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.

Ex Input:
Context: Perls' stain is routinely used to demonstrate iron in liver biopsies. We tested the hypothesis that it may be unnecessary in cases, where no iron or another similar pigment was seen on the routine hematoxylin and eosin (H and E) stained section.", "The aim of this study was to evaluate the efficiency of H and E stain in demonstrating iron in liver biopsies as well as to determine the possibility of replacing Perls' stain with H and E stain.", "Two hundred pairs of slides of liver biopsies were taken from the archival files of the Department of Pathology from 2006 to 2011. Perls' and H and E slides were independently reviewed for the presence of iron.", "Hundred and one cases showed the presence of iron using H and E stain. 84 of 86 cases showed positive iron using both Perls' and H and E stains. Seventeen cases were positive using H and E stain but negative with Perls'. Only two cases did not show the presence of iron using H and E stain. Ninety-seven cases were negative using both Perls' and H and E stains. H and E stain showed a sensitivity, specificity, accuracy, positive predictive valve, and negative predictive value of 97.67%, 85.08%, 90.5%, 83.16%, and 97.98%, respectively.\Question: Do hematoxylin and eosin stain shows a high sensitivity but sub-optimal specificity in demonstrating iron pigment in liver biopsies?

Ex Output:
We demonstrate that the H and E stain is a sensitive method to detect iron pigment in liver biopsies, particularly when present in large quantities. A negative H and E stain might obviate the need for extra Perls' staining, thus saving costs and shortening report turn-around times.

Ex Input:
Context: Proliferation of smooth muscle cells (SMCs) plays an important role in vascular pathobiology, being involved in the development of coronary restenosis and atherosclerosis. The activation of nuclear proto-oncogenes appears to be a final common pathway onto which various mitogenic signals coverage. Accordingly, we attempted to determine whether the activation of the c-myc nuclear proto-oncogene is essential for human SMC proliferation and explored the possibility of inhibiting their growth using antisense oligonucleotides directed against c-myc messenger RNA (mRNA).', 'Proliferation of human SMCs was associated with an increase in c-myc mRNA expression after growth stimulation. Using 15-mer phosphorothioate oligonucleotides (oligomers), we tested their growth-inhibitory effect in SMCs in vitro. Antisense oligomers directed against the translation initiation region of the human c-myc gene exhibited a significant antiproliferative effect, whereas sense and mismatched oligomers did not inhibit the growth. The growth-inhibitory effect of c-myc antisense oligomers was dose dependent and preventable by an excess of sense oligomers. Furthermore, growth inhibition of SMCs treated with c-myc antisense oligomers was associated with a marked decrease in the c-myc mRNA level. Phosphorothioate oligomers remained stable in medium containing 20% serum and were detectable in SMCs as early as 1 hour after cell exposure. Intact oligomers rapidly accumulated intracellularly and persisted within human SMCs for at least 16 hours.\Question: Does downregulation of c-myc expression by antisense oligonucleotides inhibit proliferation of human smooth muscle cells?

Ex Output:
c-myc antisense oligomers reduced c-myc expression and produced a significant growth inhibition of human SMCs, indicating an important role of c-myc gene activation in the process of SMC proliferation. Furthermore, extracellular stability and rapid cellular uptake provide the basis for future studies assessing the therapeutic role of the c-myc antisense approach in reducing SMC proliferation in the process of vascular restenosis.

Ex Input:
Context: The serotonin and norepinephrine transporter inhibitor sibutramine is a widely used antiobesity drug. In acute studies, the peripheral sympathomimetic effect of sibutramine was counteracted by a central sympatholytic action.', 'The objective was to test the hypothesis that blood pressure responses to long-term sibutramine therapy may be related to sympathetic nerve traffic before treatment in a prospective open-label study in an academic clinical research center.', 'This study comprised 20 obese subjects (body mass index, 30-40 kg/m2; age, 30-57 yr) receiving 5 d of placebo treatment followed by open-label 15 mg/d sibutramine and hypocaloric diet over 12 wk.', 'Body weight, blood pressure, heart rate, muscle sympathetic nerve activity (MSNA) (microneurography), plasma catecholamines, and adipose tissue gene expression were measured.', 'Open-label sibutramine treatment decreased body weight 4.1 kg (P<0.01) and MSNA 17 bursts per minute (P=0.001), and increased diastolic blood pressure 3 mm Hg (P<0.05) and heart rate 8 bpm (P<0.01). The change in blood pressure with sibutramine treatment was inversely correlated with initial MSNA (r2=0.34; P<0.01). Chronic sibutramine treatment increased adrenoreceptor gene expression and plasma catecholamines.\Question: Does sympathetic vasomotor tone determine blood pressure response to long-term sibutramine treatment?

Ex Output:
The blood pressure response to sibutramine treatment is related to initial MSNA so that subjects with higher MSNA exhibit a smaller increase or even a decrease in blood pressure. The phenomenon might be explained by a sustained reduction in central sympathetic activity with sibutramine treatment.