Stress and Coping in Youth With Spina Bifida: A Brief Longitudinal Study in a Summer Camp Setting

Introduction: It is well established that youth with chronic conditions experience elevated levels of stress; the manner in which they respond to or cope with this stress is likely to impact both health and psychosocial outcomes. The current study examined stress and coping in youth and young adults with spina bifida (SB) using the response to stress questionnaire-SB version (RSQ-SB; Connor-Smith et al., 2000). Methods: Data were collected as part of a camp-based psychosocial intervention for children (ages 7–13), adolescents (ages 14–19), and young adults (ages 20–38) with SB. Participants completed the RSQ-SB as well as questionnaires assessing demographics and condition severity. Data were collected prior to camp (T1) and 1 month (T2) after camp ended. Self-report data were collected from adolescents and young adults; parents of children and adolescents reported on their child’s stress and coping. Ratios of primary control coping, secondary control coping, disengagement coping, involuntary engagement, and involuntary disengagement coping were calculated. Descriptive statistics and t-tests were utilized to describe coping and stress responses and to determine potential change over time. T-tests were also used to compare youth and parent reported coping styles with those of youth with type 1 diabetes (T1D) and sickle cell disease (SCD). Associations between demographic/disease factors and coping styles were also examined. Results: Parent and youth report indicated that youth with SB tend to use primary control coping. Youth with SB use more primary control coping and less disengagement coping compared to youth with SCD and youth with T1D. Few significant changes in coping were found between T1 and T2. IQ and socioeconomic status were significantly associated with coping styles. Conclusion: Youth with SB use more primary control coping compared to other coping methods and as compared to other pediatric populations. Future studies should examine mechanisms by which primary control coping is advantageous for youth with SB. Future interventions should be more focused on promoting adaptive coping behaviors and be tailored to developmental age and access to resources

Genomic insights to control the emergence of vancomycin-resistant enterococci.

UNLABELLED: Nosocomial outbreaks of vancomycin-resistant Enterococcus faecium (VREfm) are thought to occur by transmission of VREfm between patients, predicting that infection control interventions will limit cross-transmission. Despite implementation of such strategies, the incidence of VREfm infections continues to rise. We aimed to use genomics to better understand the epidemiology of E. faecium within a large hospital and investigate the reasons for failure of infection control strategies. Whole-genome sequencing was performed on 61 E. faecium (36 VREfm) isolates, predominately from blood cultures collected at a single hospital between 1998 and 2009, and on five vanB-positive anaerobic commensal bacteria isolated from human feces. Phylogenomic analysis and precise mapping of the vanB gene, which contains the Tn1549 transposon, showed that at least 18 of the 36 VREfm isolates had acquired the transposon via independent insertion events, indicating de novo generation of VREfm rather than cross-transmission. Furthermore, Tn1549 sequences found in 15 of the 36 VREfm isolates were the same as the Tn1549 sequence from one of the gut anaerobes. National and international comparator E. faecium isolates were phylogenetically interspersed with isolates from our hospital, suggesting that our findings might be globally representative. These data demonstrate that VREfm generation within a patient is common, presumably occurring in the human bowel during antibiotic therapy, and help explain our inability to reduce VREfm infections. A recommendation from our findings is that infection control practices should include screening patients for specific hospital clones of vancomycin-susceptible E. faecium rather than just VREfm. IMPORTANCE: Enterococcus faecium is an increasingly important human pathogen causing predominantly antibiotic-resistant infections in hospitalized patients. Large amounts of health care funding are spent trying to control antibiotic-resistant bacteria in hospitals globally, yet in many institutions around the world, vancomycin-resistant E. faecium (VREfm) infections continue to rise. The new findings from this study help explain the failures of our current approaches to controlling vanB VREfm in health care institutions. Given the importance of this bacterium as a cause of hospital-acquired infections and the difficulties faced by infection control units in trying to prevent colonization in their institutions, the novel findings from this study provide evidence that a new approach to controlling VREfm in hospitals is required. In particular, more attention should be given to understanding the epidemiology of hospital-adapted vancomycin-susceptible E. faecium, and patients at higher risk for de novo generation of VREfm need to be identified and optimally managed

Diet-Induced Obesity Impairs Endothelium-Derived Hyperpolarization via Altered Potassium Channel Signaling Mechanisms

BACKGROUND: The vascular endothelium plays a critical role in the control of blood flow. Altered endothelium-mediated vasodilator and vasoconstrictor mechanisms underlie key aspects of cardiovascular disease, including those in obesity. Whilst the mechanism of nitric oxide (NO)-mediated vasodilation has been extensively studied in obesity, little is known about the impact of obesity on vasodilation to the endothelium-derived hyperpolarization (EDH) mechanism; which predominates in smaller resistance vessels and is characterized in this study. METHODOLOGY/PRINCIPAL FINDINGS: Membrane potential, vessel diameter and luminal pressure were recorded in 4(th) order mesenteric arteries with pressure-induced myogenic tone, in control and diet-induced obese rats. Obesity, reflecting that of human dietary etiology, was induced with a cafeteria-style diet (∼30 kJ, fat) over 16-20 weeks. Age and sexed matched controls received standard chow (∼12 kJ, fat). Channel protein distribution, expression and vessel morphology were determined using immunohistochemistry, Western blotting and ultrastructural techniques. In control and obese rat vessels, acetylcholine-mediated EDH was abolished by small and intermediate conductance calcium-activated potassium channel (SK(Ca)/IK(Ca)) inhibition; with such activity being impaired in obesity. SK(Ca)-IK(Ca) activation with cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (CyPPA) and 1-ethyl-2-benzimidazolinone (1-EBIO), respectively, hyperpolarized and relaxed vessels from control and obese rats. IK(Ca)-mediated EDH contribution was increased in obesity, and associated with altered IK(Ca) distribution and elevated expression. In contrast, the SK(Ca)-dependent-EDH component was reduced in obesity. Inward-rectifying potassium channel (K(ir)) and Na(+)/K(+)-ATPase inhibition by barium/ouabain, respectively, attenuated and abolished EDH in arteries from control and obese rats, respectively; reflecting differential K(ir) expression and distribution. Although changes in medial properties occurred, obesity had no effect on myoendothelial gap junction density. CONCLUSION/SIGNIFICANCE: In obese rats, vasodilation to EDH is impaired due to changes in the underlying potassium channel signaling mechanisms. Whilst myoendothelial gap junction density is unchanged in arteries of obese compared to control, increased IK(Ca) and Na(+)/K(+)-ATPase, and decreased K(ir) underlie changes in the EDH mechanism

The Dynamism of a MFA

I viscerally remember while reading The New Yorker article “The Dynamism of Janet McTeer,” as I sat in my cubicle in Chicago at a survival temp job turned actual fake career, sitting slack-jawed, elated, and sucker punched. McTeer talked of acting as jazz where artists re-invent every performance. I finally had words to describe the craving I longed for in my work; something I could point to and say ‘YES! See?? I want to do that!’ But with no idea how to bridge the gap from where I was to where I now dreamed to explore my craft. Admittedly, it is disorienting to look back on a MFA experience that is so vastly different from what I expected and still say… absolutely; I bridged that gap. Perhaps the incubation period is intensified when confined in isolation for most of your grad school career. Where your bed, kitchen, green screen, movement studio, shower, anger, digitalized classmates, heart aches, work, suffering students, tears, panic attacks, pee-inducing laughter, triumphs, failures, and you all manifest together like a hundred piece orchestra playing in a 425sq foot studio apartment. It is deafening. Yet, among all this is where I learned to breathe through my emotions as I speak; sustain in the power of living thought; really do what I’m doing for real, really; and forever challenge myself to embrace the free-fall of a soft belly. Held by my training, I enter back into the professional world saying ‘YES! See?? I now act jazz!