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: To investigate serum beta2-glycoprotein I-low-density lipoprotein (β2-GPI-LDL) and oxidized low-density lipoprotein (ox-LDL) levels in type 2 diabetes mellitus (T2DM) patients, and to further evaluate the associations of β2-GPI-LDL with ox-LDL in vivo and with the presence of diabetic microvascular complications.', 'We determined β2-GPI-LDL, ox-LDL and small dense low density lipoprotein cholesterol (sdLDL-C) levels in 236 T2DM patients with or without microvascular complications and 75 controls. The correlation analyses, multiple linear regression analyses and logistic regression analyses were performed, respectively.', 'Compared with controls, β2-GPI-LDL and ox-LDL levels were significantly elevated in both groups of T2DM patients and those with microvascular complications exhibited the more significant increase than those without complications. Serum β2-GPI-LDL levels were positively correlated with ox-LDL as well as sdLDL-C levels in T2DM patients. Multiple linear regression analyses showed that ox-LDL was one of the independent determinants of β2-GPI-LDL levels. Logistic regression analyses indicated that elevated β2-GPI-LDL and ox-LDL levels had significant predictive values for diabetic microvascular complications.
Answer: Elevated serum β2-GPI-LDL levels may be a serological hallmark of enhanced LDL oxidation in vivo and closely associated with the presence of diabetic microvascular complications.

A: Are elevated beta2-glycoprotein I-low-density lipoprotein levels associated with the presence of diabetic microvascular complications?
****
Q: 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.

A: Do surgeons often underestimate the amount of blood loss in replacement surgeries?
****
Q: Context: del(17p), del(11q), and associated p53 dysfunction predict for short survival and chemoresistance in B-cell chronic lymphocytic leukemia (CLL). DNA-dependent protein kinase (DNA-PK) is activated by DNA damage and mediates DNA double-strand break repair. We hypothesized that inhibiting DNA-PK would sensitize CLL cells to drug-induced DNA damage and that this approach could increase the therapeutic index of agents used to treat CLL.', 'Fifty-four CLL cases were characterized for poor prognosis markers [del(17p), del(11q), CD38, and ZAP-70]. In selected cases, DNA-PK catalytic subunit (DNA-PKcs) expression and activity and p53 function were also measured. Ex vivo viability assays established sensitivity to fludarabine and chlorambucil and also tested the ability of a novel DNA-PK inhibitor (NU7441) to sensitize CLL cells to these drugs. The effects of NU7441 on fludarabine-induced DNA damage repair were also assessed (Comet assays and detection of gammaH2AX).', 'DNA-PKcs levels correlated with DNA-PK activity and varied 50-fold between cases but were consistently higher in del(17p) (P = 0.01) and del(11q) cases. NU7441 sensitized CLL cells to chlorambucil and fludarabine, including cases with del(17p), del(11q), p53 dysfunction, or high levels of DNA-PKcs. NU7441 increased fludarabine-induced double-strand breaks and abrogated drug-induced autophosphorylation of DNA-PKcs at Ser2056. High DNA-PK levels predicted for reduced treatment-free interval.
Answer: These data validate the concept of targeting DNA-PKcs in poor risk CLL, and demonstrate a mechanistic rationale for use of a DNA-PK inhibitor. The novel observation that DNA-PKcs is overexpressed in del(17p) and del(11q) cases indicates that DNA-PK may contribute to disease progression in CLL.

A:
Is dNA-dependent protein kinase a therapeutic target and an indicator of poor prognosis in B-cell chronic lymphocytic leukemia?
****