Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Ex Input:
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.
Answer: 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.

Ex Output:
Is the anterior cingulate cortex a critical hub for pain-induced depression?


Ex Input:
Context: Genetic haploinsufficiency of SYNGAP1/Syngap1 commonly occurs in developmental brain disorders, such as intellectual disability, epilepsy, schizophrenia, and autism spectrum disorder. Thus, studying mouse models of Syngap1 haploinsufficiency may uncover pathologic developmental processes common among distinct brain disorders.', 'A Syngap1 haploinsufficiency model was used to explore the relationship between critical period dendritic spine abnormalities, cortical circuit assembly, and the window for genetic rescue to understand how damaging mutations disrupt key substrates of mouse brain development.', 'Syngap1 mutations broadly disrupted a developmentally sensitive period that corresponded to the period of heightened postnatal cortical synaptogenesis. Pathogenic Syngap1 mutations caused a coordinated acceleration of dendrite elongation and spine morphogenesis and pruning of these structures in neonatal cortical pyramidal neurons. These mutations also prevented a form of developmental structural plasticity associated with experience-dependent reorganization of brain circuits. Consistent with these findings, Syngap1 mutant mice displayed an altered pattern of long-distance synaptic inputs into a cortical area important for cognition. Interestingly, the ability to genetically improve the behavioral endophenotype of Syngap1 mice decreased slowly over postnatal development and mapped onto the developmental period of coordinated dendritic insults.
Answer: Pathogenic Syngap1 mutations have a profound impact on the dynamics and structural integrity of pyramidal cell postsynaptic structures known to guide the de novo wiring of nascent cortical circuits. These findings support the idea that disrupted critical periods of dendritic growth and spine plasticity may be a common pathologic process in developmental brain disorders.

Ex Output:
Does syngap1 haploinsufficiency damage a postnatal critical period of pyramidal cell structural maturation linked to cortical circuit assembly?


Ex Input:
Context: Although serum thyroglobulin (Tg) is an excellent marker for detecting recurrent or persistent differentiated thyroid cancer (DTC), it is unreliable in patients who have positive anti-Tg antibodies. Furthermore, a growing number of patients with DTC have elevated Tg levels but no detectable disease on radioiodine scanning or other imaging studies. The objective of this study was to determine whether a gradient in Tg protein level exists in patients with DTC.', 'Fifteen patients who underwent thyroidectomy and/or lymph node dissection for primary DTC (n = 10 patients) and recurrent or persistent DTC (n = 5 patients). A venipuncture was performed simultaneously from the internal jugular vein adjacent to the tumor and the ipsilateral antecubital vein. Venous Tg protein levels were measured by using a chemiluminescence assay. RESULTS.: The average internal jugular-to-antecubital vein Tg protein ratio was 3.4:1.0 (median Tg ratio, 2.9:1; range, 0.8-62.2). Four patients had positive anti-Tg antibodies but still had a Tg gradient. Tg levels were significantly higher in the adjacent internal jugular vein than in the antecubital vein (P = .0019). The Tg ratio between the internal jugular and antecubital veins was significantly higher in patients with recurrent or persistent DTC than in patients with primary tumors (P = .0196).
Answer: To the authors' knowledge, this is the first study to document a venous gradient in Tg protein levels in patients with DTC. The findings suggested that venous sampling for Tg may be used to localize DTC in some patients who have high or increasing serum Tg levels but negative radioiodine scans or imaging studies.

Ex Output:

Do patients with differentiated thyroid cancer have a venous gradient in thyroglobulin levels?