In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Q: Context: Cognitive impairment is a common feature of late-life bipolar disorder (BD). Yet, there is limited information on the biological mechanisms associated with this process. It is uncertain whether cognitively impaired patients with BD may present the Alzheimer's disease (AD) bio-signature in the cerebrospinal fluid (CSF), defined as a combination of low concentrations of the amyloid-beta peptide (A1-42 ) and high concentrations of total tau (T-tau) and tau phosphorylated at threonine 181 (P-tau). In this study, we sought to determine whether cognitive impairment in elderly patients with BD is associated with the AD CSF bio-signature.", 'Seventy-two participants were enrolled in the study. The test group comprised older adults with BD and mild cognitive impairment (BD-MCI; n=16) and the comparison groups comprised patients with dementia due to AD (n=17), patients with amnestic MCI (aMCI; n=14), and cognitively healthy older adults (control group; n=25). CSF samples were obtained by lumbar puncture and concentrations of A1-42 , T-tau and P-tau were determined.', 'CSF concentrations of all biomarkers were significantly different in the AD group compared to all other groups, but did not differentiate BD-MCI subjects from aMCI subjects and controls. BD-MCI patients had a non-significant reduction in CSF A1-42 compared to controls, but this was still higher than in the AD group. Concentrations of T-tau and P-tau in BD-MCI patients were similar to those in controls, and significantly lower than those in AD.\Question: Is cognitive impairment in late-life bipolar disorder associated with Alzheimer 's disease pathological signature in the cerebrospinal fluid?

A: Cognitively impaired patients with BD do not display the so-called AD bio-signature in the CSF. We therefore hypothesize that cognitive deterioration in BD is not associated with the classical pathophysiological mechanisms observed in AD, i.e., amyloid deposition and hyperphosphorylation of microtubule-associated tau protein.
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Q: Context: For patients with small bowel obstruction (SBO), who do not have strangulation obstruction or other contraindications, long tube decompression has been successful in 75% in two studies. In a 1995 prospective randomized study, comparing nasogastric suction (short tube) with long tube decompression, the short tube was successful in 51% and the long tube was successful in 75%. Using upper gastrointestinal endoscopy, a long tube can be advanced into the jejunum in 20 minutes, so the delay in function has been eliminated.', 'There were 35 patients with 37 episodes of SBO. From 1983 to 1988, three tubes then available were advanced endoscopically into the jejunum in 17 patients. From 1989 to 2002, an improved tube designed for endoscopic placement was used in 20 patients.', 'From 1983 to 1988 using three tubes, long tube decompression was successful in 12 of 17 (70%); from 1989 to 2002 with the improved tube, decompression was successful in 18 of 20 (90%).\Question: Is long tube decompression successful in 90 % of patients with adhesive small bowel obstruction?

A: For patients with SBO due to adhesions, a trial with long tube decompression for 48 to 72 hours is recommended. For those who fail a trial with the long tube, laparotomy with enterolysis or bowel resection is indicated. If the operative findings indicate a high risk for recurrent obstruction, then long tube splinting of the small bowel should be considered.
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Q: Context: Cytogenetic aberrations are of prognostic significance in childhood acute lymphoblastic leukaemias and a high detection rate could improve the biological understanding and classification of these diseases.', 'Bone-marrow samples from 92 children with acute lymphoblastic leukaemia were studied by high-resolution comparative genomic hybridisation (HRCGH) using dynamic standard reference intervals that enhance both specificity and sensitivity in the detection of aberrations.', 'In 80 patients (87%) HRCGH revealed a total of 405 aberrations, mostly whole chromosome gains (n = 265) and partial losses (n = 80). The 25 leukaemias with a gain of more than five whole chromosomes by HRCGH harboured only 7% of all losses. With G-band karyotyping 59 patients (64%) had aberrations. HRCGH revealed more aberrations per patient than did G-band karyotyping (median: 3 vs. 1, P = 0.005), revealed aberrations in 27 of the 34 patients for whom the G-band karyotyping failed or was found to be normal, and specifically revealed more 9p losses (21% vs. 5%, P < 0.005), 12p losses (12% vs. 2%, P < 0.05) and 17q gains (11% vs. 1%, P < 0.01). Compared to the present study, the frequency of patients with aberrant karyotypes was significantly lower in previous conventional CGH studies (64% vs. 87%, P < 0.0001), as was the rate of partial aberrations per patient (1.1% vs. 1.7, P < 0.001), particularly with fewer 6q losses, 9p losses and 17q gains detected.\Question: Does high-resolution comparative genomic hybridisation yield a high detection rate of chromosomal aberrations in childhood acute lymphoblastic leukaemia?

A:
HRCGH is superior to conventional CGH as an adjunct to G-band karyotyping as it detects recurrent aberrations at a significantly higher rate than both these techniques.
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