***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: BACKGROUND Induction of hypothermia in patients with brain injury was shown to improve outcomes in small clinical studies , but the results were not definitive . To study this issue , we conducted a multicenter trial comparing the effects of hypothermia with those of normothermia in patients with acute brain injury . METHODS The study subjects were 392 patients 16 to 65 years of age with coma after sustaining closed head injuries who were r and omly assigned to be treated with hypothermia ( body temperature , 33 degrees C ) , which was initiated within 6 hours after injury and maintained for 48 hours by means of surface cooling , or normothermia . All patients otherwise received st and ard treatment . The primary outcome measure was functional status six months after the injury . RESULTS The mean age of the patients and the type and severity of injury in the two treatment groups were similar . The mean ( + /-SD ) time from injury to r and omization was 4.3+/-1.1 hours in the hypothermia group and 4.1+/-1.2 hours in the normothermia group , and the mean time from injury to the achievement of the target temperature of 33 degrees C in the hypothermia group was 8.4+/-3.0 hours . The outcome was poor ( defined as severe disability , a vegetative state , or death ) in 57 percent of the patients in both groups . Mortality was 28 percent in the hypothermia group and 27 percent in the normothermia group ( P=0.79 ) . The patients in the hypothermia group had more hospital days with complications than the patients in the normothermia group . Fewer patients in the hypothermia group had high intracranial pressure than in the normothermia group . CONCLUSIONS Treatment with hypothermia , with the body temperature reaching 33 degrees C within eight hours after injury , is not effective in improving outcomes in patients with severe brain injury BACKGROUND Cardiac arrest with widespread cerebral ischemia frequently leads to severe neurologic impairment . We studied whether mild systemic hypothermia increases the rate of neurologic recovery after resuscitation from cardiac arrest due to ventricular fibrillation . METHODS In this multicenter trial with blinded assessment of the outcome , patients who had been resuscitated after cardiac arrest due to ventricular fibrillation were r and omly assigned to undergo  therapeutic hypothermia ( target temperature , 32 degrees C to 34 degrees C , measured in the bladder ) over a period of 24 hours or to receive st and ard treatment with normothermia . The primary end point was a favorable neurologic outcome within six months after cardiac arrest ; secondary end points were mortality within six months and the rate of complications within seven days . RESULTS Seventy-five of the 136 patients in the hypothermia group for whom data were available ( 55 percent ) had a favorable neurologic outcome ( cerebral-performance category , 1 [ good recovery ] or 2 [ moderate disability ] ) , as compared with 54 of 137 ( 39 percent ) in the normothermia group ( risk ratio , 1.40 ; 95 percent confidence interval , 1.08 to 1.81 ) . Mortality at six months was 41 percent in the hypothermia group ( 56 of 137 patients died ) , as compared with 55 percent in the normothermia group ( 76 of 138 patients ; risk ratio , 0.74 ; 95 percent confidence interval , 0.58 to 0.95 ) . The complication rate did not differ significantly between the two groups . CONCLUSIONS In patients who have been successfully resuscitated after cardiac arrest due to ventricular fibrillation , therapeutic mild hypothermia increased the rate of a favorable neurologic outcome and reduced mortality Background and Purpose — We undertook this study to evaluate the feasibility of inducing and maintaining moderate hypothermia with the use of endovascular rather than surface cooling . Methods — Six patients with severe acute ischemic stroke were treated with moderate hypothermia . This was induced and maintained by circulating temperature-adjusted normal saline in a closed-loop system entailing 3 balloons located near the tip of a central line , which dwelled in the inferior vena cava . Results — The mean±SD initial temperature of the patients was 37±1 ° C ( range , 35.5 ° C to 38.4 ° C ) . The pace of cooling was 1.4±0.6 ° C/h , and target temperature was reached after 3±1 hours ( range , 2 to 4.5 hours ) . During hypothermia , the maximal temperature observed was 33.4 ° C , and the minimal temperature was 32.2 ° C . Temperature deviations > 0.2 ° C or > 0.3 ° C were observed during 21 % or 10 % of the hours under hypothermia , respectively . Singultus was the only device-related complication encountered . Pulmonary infection , arterial hypotension , bradycardia , arrhythmia , and thrombocytopenia were the most common side effects . Conclusions — Induction and maintenance of hypothermia with an intravenous cooling device are feasible . The safety of this approach remains to be evaluated Objective : To report results of a r and omized pilot clinical feasibility trial of endovascular cooling in patients with ischemic stroke . Methods : Forty patients with ischemic stroke presenting within 12 hours of symptom onset were enrolled in the study . An endovascular cooling device was inserted into the inferior vena cava of those r and omized to hypothermia . A core body temperature of 33 ° C was targeted for 24 hours . All patients underwent clinical assessment and MRI initially , at days 3 to 5 and days 30 to 37 . Results : Eighteen patients were r and omized to hypothermia and 22 to receive st and ard medical management . Thirteen patients reached target temperature in a mean of 77 ± 44 minutes . Most tolerated hypothermia well . Clinical outcomes were similar in both groups . Mean diffusion-weighted imaging ( DWI ) lesion growth in the hypothermia group ( n = 12 ) was 90.0 ± 83.5 % compared with 108.4 ± 142.4 % in the control group ( n = 11 ) ( NS ) . Mean DWI lesion growth in patients who cooled well ( n = 8) was 72.9 ± 95.2 % ( NS ) . Conclusions : Induced moderate hypothermia is feasible using an endovascular cooling device in most patients with acute ischemic stroke . Further studies are needed to determine if hypothermia improves outcome Background and Purpose — Moderate hypothermia decreases ischemic damage in experimental stroke models . This multicenter study was performed to evaluate ( 1 ) the safety and feasibility of moderate hypothermia and ( 2 ) its potential to reduce intracranial hypertension in acute stroke patients . Methods — Fifty prospect i ve patients with cerebral infa rct ion involving at least the complete middle cerebral artery territory treated with moderate hypothermia were evaluated .  Hypothermia was induced with the use of cooling blankets as well as alcohol and ice bags within 22±9 hours after stroke onset and maintained for 24 to 72 hours ; subsequently , patients passively rewarmed over a mean duration of 17 hours . Outcome was assessed at 4 weeks and at 3 months . Results — Time required for cooling to < 33 ° C varied from 3.5 to 11 hours . The most frequent complications of hypothermic therapy were thrombocytopenia ( 70 % ) , bradycardia ( 62 % ) , and pneumonia ( 48 % ) . Four patients ( 8 % ) died during hypothermia as a result of severe coagulopathy , cardiac failure , or uncontrollable intracranial hypertension . An additional 15 patients ( 30 % ) died during or after rewarming because of rebound increase in intracranial pressure ( ICP ) and fatal herniation . A shorter ( < 16 hours ) rewarming period was associated with a more pronounced rise of ICP . Elevated ICP values were significantly reduced under  hypothermia . Neurological outcome according to the National Institutes of Health Stroke Scale score 4 weeks after stroke was 29 , and Rankin Scale score 3 months after stroke was 2.9 . Conclusions — Moderate hypothermia is feasible in patients with acute stroke , although it is associated with several side effects . Most deaths occur during rewarming as a result of excessive ICP rise . Our preliminary observation that a longer duration of the rewarming period limits the ICP increase remains to be confirmed in future studies Objective : To study the effects of mild hypothermia and associated changes in temperature-corrected PaCO2 ( cPaCO2 ) on intracranial pressure ( ICP ) , mean velocity of the middle cerebral artery ( Vm ) , and venous jugular saturation in O2 ( SjvO2 ) in patients with severe traumatic brain injury (TBI).¶ Design : Prospect i ve , observational study .¶ Setting : Intensive care unit.¶ Patients : Severe TBI patients mechanically ventilated , se date d and paralyzed.¶ Interventions : Twenty patients were subjected to four consecutive periods : ( a ) normocapnia-normothermia ; ( b ) hypocapnia-normothermia , where hypocapnia was induced by an increase in minute volume ; ( c ) hypocapnia-hypothermia , where hypocapnia was induced by hypothermia maintaining the ventilatory setting s constant ; ( d ) normocapnia-hypothermia , where normocapnia was achieved by a decrease in minute volume.¶ Measurements and results : cPaCO2 was 41 ± 8 mmHg in periods 1 and 4 , and 31 ± 7 mmHg in periods 2 and 3 . Core temperature was 37.1 ± 0.8 ° C in periods 1 and 2 , and 34.1 ± 1.1 ° C in periods 3 and 4 . End-tidal CO2 and cPaCO2 values showed no difference between periods 1 and 4 and periods 2 and 3 . ICP and Vm were dependent on cPaCO2 but independent of core temperature values . SjvO2 was related to cPaCO2 and was significantly higher during period 3 than during period 2 ( P < 0.05).¶ Conclusion : The decrease in ICP was similar when hypocapnia was induced by hyperventilation or as a result of hypothermia alone . The relationship between cPaCO2 and ICP might predict variations in ICP during changes in core temperature . Further studies are needed to confirm the cerebral metabolic effects of moderate hypothermia in TBI patients BACKGROUND Cardiac arrest outside the hospital is common and has a poor outcome . Studies in laboratory animals suggest that hypothermia induced shortly after the restoration of spontaneous circulation may improve neurologic outcome , but there have been no conclusive studies in humans . In a r and omized , controlled trial , we compared the effects of moderate hypothermia and normothermia in patients who remained unconscious after resuscitation from out-of-hospital cardiac arrest . METHODS The study subjects were 77 patients who were r and omly assigned to treatment with hypothermia ( with the core body temperature reduced to 33 degrees C within 2 hours after the return of spontaneous circulation and maintained at that temperature for 12 hours ) or normothermia .  The primary outcome measure was survival to hospital discharge with sufficiently good neurologic function to be discharged to home or to a rehabilitation facility . RESULTS The demographic characteristics of the patients were similar in the hypothermia and normothermia groups . Twenty-one of the 43 patients treated with hypothermia ( 49 percent ) survived and had a good outcome --that is , they were discharged home or to a rehabilitation facility -- as compared with 9 of the 34 treated with normothermia ( 26 percent , P=0.046 ) . After adjustment for base-line differences in age and time from collapse to the return of spontaneous circulation , the odds ratio for a good outcome with hypothermia as compared with normothermia was 5.25 ( 95 percent confidence interval , 1.47 to 18.76 ; P=0.011 ) . Hypothermia was associated with a lower cardiac index , higher systemic vascular resistance , and hyperglycemia . There was no difference in the frequency of adverse events . CONCLUSIONS Our preliminary observations suggest that treatment with moderate hypothermia appears to improve outcomes in patients with coma after resuscitation from out-of-hospital cardiac arrest Ischaemic preconditioning ( short periods of ischaemia with intermittent reperfusion ) has been shown paradoxically to protect the myocardium from a subsequent longer ischaemic insult . The protection associated with preconditioning is one of the most powerful mechanisms of protection known and has been shown in every animal species investigated . However , there is no direct evidence that ischaemic preconditioning occurs in the human heart . We studied whether it was possible to precondition the human heart in a setting of  coronary artery bypass surgery .  The measurement of adenosine triphosphate in biopsy specimens was used as our endpoint . We believe that our results are the first to show that it may be possible to precondition and protect the human myocardium with short controlled periods of intermittent ischaemia and reperfusion Background : We hypothesized that previous transient ischemic attack ( TIA ) had a favorable effect on early outcome after acute nonlacunar ischemic stroke . Methods : Data of 1,753 consecutive patients with ischemic stroke collected from a prospect i ve hospital-based stroke registry were studied . A comparison was made of the groups with and without previous TIA . Favorable outcome included spontaneous neurological recovery or grade s 0–2 of the modified Rankin scale at hospital discharge . Results : Previous TIA occurred in 55 ( 11.5 % ) of 484 patients with lacunar stroke and in 166 ( 13.1 % ) of 1 
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RESULTS Although the mechanisms of protection for both therapeutic strategies are multifold , both share features of downregulating metabolism .