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.
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Question: Context: To assess the ability of an adult risk screening questionnaire (RSQ), previously shown to predict attendance at hospital emergency departments, to identify impaired quality of life in adult patients with asthma in general practice.', 'Baseline data from an RCT of asthma clinics in general practice, using the St. George Respiratory Questionnaire (SGRQ) to measure quality of life.', 'Twelve general practices in Adelaide, Australia.', 'A total of 184 adult asthmatics were recruited, with a mean (standard deviation) age of 50.3 years (16.6 years). Age, gender, weight, number of comorbidities, smoking status, FEV1 and percent predicted FEV1 (pre-and post-bronchodilator), peak flow (pre and post), and RSQ were independently related to SGRQ scores. After adjusting for potential confounders, an RSQ score predictive of hospital attendance was also associated with an average increase (worsening) in SGRQ total score of 11.9 (95% CI: 7.6, 16.3), an average increase in activity score of 9.0 (2.5, 15.5), symptom score of 14.8 (8.6, 21.0), and impact score of 13.1 (8.6, 17.6). These represent clinically significant differences.\Question: Does hospital attendance prediction tool also identify impaired quality of life in adults with asthma in general practice?

Answer: An RSQ score predictive of hospital attendance should alert the general practitioner to explore and address symptom, activity, and impact domains associated with impaired quality of life in adult asthma.


Question: Context: Clinical use of doxorubicin is greatly limited by its severe cardiotoxic side effects. L-carnitine is a vitamin-like substance which has been successfully used in many cardiomyopathies, however, the intracellular mechanism(s) remain unclear. The objective of this study was set to evaluate the protective effect of L-carnitine on doxorubicin-induced cardiomyocyte apoptosis, and to explore its intracellular mechanism(s).', "Primary cultured neonatal rat cardiomyocytes were treated with doxorubicin (1 µM) with or without pretreatment with L-carnitine (1-30 mM). Lactate dehydrogenase assay, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling staining, and flow cytometry measurement were used to assess cytotoxicity and apoptosis. Fluorescent probes 2',7'-dichlorofluorescein diacetate and chemiluminescence assay of superoxide production were used to detect the production of reactive oxygen species. Western blotting was used to evaluate the quantity of cleaved caspase-3, cytosol cytochrome c, and Bcl-x(L) expression.", "L-carnitine inhibited doxorubicin-induced reactive oxygen species generation and NADPH oxidase activation, reduced the quantity of cleaved caspase-3 and cytosol cytochrome c, and increased Bcl-x(L) expression, resulting in protecting cardiomyocytes from doxorubicin-induced apoptosis. In addition, L-carnitine was found to increase the prostacyclin (PGI(2)) generation in cardiomyocytes. The siRNA transfection for PGI(2) synthase significantly reduced L-carnitine-induced PGI(2) and L-carnitine's protective effect. Furthermore, blockade the potential PGI(2) receptors, including PGI(2) receptors (IP receptors), and peroxisome proliferator-activated receptors alpha and delta (PPARα and PPARδ), revealed that the siRNA-mediated blockage of PPARα considerably reduced the anti-apoptotic effect of L-carnitine.\Question: Does l-carnitine reduce doxorubicin-induced apoptosis through a prostacyclin-mediated pathway in neonatal rat cardiomyocytes?

Answer: These findings suggest that L-carnitine protects cardiomyocytes from doxorubicin-induced apoptosis in part through PGI(2) and PPARα-signaling pathways, which may potentially protect the heart from the severe toxicity of doxorubicin.


Question: Context: Formation of branching tubes is a fundamental step in the development of glandular organs. To identify extracellular cues that orchestrate epithelial tubulogenesis, we employed an in vitro assay in which EpH4-J3B1A mammary epithelial cells form spheroidal cysts when grown in collagen gels under serum-free conditions, but form branching tubules in the presence of fetal calf serum (FCS).', 'Initial experiments showed that the tubulogenesis-inducing activity of FCS was markedly increased by heating (70 degrees C) or transient acidification to pH3. We therefore hypothesized that the tubulogenic agent was transforming growth factor-beta (TGF-beta), a cytokine that is present in serum in latent form and can be activated by heat or acid treatment. We found indeed that the tubulogenic activity of acidified FCS is abrogated by addition of either SB-431542, a selective inhibitor of the TGF-beta type I receptor, or a neutralizing antibody to TGF-beta-1. On the other hand, addition of low concentrations (20-100 pg/ml) of exogenous TGF-beta-1 recapitulated the effect of acidified FCS in inducing morphogenesis of hollow tubes. In contrast, higher concentrations of TGF-beta-1 induced the formation of thin cellular cords devoid of a detectable lumen. To gain insight into the mechanisms underlying TGF-beta-1-induced tube formation, we assessed the potential role of matrix metalloproteinases (MMPs). By western blot and gelatin zymography, we observed a dose-dependent increase in MMP-9 upon TGF-beta-1 treatment. Tube formation was suppressed by a synthetic broad-spectrum metalloproteinase inhibitor, by recombinant tissue inhibitor of metalloproteinases-2 (TIMP-2) and by a selective inhibitor of MMP-9, indicating that this morphogenetic process requires the activity of MMP-9.\Question: Do low concentrations of transforming growth factor-beta-1 induce tubulogenesis in cultured mammary epithelial cells?

Answer:
Altogether, our results provide evidence that, at low concentrations, TGF-beta-1 promotes MMP-dependent branching tubulogenesis by mammary epithelial cells in vitro, and suggest that it plays a similar role during mammary gland development in vivo.