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: Sepsis is an emergency condition with high mortality and morbidity rate. There are limited data on the association of cancer as a risk factor for mortality in sepsis patients in the emergency department (ED).', 'This retrospective study was conducted at the ED, Faculty of Medicine, Ramathibodi Hospital, Bangkok, Thailand. The study period was between January 1st and December 31st, 2014. The inclusion criteria were as follows: adult patients over 15 years of age who presented at the ED with suspicion of sepsis, received treatment at the ED, and whose blood culture was found to be positive. Clinical data were recorded from medical records including the Mortality in Emergency Department Sepsis score (MEDS score). The primary outcome of this study was mortality at one month. Multivariate logistic regression analysis was used to identify independent factors associated with death.', 'During the study period, there were 775 eligible patients. The two most common pathogens identified from blood cultures were Staphylococcus aureus (193 patients; 24.9%) and Escherichia coli (158 patients; 20.4%). At one month after presenting at the ED, 110 patients (14.2%) had died. There were four significant factors for death, having cancer, being on an endotracheal tube, initial diagnosis of bacteremia, and high MED scores. Having cancer had an adjusted OR of 2.12 (95% CI of 1.29, 3.47).\Question: Do cancer Patients Are at High Risk of Mortality if Presenting with Sepsis at an Emergency Department?
Example Output: Cancer patients have double the risk of mortality if presenting with sepsis at the ED.

Example Input: Context: In adults with growth hormone (GH) deficiency (GHD), GH treatment restores impaired endothelial function, a precursor of cardiovascular disease. Its effect in children with GHD is unknown.', 'Three months of GH (0.3 mg/kg/wk) were given to nine children with GHD. Endothelial function was measured via reactive hyperemic response. Forearm blood flow (FBF, strain gauge plethysmography) was measured before and after 5 min of upper arm arterial occlusion. Blood pressure and lipid, insulin and glucose levels were measured. Pretreatment endothelial function was compared to 18 previously studied control children.', 'Percent fall in forearm vascular resistance was greater in controls (81.2 +/- 1.9%) than in children with GHD (69.6 +/- 5.3%, p = 0.021) but was not affected by GH (60.6 +/- 7.5%). GH markedly increased HOMAIR (21 +/- 7 versus 43 +/- 8, p = 0.004). Plasma lipid levels did not significantly differ.\Question: Does growth hormone ( GH ) treatment restore endothelial function in children with GH deficiency?
Example Output: These results indicate that endothelial function is impaired in children with GHD. GH therapy does not restore the impairment.

Example Input: Context: Doxorubicin (Dox) is a potent anticancer agent that is widely used in the treatment of a variety of cancers, but its usage is limited by cumulative dose-dependent cardiotoxicity mainly due to oxidative damage. Ataxia telangiectasia mutated (ATM) kinase is thought to play a role in mediating the actions of oxidative stress. Here, we show that ATM in cardiac fibroblasts is essential for Dox-induced cardiotoxicity.', 'ATM knockout mice showed attenuated Dox-induced cardiotoxic effects (e.g. cardiac dysfunction, apoptosis, and mortality). As ATM was expressed and activated predominantly in cardiac fibroblasts, fibroblast-specific Atm-deleted mice (Atm(fl/fl);Postn-Cre) were generated to address cell type-specific effects, which showed that the fibroblast is the key lineage mediating Dox-induced cardiotoxicity through ATM. Mechanistically, ATM activated the Fas ligand, which subsequently regulated apoptosis in cardiomyocytes at later stages. Therapeutically, a potent and selective inhibitor of ATM, KU55933, when administered systemically was able to prevent Dox-induced cardiotoxicity.\Question: Does ataxia telangiectasia mutated in cardiac fibroblasts regulate doxorubicin-induced cardiotoxicity?
Example Output:
ATM-regulated effects within cardiac fibroblasts are pivotal in Dox-induced cardiotoxicity, and antagonism of ATM and its functions may have potential therapeutic implications.