instruction:
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.
question:
Context: It has been demonstrated that tumor necrosis factor-alpha (TNF alpha) induces apoptosis in cardiac myocytes. However, its mechanism of action is still not well understood. In the present study, we hypothesized that TNF alpha induces myocardial apoptosis by induction of inducible nitric oxide synthase (iNOS).', 'Neonatal cardiac myocytes were isolated from iNOS (-/-) mutant and C57BL6 wild type mice. Cells were cultured for 3 days before treatment with an NO donor or TNF alpha. Following treatment with S-nitroso-N-acetyl-penicillamine (SNAP) or TNF-alpha, cells were tested for apoptosis by terminal deoxynucleotidyl transfer-mediated end labeling (TUNEL) staining and cell death detection ELISA. NO production was measured by nitrite concentration in the culture medium. Cardiomyocyte expression of iNOS and TNF type 1 receptor (TNFR1) mRNA was determined by reverse transcriptase-polymerase chain reaction (RT-PCR).', 'SNAP (0.01-100 microM) induced apoptosis of cardiac myocytes in a concentration-dependent manner in the wild type mice (n = 5, P < 0.01). TNFR1 mRNA was expressed in neonatal cardiomyocytes from both wild type and iNOS (-/-) mutant mice. TNF alpha induced a concentration-dependent increase in iNOS mRNA expression and nitrite production as well as significant apoptosis of cardiomyocytes in the wild type mice (n = 4, P < 0.01). However, without iNOS expression, the apoptotic effects of TNF-alpha were significantly attenuated in cardiomyocytes from iNOS (-/-) mutant mice (n = 4, P < 0.05).\Question: Does tumor necrosis factor-alpha induce apoptosis via inducible nitric oxide synthase in neonatal mouse cardiomyocytes?
answer:
TNF alpha induces apoptosis via iNOS expression and NO production in neonatal mouse cardiomyocytes.

question:
Context: No previous study has examined the comorbidity of Irritable Bowel Syndrome (IBS) and Generalized Anxiety Disorder (GAD) in a general population using standardized diagnostic methods.', 'To examine the prevalence, comorbidity and risk correlates of IBS and GAD in a general population.', 'A random community-based telephone survey was conducted. The questionnaire covered symptoms of IBS, GAD, core depressive symptoms, help-seeking behaviour and functional impairment on the Sheehan Disability Scale.', 'A total of 2005 participants completed the interview. The current prevalence of IBS was 5.4% and the 12-month prevalence of GAD was 4%. GAD was five times more common among IBS respondents than non-IBS respondents (OR: 5.84, P < 0.001), whereas IBS was 4.7 times more common among GAD respondents than among non-GAD respondents (OR: 6.32, P < 0.001). Core depressive symptoms (OR: 6.25, P < 0.01) and education level (OR: 5.918, P = 0.021) were risk correlates of GAD among IBS respondents. Comorbid respondents were more impaired than respondents having either disorder alone, but were not more likely to seek professional help than IBS-only respondents.\Question: Is irritable bowel syndrome strongly associated with generalized anxiety disorder : a community study?
answer:
Irritable Bowel Syndrome and GAD comorbidity was common and added to impairment in the community. The strong association between psychiatric morbidity and IBS observed in referral centres was not a consequence of increased help-seeking behaviour.

question:
Context: 5-fluorouracil (5-FU) has been combined in the past with other drugs for the combination chemotherapy for cancers of the breast, ovary, and colon. These drug regimens were limited by the fact that 5-FU fails to kill nondividing cancer cells at the doses that are safe to deliver. The goal of the present study is to test the feasibility of replacing 5-FU in established 5-FU combination chemotherapy with the Ad-LpCDIRESE1A/5-fluorocytosine (5-FC) system for the purpose of reducing toxicity and increasing efficacy.', 'We have replaced 5-FU in the weekly combination of CPT-11, folinic acid (FA) and 5-FU chemotherapy by 5-FC and an adenoviral vector that carries the L-plastin (Lp) tumor-specific promoter-driven transcription unit encoding the cytosine deaminase gene linked to the E1A gene by an internal ribosomal entry site element. This combination is called "genetic combination therapy." The goal of using the vector was to decrease the toxicity to normal tissue and to increase the efficacy of therapy in the cancer cells by increasing the concentration of 5-FU sufficiently high that even nondividing cancer cells would be killed by 5-FU through its incorporation into mRNA and consequent inhibition of synthesis of functional proteins. We compared the in vivo efficacy of the genetic combination therapy with the conventional combination chemotherapy in a mouse colon cancer model.', 'Both replication-competent and -noncompetent adenoviral vectors carrying an L-plastin-driven cytosine deaminase transcription unit when combined with 5-FC, CPT-11, and FA showed increased in vitro therapeutic activity that was significantly higher than that of the conventional chemotherapy combination. Tumor-bearing mice treated with the genetic combination therapy showed a statistically significant advantage in terms of increased response rate, response duration, survival, and reduced toxicity when compared with tumor-bearing mice treated with the conventional combination chemotherapy.\Question: Does vector targeting make 5-fluorouracil chemotherapy less toxic and more effective in animal models of epithelial neoplasms?
answer:
Replacement of 5-FU in 5-FU-based combination chemotherapy with the Ad-LpCDIRESE1A vector and 5-FU reduces toxicity and increases efficacy. This is a concept that could be potentially applied widely for many forms of cancer treatment.