***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: Summary We investigated the effect of mild hypothermia ( 32–34 ° C ) , mannitol and insulin – induced hypoglycaemia on the ischaemic infa rct volume on permanent middle cerebral artery occlusion with bilateral carotid artery ligation in rats . Temporalis muscle temperature as an indicator of brain temperature was monitored throughout the experiment in all rats , which were r and omly divided into seven groups . During ischaemia , control rats received intravenous saline in a normothermic condition ; treated rats had hypothermia and intravenous saline , hypothermia and mannitol , normothermia and mannitol , normothermia and insulin , normothermia , insulin and glucose , and hypothermia and insulin applied . After the experiment , the animals were killed , and brain sections were stained with haematoxylin and eosin . Images of infa rct areas were determined using a camera attached to the microscope , and analysed by image analysis software . The total volume of infa rct ed tissue , right hemispheric volume , and the percentage of infa rct ion were determined at the end of the image analysis investigation . The infa rct volume on the control group was found to be 128.16±6.67 mm3 . Infa rct volumes in hypothermic groups were significantly smaller than those of the control group ( p<0.05 ) . There were no significant differences between infa rct volumes in the hypothermic groups . However , we found that hypothermia plus mannitol have the greatest neuro-protective effect . In normothermic rats , the infa rct volume decreased proportionally but not statistically ( p>0.05 ) whether mannitol or insulin was given . Our results also demonstrate that pre- , and post-ischaemic serum glucose concentrations influence the volume of infa rct ion . Rats that had had pre-ischaemic high serum glucose concentrations had a higher volume of infa rct than the hypothermic rats ( p<0.05 ) , while rats with post-ischaemic low serum glucose concentrations had a lower volume of infa rct than the control rats BACKGROUND AND PURPOSE Hyperglycemia at the time of ischemic stroke is associated with increased mortality and morbidity . Animal studies suggest that infa rct expansion may be responsible . The influence of persisting hyperglycemia after stroke has not previously been examined . We measured the blood glucose profile after acute ischemic stroke and correlated it with infa rct volume changes using T2- and diffusion-weighted MRI . METHODS We recruited 25 subjects within 24 hours of ischemic stroke symptoms .  Continuous glucose monitoring was performed with a glucose monitoring device ( CGMS ) , and 4-hour capillary glucose levels ( BGL ) were measured for 72 hours after admission .  MRI and clinical assessment s were performed at acute ( median , 15 hours ) , subacute ( median , 5 days ) , and outcome ( median , 85 days ) time points . RESULTS Mean CGMS glucose and mean BGL glucose correlated with infa rct volume change between acute and subacute diffusion-weighted MRI ( r > or=0.60 , P<0.01 ) , acute and outcome MRI ( r=0.56 , P=0.01 ) , outcome National Institutes of Health Stroke Scale ( NIHSS ; r > or=0.53 , P<0.02 ) , and outcome modified Rankin Scale ( mRS ; r > or=0.53 , P=0.02 ) . Acute and final infa rct volume change and outcome NIHSS and mRS were significantly higher in patients with mean CGMS or mean BGL glucose > or=7 mmol/L. Multiple regression analysis indicated that both mean CGMS and BGL glucose levels > or=7 mmol/L were independently associated with increased final infa rct volume change . CONCLUSIONS Persistent hyperglycemia on serial glucose monitoring is an independent determinant of infa rct expansion and is associated with worse functional outcome . There is an urgent need to study normalization of blood glucose after stroke OBJECTIVES We tested how insulin-glucose infusion followed by multidose insulin treatment in diabetic patients with acute myocardial infa rct ion affected mortality during the subsequent 12 months of follow-up . BACKGROUND Despite significant improvements in acute coronary care , diabetic patients with acute myocardial infa rct ion still have a high mortality rate . METHODS A total of 620 patients were studied : 306 r and omized to treatment with insulin-glucose infusion followed by multidose subcutaneous insulin for > or = 3 months and 314 to conventional therapy .  RESULTS The two groups were well matched for baseline characteristics . Blood glucose decreased from 15.4 + /- 4.1 to 9.6 + /- 3.3 mmol/liter ( mean + /- SD ) in the infusion group during the 1st 24 h , and from 15.7 + /- 4.2 to 11.7 + /- 4.1 among control patients ( p < 0.0001 ) . After 1 year 57 subjects ( 18.6 % ) in the infusion group and 82 ( 26.1 % ) in the control group had died ( relative mortality reduction 29 % , p = 0.027 ) . The mortality reduction was particularly evident in patients who had a low cardiovascular risk profile and no previous insulin treatment ( 3-month mortality rate 6.5 % in the infusion group vs. 13.5 % in the control group [ relative reduction 52 % , p = 0.046 ] ; 1-year mortality rate 8.6 % in the infusion group vs. 18.0 % in the control group [ relative reduction 52 % , p = 0.020 ] ) . CONCLUSIONS Insulin-glucose infusion followed by a multidose insulin regimen improved long-term prognosis in diabetic patients with acute myocardial infa rct ion Background —The clinical benefits of insulin previously observed in acute ST-segment – elevation myocardial infa rct ion ( STEMI ) may be partially explained by an anti-inflammatory effect . We assessed this potential effect of insulin in STEMI patients treated with fibrinolytics .  Methods and Results —Thirty-two patients receiving reteplase were r and omly assigned infusions of either insulin at 2.5 U/h , dextrose , and potassium ( GIK ) or normal saline and potassium ( C ) for 48 hours . Plasma concentrations of high-sensitivity C-reactive protein ( CRP ) , serum amyloid A ( SAA ) , plasminogen activator inhibitor-1 ( PAI-1 ) , creatine kinase ( CK ) , and CK-MB were measured at baseline and sequentially for 48 hours . Total p47phox protein in mononuclear cells was measured in a subgroup of 13 subjects . Baseline CRP and SAA were significantly increased ( 2- to 4-fold ) at 24 and 48 hours in each group ( P < 0.01 ) . However , in the insulin group , there was a significant ( P < 0.05 ) attenuation of the absolute rise in concentration of CRP and SAA from baseline . The absolute increase of CRP and SAA was reduced by 40 % ( CRP ) and 50 % ( SAA ) at 24 hours and at 48 hours compared with the control group . The absolute increase in PAI-1 from baseline and the percentage increase in p47phox over 48 hours were significantly ( P < 0.05 ) lower in the insulin-treated group . CK-MB peaked earlier and tended to be lower in insulin-treated subjects , especially in patients with inferior MI . Conclusions —Insulin has an anti-inflammatory and profibrinolytic effect in patients with acute MI . These effects may contribute to the clinical benefits of insulin in STEMI Objective : To analyze the frequency , clinical characteristics , and predictors of symptomatic intracerebral hemorrhage ( ICH ) after intraarterial ( IA ) thrombolysis with recombinant pro-urokinase ( r-proUK ) in acute ischemic stroke . Method : The authors conducted an exploratory analysis of  symptomatic ICH  from a r and omized , controlled clinical trial of IA thrombolysis with r-proUK for patients with angiographically documented occlusion of the middle cerebral artery within 6 hours from stroke onset . Patients ( n = 180 ) were r and omized in a ratio of 2:1 to either 9 mg IA r-proUK over 120 minutes plus IV fixed-dose heparin or IV fixed-dose heparin alone . As opposed to intention to treat , this analysis was based on “ treatment received ” and includes 110 patients given r-proUK and 64 who did not receive any thrombolytic agent .  The remaining six patients received out-of- protocol urokinase and were excluded from analysis . The authors analyzed central ly adjudicated ICH with associated neurologic deterioration ( increase in NIH Stroke Scale [ NIHSS ] score of ≥4 points ) within 36 hours of treatment initiation . Results : Symptomatic ICH occurred in 12 of 110 patients ( 10.9 % ) treated with r-proUK and in two of 64 ( 3.1 % ) receiving heparin alone . ICH symptoms in r-proUK – treated patients occurred at a mean of 10.2 ± 7.4 hours after the start of treatment . Mortality after symptomatic ICH was 83 % ( 10/12 patients ) . Only blood glucose was significantly associated with symptomatic ICH  in r-proUK – treated patients based on univariate analyses of 24 variables : patients with baseline glucose > 200 mg/dL experienced a 36 % risk of symptomatic ICH compared with 9 % for those with ≤200 mg/dL ( p = 0.022 ; relative risk , 4.2 ; 95 % CI , 1.04 to 11.7 ) . Conclusions : Symptomatic ICH after IA thrombolysis with r-proUK for acute ischemic stroke occurs early after treatment and has high mortality . The risk of symptomatic ICH may be increased in patients with a blood glucose > 200 mg/dL at stroke onset Eleven Type 2 diabetic subjects ( 10 male 1 female : age 56.2 + /- 9.7 ( SD ) yr ) were treated in r and om order either with insulin or with sulphonylureas for 8 weeks each , without attempting to alter glycaemic control between the two treatment periods . Insulin treatment was associated with suppression of endogenous insulin secretion ( fasting C-peptide levels -35.0 + /- 24.2 % ; p = 0.006 ) , and of intact proinsulin ( -43.1 + /- 36.8 % ; p = 0.03 ) and 32,33 split proinsulin -20.1 + /- 27.0 % ; p = 0.03 ) . Activity of plasminogen activator inhibitor ( PAI-1 ) , a fast acting inhibitor of fibrinolysis , decreased significantly ( -14.3 % + /- 27.5 % ; p = 0.02 ) but no changes occurred in concentration of lipoproteins or apoproteins between therapies . Changes in concentrations of 32,33 split and intact proinsulin were closely and significantly related ( rs = 0.83 ; p < 0.001 ) to each other but not with changes in concentrations of C-peptide ( intact proinsulin rs = -0.41 ; p = 0.11 ) and 32,33 split proinsulin rs = -0.27 ; ( p = 0.21 ) . Percentage changes in intact proinsulin concentrations were positively correlated with those in PAI-1 ( rs = 0.51 ; p = 0.05 ) . There was , however a paradoxical negative relationship between changes in C-peptide concentrations and those of PAI-1 ( rs = -0.73 ; p = 0.006 ) . These preliminary observations suggest that insulin treatment in Type 2 diabetic subjects without any changes in glycaemic control is associated with a reduced activity of PAI-1 , but is without effect on any other cardiovascular risk factors . Concentrations of insulin precursor molecules may play a role in determining fibrinolytic activity CONTEXT Glucose-insulin-potassium ( GIK ) infusion is a widely applicable , low-cost therapy that has been postulated to improve mortality in patients with acute ST-segment elevation myocardial infa rct ion ( STEMI ) . Given the potential global importance of GIK infusion , a large , adequately powered r and omized trial is required to determine the effect of GIK on mortality in patients with STEMI . OBJECTIVE To determine the effect of high-dose GIK infusion on mortality in patients with STEMI . DESIGN , SETTING , AND PARTICIPANTS R and omized controlled trial conducted in 470 centers worldwide among 20,201 patients with STEMI who presented within 12 hours of symptom onset . The mean age of patients was 58.6 years , and evidence -based therapies were commonly used . INTERVENTION Patients were r and omly assigned to receive GIK intravenous infusion for 24 hours plus usual care  ( n = 10,091 ) or to receive usual care alone  ( controls ; n = 10,110 
    Output:
    
Using MRI it has been demonstrated that in patients with acute perfusion diffusion mismatch within 24 hours of stroke onset , acute hyperglycemia correlates with reduced salvage of mismatch tissue from infa rct ion , greater final infa rct size , and worse functional outcome .4 As a consequence , not only has a causal relationship between hyperglycemia and poor outcome been assumed , but also a benefical treatment effect from control of