Interactions between metabolic, reward and cognitive processes in appetite control:Implications for novel weight management therapies

Traditional models of appetite control have emphasised the role of parallel homeostatic and hedonic systems, but more recently the distinction between independent homeostatic and hedonic systems has been abandoned in favour of a framework that emphasises the cross talk between the neurochemical substrates of the two systems. In addition, evidence has emerged more recently, that higher level cognitive functions such as learning, memory and attention play an important role in everyday appetite control and that homeostatic signals also play a role in cognition. Here, we review this evidence and present a comprehensive model of the control of appetite that integrates cognitive, homeostatic and reward mechanisms. We discuss the implications of this model for understanding the factors that may contribute to disordered patterns of eating and suggest opportunities for developing more effective treatment approaches for eating disorders and weight management

Multidisciplinary approaches to the study of eating disorders and obesity: recent progress in research and development and future prospects

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TRIP13 and APC15 drive mitotic exit by turnover of interphase- and unattached kinetochore-produced MCC

The mitotic checkpoint ensures accurate chromosome segregation through assembly of the mitotic checkpoint complex (MCC), a soluble inhibitor of the anaphase-promoting complex/cyclosome (APC/C) produced by unattached kinetochores. MCC is also assembled during interphase by Mad1/Mad2 bound at nuclear pores, thereby preventing premature mitotic exit prior to kinetochore maturation and checkpoint activation. Using degron tagging to rapidly deplete the AAA+ ATPase TRIP13, we show that its catalytic activity is required to maintain a pool of open-state Mad2 for MCC assembly, thereby supporting mitotic checkpoint activation, but is also required for timely mitotic exit through catalytic disassembly of MCC. Strikingly, combining TRIP13 depletion with elimination of APC15-dependent Cdc20 ubiquitination/degradation results in a complete inability to exit mitosis, even when MCC assembly at unattached kinetochores is prevented. Thus, mitotic exit requires MCC produced either in interphase or mitosis to be disassembled by TRIP13-catalyzed removal of Mad2 or APC15-driven ubiquitination/degradation of its Cdc20 subunit

Attention Deficit Hyperactivity Disorder (ADHD) and disordered eating behaviour: A systematic review and a framework for future research

Preliminary findings suggest that Attention Deficit Hyperactivity Disorder (ADHD) may be associated with disordered eating behaviour, but whether there is sufficient evidence to suggest an association between ADHD and specific types of disordered eating behaviour is unclear. Furthermore, it is uncertain whether specific features associated with ADHD are differentially associated with disordered eating behaviour. A systematic review of seventy-five studies was conducted to evaluate the potential association between ADHD symptomatology and disordered eating behaviour and to provide an estimate of the strength of evidence for any association. Overall, a moderate strength of evidence exists for a positive association between ADHD and disordered eating and with specific types of disordered-eating behaviour, in particular, overeating behaviour. There is consistent evidence that impulsivity symptoms of ADHD are positively associated with overeating and bulimia nervosa and more limited evidence for an association between hyperactivity symptoms and restrictive eating in males but not females. Further research is required to assess the potential direction of the relationship between ADHD and disordered eating, the underlying mechanisms and the role of specific ADHD symptoms in the development and/or maintenance of disordered eating behaviour. We propose a framework that could be used to guide the design of future studies

Associations between core symptoms of attention deficit hyperactivity disorder and both binge and restrictive eating

It is unclear whether core symptoms of attention deficit hyperactivity disorder (ADHD) relate to specific types of disordered eating and little is known about the mediating mechanisms. We investigated associations between core symptoms of ADHD and binge/disinhibited eating and restrictive eating behavior and assessed whether negative mood and/or deficits in awareness and reliance on internal hunger/satiety cues mediate these relationships.In two independent studies, we used a dimensional approach to study ADHD and disordered eating. In Study 1, a community-based sample of 237 adults (72.6% female, 18-60 years [M = 26.8, SE = 0.6]) completed an online questionnaire, assessing eating attitudes/behaviors, negative mood, awareness, and reliance on internal hunger/satiety cues and ADHD symptomatology. In Study 2, 142 students (80.3% female, 18-32 years [M = 19.3, SE = 0.1]) were recruited to complete the same questionnaires and complete tasks assessing interoceptive sensitivity and impulsivity in the laboratory.In each study, core symptoms of ADHD correlated positively with both binge/disinhibited and restrictive eating and negative mood mediated the relationships. Deficits in awareness and reliance on internal hunger/satiety signals also mediated the association between inattentive symptoms of ADHD and disordered eating, especially binge/disinhibited eating. The results from both studies demonstrated that inattentive symptoms of ADHD were also directly related to binge/disinhibited eating behavior, while accounting for the indirect pathways of association via negative mood and awareness and reliance on internal hunger/satiety signals.This research provides evidence that core symptoms of ADHD are associated with both binge/disinhibited eating and restrictive eating behavior. Further investigation of the role of inattentive symptoms of ADHD in disordered eating may be helpful in developing novel treatments for both ADHD and binge eating

Central line-associated bloodstream infections in pediatric patients: Results from a national nosocomial infections surveillance program

ΟBJECTIVE To provide updated data on the rates of central line-associated bloodstream infections (CLABSI) in Greek neonatal intensive care units (NICUs), pediatric intensive care units (PICUs) and pediatric oncology units (PONCs), and to describe pathogen distribution and antimicrobial resistance patterns for CLABSIs. METHOD Active surveillance for CLABSI was conducted from June 2016 to December 2019 (43 months). A consortium of 14 NICUs, 3 PICUs, and 6 PONCs participated in the program. Surveillance definitions of central line (CL), central line utilization (CLU) ratio, CLABSI event, and CLABSI rate were based on the 2014 National Healthcare Safety Network criteria of the US Centers for Disease Control and Prevention (CDC). Medical records were assessed daily for calculation of CL-days, pa-tient-days, and susceptibility to isolated organisms. RESULTS A total of 519 CLABSI episodes were recorded in the 43 months. Mean CLABSI rates were 7.15 in NICUs, 5.19 in PICUs, and 2.20, per 1,000 CL-days in PONCs. A higher mean CLU ratio was reported in PONCs (0.83) and a lower mean ratio was found in NICUs (0.15). A total of 567 pathogens were isolated, the most common of which were Enterobacterales (42.1%), followed by Gram-positive cocci (29%), non-fermenting Gram-negative bacteria (14.6%), and fungi (11.5%). Among 239 (63.1%) Enterobacterales isolated, 151 were multidrug resistant. Overall, 14.8% of Gram-negative pathogens were resistant to third generation ceph-alosporins and 23.7% to carbapenems. CONCLUSIONS The rates of CLABSI and antibiotic resistance among organ-isms causing CLABSI are high in high-risk hospitalized children. These data highlight the significance of this problem and emphasize the need for implementation of infection prevention interventions. The methodology used for this surveillance program could be applied in other pediatric or adult units across Greece. © Athens Medical Society