***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 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Objective : To prospect ively study S-100B and neuron specific enolase ( NSE ) levels in subjects treated for severe head injury ( sTBI ) , and investigate the prognostic value of these biomarkers . Methods : Subjects included in a prospect i ve double blind r and omised study for sTBI . Inclusion criteria : Glasgow Coma Score ( GCS ) ⩽8 , age 15–70 years , first recorded cerebral perfusion pressure of > 10 mm Hg and arrival < 24 h after trauma . Subjects were treated with an intracranial pressure ( ICP ) targeted therapy . Blood sample s for S-100B and NSE were drawn immediately after arrival and every 12 h for 5 days . Outcome was evaluated as Glasgow Outcome Scale ( GOS ) by independent staff at 3 and 12 months . Results : 48 subjects , mean age 35.5 years , and median GCS 6 were included . The first blood sample was drawn at 15.6 ( 1.4 ) h after injury . Initial concentration of S-100B was 1.04 ( 0.21 ) μg/l and for NSE 18.94 ( 2.32 ) μg/l . The biomarkers were significantly higher in subjects with GCS 3 and in those who died compared with those with GCS 4–8 and GOS 2–5 , respectively . Receiver operated characteristic curve analyses of the initial S-100B and NSE levels to GOS dichotomised as unfavourable ( GOS 1–3 ) and favourable ( GOS 4–5 ) showed a weak correlation : AUC 0.585 and 0.555 , respectively . Using the dichotomisation dead ( GOS 1)/alive ( GOS 2–5 ) , the AUC values were 0.687 and 0.734 , respectively . Furthermore , a correlation was found between the biomarkers themselves and the biomarkers and ICP . Conclusion : At 3 and 12 months after trauma , no differences in prognostic values between the markers were apparent nor was there any clinical significant value of the markers as predictors of clinical outcome Purpose To identify factors associated with decisions to withdraw life-sustaining therapies in patients with severe traumatic brain injury ( TBI ) . Material s and Methods We conducted a 2-year multicenter retrospective cohort study ( 2005–2006 ) in mechanically ventilated patients aged 16 years and older admitted to the intensive care units ( ICUs ) of six Canadian level I trauma centers following severe TBI . One hundred and twenty charts were r and omly selected at each center ( n = 720 ) .  Data on ICU management strategies , patients ’ clinical condition , surgical procedures , diagnostic imaging , and decision to withdraw life-sustaining therapies  were collected . The association of factors pertaining to the injury , interventions , and management strategies with decisions to withdraw life-sustaining therapies  was evaluated among non-survivors . Results Among the 228 non-survivors , 160 died following withdrawal of life-sustaining therapies .  Patients were predominantly male ( 69.7 % ) with a mean age of 50.7 ( ±21.7 ) years old . Brain herniation was more often reported in patients who died following decisions to withdraw life-sustaining therapies ( odds ratio [ OR ] 2.91 , 95 % confidence interval [ CI ] 1.16–7.30 , p = 0.02 ) compared to those who died due to other causes ( e.g. , cardiac arrest , shock , etc . ) . Epidural hematomas ( OR 0.18 , 95 % CI 0.06–0.56 , p < 0.01 ) , craniotomies ( OR 0.12 , 95 % CI 0.02–0.68 , p = 0.02 ) , and other non-neurosurgical procedures ( OR 0.08 , 95 % CI 0.02–0.43 , p < 0.01 ) were less often associated with death following withdrawal of life-sustaining therapies than death from other causes . Conclusions Death following decisions to withdraw life-sustaining therapies is associated with specific patient and clinical factors , and the intensity of care Background : Severe traumatic brain injury often leads to death from withdrawal of life-sustaining therapy , although prognosis is difficult to determine . Methods : To evaluate variation in mortality following the withdrawal of life-sustaining therapy and hospital mortality in patients with critical illness and severe traumatic brain injury , we conducted a two-year multicentre retrospective cohort study in six Canadian level-one trauma centres . The effect of centre on hospital mortality and withdrawal of life-sustaining therapy was evaluated using multivariable logistic regression adjusted for baseline patient-level covariates ( sex , age , pupillary reactivity and score on the Glasgow coma scale ) . Results : We r and omly selected 720 patients with traumatic brain injury for our study . The overall hospital mortality among these patients was 228/720 ( 31.7 % , 95 % confidence interval [ CI ] 28.4%–35.2 % ) and ranged from 10.8 % to 44.2 % across centres ( χ2 test for overall difference , p < 0.001 ) . Most deaths ( 70.2 % [ 160/228 ] , 95 % CI 63.9%–75.7 % ) were associated with withdrawal of life-sustaining therapy , ranging from 45.0 % ( 18/40 ) to 86.8 % ( 46/53 ) ( χ2 test for overall difference , p < 0.001 ) across centres . Adjusted odd ratios ( ORs ) for the effect of centre on hospital mortality ranged from 0.61 to 1.55 ( p < 0.001 ) . The incidence of withdrawal of life-sustaining therapy  varied by centre , with ORs ranging from 0.42 to 2.40 ( p = 0.001 ) . About one half of deaths that occurred following the withdrawal of life-sustaining therapies happened within the first three days of care . Interpretation : We observed significant variation in mortality across centres . This may be explained in part by regional variations in physician , family or community approaches to the withdrawal of life-sustaining therapy . Considering the high proportion of early deaths associated with the withdrawal of life-sustaining therapy and the limited accuracy of current prognostic indicators , caution should be used regarding early withdrawal of life-sustaining therapy following severe traumatic brain injury Elevated serum neuron-specific enolase  levels are correlated with brain cell damage . Low scores according to Glasgow Coma Scale are also considered as serious poor prognostic factor . The aims of the study were to investigate whether there is a correlation between the two measurements in patients with traumatic brain injury and whether serum neuron-specific enolase levels have potential as a screening test to predict outcome . A total of 169 consecutive patients with traumatic brain injury admitted to our clinic between 2002 and 2005 are included in this study . Those patients , who had any major health problem before trauma , were excluded from the study . However , patients with isolated head injury were included in the study . Serial serum neuron-specific enolase concentrations taken at the first 2 , 24 , and 48 h after traumatic brain injury were analyzed . A computed tomography was performed on each patient on admission . Their Glasgow Coma Scale scores were recorded serially . The relationship between Glasgow Coma Scale scores and the serum neuron-specific enolase levels were assessed by statistical methods . There was a significant negative correlation between the serum neuron-specific enolase levels and Glasgow Coma Scale scores . The levels of neuron-specific enolase were significantly higher in the patients who died in 30 days after trauma and whose scores were lower than or equal to 8 points in Glasgow Coma Scale . Although there are several serious limitations of the use of neuron-specific enolase as a biomarker in traumatic brain injury ( i.e. , hypoperfusion , extracranial trauma , bleeding , liver , or kidney damage also increase the level of neuron-specific enolase ) , its concentrations may be useful as a practical and helpful screening test to identify neurotrauma patients who are at increased risk and may provide supplementary estimation with radiological and clinical findings In recent years , in addition to neurological examination and neuroradiologic examinations , attempts have been made to assess the severity of post-traumatic brain injury and to obtain an early idea of patient prognosis using biochemical markers with a high degree of brain tissue specificity . One such enzyme is neuron-specific enolase ( NSE ) . This study investigates the correlation between serum NSE levels , Glasgow Coma Score , and prognosis measured by Glasgow Outcome Scores in head trauma patients . This was a prospect i ve study conducted with 80 trauma patients presenting to the Emergency Department . Patients were divided into four groups . The first group consisted of patients with general body trauma , but no head trauma . The second group had minor head trauma .  The third group had moderate head trauma  , and the fourth group had severe head trauma .  The relationship between subjects ' admission NSE levels and admission and discharge Glasgow Coma Scores ( GCS ) and Glasgow Outcome Scores ( GOS ) 1 month later was examined . A receiver operating characteristic ( ROC ) analysis was performed using a serum NSE cutoff level of 20.52 ng/mL and a GOS of 3 or less as the definition of poor neurologic outcome . There was a significant difference in the NSE levels between group 1 ( general trauma ) and group 3 ( moderate head trauma ) . There was also a statistically significant difference in NSE levels between group 1 ( general trauma ) and group 4 ( severe head trauma ) ( p < 0.05 ) . There was a statistically significant inverse relationship between NSE levels and GOS as determined within groups 3 ( moderate ) and 4 ( severe head trauma ) ( p < 0.05 ) . When NSE levels were compared with admission GCS , it was found that GCS fell as NSE levels rose . There was no significant correlation between NSE and GCS within groups 3 ( moderate ) or 4 ( severe ) . There was a statistically significant correlation within group 2 ( mild ) ( p < 0.05 ) . By ROC analysis , serum NSE  was 87 % sensitive and 82.1 % specific in predicting poor neurologic outcome in the study patients . The area under the curve was 0.931 . This study shows that initial serum NSE levels in moderate and severe head trauma patients correlate inversely with GOS 1 month later , but only within the moderate and severe head trauma groups . However , serum NSE  was 87 % sensitive and 82.1 % specific in predicting poor neurologic outcome in all of the study patients . This derived cutoff value now needs to be prospect ively vali date OBJECTIVE The aim of this study was to investigate S-100B protein and NSE as a serum marker of brain cell damage after traumatic brain injury . MATERIAL AND METHODS Forty-one patients with traumatic brain injury were included in this prospect i ve study . Venous blood sample s for S-100B protein and NSE were taken after admission and on the next day . Serum levels of S-100 protein and NSE were compared with Glasgow Coma Scale score , computed tomographic findings and outcome after 3 months . RESULTS Serum S-100B protein and NSE were significantly correlated with Glasgow Coma Scale score and outcome after 3 months . The significant correlation was found between the initial S-100B and NSE ( P < 0.001 ) . In patients without parenchymal injuries on computed tomographic scan such as epidural hematoma and concussion , the elevation of S-100B protein and NSE was observed . The initial values of S-100B and NSE  in acute subdural hematomas with unfavorable outcome were significantly higher than in those with favorable outcome . Secondary increase of serum markers was associated with the presence of secondary insult such as hypoxia or hypotension , and was found to have an unfavorable outcome . CONCLUSIONS Serum concentration and kinetics of S-100B protein and NSE  provide the clinical assessment of the primary brain damage and have a predictive value for outcome after traumatic brain injury Summary We investigated the time course of  neuron specific enolase ( NSE ) and S-100 protein after severe head injury in correlation to outcome . We included 30 patients ( GCS<9 ) , who had been admitted within 5 hours after injury , in a prospect i ve study .  Blood sample s were taken on admission , 6 , 12 . and 24 hours and every 24 hours up to the fifth day after injury . The outcome was estimated on discharge using the Glasgow Outcome Scale . 70 % reached a good outcome . All concentrations of NSE and 83 % of the S-100 sample s were elevated concerning the first probe ( 30.2 μg/l NSE mean and 2.6 μg/l S-100 mean ) . Patients with bad outcome had an NSE concentration of 38 μg/l ( mean ) compared with 26.9 μg/l ( mean ) in patients with good outcome . Patients with bad outcome had an S-100 concentration of 4.9 μg/l ( mean ) compared with 1.7 μg/l ( mean ) in patients with good outcome ( p<0.05 ) . The mean values of NSE and S-100 decreased during the first 5 days . Four patients with increasing intracranial pressure showed a quick increasing concentration of NSE , in two patients the S-100 level showed a slower rise . The NSE serum levels did not correlate with intracranial pressure values . Our results show that the first serum concentration of S-100 seems to be predictive for outcome after severe head injury Neuron-specific en 
    Output:
    
INTERPRETATION In patients with moderate or severe traumatic brain injury , increased neuron-specific enolase serum levels are associated with unfavourable outcomes .