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: Chronic marijuana use has been associated with impairments of learning, memory, and executive functions. Little is known, however, about the effects of marijuana use on other cognitive domains, such as decision-making, which are thought to play an important role in addiction and drug abuse.', 'The purpose of the present study was to determine if long-term heavy marijuana users employ different decision-making strategies than individuals with minimal marijuana exposure.', 'Volunteers were assigned to a cannabis (n = 10) or control group (n = 10) based upon history of prior marijuana use. Demographic and neuropsychological variables were evaluated, and a decision-making task--the gambling task (GT) was administered.', 'Although few demographic and neuropsychological differences were noted between groups, marijuana users made more decisions that led to larger immediate gains despite more costly losses than controls.\Question: Do long-term heavy marijuana users make costly decisions on a gambling task?

A: These data suggest that long-term heavy marijuana users may have specific deficits in the ability to balance rewards and punishments that may contribute to continued drug-taking behavior. It is unknown, however, whether the basis for such deficits might be attributed directly to marijuana exposure or pre-existing genetic or behavioral differences.
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Q: Context: Animal models for hepatic metastases can facilitate the investigation of lymphokine-activated killer (LAK) cell-based immunotherapy. The aim of this study was to investigate the efficacy of ccM4 antibody-targeted LAK cells in inhibiting hepatic micrometastases.', 'Hepatic micrometastases were generated after the intrasplenic injection of HM7 colon carcinoma cells. TAG72 expression was detected in these hepatic micrometastases using ccM4 antibody. The ccM4 antibody was conjugated onto LAK cells by treatment with 17.5% polyethylene glycol 8000. After the intrasplenic injection of HM7 cells, severe combined immunodeficient mice were randomized into five groups (i-v) and received either 10(7) ccM4-LAK cells plus 1000 U interleukin 2 (IL-2; group i), LAK cells plus 50 micrograms ccM4 and IL-2 (group ii), LAK cells plus IL-2 (group iii), IL-2 alone (group iv), or only phosphate-buffered saline (group v).', 'The ccM4-LAK cells retained cytolytic activity and acquired TAG72-binding reactivity. The results showed that group i had significantly fewer hepatic metastases compared with group ii or group iii (P < 0.05) and even fewer hepatic metastases compared with group iv or group v (P < 0.001).\Question: Do antibody-targeted lymphokine-activated killer cells inhibit liver micrometastases in severe combined immunodeficient mice?

A: These results show that ccM4 antibody-targeted LAK cells significantly inhibited tumor growth in vivo; thus, they can be potentially useful in treatment of hepatic micrometastases.
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Q: Context: Chronic alcohol intake affects liver function and causes hepatic pathological changes. It has been shown that peroxisome proliferator-activated receptor α (PPARα)-null mice developed more pronounced hepatic changes than wild-type (WT) mice after chronic exposure to a diet containing 4% alcohol. The remarkable similarity between the histopathology of alcoholic liver disease (ALD) in Ppara-null model and in humans, and the fact that PPARα expression and activity in human liver are less than one-tenth of those in WT mouse liver make Ppara-null a good system to investigate ALD.', 'In this study, the Ppara-null model was used to elucidate the dynamic regulation of PPARα activity during chronic alcohol intake. Hepatic transcriptomic and metabolomic analyses were used to examine alterations of gene expression and metabolites associated with pathological changes. The changes triggered by alcohol consumption on gene expression and metabolites in Ppara-null mice were compared with those in WT mice.', 'The results showed that in the presence of PPARα, 3 major metabolic pathways in mitochondria, namely the fatty acid β-oxidation, the tricarboxylic acid cycle, and the electron transfer chain, were induced in response to a 2-month alcohol feeding, while these responses were greatly reduced in the absence of PPARα. In line with the transcriptional modulations of these metabolic pathways, a progressive accumulation of triglycerides, a robust increase in hepatic cholic acid and its derivatives, and a strong induction of fibrogenesis genes were observed exclusively in alcohol-fed Ppara-null mice.\Question: Does modulation of fatty acid and bile acid metabolism by peroxisome proliferator-activated receptor α protect against alcoholic liver disease?

A:
These observations indicate that PPARα plays a protective role to enhance mitochondrial function in response to chronic alcohol consumption by adaptive transcriptional activation and suggest that activation of this nuclear receptor may be of therapeutic value in the treatment for ALD.
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