TASK DEFINITION: Given a passage, 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.
PROBLEM: The objective of this study was to compare health-related quality of life (HR-QoL), disability/work productivity, and health care utilization in a variety of medical disorders with and without comorbid major depressive disorder (MDD) in the general population.', 'Twelve-month MDD (Composite International Diagnostic Interview) diagnosis was determined among 4181 participants from a community sample. Medical diagnoses (respiratory, cardiovascular, allergic, endocrine/metabolic, gastrointestinal, and neurological diseases) were made after medical examination. HR-QoL was evaluated with the MOS-SF-36. Outpatient doctor visits and disability/work productivity were assessed by self-report.', 'Comorbid MDD was associated with a lower SF-36 mental summary score in all medical diagnoses and with a lower physical summary score in comorbid allergic and neurological disorders. The number of coexisting medical disorders was strongly related to lower physical and mental summary scores in cases without comorbid depression. The number of outpatient doctor visits increased by 42% when any of the medical disorders without comorbid MDD was present, and comorbid MDD was associated with a further 24-42% increase, depending on the medical disorder. Comorbid MDD was strongly associated with lower full-time working status (37.1% with MDD vs. 51.0% without MDD) and with a significant increase in disability days (45%) in the presence of any medical disorder.

SOLUTION: Do medical disorders affect health outcome and general functioning depending on comorbid major depression in the general population?

PROBLEM: To determine whether granulocyte colony-stimulating factor (G-CSF) could prevent loss of spermatogenesis induced by busulfan chemotherapy via protection of undifferentiated spermatogonia, which might serve as an adjuvant approach to preserving male fertility among cancer patients.', 'Laboratory animal study.', 'University.', 'Laboratory mice.', 'Five-week-old mice were treated with a sterilizing busulfan dose and with 7 days of G-CSF or vehicle treatment and evaluated 10 weeks later (experiment 1) or 24 hours after treatment (experiment 2).', 'Experiment 1: testis weights, epididymal sperm counts, testis histology. Experiment 2: PLZF immunofluorescent costaining with apoptotic markers. Molecular analysis of G-CSF receptor expression in undifferentiated spermatogonia.', 'Ten weeks after treatment, busulfan-treated mice that also received treatment with G-CSF exhibited significantly better recovery of spermatogenesis and epididymal sperm counts than animals receiving busulfan alone. G-CSF led to increased numbers of PLZF+ spermatogonia 24 hours after treatment that was not accompanied by changes in apoptosis. To address the cellular target of G-CSF, mRNA for the G-CSF receptor, Csf3r, was found in adult mouse testes and cultured THY1+ (undifferentiated) spermatogonia, and cell-surface localized CSF3R was observed on 3% of cultured THY1+ spermatogonia.

SOLUTION: Does granulocyte colony-stimulating factor prevent loss of spermatogenesis after sterilizing busulfan chemotherapy?

PROBLEM: Angiotensin II (AngII), a vasoconstrictive peptide of the renin-angiotensin system (RAS), promotes hepatic fibrogenesis and induces microRNA-21(mir-21) expression. Angiotensin-(1-7) [Ang-(1-7)] is a peptide of the RAS, which attenuates liver fibrosis. Recently, it was reported that the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome participated in liver fibrosis. However, it remains unclear how mir-21 mediates AngII-induced NLRP3 inflammasome activation. We investigate the role of AngII-induced mir-21 in the regulation of NLRP3 inflammasome/IL-1 axis in liver fibrosis.', 'In vivo, circulating mir-21 was upregulated in patients with liver fibrosis and was positively correlated with liver fibrosis and oxidation. Treatment with Ang-(1-7) inhibited mir-21, NLRP3 inflammasome, and liver fibrosis after bile duct ligation (BDL) or AngII infusion. Inhibition of mir-21 suppressed the Smad7/Smad2/3/NOX4, Spry1/ERK/NF-B pathway, NLRP3 inflammasome, and liver fibrosis induced by AngII infusion. In vitro, AngII upregulated mir-21 expression via targeting Smad7 and Spry1 in primary hepatic stellate cells (HSCs). In contrast, Ang-(1-7) suppressed mir-21 expression and oxidation induced by AngII. Overexpression of mir-21 promoted oxidation, and collagen production enhanced the effect of AngII on NLRP3 inflammasome activation via the Spry1/ERK/NF-B, Smad7/Smad2/3/NOX4 pathways. However, downregulation of mir-21 exerted the opposite effects.

SOLUTION:
Does microRNA-21 mediate Angiotensin II-Induced Liver Fibrosis by Activating NLRP3 Inflammasome/IL-1 Axis via Targeting Smad7 and Spry1?