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.
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Question: Context: Rhinovirus (RV) infection in asthma induces varying degrees of airway inflammation (e.g. neutrophils), but the underlying mechanisms remain unclear.', 'The major goal was to determine the role of genetic variation [e.g. single nucleotide polymorphisms (SNPs)] of Toll-interacting protein (Tollip) in airway epithelial responses to RV in a type 2 cytokine milieu.', 'DNA from blood of asthmatic and normal subjects was genotyped for Tollip SNP rs5743899 AA, AG and GG genotypes. Human tracheobronchial epithelial (HTBE) cells from donors without lung disease were cultured to determine pro-inflammatory and antiviral responses to IL-13 and RV16. Tollip knockout and wild-type mice were challenged with house dust mite (HDM) and infected with RV1B to determine lung inflammation and antiviral response.', 'Asthmatic subjects carrying the AG or GG genotype (AG/GG) compared with the AA genotype demonstrated greater airflow limitation. HTBE cells with AG/GG expressed less Tollip. Upon IL-13 and RV16 treatment, cells with AG/GG (vs. AA) produced more IL-8 and expressed less antiviral genes, which was coupled with increased NF-κB activity and decreased expression of LC3, a hallmark of the autophagic pathway. Tollip co-localized and interacted with LC3. Inhibition of autophagy decreased antiviral genes in IL-13- and RV16-treated cells. Upon HDM and RV1B, Tollip knockout (vs. wild-type) mice demonstrated higher levels of lung neutrophilic inflammation and viral load, but lower levels of antiviral gene expression.
Answer: Our data suggest that Tollip SNP rs5743899 may predict varying airway response to RV infection in asthma.

Answer: Does tollip SNP rs5743899 modulate human airway epithelial responses to rhinovirus infection?


Question: Context: Sit-to-stand tasks are commonly facilitated by modifying the initial position of the center of mass relative to the feet. It was hypothesized that modifications in the center of mass trajectory during sit-to-stand tasks altered the total body momentum at seat departure and redistributed the lower extremity net joint moments.', 'Between-task within-subject comparison was employed using a robust statistical method to accommodate for small sample size.', 'Six individuals performed four sit-to-stand tasks with systematic modifications in the initial center of mass position by varying the orientation of the lower extremity segments. The momentum of the center of mass and lower extremity net joint moments were quantified and compared.', 'Reducing the horizontal center of mass displacement significantly reduced horizontal total body momentum required at seat departure. Sit-to-stand tasks initiated with more horizontal shank and thigh positions required significantly greater knee and hip extensor net joint moments than those with more vertical shank and thigh positions. Sit-to-stand tasks initiated with vertical shank positions also required significantly greater hip extensor net joint moments as compared to those with more horizontal shank orientations.
Answer: When changes in initial center of mass position are made, alteration in center of mass horizontal momentum and the orientation of the lower extremity segments relative to the reaction force are observed. Consequently, mechanical demand imposed on the ankle, knee, and hip joint is redistributed. The magnitude of the net joint moments is dependent on the segment orientation, the reaction force, and the adjacent net joint moment.

Answer: Does modifying center of mass trajectory during sit-to-stand tasks redistribute the mechanical demand across the lower extremity joints?


Question: Context: Proliferative vitreoretinopathy (PVR) is a blinding disorder that develops after a retinal tear or detachment. Activation of the retinal pigmented epithelium (RPE) is implicated in PVR; however, the mechanisms leading to enhanced RPE proliferation, migration, and contraction remain largely unknown. This study utilized an in vitro model of PVR to investigate the role of acetylation in RPE activation and its contribution to the progression of this disease.', 'ARPE-19 cells, primary cultures of porcine RPE, and induced pluripotent stem cell-derived RPE (iPS-RPE) were utilized for cellular and molecular analyses. Cells treated with transforming growth factor beta 2 (TGFβ2; 10\u2009ng/mL) alone or in the presence of the broad-spectrum histone deacetylase (HDAC) inhibitor, trichostatin A (TSA; 0.1\u2009μM), were assessed for contraction and migration through collagen contraction and scratch assays, respectively. Western blotting and immunofluorescence analysis were performed to assess α-smooth muscle actin (α-SMA) and β-catenin expression after TGFβ2 treatment alone or in combination with TSA.', 'TGFβ2 significantly increased RPE cell contraction in collagen matrix and this effect was inhibited in the presence of TSA (0.1\u2009μM). In agreement with these data, immunofluorescence analysis of TSA-treated iPS-RPE wounded monolayers revealed decreased α-SMA as compared with control. Scratch assays to assess wound healing revealed TSA inhibited TGFβ2-mediated iPS-RPE cell migration.
Answer: Our findings indicate a role of acetylation in RPE activation. Specifically, the HDAC inhibitor TSA decreased RPE cell proliferation and TGFβ2-mediated cell contraction and migration. Further investigation of pharmacological compounds that modulate acetylation may hold promise as therapeutic agents for PVR.

Answer:
Does trichostatin A inhibit Retinal Pigmented Epithelium Activation in an In Vitro Model of Proliferative Vitreoretinopathy?