The "chicken-leg anastomosis": Low-cost tissue-realistic simulation model for esophageal atresia training in pediatric surgery.

Introduction: Shifting the training from the operating room (OR) to simulation models has been proven effective in enhancing patient safety and reducing the learning time to achieve competency and increase the operative efficiency. Currently the field of pediatric surgery only offers few low-cost trainers for specialized training and these feature predominantly artificial and often unrealistic tissue. The aim of this study was to develop an easy access low-cost tissue-realistic simulation model for open training of esophageal atresia and to evaluate the acceptance in trainees and junior pediatric surgeons. Materials and methods: The model is fashioned using reconfigured chicken skin from a chicken leg. To create a model of esophageal atresia, the chicken skin is dissected off the muscle and reconfigured around a foley catheter balloon to recreate the proximal pouch and a feeding tube to recreate the distal pouch. Surrounding structures such as the tracheo-esophageal fistula and the azygos vein can be easily added, obtaining a realistic esophageal atresia (Type C) prototype. Evaluation of model construction, usage and impact on user were performed by both a self-assessment questionnaire with pre- and post-training questions as well as observer-based variables and a revised Objective Structured Assessment of Technical Skills (OSATS) score. Results: A total of 10 participants were constructing and using the model at two different timepoints. OSATS score for overall performance was significantly higher (p = 0.005, z = -2.78) during the second observational period [median (MD): 4,95% confidence interval CI: 3.4, 5.1] compared to the first (MD: 3, 95% CI 2.4, 4.1). Self-reported boost in confidence after model usage for performing future esophageal atresia (EA) repair and bowel anastomosis (BA) in general was significantly higher (EA: U = 1, z = -2.3, p = 0.021, BA: U = 1, z = -2.41, p = 0.016) in participants with more years in training/attending status (EA MD:5, BA MD: 5.5) compared to less experienced participants (EA MD: 1.5, BA: 1). Conclusion: Our easy access low-cost simulation model represents a feasible and tissue realistic training option to increase surgical performance of pediatric surgical trainees outside the OR.

Is fetal magnetic resonance imaging volumetry of eventrated organs in gastroschisis predictive for surgical treatment?

BACKGROUND: Fetal MRI is increasingly used in congenital abdominal wall defects. In gastroschisis, the role of fetal MRI in surgical therapy is poorly understood. Currently, the type of repair is determined primarily by clinical presentation and institutional preference. OBJECTIVE: To evaluate the feasibility of fetal MRI volumetry in gastroschisis treatment. MATERIALS AND METHODS: We included 22 cases of gastroschisis in this retrospective single-center study. Routine fetal MRI scans were acquired between Jan. 1, 2006, and July 1, 2018, at gestational ages of 19-34 postmenstrual weeks. Fetal-MRI-based manual segmentation and volumetry were performed utilizing steady-state free precision and T2-weighted sequences. Acquired parameters included intraabdominal volume, eventrated organ volume and total fetal body volume, and we calculated a volume ratio between eventrated organ volume and intraabdominal volume (E/I ratio). RESULTS: Primary closure was conducted in 13 cases and silo bag treatment with delayed closure in 9 cases. Prenatal MRI volumetry showed a significantly higher E/I ratio in patients with silo bag treatment with delayed closure (mean [M]=0.34; 95% confidence interval [CI] 0.30, 0.40) than in primary closure (M=0.23, 95% CI 0.19, 0.27; P=0.004). We propose a volume ratio cutoff value of 0.27 for predicting silo bag treatment. CONCLUSION: Fetal MRI predicted silo bag treatment in patients with gastroschisis in 90% of the cases in our cohort and might facilitate prenatal counseling and treatment planning.

Dopaminergic and opioidergic regulation during anticipation and consumption of social and nonsocial rewards.

The observation of animal orofacial and behavioral reactions has played a fundamental role in research on reward but is seldom assessed in humans. Healthy volunteers (N = 131) received 400 mg of the dopaminergic antagonist amisulpride, 50 mg of the opioidergic antagonist naltrexone, or placebo. Subjective ratings, physical effort, and facial reactions to matched primary social (affective touch) and nonsocial (food) rewards were assessed. Both drugs resulted in lower physical effort and greater negative facial reactions during reward anticipation, especially of food rewards. Only opioidergic manipulation through naltrexone led to a reduction in positive facial reactions to liked rewards during reward consumption. Subjective ratings of wanting and liking were not modulated by either drug. Results suggest that facial reactions during anticipated and experienced pleasure rely on partly different neurochemical systems, and also that the neurochemical bases for food and touch rewards are not identical.

Studies in rats and other species have shown that two chemical messengers in the brain regulate how much an animal desires a reward, and how pleasant receiving the reward is. In this context, chemicals called opioids control both wanting and enjoying a reward, whereas a chemical called dopamine only regulates how much an animal desires it. However, since these results were obtained from research performed on animals, further studies are needed to determine if these chemicals play the same roles in the human brain. Korb et al. show that the same brain chemicals that control reward anticipation and pleasure in rats are also at work in humans. In the experiment, 131 healthy volunteers received either a drug that blocks opioid signaling in the brain, a drug that blocks dopamine signaling, or a placebo, a pill with no effect. Then, participants were given, on several occasions, either sweet milk with chocolate or a gentle caress on the forearm. Participants rated how much they wanted each of the rewards before receiving it, and how much they liked it after experiencing it. To measure their implicit wanting of the reward, participants also pressed a force-measuring device to increase their chances of receiving the reward. Additionally, small electrodes measured the movement of the volunteer's smiling or frowning muscles to detect changes in facial expressions of pleasure. Volunteers taking either drug pressed on the device less hard than the participants taking the placebo, suggesting they did not want the rewards as much, and they frowned more as they anticipated the reward, indicating less anticipatory pleasure. However, only the volunteers taking the opioid-blocking drug smiled less when they received a reward, indicating that these participants did not get as much pleasure as others out of receiving it. These differences were most pronounced when volunteers looked at or received the sweet milk with chocolate. This experiment helps to shed light on the chemicals in the human brain that are involved in reward-seeking behaviors. In the future, the results may be useful for developing better treatments for addictions.

On the relationship of first-episode psychosis to the amphetamine-sensitized state: a dopamine D2/3 receptor agonist radioligand study.

Schizophrenia is characterized by increased behavioral and neurochemical responses to dopamine-releasing drugs. This prompted the hypothesis of psychosis as a state of "endogenous" sensitization of the dopamine system although the exact basis of dopaminergic disturbances and the possible role of prefrontal cortical regulation have remained uncertain. To show that patients with first-episode psychosis release more dopamine upon amphetamine-stimulation than healthy volunteers, and to reveal for the first time that prospective sensitization induced by repeated amphetamine exposure increases dopamine-release in stimulant-naïve healthy volunteers to levels observed in patients, we collected data on amphetamine-induced dopamine release using the dopamine D2/3 receptor agonist radioligand [11C]-(+)-PHNO and positron emission tomography. Healthy volunteers (n = 28, 14 female) underwent a baseline and then a post-amphetamine scan before and after a mildly sensitizing regimen of repeated oral amphetamine. Unmedicated patients with first-episode psychosis (n = 21; 6 female) underwent a single pair of baseline and then post-amphetamine scans. Furthermore, T1 weighted magnetic resonance imaging of the prefrontal cortex was performed. Patients with first-episode psychosis showed larger release of dopamine compared to healthy volunteers. After sensitization of healthy volunteers their dopamine release was significantly amplified and no longer different from that seen in patients. Healthy volunteers showed a negative correlation between prefrontal cortical volume and dopamine release. There was no such relationship after sensitization or in patients. Our data in patients with untreated first-episode psychosis confirm the "endogenous sensitization" hypothesis and support the notion of impaired prefrontal control of the dopamine system in schizophrenia.

Prefrontal networks dynamically related to recovery from major depressive disorder: a longitudinal pharmacological fMRI study.

Due to lacking predictors of depression recovery, successful treatment of major depressive disorder (MDD) is frequently only achieved after therapeutic optimization leading to a prolonged suffering of patients. This study aimed to determine neural prognostic predictors identifying non-remitters prior or early after treatment initiation. Moreover, it intended to detect time-sensitive neural mediators indicating depression recovery. This longitudinal, interventional, single-arm, open-label, phase IV, pharmacological functional magnetic resonance imaging (fMRI) study comprised four scans at important stages prior (day 0) and after escitalopram treatment initiation (day 1, 28, and 56). Totally, 22 treatment-free MDD patients (age mean ± SD: 31.5 ± 7.7; females: 50%) suffering from a concurrent major depressive episode without any comorbid DSM-IV axis I diagnosis completed the study protocol. Primary outcome were neural prognostic predictors of depression recovery. Enhanced de-activation of anterior medial prefrontal cortex (amPFC, single neural mediator) indicated depression recovery correlating with MADRS score and working memory improvements. Strong dorsolateral PFC (dlPFC) activation and weak dlPFC-amPFC, dlPFC-posterior cingulate cortex (PCC), dlPFC-parietal lobe (PL) coupling (three prognostic predictors) hinted at depression recovery at day 0 and 1. Preresponse prediction of continuous (dlPFC-PL: R2day1 = 55.9%, 95% CI: 22.6-79%, P < 0.005) and dichotomous (specificity/sensitivity: SP/SNday1 = 0.91/0.82) recovery definitions remained significant after leave-one-out cross-validation. Identified prefrontal neural predictors might propel the future development of fMRI markers for clinical decision making, which could lead to increased response rates and adherence during acute phase treatment periods. Moreover, this study underscores the importance of the amPFC in depression recovery.