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: Although Alzheimer's disease (AD) is associated with early death, its life expectancy differs greatly between patients. A better understanding of this heterogeneity may reveal important disease mechanisms underlying the malignancy of AD. The aim of this study was to examine the relation between AD pathologies and early death in AD caused by dementia.", 'At a memory clinic, 247 referred consecutive patients with AD were monitored during 12.61.6 years. Multivariate Cox regression analyses were performed with baseline measures of amyloid beta (A) pathology (APOE genotype, cerebrospinal fluid (CSF) A42) tau pathology (CSF phosphorylated tau and total tau), cerebrovascular pathology (white-matter lesions and CSF/serum albumin ratio), neuroinflammatory pathology (CSF soluble vascular cell adhesion molecule-1, sVCAM-1), frontal, temporal, and central brain atrophies, global cognition, sex, and age. Comorbidities and medications also were analyzed. All continuous variables were transformed to z scores to compare hazard ratios (HRs) and 95% confidence intervals (CIs).', 'At follow-up, 89% of the patients had died. The mean survival time was 6.43.0 years. The AD pathology that independently predicted an early death caused by dementia was cerebral inflammation (sVCAM-1; HR, 1.32; 95% CI, 1.07-1.64). Other independent predictors were lower global cognition (HR, 0.51; 95% CI, 0.43-0.61), frontal atrophy (HR, 1.38; 95% CI, 1.12-1.70), and medial temporal atrophy (HR, 1.23; 95% CI, 1.02-1.49). When examining death caused by dementia and related causes (vascular diseases and infections), age (HR, 1.23; 95% CI, 1.04-1.46) and cerebrovascular pathology (white-matter lesions: HR, 1.17; 95% CI, 1.01-1.36; and CSF/serum albumin ratio: HR, 1.16; 95% CI, 1.001-1.34) were also significant risk factors in addition to the previous variables. No comorbidity or medication was significant in the specific-cause models.
Answer: This is the first study to link neuroinflammation independently to early death in AD and, hence, a rapidly progressing disease. Frontal and medial temporal atrophies and low cognition were also significant predictors. These are probably downstream biomarkers that reflect neuronal degeneration and late-stage disease. Our results suggest that inflammation, and not amyloid or tau pathology, is an independent underlying mechanism in the malignancy of AD.

Ex Output:
Is cerebral inflammation an underlying mechanism of early death in Alzheimer 's disease : a 13-year cause-specific multivariate mortality study?

Ex Input:
Context: Approximately 12% of bound blood calcium is linked to various anions including phosphate. In patients with end-stage kidney disease (ESKD), serum phosphate is highly variable. We propose that establishing a formula to calculate albumin- and phosphate-corrected total calcium would be more appropriate to estimate free calcium in ESKD patients.', 'In 82 haemodialysis patients, serum ionized calcium (Ca(ion)) and pH were measured by blood gas analyser with ion-selective electrodes at the point-of-care, while bicarbonate, phosphate, albumin, magnesium and total calcium (Ca(tot)) were measured at the central laboratory. Linear regression analysis of measured variables was used to best fit adjusted calcium versus Ca(ion).', 'The most parsimonious multiple linear regression model (r(2) = 0.81) of variables associated with Ca(ion) included Ca(tot) (coeff 0.820, P < 0.0001), albumin (coeff -0.016, P < 0.0001) and phosphate (coeff -0.063, P < 0.002). Modelling of available variables yielded the following equation to adjust calcium for albumin and phosphate: Ca(albPh) = Ca(tot) + (0.015 x (40 - [albumin]) + 0.07 x (1.5 - [phosphate])). At an ambient albumin of 40 g/L, Ca(albPh) would be 0.07 mmol/L lower than Ca(tot) for every mmol/L of phosphate. In vitro data using three different albumin levels and increasing phosphate concentrations demonstrated this relationship, with the slope of the phosphate effect being stronger at lower albumin concentrations.
Answer: Because guidelines recommendations indicate that corrected serum calcium should be maintained within the normal range in ESKD patients, inclusion of phosphate to correct Ca(tot) in these patients may have clinical implications on the choice of phosphate binders and the prescription of vitamin D or calcimimetic agents.

Ex Output:
Is serum phosphate an important determinant of corrected serum calcium in end-stage kidney disease?

Ex Input:
Context: Peritoneal dialysis (PD) is associated with functional and structural alterations of the peritoneal membrane. However, the (ir)reversibility of these pathological changes of the peritoneum is not understood fully.', 'In an experimental PD model, rats (n = 15) received daily 10 ml conventional glucose containing PD fluid, via peritoneal catheters connected to implanted subcutaneous mini vascular access ports. After 5 weeks of treatment, the first group of animals (PDF; n = 10) was sacrificed, while peritoneal catheters of the remaining group of rats (PD-rest; n = 5) were removed 1 week later. The latter group (PD-rest) was sacrificed 12 weeks after removing catheters. At both time points, untreated rats were included as controls. Cellular and morphological parameters were analysed by light and electron microscopy.', "Rats exposed to PD fluid for 5 weeks showed a severe angiogenesis in various peritoneal tissues. Peritoneal rest resulted in a significant reduction in blood vessel density in visceral (mesentery, P<0.05), but not in parietal peritoneum. Five weeks' exposure to PD fluid resulted in a profound fibrosis in the parietal peritoneum, whereas the degree of fibrosis was significantly reduced in the PD-rest group (P<0.02). Daily exposure to PD fluid induced a higher number of mast cells in the omentum compared with untreated rats, whereas peritoneal rest normalized the increased mast cell density completely (P<0.03). Likewise, continued PD fluid instillation evoked a strong omental milky spot response, which was returned to the control level after peritoneal rest (P<0.009). Furthermore, the number of mesothelial cells on the liver was significantly increased in rats treated with PD fluid, whereas animals from the PD-rest group had a lower number of mesothelial cells, although this was not statistically significant (P = 0.08). Finally, as evidenced by electron microscopy, daily exposure to PD fluid resulted in severe damage to the mesothelial cell layer covering the peritoneum, whereas this cell layer was completely recovered after peritoneal rest.
Answer: We show that PD fluid-induced cellular and morphological alterations of the peritoneal membrane are generally reversible.

Ex Output:
Are peritoneal dialysis fluid-induced changes of the peritoneal membrane reversible after peritoneal rest in rats?