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: Extended-release niacin effectively lowers plasma TG levels and raises plasma high-density lipoprotein (HDL) cholesterol levels, but the mechanisms responsible for these effects are unclear.', 'We examined the effects of extended-release niacin (2 g/d) and extended-release niacin (2 g/d) plus lovastatin (40 mg/d), relative to placebo, on the kinetics of apolipoprotein (apo) A-I and apoA-II in HDL, apoB-100 in TG-rich lipoproteins (TRL), intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL), and apoB-48 in TRL in 5 men with combined hyperlipidemia. Niacin significantly increased HDL cholesterol and apoA-I concentrations, associated with a significant increase in apoA-I production rate (PR) and no change in fractional catabolic rate (FCR). Plasma TRL apoB-100 levels were significantly lowered by niacin, accompanied by a trend toward an increase in FCR and no change in PR. Niacin treatment significantly increased TRL apoB-48 FCR but had no effect on apoB-48 PR. No effects of niacin on concentrations or kinetic parameters of IDL and LDL apoB-100 and HDL apoA-II were noted. The addition of lovastatin to niacin promoted a lowering in LDL apoB-100 attributable to increased LDL apoB-100 FCR.\Question: Does extended-release niacin alter the metabolism of plasma apolipoprotein ( Apo ) A-I and ApoB-containing lipoproteins?

Ex Output:
Niacin treatment was associated with significant increases in HDL apoA-I concentrations and production, as well as enhanced clearance of TRL apoB-100 and apoB-48.


Ex Input:
Context: Intrathecal adenosine is antinociceptive under conditions of central sensitization, but not in response to acute stimuli in normals. The reasons for this selective circumstance of action remain unclear, but some evidence links adenosine's antinociceptive effects to release of norepinephrine by terminals in the spinal cord. The purpose of this study was to test whether spinal adenosine induces norepinephrine release selectively in settings of hypersensitivity.", 'Rats randomly assigned to spinal nerve ligation, sham operation, or no operation were anesthetized. A microdialysis fiber was implanted in the spinal cord dorsal horn at the L5-L6 level and perfused with artificial cerebrospinal fluid. After washout and a baseline sample period, adenosine at various concentrations was infused through the fiber for 150 min, and samples were collected every 15 min.', "In ligated, but not in sham or normal animals, adenosine perfusion increased norepinephrine in spinal cord microdialysates in a concentration-dependent manner. The effects of adenosine plateaued after 75 min and remained stable until the end of the experiment. Intravenous injection of selective adenosine A1 and A2 receptor antagonists revealed that adenosine's effect on spinal norepinephrine release was A1 receptor mediated.\Question: Does intraspinal adenosine induce spinal cord norepinephrine release in spinal nerve-ligated rats but not in normal or sham controls?

Ex Output:
This is the first study to provide direct evidence that adenosine is able to release norepinephrine in spinal cord dorsal horns in living animals. However, this effect was only seen in animals after spinal nerve ligation. These data are consistent with behavioral studies demonstrating that adenosine's antinociceptive effects in rats after spinal nerve ligation is totally dependent on intact spinal noradrenergic terminals and can be blocked by spinal alpha 2-adrenergic receptor antagonists.


Ex Input:
Context: The treatment of persistent epithelial defects (PED) with autologous serum eye drops is often combined with conventional medication such as artificial tears and topical antibiotics, but until now no report exists on the use of a bandage contact lens (BCL) in combination with autologous serum eye drops in the treatment of PEDs. We report six eyes (five patients) which were all treated with autologous serum eye drops in combination with an FDA group IV hydrogel contact lens.', 'Five patients aged 36-88 years, were suffering from six PEDs for 73.5+/-46.9 days due to rheumatoid sterile corneal ulcer (n=1), neurotrophic keratopathy (n=3) or partial limbal stem cell deficiency (n=1). All patients had been unsuccessfully treated with conventional therapy before. Three of them had already had an amniotic membrane transplantation and two had undergone a keratoplasty; however, the epithelial defect persisted or recurred. In all cases, an FDA group IV hydrogel contact lens (Biomedics 55, ocufilcon D, 55% water content) was fitted and serum eye drops applied 8 times a day.', 'The PED healed in five of six eyes after a treatment period of 14.2+/-8.9 days. In one eye the PED became smaller, but it took 90 days until the lesion healed completely. In three eyes (two patients) white deposits appeared on the surface of the BCL during the treatment after 12.3+/-5.1 days. Because no signs of inflammation were observed and since the epithelial defect improved, a new identical lens was applied and the medication continued unaltered. The surface of contaminated and non-contaminated BCLs were analyzed by scanning electron microscopy and SDS gel-electrophoresis. The scanning electron microscopic examination presented a coating of amorphous material with a wrinkled appearance and many corpuscular deposits. There was no indication of bacterial colonisation. The SDS gel-electrophoresis showed a small band at 65 kDa, probably albumin.\Question: Does combination of serum eye drop with hydrogel bandage contact lenses in the treatment of persistent epithelial defects?

Ex Output:

These findings suggest that the combination of a therapeutic contact lens and serum eye drops can be successfully used in the treatment of persistent epithelial defects. Deposition of albumin may occur on the surface of the contact lenses, which, in the small group presented here, caused no unwanted effects.