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: Cyclosporine causes intrarenal vasoconstriction, which may account for its nephrotoxic side effects. Plasma levels of the vasoconstrictor peptide endothelin-1 are increased after cyclosporine administration, and endothelin-1 has been shown to cause renal vasoconstriction. In this study we used in vivo microscopy to investigate the role of endothelin-1 in cyclosporine-induced vasoconstriction.', 'Hydronephrotic kidneys in decerebrate rats were suspended in an environmentally controlled tissue bath with neurovascular supply intact. Interlobular, afferent, and efferent arteriolar diameters and flow were measured by videomicroscopy and Doppler velocimetry. Cyclosporine was added to the tissue bath, and measurements were repeated for 60 minutes. In study groups endogenous endothelin-1 was blocked by infusion of either specific endothelin antiserum or an endothelin-1 receptor antagonist.', 'Cyclosporine caused constriction of the interlobular artery by 20% +/- 2% and a corresponding decrease in blood flow by 66% +/- 4%. The afferent and efferent arterioles constricted to a similar degree. This vasoconstriction was entirely prevented by infusion of either the endothelin antiserum or the receptor antagonist. The antagonist reagents alone had no effect on hemodynamic parameters or renal microvessel diameters.
Answer: The acute renal vasoconstriction induced by cyclosporine is mediated by endothelin-1. Endogenous endothelin-1 has little role in maintaining basal vascular tone.

Ex Output:
Is acute cyclosporine-induced renal vasoconstriction mediated by endothelin-1?


Ex Input:
Context: We utilized whole-genome mapping of promoters that are activated by DNA hypomethylation in hepatocellular carcinoma (HCC) clinical samples to shortlist novel targets for anticancer therapeutics. We provide a proof of principle of this approach by testing six genes short-listed in our screen for their essential role in cancer growth and invasiveness.', 'We used siRNA- or shRNA-mediated depletion to determine whether inhibition of these genes would reduce human tumor xenograft growth in mice as well as cell viability, anchorage-independent growth, invasive capacities, and state of activity of nodal signaling pathways in liver, breast, and bladder cancer cell lines.', 'Depletion of EXOSC4, RNMT, SENP6, WBSCR22, RASAL2, and NENF effectively and specifically inhibits cancer cell growth and cell invasive capacities in different types of cancer, but, remarkably, there is no effect on normal cell growth, suggesting a ubiquitous causal role for these genes in driving cancer growth and metastasis. Depletion of RASAL2 and NENF in vitro reduces their growth as explants in vivo in mice. RASAL2 and NENF depletion interferes with AKT, WNT, and MAPK signaling pathways as well as regulation of epigenetic proteins that were previously demonstrated to drive cancer growth and metastasis.
Answer: Our results prove that genes that are hypomethylated and induced in tumors are candidate targets for anticancer therapeutics in multiple cancer cell types. Because these genes are particularly activated in cancer, they constitute a group of targets for specific pharmacologic inhibitors of cancer and cancer metastasis. Clin Cancer Res; 20(12); 3118-32. ©2014 AACR.

Ex Output:
Does genome-wide study of hypomethylated and induced genes in patients with liver cancer unravel novel anticancer targets?


Ex Input:
Context: Adolescents with type 1 diabetes are at increased risk for deteriorating glycemic control, poor quality of life, and depressive symptoms. Stress and coping are related to these outcomes in adolescents with diabetes, yet few studies have examined these constructs longitudinally.', 'This study aimed to describe stress and coping in adolescents with type 1 diabetes and to examine coping strategies as predictors of adolescent adjustment (i.e., depressive symptoms, quality of life) and glycemic control.', "Adolescents with type 1 diabetes completed measures of diabetes-related stress, coping, symptoms of depression, and quality of life at baseline, 6\xa0months, and 12\xa0months. Data on glycemic control were collected from the adolescents' medical charts.", "The adolescents' use of primary control coping (e.g., problem solving) and secondary control engagement coping (e.g., positive thinking) strategies predicted significantly fewer problems with quality of life and fewer depressive symptoms over time. In contrast, the use of disengagement coping strategies (e.g., avoidance) predicted more problems with quality of life and depressive symptoms. Coping was not a significant predictor of glycemic control. Coping mediated the effects of diabetes-related stress on depressive symptoms and quality of life.
Answer: The ways in which adolescents with type 1 diabetes cope with diabetes-related stress predict quality of life and symptoms of depression but not glycemic control. Through the use of screening to identify adolescent's diabetes-related stress and targeted interventions to improve coping strategies, there is potential to improve outcomes.

Ex Output:

Does stress and Coping predict Adjustment and Glycemic Control in Adolescents with Type 1 Diabetes?