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.

Example Input: Context: Transcranial direct current stimulation (tDCS) of the primary motor cortex has been shown to modulate pain and trigeminal nociceptive processing.', 'Ten patients with classical trigeminal neuralgia (TN) were stimulated daily for 20\xa0minutes over two weeks using anodal (1\xa0mA) or sham tDCS over the primary motor cortex (M1) in a randomized double-blind cross-over design. Primary outcome variable was pain intensity on a verbal rating scale (VRS 0-10). VRS and attack frequency were assessed for one month before, during and after tDCS. The impact on trigeminal pain processing was assessed with pain-related evoked potentials (PREP) and the nociceptive blink reflex (nBR) following electrical stimulation on both sides of the forehead before and after tDCS.', 'Anodal tDCS reduced pain intensity significantly after two weeks of treatment. The attack frequency reduction was not significant. PREP showed an increased N2 latency and decreased peak-to-peak amplitude after anodal tDCS. No severe adverse events were reported.\Question: Does patient-conducted anodal transcranial direct current stimulation of the motor cortex alleviate pain in trigeminal neuralgia?
Example Output: Anodal tDCS over two weeks ameliorates intensity of pain in TN. It may become a valuable treatment option for patients unresponsive to conventional treatment.

Example Input: Context: To assess the effects of protein C activator (PCA) from Agkistrodon halys snake venom on cardiac fibrosis in streptozotocin (STZ) induced diabetic rat model, and investigate the mechanisms of its action.', 'PCA was identified by one-dimensional reversed phase liquid chromatography - mass spectrometry/mass spectrometry. Male Sprague-Dawley rats (120-140 g) were randomly assigned to negative control (NC) and diabetic group. Diabetes was induced by STZ in high-fat diet fed rats. Diabetic group was subdivided into three groups: diabetic group (DM), diabetic group treated with PCA (0.5, 2, and 8 mg/kg), and diabetic group treated with metformin (5 mg/kg, positive control). NC and DM groups received the same volume of distilled water. Left ventricular mass index (LVWI) and collagen volume fraction were measured by hematoxylin and eosin and Masson staining. Transforming growth factor beta-1 (TGF-β1) and interleukin 1 beta (IL-1β) levels were determined by enzyme-linked immunosorbent assay.', 'The diabetic rat model was successfully established by STZ induction and high-fat diet. Glucose level, LVWI, TGF-β1 and IL-1β level, and collagen volume fraction were significantly reduced in diabetic rats treated by PCA in a dose-dependent manner (P<0.050), especially in the high dose (8 mg/kg) group (P<0.010), compared to diabetes group. The high dose PCA had the same effect as metformin positive control in reducing the level of fasting blood glucose. PCA decreased the expression of MMP-2 and reduced that of TIMP-2.\Question: Does a new Agkistrodon halys venom-purified protein C activator prevent myocardial fibrosis in diabetic rats?
Example Output: Our results indicate that PCA has anti-fibrotic effects and that it may be used to treat myocardial fibrosis.

Example Input: Context: The antileukemic drug asparaginase, a key component in the treatment of acute lymphoblastic leukemia, acts by depleting asparagine from the blood. However, little is known about its pharmacokinetics and mechanisms of therapy resistance are poorly understood. Here, we explored the in vivo biodistribution of radiolabeled asparaginase, using a combination of in vivo imaging and biochemical techniques, and provide evidence for tissue specific clearance mechanisms, which could reduce effectiveness of the drug at these specific sites.', 'In vivo localization of Indium-111-labeled E.coli asparaginase was carried out in C57Bl/6 mice by both microSPECT/CT and by ex vivo biodistribution studies. Mice were treated with liposomal clodronate to investigate the effect of macrophage depletion on tracer localization and drug clearance in vivo. Moreover, macrophage cell line models RAW264.7 and THP-1, as well as cathepsin B deficient mice, were used to identify the cellular and molecular components controlling asparaginase pharmacokinetics.', 'In vivo imaging and biodistribution studies showed a rapid accumulation of asparaginase in macrophage-rich tissues such as liver, spleen and in particular bone marrow. Clodronate-mediated depletion of phagocytic cells markedly prolonged the serum half-life of asparaginase in vivo and decreased drug uptake in target organs. Immunohistochemistry and in vitro binding assays confirmed the involvement of macrophage-like cells in the uptake of asparaginase. We identified the activity of the lysosomal protease cathepsin B in macrophages as a rate-limiting factor in degrading asparaginase both in vitro and in vivo.\Question: Does in vivo imaging of antileukemic drug asparaginase reveal a rapid macrophage mediated clearance from the bone marrow?
Example Output:
We show that asparaginase is rapidly cleared from the serum by liver, spleen and bone marrow-resident phagocytic cells. As a consequence of this efficient uptake and protease mediated degradation, particularly bone marrow resident macrophages may provide a protective niche to leukemic cells.