Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.

[EX Q]: A prospective cohort study at our institution demonstrated a 48% mortality rate in warfarin anticoagulated trauma patients sustaining intracranial hemorrhage (ICH) compared with a 10% mortality rate in nonanticoagulated patients. Forty percent of patients demonstrated progression of their ICH, despite anticoagulation reversal, with a resultant 65% mortality rate. Seventy-one percent of these patients initially presented with a Glasgow Coma Scale (GCS) score > or = 14 and a 'minor' ICH. We postulated that early diagnosis of ICH and rapid anticoagulation reversal would reduce ICH progression rates and mortality.", 'All anticoagulated patients with known or suspected head trauma were entered into the Coumadin protocol. The protocol ensured immediate triage and physician evaluation, head computed tomography (CT) scan, and fresh frozen plasma administration in patients with documented ICH.', 'Eighty-two patients were entered into the protocol with ICH documented in 19 (23%). Sixteen of 19 patients (84%) presented with GCS > or = 14. Median international normalized ratio (INR) for treated patients with ICH was 2.7 versus 2.5 for patients without ICH (p = 0.546). Mean time to initiate warfarin reversal was 1.9 hours for protocol patients versus 4.3 hours for preprotocol patients (p < 0.001). Two of 19 (10%) protocol patients with ICH died. However, both patients presented >10 hours after injury with a severe ICH. This 10% mortality rate is significantly less than the 48% mortality rate seen previously (p < 0.001) and is now consistent with that observed in similarly injured patients not on anticoagulation.
[EX A]: 0

[EX Q]: Cetuximab is a monoclonal epidermal growth factor receptor (EGFR)-targeting antibody, used in the treatment of colon cancer. KRAS mutation status is strongly predictive of cetuximab efficacy, but more predictive factors are needed for better patient selection. PTEN is a downstream inhibitor of the EGFR pathway and has been evaluated as a predictive factor of cetuximab efficacy in colorectal cancer.', "Formalin-fixed paraffin-embedded tumor tissue samples were collected from 226 patients with advanced or metastatic colorectal cancer that had been treated with cetuximab. Clinical information was collected retrospectively from the patients' medical records. After central evaluation, 147 cases with adequate material were eligible for further evaluation. EGFR and PTEN status was evaluated with immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH). Data were associated with cetuximab treatment outcome. Additional analysis was performed with previously published data on PIK3CA, BRAF and KRAS mutation status and EGFR ligand amphiregulin (AREG) and epiregulin intratumoral mRNA expression levels. PIK3CA mutation status and PTEN protein expression were also analyzed as a single complex parameter, to evaluate the predictive value of PI3K/PTEN axis dysfunction as one entity.", 'Analysis showed a borderline association of overall response rate (ORR) and time to progression (TTP) with EGFR protein overexpression by IHC (p = 0.059 and p = 0.057, respectively) and a positive association of EGFR gain by FISH (found in only five cases) with longer TTP (p = 0.026). No association was found between ORR or TTP and PTEN IHC or FISH status. Comparative analysis with previously published data showed that PTEN protein expression is associated with longer TTP in patients with wild-type (WT) KRAS (p = 0.036) and especially in the ones with elevated AREG levels (p = 0.046), as well as in patients with both KRAS and BRAF WT (p = 0.019). Patients with both PIK3CA WT and PTEN protein expression had significantly longer TTP (p = 0.010) versus all others, in the absence of BRAF and KRAS mutations, a finding which persisted in the KRAS WT/AREG high subgroup (p = 0.046).
[EX A]: 0

[EX Q]: While antiretroviral therapies have improved life expectancy and reduced viral loads in HIV-1-positive individuals, the cessation of treatment results in a rebound of viral replication. This suggests that a reservoir of latently-infected cells remains within these patients, the identity of which is ill-defined and therefore difficult to target therapeutically. Current strategies are aimed at using drugs such as histone deacetylase (HDAC) inhibitors to induce the expression of latent HIV-1 proviruses in order to activate and ultimately eradicate this reservoir of infected cells. One concern with the use of HDAC inhibitors is that they could up-regulate human endogenous retroviruses (HERVs), as well as HIV-1, with potentially pathophysiological consequences.', 'In this study, we analysed the transcription of HERV genes in HIV-1 latency T cell (J-LAT 8.4) and monocyte (U1) models following treatment with the HDAC inhibitors, vorinostat, panobinostat and romidepsin. We examined the expression of HERV-K (HML-2) env and pol, as well as the co-opted genes HERV-W env (syncytin-1), HERV-FRD env (syncytin-2), in these cell lines. Finally, we investigated HERV expression in primary human T cells.
[EX A]:
0