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.

Input: Consider Input: Context: Several studies have shown excess mortality among hip fracture patients compared with the normal population of the same age. Finnish guidelines for medical treatment of hip fracture patients recommend anti-osteoporosis medication and the daily concomitant use of prescribed calcium and vitamin D supplements. However, whether post-fracture use of calcium and vitamin D supplements is associated with survival in such patients has not been evaluated.', "To study the association between survival in hip fracture patients and patients' sex and age, pre-fracture vitamin D status, American Society of Anesthesiologists - Physical Status (ASA-PS) class, type of fracture and post-fracture use of prescribed calcium plus vitamin D and anti-osteoporotic medication.", "The study population was 221 hip fracture patients primarily treated in acute care for a new hip fracture in 2003-4 in two Finnish hospitals. After a median of 27.5 months from the fracture, a questionnaire was sent to all patients who were still alive at the time (n = 137). The patients were queried about their use of prescribed calcium plus vitamin D supplementation and of anti-osteoporotic drugs. The follow-up time for use of anti-osteoporotic medication and prescribed calcium and vitamin D was 19.5-36 months (median 27.5 months). Data on the use of prescribed calcium plus vitamin D supplementation and anti-osteoporotic drugs were checked against information on reimbursement of drug prescriptions held by the Finnish Social Insurance Institution. A total of 4 years' (48 months') survival data for all patients in the study population was also obtained, with the dates of patient deaths being checked against Official National and Regional population statistics. Patient survival was analysed using both the Bayesian multivariate analysis and the life table method.", 'In the multivariate analysis, the combination of variables that best explained post-fracture survival was as follows: age <80 years; ASA-PS class 1-2 (ASA-PS class 1 and 2 data were combined in calculations); post-fracture use of prescribed calcium plus vitamin D supplements concomitantly with anti-osteoporotic drugs; post-fracture use of prescribed calcium plus vitamin D supplements; post-fracture use of anti-osteoporotic drugs only; and type of fracture (femoral neck or subtrochanteric). This model correctly predicted 74% of cases. At 36 months, we observed a 36% reduction in deaths in females who used prescribed calcium plus vitamin D supplementation and a corresponding 43% reduction in males. Survival of females who used anti-osteoporotic drugs concomitantly was even greater (43% reduction in deaths) over the entire follow-up period. Excess mortality was highest in females and males who used neither anti-osteoporotic drugs nor prescribed calcium and vitamin D.
Answer: Our results indicate a potential relationship between reduced mortality and post-fracture use of prescribed calcium plus vitamin D supplementation and, in females, concomitant use of anti-osteoporotic drugs. However, further investigations are needed to understand the reason for the reduction in the risk of death. Population-based, randomized, placebo-controlled trials with total mortality as the main endpoint should be conducted to verify our results.

Output: Is post-fracture prescribed calcium and vitamin D supplements alone or , in females , with concomitant anti-osteoporotic drugs associated with lower mortality in elderly hip fracture patients : a prospective analysis?

Input: Consider Input: Context: Environmental conditions (eg, latitude) play a critical role in the susceptibility and severity of many autoimmune disorders, including multiple sclerosis (MS). Here, we investigated the mechanisms underlying the beneficial effects of immune regulatory processes induced in the skin by moderate ultraviolet B (UVB) radiation on central nervous system (CNS) autoimmunity.', 'Effects of UVB light were analyzed in a murine model of CNS autoimmunity (experimental autoimmune encephalomyelitis). Additionally, patients with relapsing-remitting MS were treated with narrowband UVB phototherapy. Immunomodulatory effects were examined in skin biopsies, serum samples, and immune cells of the peripheral blood.', 'Regulatory T cells (Tregs), which are induced locally in the skin-draining lymph nodes in response to UVB exposure, connect the cutaneous immune response to CNS immunity by migration to the sites of inflammation (blood, spleen, CNS). Here, they attenuate the inflammatory response and ameliorate disease symptoms. Treg-inducing tolerogenic dendritic cells (DCs) were further necessary for induction of this systemic immune regulation by UVB radiation, because ablation of Langerhans cells abolished the UVB-induced phenotype. MS patients treated with UVB phototherapy showed an increase in induced Tregs and tolerogenic DCs accompanied by the downregulation of the T-cell effector cytokine interleukin 21. The treatment further induced elevated serum levels of vitamin D.
Answer: Local UVB radiation of the skin influences systemic immune reactions and attenuates systemic autoimmunity via the induction of skin-derived tolerogenic DCs and Tregs. Our data could have implications for the understanding or therapeutic modulation of environmental factors that influence immune tolerance.

Output: Does ultraviolet B light attenuate the systemic immune response in central nervous system autoimmunity?

Input: Consider Input: Context: Macrophage accumulation of cholesterol leads to foam cell formation which is a major pathological event of atherosclerosis. Recent studies have shown that microRNA (miR)-19b might play an important role in cholesterol metabolism and atherosclerotic diseases. Here, we have identified miR-19b binding to the 3'UTR of ATP-binding cassette transporter A1 (ABCA1) transporters, and further determined the potential roles of this novel interaction in atherogenesis.", 'To investigate the molecular mechanisms involved in a miR-19b promotion of macrophage cholesterol accumulation and the development of aortic atherosclerosis.', "We performed bioinformatics analysis using online websites, and found that miR-19b was highly conserved during evolution and directly bound to ABCA1 mRNA with very low binding free energy. Luciferase reporter assay confirmed that miR-19b bound to 3110-3116 sites within ABCA1 3'UTR. MiR-19b directly regulated the expression levels of endogenous ABCA1 in foam cells derived from human THP-1 macrophages and mouse peritoneal macrophages (MPMs) as determined by qRT-PCR and western blot. Cholesterol transport assays revealed that miR-19b dramatically suppressed apolipoprotein AI-mediated ABCA1-dependent cholesterol efflux, resulting in the increased levels of total cholesterol (TC), free cholesterol (FC) and cholesterol ester (CE) as revealed by HPLC. The excretion of (3)H-cholesterol originating from cholesterol-laden MPMs into feces was decreased in mice overexpressing miR-19b. Finally, we evaluated the proatherosclerotic role of miR-19b in apolipoprotein E deficient (apoE(-/-)) mice. Treatment with miR-19b precursor reduced plasma high-density lipoprotein (HDL) levels, but increased plasma low-density lipoprotein (LDL) levels. Consistently, miR-19b precursor treatment increased aortic plaque size and lipid content, but reduced collagen content and ABCA1 expression. In contrast, treatment with the inhibitory miR-19b antisense oligonucleotides (ASO) prevented or reversed these effects.
Answer: MiR-19b promotes macrophage cholesterol accumulation, foam cell formation and aortic atherosclerotic development by targeting ABCA1.
Output: Does microRNA-19b promote macrophage cholesterol accumulation and aortic atherosclerosis by targeting ATP-binding cassette transporter A1?