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: This study tested the hypothesis that patients with more severe substance use disorders (SUDs) at intake respond better when treated in more structured and intensive settings (i.e. in-patient/residential versus out-patient), whereas patients with less severe SUD problems have similar outcomes regardless of treatment setting.', 'Up to 50 new patients were selected randomly from each of a random and representative sample of 50 Department of Veterans Affairs (VA) SUD treatment programs (total n = 1917 patients), and were followed-up an average of 6.7 months later (n = 1277).', 'Patients completed a brief self-report version of the Addiction Severity Index (ASI) at baseline and at follow-up.', 'In mixed-model regression analyses, baseline substance use severity predicted follow-up substance use severity and there were no main effects of treatment setting. However, interaction effects were found, such that more severe patients experienced better alcohol and drug outcomes following in-patient/residential treatment versus out-patient treatment; on the other hand, patients with lower baseline ASI drug severity had better drug outcomes following out-patient treatment than in-patient treatment. Treatment setting was unrelated to alcohol outcomes in patients with less severe ASI alcohol scores.\Question: Do treatment setting and baseline substance use severity interact to predict patients ' outcomes?
Example Output: Results provide some support to the matching hypothesis that for patients who have higher levels of substance use severity at intake, treatment in in-patient/residential treatment settings is associated with better outcomes than out-patient treatment. More research needs to be conducted before in-patient/residential settings are further reduced as a part of the SUD continuum of care in the United States.

Example Input: Context: Hepatic expression of growth hormone (GH)-inducible genes serine protease inhibitor (Spi 2.1) and insulin-like growth factor (IGF)-I are inhibited by interleukin (IL)-1. The current study examines the role of the nuclear factor kappaB (NFkappaB) pathway and suppressor of cytokine signaling (SOCS)-3 expression as potential mechanisms for IL-1-mediated GH resistance.', 'CWSV-1 hepatocytes were cotransfected with Spi 2.1 or IGF-1 promoter luciferase constructs and empty pCMV4 vector or dominant negative inhibitor-kappaBalpha (IkappaBalpha)S/A construct. Cells were treated with or without IL-1 and then stimulated with or without recombinant human GH. Cell extracts were assayed for luciferase activity and protein, normalized and expressed as fold-induction. CWSV-1 cells transfected with pCMV4 or IkappaBalphaS/A were treated with or without IL-1 then SOCS-3 mRNA was measured. Finally, CWSV-1 cells were cotransfected with a SOCS-3 promoter construct with or without pCMV4 or IkappaBalphaS/A and then stimulated with or without IL-1 to investigate SOCS-3 promoter activity.', 'CWSV-1 cells cotransfected with pCMV4 demonstrated a three- to fivefold induction of Spi 2.1 or IGF-1 promoter activity after GH stimulation that was almost completely inhibited by IL-1. Cotransfection with IkappaBalphaS/A increased GH-inducible Spi 2.1 and IGF-1 promoter activity, but the inhibitory effects of IL-1 on both promoters were attenuated by cotransfection with IkappaBalphaS/A. IL-1 stimulated SOCS-3 mRNA expression and promoter activity. Cotransfection with IkappaBalphaS/A increased IL-1-inducible SOCS-3 promoter activity, but not SOCS-3 mRNA or protein.\Question: Does nuclear factor kappaB mediate the inhibitory effects of interleukin-1 on growth hormone-inducible gene expression?
Example Output: Signaling via the NFkappaB pathway is responsible for the inhibitory effects of IL-1 on GH-inducible gene expression by a mechanism that does not seem to involve increased SOCS-3 expression.

Example Input: Context: Vitamin C can be metabolized to oxalate. Case reports have suggested an association between IV vitamin C and urinary oxalate excretion. Recently, the US Food and Drug Administration required the dose of vitamin C in IV multivitamin preparations to be increased from 100 mg to 200 mg/d. We compared the urinary oxalate excretion level in stable home total parenteral nutrition (TPN) patients receiving both doses of vitamin C.', 'Each participant provided a 24-hour urine sample for oxalate determination on the vitamin C dose (100 mg/d), and again after at least 1 month on the increased vitamin C dose (200 mg/d). A 2-day diet diary was completed covering the day before and the day of the urine collection and was analyzed for oxalate and vitamin C content. Comparisons were made using Student paired t test and Wilcoxon signed rank.', 'Thirteen patients (7 males/6 females) aged 63.1 +/- 12.2 years who had no history of nephrolithiasis and had received TPN for 55.9 +/- 78.8 months were enrolled. The most common indication for TPN was short bowel syndrome (38.5%). Eight patients had an intact colon. Urinary oxalate excretion increased on the 200-mg vitamin C dose, from 0.34 +/- 0.13 to 0.44 +/- 0.17 mmol/d (mean increase = 0.10 mmol/d; p = .04; 95% confidence interval 0.004 to 0.19 mmol/d). Oral intake of vitamin C and oxalate did not differ between the 2 collection periods.\Question: Does urinary oxalate excretion increase in home parenteral nutrition patients on a higher intravenous ascorbic acid dose?
Example Output:
In therapeutically used doses, IV vitamin C increases urinary oxalate excretion, potentially predisposing susceptible individuals to nephrolithiasis. This factor should be considered in patients receiving home TPN.