.

Ischemic damage is recognized to cause cardiomyocyte (CM) death and myocardial dysfunction, but the role of cell-matrix interactions and integrins in this process has not been extensively studied. Expression of α7β1D integrin, the dominant integrin in normal adult CMs, increases during ischemia/reperfusion (I/R), while deficiency of β1 integrins increases ischemic damage. We hypothesized that the forced overexpression of integrins on the CM would offer protection from I/R injury. Tg mice with CM-specific overexpression of integrin α7β1D exposed to I/R had a substantial reduction in infarct size compared with that of α5β1D-overexpressing mice and WT littermate controls. Using isolated CMs, we found that α7β1D preserved mitochondrial membrane potential during hypoxia/reoxygenation (H/R) injury via inhibition of mitochondrial Ca 2+ overload but did not alter H/R effects on oxidative stress. Therefore, we assessed Ca 2+ handling proteins in the CM and found that β1D integrin colocalized with ryanodine receptor 2 (RyR2) in CM T-tubules, complexed with RyR2 in human and rat heart, and specifically bound to RyR2 amino acids 165-175. Integrins stabilized the RyR2 interdomain interaction, and this stabilization required integrin receptor binding to its ECM ligand. These data suggest that α7β1D integrin modifies Ca 2+ regulatory pathways and offers a means to protect the myocardium from ischemic injury.