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https://www.selleckchem.com/products/NVP-BHG712.html Depression is a debilitating disorder with high prevalence and socioeconomic cost, but the brain-physiological processes that are altered during depressive states are not well understood. Here, we build on recent findings in macaques that indicate a direct causal relationship between pupil dilation and anterior cingulate cortex mediated arousal during anticipation of reward. We translated these findings to human subjects with concomitant pupillometry/fMRI in a sample of unmedicated participants diagnosed with major depression and healthy controls. We could show that the upregulation and maintenance of arousal in anticipation of reward was disrupted in patients in a symptom-load dependent manner. We could further show that the failure to maintain reward anticipatory arousal showed state-marker properties, as it tracked the load and impact of depressive symptoms independent of prior diagnosis status. Further, group differences of anticipatory arousal and continuous correlations with symptom load were not traceable only at the level of pupillometric responses, but were mirrored also at the neural level within salience network hubs. The upregulation and maintenance of arousal during reward anticipation is a novel translational and well-traceable process that could prove a promising gateway to a physiologically informed patient stratification and targeted interventions.Wernicke's encephalopathy (WE) is an acute neurological disorder resulting from thiamine deficiency, commonly found in alcohol use disorder (AUD) patients. Liver transplantation (LT) could represent a risk factor for the onset of WE in AUD patients, due to the onset of chronic depletion of thiamine in this population and the high metabolic demand of surgery and the postoperative period. However, few data are available about the risk of the onset of WE in AUD patients after LT. Here we report three cases of AUD patients who developed WE with confusion and

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