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.

[EX Q]: To investigate the association between adenoidectomy and/or tonsillectomy in childhood and asthma, allergic rhinitis (AR), and eczema in adolescence.', 'Longitudinal birth cohort study of 1328 members born in the city of Nijmegen. Information on ear-nose-throat surgery was documented at 2, 4, and 8 years of age. In 1055 cohort members the incidence of asthma, AR, and eczema at 21 years of age was determined using the International Study of Asthma and Allergic disease in Childhood Core Questionnaire. To analyse the association between adenoidectomy and/or tonsillectomy in childhood and asthma, AR, and eczema at age 21 years, relative risks (RR) were calculated.', 'Six hundred and ninety-three (66%) members completed the questionnaire at age 21 years, of whom 104 (15%) had undergone adenoidectomy and/or tonsillectomy and 262 (38%) reported atopic disease. Children who underwent adenoidectomy and/or tonsillectomy before the age of 8 years were not more likely to develop asthma, AR, or eczema at the age of 21 years than children who did not; RR 0.93 (95% confidence limits (CL) 0.52-1.64), RR 0.94 (CL 0.68-1.30), and RR 1.00 (CL 0.59-1.68), respectively.
[EX A]: Is adenoidectomy and/or tonsillectomy in childhood associated with atopic disease later in life?

[EX Q]: Increased placental growth secondary to reduced apoptosis may contribute to the development of macrosomia in GDM pregnancies. We hypothesize that reduced apoptosis in GDM placentas is caused by dysregulation of apoptosis related genes from death receptors or mitochondrial pathway or both to enhance placental growth in GDM pregnancies.', 'Newborn and placental weights from women with no pregnancy complications (controls; N=5), or with GDM (N=5) were recorded. Placental villi from both groups were either fixed for TUNEL assay, or snap frozen for gene expression analysis by apoptosis PCR microarrays and qPCR.', 'Maternal, placental and newborn weights were significantly higher in the GDM group vs. Controls. Apoptotic index of placentas from the GDM group was markedly lower than the Controls. At a significant threshold of 1.5, seven genes (BCL10, BIRC6, BIRC7, CASP5, CASP8P2, CFLAR, and FAS) were down regulated, and 13 genes (BCL2, BCL2L1, BCL2L11, CASP4, DAPK1, IκBκE, MCL1, NFκBIZ, NOD1, PEA15, TNF, TNFRSF25, and XIAP) were unregulated in the GDM placentas. qPCR confirmed the consistency of the PCR microarray. Using Western blotting we found significantly decreased placental pro-apoptotic FAS receptor and FAS ligand (FASL), and increased mitochondrial anti-apoptotic BCL2 post GDM insult. Notably, caspase-3, which plays a central role in the execution-phase of apoptosis, and its substrate poly (ADP-ribose) polymerase (PARP) were significantly down regulated in GDM placentas, as compared to non-diabetic Control placentas.
[EX A]: Does gestational diabetes mellitus alter apoptotic and inflammatory gene expression of trophobasts from human term placenta?

[EX Q]: Lactate dehydrogenase-elevating virus (LDV) is a natural infectious agent of mice. Like several other viruses, LDV causes widespread and very rapid but transient activation of both B cells and T cells in lymphoid tissues and the blood. The mechanism of this activation has not been fully described and is the focus of the current studies.', "A known inducer of early lymphocyte activation is IFNalpha, a cytokine strongly induced by LDV infection. Neutralization of IFNalpha in the plasma from infected mice ablated its ability to activate lymphocytes in vitro. Since the primary source of virus-induced IFNalpha in vivo is often plasmacytoid dendritic cells (pDC's), we depleted these cells prior to LDV infection and tested for lymphocyte activation. Depletion of pDC's in vivo eradicated both the LDV-induced IFNalpha response and lymphocyte activation. A primary receptor in pDC's for single stranded RNA viruses such as LDV is the toll-like receptor 7 (TLR7) pattern recognition receptor. Infection of TLR7-knockout mice revealed that both the IFNalpha response and lymphocyte activation were dependent on TLR7 signaling in vivo. Interestingly, virus levels in both TLR7 knockout mice and pDC-depleted mice were indistinguishable from controls indicating that LDV is largely resistant to the systemic IFNalpha response.
[EX A]:
Does lactate dehydrogenase-elevating virus induce systemic lymphocyte activation via TLR7-dependent IFNalpha responses by plasmacytoid dendritic cells?