In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Q: Context: Besides chronic stress, chronic pain is a prevalent determinant for depression. Changes induced in specific brain regions by sustained pain may alter the processing of affective information, thus resulting in anxiodepressive disorders. Here, we compared the role of the anterior cingulate cortex (ACC) and the posterior insular cortex in the anxiodepressive, sensory, and affective aspects of chronic pain.', 'Neuropathic pain was induced by cuffing the right sciatic nerve of C57BL/6J mice. Lesions were performed by local injection of ibotenic acid and chronic activation of the ACC by optogenetic stimulation. Anxiodepressive-related behaviors were evaluated through the novelty suppressed feeding, marble burying, splash, and forced swimming tests. Mechanical thresholds were determined using von Frey filaments, and the relief of spontaneous pain was determined by using place conditioning.', 'The ACC lesion prevented the anxiodepressive consequences of chronic pain without affecting the sensory mechanical allodynia. Conversely, the tonic or spontaneous pain and the anxiodepressive consequences of pain remained present after posterior insular cortex lesion, even though the mechanical allodynia was suppressed. Furthermore, optogenetic stimulation of the ACC was sufficient to induce anxiety and depressive-like behaviors in naïve animals.\Question: Is the anterior cingulate cortex a critical hub for pain-induced depression?

A: Our results show that, at cortical level, the sensory component of chronic pain remains functionally segregated from its affective and anxiodepressive components. Spontaneous tonic pain and evoked allodynia can be experimentally dissociated. Furthermore, the ACC appears as a critical hub for mood disorders, including for the anxiodepressive consequences of chronic pain, and thus constitutes an important target for divulging the underlying mechanism.
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Q: Context: Transport across the blood-brain barrier (BBB) is an important mediator of beta-amyloid (Aβ) accumulation in the brain and a contributing factor in the pathogenesis of Alzheimer's disease (AD). One of the receptors responsible for the transport of Aβ in the BBB is the low density lipoprotein receptor-related protein 1 (LRP1). LRP1 is susceptible to proteolytic shedding at the cell surface, which prevents endocytic transport of ligands. Previously, we reported a strong inverse correlation between LRP1 shedding in the brain and Aβ transit across the BBB. Several proteases contribute to the ectodomain shedding of LRP1 including the α-secretase, a desintegrin and metalloproteinase domain containing protein 10 (ADAM10).", 'The role of ADAM10 in the shedding of LRP1 and Aβ BBB clearance was assessed through pharmacological inhibition of ADAM10 in an in vitro model of the BBB and through the use of ADAM10 endothelial specific knock-out mice. In addition, an acute treatment paradigm with an ADAM10 inhibitor was also tested in an AD mouse model to assess the effect of ADAM10 inhibition on LRP1 shedding and Aβbrain accumulation.', 'In the current studies, inhibition of ADAM10 reduced LRP1 shedding in brain endothelial cultures and increased Aβ42 transit across an in vitro model of the BBB. Similarly, transgenic ADAM10 endothelial knockout mice displayed lower LRP1 shedding in the brain and significantly enhanced Aβ clearance across the BBB compared to wild-type animals. Acute treatment with the ADAM10-selective inhibitor GI254023X in an AD mouse model substantially reduced brain LRP1 shedding and increased Aβ40 levels in the plasma, indicating enhanced Aβ transit from the brain to the periphery. Furthermore, both soluble and insoluble Aβ40 and Aβ42 brain levels were decreased following GI254023X treatment, but these effects lacked statistical significance.\Question: Does inhibition of ADAM10 promote the clearance of Aβ across the BBB by reducing LRP1 ectodomain shedding?

A: These studies demonstrate a role for ADAM10 in the ectodomain shedding of LRP1 in the brain and the clearance of Aβ across the BBB, which may provide a novel strategy for attenuating Aβ accumulation in the AD brain.
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Q: Context: Delirium is an important morbidity following heart surgery. We sought to determine whether dopamine infusion is associated with increased risk of delirium in patients undergoing coronary artery bypass grafting.', 'A total of 137 patients (mean age; 61.02±7.83, 105 males) were included in the study. Patients undergoing isolated coronary artery bypass grafting were considered eligible and those with preoperative neurological deficit or significant neurocognitive disorders, dementia or psychiatric disorders were excluded. Primary outcome measure was occurrence of delirium within 72 hours after operation. The diagnosis of delirium was made using confusion assessment method for the intensive care unit questionnaire. Both administration of dopamine as a dichotomised variable and the total amount of dopamine per kg body-weight were included in two different logistic regression models.', 'Delirium occurred in 18 (13.1%) patients. Age adjusted Mantel-Haenszel relative risk for delirium with receiving dopamine was 4.62. Relative risk was 2.37 (0.18 to 31.28, 95% CI, p=0.51) in total doses over 10mg whereas it was 3.55 (1.16 to 10.89 95% CI, p=0.02) in total doses over 30 mg per kg body-weight. Older age (p=0.03), dopamine administration (OR: 9.227 95% CI, 2.688-32.022, p<0.001) and the amount of dopamine administered (OR: 1.072, 95% CI, 1.032-1.115, p<0.001) were independent predictors for delirium 72 hours after surgery.\Question: Is dopamine Administration a Risk Factor for Delirium in Patients Undergoing Coronary Artery Bypass Surgery?

A:
Along with older age, dopamine infusion--even in low doses but more probably in higher doses--emerged as an independent risk factor for delirium in patients undergoing CABG. Further study is needed to confirm the validity of results presented.
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