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: To investigate serum beta2-glycoprotein I-low-density lipoprotein (2-GPI-LDL) and oxidized low-density lipoprotein (ox-LDL) levels in type 2 diabetes mellitus (T2DM) patients, and to further evaluate the associations of 2-GPI-LDL with ox-LDL in vivo and with the presence of diabetic microvascular complications.', 'We determined 2-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, 2-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 2-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 2-GPI-LDL levels. Logistic regression analyses indicated that elevated 2-GPI-LDL and ox-LDL levels had significant predictive values for diabetic microvascular complications.
Answer: Elevated serum 2-GPI-LDL levels may be a serological hallmark of enhanced LDL oxidation in vivo and closely associated with the presence of diabetic microvascular complications.

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

Input: Consider Input: Context: The aim of the present study was to evaluate baseline regional cerebral oxygen saturation (rSO2) values and identify factors influencing preoperative rSO2 in elective minor surgery.', 'Observational analysis post-hoc.', 'Observational post-hoc analysis of data for the patient sample (n=50) of a previously conducted clinical trial in patients undergoing tumourectomy for breast cancer or inguinal hernia repair. Exclusion criteria included pre-existing cerebrovascular diseases, anaemia, baseline pulse oximetry <97% and low quality rSO2 sensor signals. Demographic data, comorbidities, and ASA physical status as well as height and weight were collected prospectively from all patients. Baseline rSO2 values were recorded while the patient breathed room air, using the INVOS 5100C monitor™️ (Covidien, Dublin, Ireland).', 'Thirty-seven women (72%) and 13 men (28%) 48 13 years of age were enrolled in this study. Baseline rSO2 was 62.01 10.38%. Baseline rSO2 was significantly different between men (67.6 11.2%) and women (60 9.4%), (P=0.023). There were also differences between baseline rSO2 and ASA physical status (ASA I: 67.6 10.7%, ASA II: 61.6 8.4%, ASA III: 55.8 13.9%, P=0.045). Baseline rSO2 had a positive correlation with body weight (r=0.347, P=0.014) and height (r=0.345, P=0.014). We also found significant differences in baseline rSO2 among patients with and without chronic renal failure (P=0.005). No differences were found in any other studied variables.
Answer: Non-modifiable patient characteristics (ASA physical status, sex, chronic renal failure, body weight and height) influence baseline rSO2.

Output: Do baseline cerebral oximetry values depend on non-modifiable patient characteristics?

Input: Consider Input: Context: On the basis of our previous work with triheptanoin, which provides key substrates to the Krebs cycle in the brain, we wished to assess its therapeutic effect in patients with glucose transporter type 1 deficiency syndrome (GLUT1-DS) who objected to or did not tolerate ketogenic diets.', 'We performed an open-label pilot study with three phases of 2 months each (baseline, treatment and withdrawal) in eight patients with GLUT1-DS (7-47 years old) with non-epileptic paroxysmal manifestations. We used a comprehensive patient diary to record motor and non-motor paroxysmal events. Functional (31)P-NMR spectroscopy was performed to quantify phosphocreatine (PCr) and inorganic phosphate (Pi) within the occipital cortex during (activation) and after (recovery) a visual stimulus.', 'Patients with GLUT1-DS experienced a mean of 30.8 ( 27.7) paroxysmal manifestations (52% motor events) at baseline that dropped to 2.8 ( 2.9, 76% motor events) during the treatment phase (p = 0.028). After withdrawal, paroxysmal manifestations recurred with a mean of 24.2 ( 21.9, 52% motor events; p = 0.043). Furthermore, brain energy metabolism normalised with triheptanoin, that is, increased Pi/PCr ratio during brain activation compared to the recovery phase (p = 0.021), and deteriorated when triheptanoin was withdrawn.
Answer: Treatment with triheptanoin resulted in a 90% clinical improvement in non-epileptic paroxysmal manifestations and a normalised brain bioenergetics profile in patients with GLUT1-DS.
Output: Does triheptanoin dramatically reduce paroxysmal motor disorder in patients with GLUT1 deficiency?