instruction:
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.
question:
Bradykinin is a neuropeptide released after tissue damage which plays an important role in inflammatory pain. The up-regulation of the bradykinin B1 receptor in response to inflammation makes it an attractive target for drug development. Aim was to investigate if the selective B1 receptor antagonist BI113823 reduces inflammation-induced mechanical hyperalgesia and if the effect is mediated via peripheral and/or spinal B1 receptor antagonism.', "Electrophysiological recordings of peripheral afferents and spinal neurons were combined with behavioural experiments to better understand the underlying mechanisms of B1 receptor antagonism. Experiments were performed 24h after injection of complete Freund's adjuvant (CFA) or saline into the paw of Wistar rats. A gene expression analysis for the B1 receptor was performed in different tissues. BI113823 was administered orally or intrathecally to assess effects on CFA-induced hyperalgesia. Peripheral afferents of the saphenous nerve as well as spinal wide dynamic range (WDR) and nociceptive-specific (NS) neurons were recorded, and mechanosensitivity was measured before and after BI113823 administration.", 'BI113823 reduced CFA-induced mechanical hyperalgesia when administered orally or intrathecally. An increased B1 receptor gene expression was found in peripheral and spinal neural tissue. BI113823 significantly reduced mechanosensitivity of peripheral afferents and spinal NS neurons, but had no effect on WDR neurons.
answer:
0

question:
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.
answer:
0

question:
During cardiopulmonary resuscitation (CPR), myocardial blood flow generated by chest compression rarely exceeds 35% of its normal level. Cardiac output generated by chest compression decreases gradually with the prolongation of cardiac arrest and resuscitation. Early studies have demonstrated that myocardial blood flow during CPR is largely dependent on peripheral vascular resistance. In this study, we investigated the effects of chest compression in combination with physical control of peripheral vascular resistance assisted by tourniquets on myocardial blood flow during CPR.', 'Ventricular fibrillation was induced and untreated for 7 min in ten male domestic pigs weighing between 33 and 37 kg. The animals were then randomized to receive CPR alone or a tourniquet assisted CPR (T-CPR). In the CPR alone group, chest compression was performed by a miniaturized mechanical chest compressor. In the T-CPR group, coincident with the start of resuscitation, the thin elastic tourniquets were wrapped around the four limbs from the distal end to the proximal part. After 2 min of CPR, epinephrine (20 g/kg) was administered via the femoral vein. After 5 min of CPR, defibrillation was attempted by a single 150 J shock. If resuscitation was not successful, CPR was resumed for 2 min before the next defibrillation. The protocol was continued until successful resuscitation or for a total of 15 min. Five minutes after resuscitation, the elastic tourniquets were removed. The resuscitated animals were observed for 2h.', 'T-CPR generated significantly greater coronary perfusion pressure, end-tidal carbon dioxide and carotid blood flow. There was no difference in both intrathoracic positive and negative pressures between the two groups. All animals were successfully resuscitated with a single shock in both groups. There were no significant changes in hemodynamics observed in the animals treated in the T-CPR group before-and-after the release of tourniquets at post-resuscitation 5 min.
answer:
1