The utilization of hyperbaric oxygenation therapy in hypospadias repair: a systematic review and meta-analysis

International Urology and Nephrology - This study aimed to evaluate the efficacy and safety of Hyperbaric Oxygen Therapy (HBOT) use in hypospadias repair through systematic review and meta-analysis...     

Attaining competency and proficiency in open pyeloplasty: a learning curve configuration using cumulative sum analysis

International Urology and Nephrology - The learning curves for minimally invasive pyeloplasty techniques have been described in the past. However, the learning curve in achieving competency in open...     

Association of intraoperative dexmedetomidine use with postoperative hypotension in unilateral hip and knee arthroplasties: a historical cohort study

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - Dexmedetomidine is frequently used as a sedative agent for orthopedic surgery patients undergoing total hip or knee...     

The Long‐Term Use of a Low‐Phenylalanine Diet in Late‐Treated Phenylketonuria: A Single Case Report

Background When phenylketonuria (PKU) is not diagnosed and long‐term treatment commenced within the first few weeks of life, permanent brain damage will occur. There is some evidence to show that late diagnosed or untreated people with PKU who have severe challenging behaviours may benefit from a low phenylalanine diet [ Harper & Reid (1987) Journal of Mental Deficiency Research vol. 31, pp. 209–212; Hoskins et al. (1992) Journal of Intellectual Disability Research vol. 36, pp. 183–191; Baumeister & Baumeister (1998) Clinical Neuropharmacology vol. 21, pp. 18–27; Fitzgerald et al. (2000) Journal of Intellectual Disability Research vol. 44, pp. 53–59]. Method In the light of this evidence, a woman with late‐diagnosed PKU was treated with a low‐phenylalanine diet in an attempt to reduce her severe challenging behaviour. Results A reduction in challenging behaviours was observed when phenylalanine levels were maintained within a specific narrow range. Data are reported over a 2‐year period. A dramatic rise in severe challenging behaviour was noticed when her blood phenylalanine levels fell below a certain level. Conclusions This case report suggests that blood phenylalanine levels need to be maintained within a specific range for maximum benefit.     

Neural signature of behavioural inhibition in women with bulimia nervosa

BackgroundImpaired inhibitory control is considered a behavioural phenotype in patients with bulimia nervosa. However, the underlying neural correlates of impaired general and food-specific behavioural inhibition are largely unknown. Therefore, we investigated brain activation during the performance of behavioural inhibition to general and food-related stimuli in adults with bulimia nervosa.MethodsWomen with bulimia and healthy control women underwent event-related fMRI while performing a general and a food-specific no-go task.ResultsWe included 28 women with bulimia nervosa and 29 healthy control women in our study. On a neuronal level, we observed significant group differences in response to general no-go stimuli in women with bulimia nervosa with high symptom severity; compared with healthy controls, the patients showed reduced activation in the right sensorimotor area (postcentral gyrus, precentral gyrus) and right dorsal striatum (caudate nucleus, putamen).LimitationsThe present results are limited to adult women with bulimia nervosa. Furthermore, it remains unclear whether impaired behavioural inhibition in patients with this disorder are a cause or consequence of chronic illness.ConclusionOur findings suggest that diminished frontostriatal brain activation in patients with bulimia nervosa contribute to the severity of binge eating symptoms. Gaining further insight into the neural mechanisms of behavioural inhibition problems in individuals with this disorder may inform brain-directed treatment approaches and the development of response inhibition training approaches to improve inhibitory control in patients with bulimia nervosa. The present study does not support greater behavioural and neural impairments to food-specific behavioural inhibition in these patients.