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Long F.R.,Childrens Radiological Institute | Flucke R.L.,Nationwide Childrens Hospital | Castile R.G.,Research Institute at Nationwide
Pediatric Radiology | Year: 2010

Background: Lung inflation and respiratory motion during chest CT affect diagnostic accuracy and reproducibility. Objective: To describe a simple volume-monitored (VM) method for performing reproducible, motion-free full inspiratory and end expiratory chest CT examinations in children. Materials and methods: Fifty-two children with cystic fibrosis (mean age 8.8±2.2 years) underwent pulmonary function tests and inspiratory and expiratory VM-CT scans (1.25-mm slices, 80-120 kVp, 16-40 mAs) according to an IRB-approved protocol. The VM-CT technique utilizes instruction from a respiratory therapist, a portable spirometer and real-time documentation of lung volume on a computer. CT image quality was evaluated for achievement of targeted lung-volume levels and for respiratory motion. Results: Children achieved 95% of vital capacity during full inspiratory imaging. For end expiratory scans, 92% were at or below the child's end expiratory level. Two expiratory exams were judged to be at suboptimal volumes. Two inspiratory (4%) and three expiratory (6%) exams showed respiratory motion. Overall, 94% of scans were performed at optimal volumes without respiratory motion. Conclusion: The VM-CT technique is a simple, feasible method in children as young as 4 years to achieve reproducible high-quality full inspiratory and end expiratory lung CT images. © 2010 Springer-Verlag. Source

Shen J.,Cleveland Clinic | Shen J.,Auburn University | Chandrasekharan U.M.,Cleveland Clinic | Ashraf M.Z.,Cleveland Clinic | And 5 more authors.
Circulation Research | Year: 2010

Rationale: Multiple protein kinases have been implicated in cardiovascular disease; however, little is known about the role of their counterparts: the protein phosphatases. Objective: To test the hypothesis that mitogen-activated protein kinase phosphatase (MKP)-1 is actively involved in atherogenesis. Methods and Results: Mice with homozygous deficiency in MKP-1 (MKP-1 -/-) were bred with apolipoprotein (Apo)E-deficient mice (ApoE -/-) and the 3 MKP-1 genotypes (MKP-1+/+/ApoE -/-; MKP-1+/-/ApoE-/- and MKP-1 -/-/ApoE-/-) were maintained on a normal chow diet for 16 weeks. The 3 groups of mice exhibited similar body weight and serum lipid profiles; however, both MKP-1+/- and MKP-1-/- mice had significantly less aortic root atherosclerotic lesion formation than MKP-1 +/+ mice. Less en face lesion was observed in 8-month-old MKP-1 -/- mice. The reduction in atherosclerosis was accompanied by decreased plasma levels of interleukin-1α and tumor necrosis factor a, and preceded by increased antiinflammatory cytokine interleukin-10. In addition, MKP-1-null mice had higher levels of plasma stromal cell-derived factor-1a, which negatively correlated with atherosclerotic lesion size. Immuno-histochemical analysis revealed that MKP-1 expression was enriched in macrophage-rich areas versus smooth muscle cell regions of the atheroma. Furthermore, macrophages isolated from MKP-1-null mice showed dramatic defects in their spreading/migration and impairment in extracellular signal-regulated kinase, but not c-Jun N-terminal kinase and p38, pathway activation. In line with this, MKP-1-null atheroma exhibited less macrophage content. Finally, transplantation of MKP-1-intact bone marrow into MKP-1-null mice fully rescued the wild-type atherosclerotic phenotype. Conclusion: These findings demonstrate that chronic deficiency of MKP-1 leads to decreased atherosclerosis via mechanisms involving impaired macrophage migration and defective extracellular signal-regulated kinase signaling. © 2010 American Heart Association, Inc. Source

Kerr Z.Y.,University of North Carolina at Chapel Hill | Casa D.J.,University of Connecticut | Marshall S.W.,University of North Carolina at Chapel Hill | Comstock R.D.,Ohio State University | Comstock R.D.,Research Institute at Nationwide
American Journal of Preventive Medicine | Year: 2013

Background: It is estimated that more than 9000 high school athletes are treated for exertional heat illness annually. Risk factors include being obese and beginning practice during hot and humid weather, when athletes are not yet acclimated to physical exertion in heat. Purpose: To describe the epidemiology of exertional heat illness in high school athletes. Methods: National High School Sports-Related Injury Surveillance System data (2005/2006-2010/2011) were analyzed in 2012 to calculate rates and describe circumstances of exertional heat illness. Results: Exertional heat illness occurred at a rate of 1.20 per 100,000 athlete exposures (95% CI=1.12, 1.28). Exertional heat illnesses were widely distributed geographically, and most occurred in August (60.3%). Of the exertional heat illnesses reported during practice, almost one third (32.0%) occurred more than 2 hours into the practice session. The exertional heat illness rate in football (4.42 per 100,000 athlete exposures) was 11.4 times that in all other sports combined (95% CI=8.3, 15.5, p<0.001). In addition, approximately one third (33.6%) of exertional heat illnesses occurred when a medical professional was not onsite at the time of onset. Conclusions: Although most exertional heat illnesses occurred in football, athletes in all sports and all geographic areas are at risk. Because exertional heat illness frequently occurs when medical professionals are not present, it is imperative that high school athletes, coaches, administrators, and parents are trained to identify and respond to it. Implementing effective preventive measures depends on increasing awareness of exertional heat illness and relevant preventive and therapeutic countermeasures. © 2013 American Journal of Preventive Medicine. Source

Perlman S.B.,University of Pittsburgh | Fournier J.C.,University of Pittsburgh | Bebko G.,University of Pittsburgh | Bertocci M.A.,University of Pittsburgh | And 22 more authors.
Journal of the American Academy of Child and Adolescent Psychiatry | Year: 2013

Objective Pediatric bipolar disorder involves poor social functioning, but the neural mechanisms underlying these deficits are not well understood. Previous neuroimaging studies have found deficits in emotional face processing localized to emotional brain regions. However, few studies have examined dysfunction in other regions of the face processing circuit. This study assessed hypoactivation in key face processing regions of the brain in pediatric bipolar disorder. Method Youth with a bipolar spectrum diagnosis (n = 20) were matched to a nonbipolar clinical group (n = 20), with similar demographics and comorbid diagnoses, and a healthy control group (n = 20). Youth participated in a functional magnetic resonance imaging (fMRI) scanning which employed a task-irrelevant emotion processing design in which processing of facial emotions was not germane to task performance. Results Hypoactivation, isolated to the fusiform gyrus, was found when viewing animated, emerging facial expressions of happiness, sadness, fearfulness, and especially anger in pediatric bipolar participants relative to matched clinical and healthy control groups. Conclusions The results of the study imply that differences exist in visual regions of the brain's face processing system and are not solely isolated to emotional brain regions such as the amygdala. Findings are discussed in relation to facial emotion recognition and fusiform gyrus deficits previously reported in the autism literature. Behavioral interventions targeting attention to facial stimuli might be explored as possible treatments for bipolar disorder in youth. Source

Guzeloglu-Kayisli O.,University of South Florida | Kayisli U.A.,University of South Florida | Semerci N.,University of South Florida | Basar M.,Yale University | And 9 more authors.
Journal of Pathology | Year: 2015

In chorioamnionitis (CAM), a major cause of preterm birth (PTB), maternal-fetal inflammation of the decidua and amniochorion cause the release of cytokines that elicit cervical ripening, fetal membrane rupture and myometrial activation. We posit that this inflammatory milieu triggers PTB by inhibiting progesterone receptor (PR) expression and increasing decidual prostaglandin (PG) production. Immunohistochemical staining of decidua detected significantly lower PR levels in decidual cells (DCs) from CAM-complicated PTB. Incubation of DCs with IL-1β decreased PR expression and significantly increased PGE2 and PGF2α production and COX-2 expression. The addition of PGF2α to DC cultures also suppressed PR expression. However, the COX inhibitor, indomethacin, did not reverse IL-1β suppression of PR expression in DC cultures. Although IL-1β treatment activated the NF-KB, ERK1/2 and p38 MAPK signalling cascades in DCs, inhibition of ERK1/2 MAPK signalling alone was sufficient to completely reverse the suppression of PR levels by IL-1β. These findings suggest that CAM-associated PTB is induced at least in part by IL-1β-mediated functional progesterone withdrawal. © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. Source

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