instruction:
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.
question:
Context: Hepatic expression of growth hormone (GH)-inducible genes serine protease inhibitor (Spi 2.1) and insulin-like growth factor (IGF)-I are inhibited by interleukin (IL)-1. The current study examines the role of the nuclear factor kappaB (NFkappaB) pathway and suppressor of cytokine signaling (SOCS)-3 expression as potential mechanisms for IL-1-mediated GH resistance.', 'CWSV-1 hepatocytes were cotransfected with Spi 2.1 or IGF-1 promoter luciferase constructs and empty pCMV4 vector or dominant negative inhibitor-kappaBalpha (IkappaBalpha)S/A construct. Cells were treated with or without IL-1 and then stimulated with or without recombinant human GH. Cell extracts were assayed for luciferase activity and protein, normalized and expressed as fold-induction. CWSV-1 cells transfected with pCMV4 or IkappaBalphaS/A were treated with or without IL-1 then SOCS-3 mRNA was measured. Finally, CWSV-1 cells were cotransfected with a SOCS-3 promoter construct with or without pCMV4 or IkappaBalphaS/A and then stimulated with or without IL-1 to investigate SOCS-3 promoter activity.', 'CWSV-1 cells cotransfected with pCMV4 demonstrated a three- to fivefold induction of Spi 2.1 or IGF-1 promoter activity after GH stimulation that was almost completely inhibited by IL-1. Cotransfection with IkappaBalphaS/A increased GH-inducible Spi 2.1 and IGF-1 promoter activity, but the inhibitory effects of IL-1 on both promoters were attenuated by cotransfection with IkappaBalphaS/A. IL-1 stimulated SOCS-3 mRNA expression and promoter activity. Cotransfection with IkappaBalphaS/A increased IL-1-inducible SOCS-3 promoter activity, but not SOCS-3 mRNA or protein.\Question: Does nuclear factor kappaB mediate the inhibitory effects of interleukin-1 on growth hormone-inducible gene expression?
answer:
Signaling via the NFkappaB pathway is responsible for the inhibitory effects of IL-1 on GH-inducible gene expression by a mechanism that does not seem to involve increased SOCS-3 expression.


question:
Context: Depression is a prevalent comorbidity of chronic respiratory disease (CRD), and may indicate worse clinical outcomes. The relationship between depression and living with chronic hypoxia due to CRD or residence at altitude has received little attention in resource-poor settings.', 'To investigate the association between CRD conditions and depressive symptoms in four settings in Peru.', 'We collected data on CRD and depressive symptoms in adults aged ⩾35 years. Depressive symptoms were measured according to the Center for Epidemiologic Studies Depression scale. Multivariable ordinal logistic regression was used to assess the adjusted odds of being in a higher category of depressive symptoms as a function of CRD.', 'We analyzed data from 2953 participants (mean age 55.3 years, 49% male). The prevalence of major depressive symptoms was 19%, with significant variation according to setting. Participants with at least one CRD (OR 1.34, 95%CI 1.06-1.69) and those living at altitude (OR 1.64, 95%CI 1.10-2.43) had an increased adjusted odds of being in a higher category of depressive symptoms.\Question: Are chronic respiratory disease and high altitude associated with depressive symptoms in four diverse settings?
answer:
We found a high prevalence of depressive symptoms, and a positive association between depressive symptoms with CRD and with living at altitude, both of which cause chronic hypoxia.


question:
Context: 22q11 deletion syndrome arises from recombination between low-copy repeats on chromosome 22. Typical deletions result in hemizygosity for TBX1 associated with congenital cardiovascular disease. Deletions distal to the typically deleted region result in a similar cardiac phenotype but lack in extracardiac features of the syndrome, suggesting that a second haploinsufficient gene maps to this interval.', 'The transcription factor HIC2 is lost in most distal deletions, as well as in a minority of typical deletions. We used mouse models to test the hypothesis that HIC2 hemizygosity causes congenital heart disease.', 'We created a genetrap mouse allele of Hic2. The genetrap reporter was expressed in the heart throughout the key stages of cardiac morphogenesis. Homozygosity for the genetrap allele was embryonic lethal before embryonic day E10.5, whereas the heterozygous condition exhibited a partially penetrant late lethality. One third of heterozygous embryos had a cardiac phenotype. MRI demonstrated a ventricular septal defect with over-riding aorta. Conditional targeting indicated a requirement for Hic2 within the Nkx2.5+ and Mesp1+ cardiovascular progenitor lineages. Microarray analysis revealed increased expression of Bmp10.\Question: Is hIC2 a novel dosage-dependent regulator of cardiac development located within the distal 22q11 deletion syndrome region?
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Our results demonstrate a novel role for Hic2 in cardiac development. Hic2 is the first gene within the distal 22q11 interval to have a demonstrated haploinsufficient cardiac phenotype in mice. Together our data suggest that HIC2 haploinsufficiency likely contributes to the cardiac defects seen in distal 22q11 deletion syndrome.