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.

[Q]: 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.
[A]: Is serum phosphate an important determinant of corrected serum calcium in end-stage kidney disease?

[Q]: Context: Although diabetic patients often have gastrointestinal complications, the gastric mucosal function in diabetes has not been well documented.', 'To investigate the effect of fasting on the gastric mucosa in C57BL/KsJ-db +/+ db (db/db) mice, genetically non-insulin-dependent diabetic animals.', 'Blood glucose levels, gastric mucosal morphology, and the amount of gastric mucin were examined before and after 18 h of fasting with free access to water in db/db mice and their non-diabetic littermates (db/m).', 'Although 18 h of fasting reduced the blood glucose levels of both db/db and db/m mice, fasting decreased the amount of gastric adherent mucin and caused haemorrhagic gastric lesions only in db/db mice. After fasting, oral administration of ethanol induced much more severe gastric damage in db/db than in db/m mice. The above fasting-induced gastric damage such as haemorrhagic lesions, loss of the mucin, and the increased sensitivity to ethanol worsened as the duration of diabetes became longer. Glucose ingestion in drinking water during the fasting counteracted the fall in blood glucose and prevented the decrease in the amount of gastric mucin and the formation of gastric mucosal lesions in db/db mice.
Answer: These findings indicate that fasting-induced glucose deficit causes gastric mucosal lesions and increases the susceptibility of gastric mucosa to noxious agents owing to the loss of mucus glycoprotein in db/db mice. Prolonged diabetes is likely to augment the severity of fasting-induced impairment of the gastric mucosal function.
[A]: Does fasting induce impairment of gastric mucosal integrity in non-insulin-dependent diabetic ( db/db ) mice?

[Q]: Context: Although moderate (conscious) sedation is intended during elective gastrointestinal endoscopy, unintended levels of deep sedation occur. The aims of this study were to prospectively evaluate the incidence and risk factors of deep sedation during elective endoscopy with meperidine and midazolam intended to maintain a level of moderate sedation.', "Eighty American Society of Anesthesiology class 1-2, outpatients presenting for elective esophagogastroduodenoscopy (EGD), colonoscopy, endoscopic retrograde cholangiopancreatography (ERCP), and endoscopic ultrasonography (EUS) were offered enrollment. Intravenous meperidine and midazolam were administered according to a standardized protocol. Hemodynamic parameters and levels of sedation were assessed and recorded by a single observer at 3-min intervals. The Modified Observer's Assessment of Alertness/Sedation (MOAA/S) scale (ranging 1-5) is a subjective sedation assessment scale used to assess sedation levels. Occurrence of deep sedation, defined by MOAA/S 1-2, was recorded. Univariable and multivariable analyses were used to assess predictors of deep sedation.", 'Deep sedation occurred in 54/80 (68%) patients for a total of 204/785 (26%) of total sedation assessments. The percentage of deep sedation episodes of all sedation-level observations by procedure was 26% for EGD, 11% for colonoscopy, 35% for ERCP, and 29% for EUS. Deep sedation occurred at least once in 60% of EGD, 45% of colonoscopy, 85% of ERCP, and 80% of EUS. Multivariable analysis showed that only ERCP and EUS were independent risk factors of deep sedation.
Answer: Deep sedation occurs frequently during elective endoscopy with meperidine and midazolam used with the intent of moderate sedation. ERCP and EUS are risk factors for the occurrence of deep sedation, independent of sedation dose or length of procedure.
[A]:
Does deep sedation occur frequently during elective endoscopy with meperidine and midazolam?