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: p38 mitogen-activated protein kinase is associated with many clinical entities characterized by inflammation. We postulated that inhibition of p38 mitogen-activated protein kinase with FR167653 attenuates inflammation and the development of pulmonary hypertension in monocrotaline-treated rats.', 'Rats were divided into 4 groups: (1) the control group (daily 0.9% saline), (2) the FR group (daily FR167653, 2 mg . kg(-1) . d(-1)), (3) the MCT group (daily 0.9% saline the day after a single monocrotaline dose, 60 mg/kg), and (4) the MCT+FR group (daily FR167653, 2 mg . kg(-1) . d(-1), the day after a single MCT dose). Body weight, pulmonary artery pressure, and morphometric changes of the pulmonary artery with the histopathologic method were observed weekly for 4 weeks. Also, p38 mitogen-activated protein kinase activity and inflammatory cytokine expression in the lung were measured.', 'Four weeks after monocrotaline administration, mean pulmonary artery pressure in the MCT+FR group was lower than in the MCT group (MCT+FR vs MCT: 24.7 +/- 1.9 vs 36.5 +/- 2.1 mm Hg; P < .05). In morphometric analysis the percentage of medial wall thickness and the percentage of muscularization in the MCT+FR group were reduced compared with those in the MCT group after 4 weeks (P < .05); however, the number of macrophages was not significantly different. p38 mitogen-activated protein kinase activity was significantly attenuated in the MCT+FR group compared with in the MCT group (7.2 +/- 0.52 vs 2.1 +/- 0.23 fold-increase, P < .05, at 1 week). Although mRNA levels of tumor necrosis factor alpha and interleukin 1beta were reduced in the MCT+FR group compared with in the MCT group (tumor necrosis factor alpha: 1.18 +/- 0.36 vs 3.05 +/- 1.12 fold-increase, P < .05, at 2 weeks; interleukin 1beta: 2.2 +/- 0.34 vs 4.4 +/- 1.09 fold-increase, P < .05, at 1 week), FR167653 did not suppress increased monocyte chemotactic protein 1 mRNA expression induced by monocrotaline (3.2 +/- 0.62 vs 3.1 +/- 0.42 fold-increase, at 1 week).
Answer: FR167653 significantly attenuates the expression of inflammatory cytokines, ultimately preventing the progression of pulmonary hypertension. These results suggest that p38 mitogen-activated protein kinase might play a central role in the molecular events that underlie the development and progression of pulmonary hypertension.

Ex Output:
Does specific inhibition of p38 mitogen-activated protein kinase with FR167653 attenuate vascular proliferation in monocrotaline-induced pulmonary hypertension in rats?


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: Evacuation disorders associated with a rectocele can be improved by rectocele repair. This study investigated whether anorectal function tests results change after rectocele repair.', 'Fourteen patients with 2nd or 3rd degree rectocele and evacuation disorder were treated by posterior colporrhaphy and evaluated pre- and postoperatively (after 8 months, range 3-14) using questionnaires, anal manometry and endosonography, rectal barostat testing, and colonic transit time measurement with radio-opaque markers. Results from female controls were used for comparison.', 'Preoperatively, rectocele patients had high maximal basal sphincter pressures, large sphincter lengths, and low maximal squeeze pressures, with an anal sphincter defect in seven and lower visceral sensitivity scores than in controls. Postprandial rectal responses (more than 10% decrease in postprandial volume after 1 h) were found in 3 of 14 patients compared to 2 of 11 parous and 9 of 11 nulliparous controls. After repair, a rectocele of 2nd degree was found in four patients. Questionnaire scores were significantly decreased for straining, evacuation disorder, manual support, and protrusion. Overall patient satisfaction with the operation scored 8.25 (range 3-10). Defecation frequencies and stool consistencies were unaltered. Anal pressures, rectal compliance-curves, visceral sensitivity, and colonic transit times were unaltered after the rectocele repair.
Answer: Rectocele repair improved complaints of evacuation disorder and protrusion, but defecation frequency and stool consistency were not affected. Anorectal function was unaltered after rectocele repair. Selection of patients for rectocele repair should be performed based on evacuation and protrusion complaints, anorectal function, or colonic transit time measurements have a limited role.

Ex Output:

Does rectocele repair improve evacuation and prolapse complaints independent of anorectal function and colonic transit time?