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: To assess the accuracy of the clinically estimated blood loss (EBL) when compared with the actual blood loss (ABL) in replacement surgeries.', "This prospective study was done in Sri Ramachandra Medical Centre from April 2011 to April 2013. Altogether 140 patients undergoing total hip replacement or total knee replacement were included with the inclusion criteria being patients with haemoglobin higher than 100 g/ml and coagulation profile within normal limits. Exclusion criteria were intake of anti-platelet drug or anti-coagulant, bleeding disorders, thrombotic episode, and haematological disorders. There were 65 men and 75 women. In this study, the consultants were free to use any clinical method to estimate the blood loss, including counting the blood-soaked mops and gauze pieces (estimating the volume of blood carried in all the mops and gauzes), measuring blood lost to suction bottles and blood in and around the operative field. The ABL was calculated based on a modification of the Gross's formula using haematocrit values.", 'In 42 of the 140 cases, the EBL exceeded the ABL. These cases had a negative difference in blood loss (or DIFF-BL<0) and were included in the overestimation group, which accounted for 30% of the study population. Of the remaining 98 cases (70%), the ABL exceeded the EBL. Therefore they were put into the underestimation group who had a positive difference in blood loss (DIFF-BL>0). We found that when the average blood loss was small, the accuracy of estimation was high. But when the average blood loss exceeded 500 ml, the accuracy rate decreased significantly. This suggested that clinical estimation is inaccurate with the increase of blood loss.
Answer: This study has shown that using clinical estimation alone to guide blood transfusion is inadequate. In this study, 70% of patients had their blood loss underestimated, proving that surgeons often underestimate blood loss in replacement surgeries.

Answer: Do surgeons often underestimate the amount of blood loss in replacement surgeries?


Question: 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.

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


Question: Context: Peroxisome proliferator-activated receptor alpha (PPARα) is a key regulator of hepatic fat oxidation that serves as an energy source during starvation. Vanin-1 has been described as a putative PPARα target gene in liver, but its function in hepatic lipid metabolism is unknown.', 'We investigated the regulation of vanin-1, and total vanin activity, by PPARα in mice and humans. Furthermore, the function of vanin-1 in the development of hepatic steatosis in response to starvation was examined in Vnn1 deficient mice, and in rats treated with an inhibitor of vanin activity.', 'Liver microarray analyses reveals that Vnn1 is the most prominently regulated gene after modulation of PPARα activity. In addition, activation of mouse PPARα regulates hepatic- and plasma vanin activity. In humans, consistent with regulation by PPARα, plasma vanin activity increases in all subjects after prolonged fasting, as well as after treatment with the PPARα agonist fenofibrate. In mice, absence of vanin-1 exacerbates the fasting-induced increase in hepatic triglyceride levels. Similarly, inhibition of vanin activity in rats induces accumulation of hepatic triglycerides upon fasting. Microarray analysis reveal that the absence of vanin-1 associates with gene sets involved in liver steatosis, and reduces pathways involved in oxidative stress and inflammation.
Answer: We show that hepatic vanin-1 is under extremely sensitive regulation by PPARα and that plasma vanin activity could serve as a readout of changes in PPARα activity in human subjects. In addition, our data propose a role for vanin-1 in regulation of hepatic TG levels during fasting.

Answer:
Does pPAR-alpha dependent regulation of vanin-1 mediate hepatic lipid metabolism?