Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Input: Consider Input: Context: To analyze the effect of antiretroviral therapy, including drugs that have good penetration in cerebrospinal fluid (CSF), on neuropsychologic performance.', 'One hundred sixty-five HIV-1-infected patients exposed to a stable highly active antiretroviral therapy (HAART) regimen were studied. Neuropsychologic examinations were performed for all patients.', "A total of 50.3% of patients were impaired. In multivariate analysis, older age (for 10-year increase, odds ratio [OR] = 4.8, 95% confidence interval [CI]: 2.2 to 10.4; P< 0.0001) and higher plasma HIV-1 RNA levels (OR = 1.90, 95% CI: 1.1 to 3.2; P = 0.021) at testing were independently associated with an increased probability of impaired neurocognitive performance, whereas higher educational level was a protective factor (OR = 0.76, 95% CI: 0.65 to 0.90; P=0.001). A significant linear correlation was observed between the neuropsychologic z score for 8 tests (NPZ8) score, a quantitative parameter of neurocognitive impairment, and CD4 cell count at neuropsychologic testing (R = 0.273, P = 0.001) and between the NPZ8 score and the patient's age (R = 0.288, P = 0.001).
Answer: Our study indicates that the use of stable HAART, including multiple drugs that have good CSF penetration, was not associated with neuropsychologic performance. To prevent independent replication of HIV in CSF with better control of a relevant reservoir of HIV is one of the crucial aims of therapeutic strategy.

Output: Do neuroactive antiretroviral drugs influence neurocognitive performance in less advanced HIV-infected patients responding to highly active antiretroviral therapy?


Input: Consider Input: Context: Cancer cells frequently exhibit resistance to the cytotoxic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Pretreatment of TRAIL-resistant cells with cisplatin sensitizes them to this ligand. Cisplatin also has been shown to enhance adenoviral transgene expression.', 'This study aims to evaluate the ability of cisplatin to enhance the expression and the cytotoxic effect of the tumor-specific adenoviral vector Ad/gTRAIL, which expresses a green fluorescent protein-TRAIL fusion protein.', 'Cultured cancer cells and normal human cells were infected with Ad/gTRAIL with or without cisplatin pretreatment. Adenoviral transgene expression was determined by using flow cytometry to measure green fluorescent protein fluorescence. Cytotoxicity was measured by using thiazolyl blue tetrazolium bromide assays and an apoptosis enzyme-linked immunosorbent assay kit.', 'Green fluorescent protein-TRAIL fusion protein expression was significantly enhanced by cisplatin pretreatment in cancer cells. Cisplatin treatment before Ad/gTRAIL infection resulted in a 2- to 12-fold increase in green fluorescent protein fluorescence intensity across cancer lines. Although Ad/gTRAIL induced mild cytotoxicity in all cancer lines (inhibitory concentration of 50% values of >500 pfu/cell), pretreatment with cisplatin resulted in a dose-dependent enhancement of Ad/gTRAIL-mediated cytotoxicity, as indicated by the drastic reduction of inhibitory concentration of 50% values to 4 to 42 pfu/cell in all cell lines. There was no cytotoxicity noted in normal cells treated with both cisplatin and Ad/gTRAIL.
Answer: Cisplatin pretreatment enhances Ad/gTRAIL cytotoxicity in malignant cells while not affecting normal cells. The mechanisms underlying this effect might include both enhancement of the susceptibility of cisplatin-treated cells to TRAIL and cisplatin-mediated enhancement of TRAIL expression in Ad/gTRAIL infected cells. These findings provide a rationale for development of Ad/gTRAIL-based therapy for thoracic malignancies.

Output: Does cisplatin enhance apoptosis induced by a tumor-selective adenovirus expressing tumor necrosis factor-related apoptosis-inducing ligand?


Input: Consider Input: Context: The underlying genetic factors for the development and progression of hepatocellular carcinoma (HCC) are largely unknown. TNFalpha is a well characterized inflammatory mediator and is implicated in the development of HCC. We investigated TNFalpha polymorphisms for association with HCC.', 'The study population consisted of 227 HCC patients and 365 age and sex matched Korean controls. TNFalpha polymorphisms (G-238A, C-857T, and C-863A) were genotyped using pyrosequencing analysis. TNFalpha levels in patients with HCC were determined by enzyme linked immunosorbent assay (ELISA). Logistic regression analysis was used to determine the association with HCC and haplotype was calculated using EH program.', 'Of three TNFalpha polymorphisms investigated in our study, C-863A did not correlate with HCC. However, both G-238A and C-857T were found to be significantly associated with HCC. TNFalpha -238A allele was more frequent in HCC patients than in control [P=0.012; odds ratio (OR), 1.89; 95% confidence interval (CI), 1.14-3.13]. TNFalpha -857T was significantly associated with HCC patients (P=0.001; OR, 1.63; 95% CI, 1.21-2.19). Haplotype analysis revealed that the GTC haplotype (G-238A, C-857T, C-863A) was a risk marker for HCC (P=0.0021). Serum TNFalpha level was significantly increased in HCC patients with CT+TT genotype for TNFalpha -857 (P=0.018).
Answer: Our data imply that TNFalpha G-238A and C-857T, not C-863A, polymorphisms may confer different susceptibilities to the development of HCC with TNFalpha -238A and -857T alleles playing as risk factors.


Output: Is tNFalpha promoter polymorphism a risk factor for susceptibility in hepatocellular carcinoma in Korean population?