***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: Background The enzyme heme oxygenase-1 ( HO-1 ) de grade s heme and protects against ischemia-reperfusion injury . Monocytes/macrophages are the major source of HO-1 and higher levels improve renal transplant outcomes . Heme arginate ( HA ) safely induces HO-1 in humans . Methods The Heme Oxygenase-1 in renal Transplantation study was a r and omized , placebo-controlled , IIb trial to evaluate HA effect on HO-1 upregulation after deceased donor kidney transplantation . 40 recipients were r and omized to either 3 mg kg−1 HA or placebo ( 0.9 % NaCl )  , given preoperatively ( day 0 ) and again on day 2 . Recipient blood and urine were collected daily . Graft biopsies were taken preoperatively and on day 5 . Primary outcome was HO-1 upregulation in peripheral blood mononuclear cells ( P BMC s ) . Secondary outcomes were graft HO-1 upregulation and injury , urinary biomarkers , and renal function . Results The HA upregulated P BMC HO-1 protein more than placebo at 24 hours : HA 11.1 ng/mL versus placebo 0.14 ng/mL ( P = < 0.0001 ) . The P BMC HO-1 messenger RNA also increased : HA 2.73-fold versus placebo 1.41-fold ( P = 0.02 ) . Heme arginate increased day 5 tissue HO-1 protein immunopositivity compared with placebo : HA 0.21 versus placebo −0.03 ( P = 0.02 ) and % HO-1–positive renal macrophage also increased : HA 50.8 cells per high power field versus placebo 22.3 ( P = 0.012 ) . Urinary biomarkers were reduced after HA but not significantly . Histological injury and renal function were similar but the study was not powered for this . Adverse events were equivalent between groups . Conclusions The primary outcome was achieved and demonstrated for the first time that HA safely induces HO-1 in transplant recipients . Planned larger studies will determine the impact of HO-1 upregulation on clinical outcomes and evaluate the benefit to patients at risk of ischemia-reperfusion injury Objective To investigate the adrenocortical function in brain-dead patients , potential organ donors . Design Prospect i ve study . Setting Intensive care units in two teaching hospitals . Patients A total of 37 patients ( 28 men , nine women ) with severe brain injury , having a mean age of 42 ± 18 yrs , were included in the study . Group A consisted of 20 brain-injured patients who did not deteriorate to brain death . Group B included 17 brain-injured patients who were brain dead ; of these , ten patients developed brain death during ICU stay and seven patients were admitted to the ICU after clinical brain death . Interventions In all patients ( group A and group B ) , a morning blood sample was obtained at admission to the ICU to determine baseline plasma cortisol . Subsequently , 1 & mgr;g of corticotropin ( adrenocorticotropic hormone , Synacthen ) was administered intravenously , and a blood sample was taken 30 mins after the injection . In group B patients who became brain dead while being treated in the ICU ( n = 10 ) , the same procedure was repeated the morning after the confirmation of brain death . Patients having a cortisol level of at least 18 & mgr;g/dL after the administration of adrenocorticotropic hormone were defined as responders . Measurements and Main Results After the occurrence of brain death , group B patients had significantly lower values for baseline ( 8.5 ± 6.2 vs. 17.0 ± 6.6 & mgr;g/dL , p < .001 ) and stimulated ( 16.9 ± 6.3 vs. 23.9 ± 5.7 & mgr;g/dL , p = .001 ) plasma cortisol compared with group A patients . Thirteen group B patients ( 76 % ) and two group A patients ( 10 % ) were nonresponders to adrenocorticotropic hormone ( p < .001 ) . In group B patients , baseline and stimulated cortisol concentrations were significantly related ( r = .71 , p = .001 ) , whereas there was no correlation between baseline cortisol and the increment in cortisol ( r = −.37 , p = .15 ) . Mean hormonal data of the ten brain-dead patients studied at admission in the ICU and after the occurrence of brain death were the following : baseline plasma cortisol ( 23.5 ± 11.4 vs. 6.8 ± 4.2 & mgr;g/dL , p = .003 ) and stimulated serum cortisol ( 28.8 ± 9.9 vs. 16.3 ± 4.3 & mgr;g/dL , p = .008 ) . Conclusions Adrenal cortisol secretion after dynamic stimulation is deficient in a substantial proportion of brain-dead potential organ donors CONTEXT After brain stem death ( BSD ) , a low T(3 ) state is common , and T(3 ) supplementation has been advocated to improve heart function and yield for transplantation . OBJECTIVES The aim of the study was to assess the effects of T(3 ) on expression of mRNAs encoding T(3)-responsive genes in the post-BSD human heart . DESIGN Within a prospect i ve double-blind trial , potential BSD cardiac donors undergoing hemodynamic optimization were r and omized to T(3 ) ( 0.8 microg . kg(-1 ) bolus ; infusion 0.113 microg . kg(-1 ) . h(-1 ) ) or placebo ( 5 % dextrose ) for up to 6 h. Left ventricular biopsies were obtained at end- assessment from 30 donors ( T(3 ) ; n=16 ) . TaqMan real-time PCR was performed to investigate mRNA expression of the voltage-gated potassium channel Kv1.5 , beta-1 adrenergic receptor ( ADRB1 ) , sarcoplasmic reticulum calcium ATPase type 2a ( SERCA2a ) , and phospholamban ( PLB ) . RESULTS Time between diagnosis of BSD and donor management was 13.2 h ( range , 9.7 - 16.8 h ) . T(3 ) donors were managed for 7.6 ( 6.9 - 8.3 ) h. Median serum free T(3 ) ( fT3 ) at baseline was 2.9 ( 2.3 - 3.8 ) pmol . liter(-1 ) ( reference range , 3.3 - 7.5 pmol . liter(-1 ) ) . At baseline , 19 of 30 ( 56.7 % ) had low serum fT3 , and T(3 ) treatment increased fT3 to supraphysiological levels ( P < 0.001 ) . Expression of mRNAs encoding Kv1.5 and SERCA2a was increased 1.99-fold and 1.51-fold ( P = 0.015 and 0.043 ) . There was no significant change in the expression of mRNAs encoding ADRB1 and PLB . Treatment with T(3 ) did not improve hemodynamic function compared with placebo . CONCLUSIONS Acute administration of T(3 ) in the BSD cardiac donor reverses the low T(3 ) state and increases expression of the mRNAs encoding Kv1.5 and SERCA2a , but not ADRB1 or PLB and is not associated with any improvement in hemodynamic performance 34 cadaveric donor grafts were r and omized in a blind study of the effect of pretreatment of 5 g each of methylprednisolone and cyclophosphamide on kidney graft outcome . There was no difference in overall survival or functioning after 3 , 6 or 12 months between grafts from pretreated ( 33 kidneys ) or control ( 29 kidneys ) cadaveric donors . In addition , this pretreatment protocol did not modify the recipient immune response against B-lymphocyte alloantigens which developed in unsuccessful transplants . Our data , thus , neither confirm the high rate of kidney graft survival attributed to cadaveric donor treatment nor the supposition that treatment is effective in suppressing recipient antidonor B-lymphocyte antibodies BACKGROUND  Posttransplantation acute renal failure ( ARF ) occurs in roughly 25 % of recipients of organs from deceased donors . Inflammation in the donor organ is associated with risk for ARF . OBJECTIVE To determine whether administering corticosteroids to deceased organ donors reduces the incidence and duration of ARF in organ recipients more than placebo . DESIGN Parallel , blocked r and omized trial , performed between February 2006 and November 2008 , with computer-generated r and omization and central ized allocation . Investigators were masked to group assignment . ( Controlled-trials.com registration number : IS RCT N78828338 ) SETTING : 3 renal transplantation centers in Austria and Hungary . PATIENTS 306 deceased heart-beating donors and 455 renal transplant recipients . INTERVENTIONS Organ donors were administered an intravenous infusion of either 1000 mg of methylprednisolone ( 136 donors ) or placebo ( 0.9 % saline ) ( 133 donors ) at least 3 hours before organ harvesting . MEASUREMENTS Incidence of ARF , defined as more than 1 dialysis session in the first week after transplantation , was the primary end point . Secondary and other end points included duration of ARF and trajectories of serum creatinine level . The suppression of immune response and inflammation by the intervention was assessed in the donor organ on a genome-wide basis . RESULTS 52 of 238 recipients ( 22 % ) of kidneys from steroid-treated donors and 54 of 217 recipients ( 25 % ) of kidneys from placebo-treated donors had ARF ( difference , 3 percentage points [ 95 % CI , -11 to 5 percentage points ] ) . One graft was lost on day 1 in each group , and 1 recipient in the placebo group died of cardiac arrest on day 2 . The median duration of ARF was 5 days ( interquartile range , 2 days ) in the steroid group and 4 days ( interquartile range , 2 days ) in the placebo group ( P = 0.31 ) . The groups had similar trajectories of serum creatinine level in the first week ( P = 0.72 ) . Genomic analysis showed suppressed inflammation and immune response in kidney biopsies from deceased donors who received corticosteroids . LIMITATION Donors and recipients were mainly white , and all were from 3 transplantation centers in central Europe , which may limit generalizability . CONCLUSION Systemic suppression of inflammation in deceased donors by corticosteroids did not reduce the incidence or duration of posttransplantation ARF in allograft recipients . PRIMARY FUNDING SOURCE Austrian Science Fund and Austrian Academy of Science BACKGROUND Traditional approaches to mechanical ventilation use tidal volumes of 10 to 15 ml per kilogram of body weight and may cause stretch-induced lung injury in patients with acute lung injury and the acute respiratory distress syndrome . We therefore conducted a trial to determine whether ventilation with lower tidal volumes would improve the clinical outcomes in these patients . METHODS Patients with acute lung injury and the acute respiratory distress syndrome were enrolled in a multicenter , r and omized trial . The trial compared traditional ventilation treatment , which involved an initial tidal volume of 12 ml per kilogram of predicted body weight and an airway pressure measured after a 0.5-second pause at the end of inspiration ( plateau pressure ) of 50 cm of water or less , with ventilation with a lower tidal volume , which involved an initial tidal volume of 6 ml per kilogram of predicted body weight and a plateau pressure of 30 cm of water or less . The primary outcomes were death before a patient was discharged home and was breathing without assistance and the number of days without ventilator use from day 1 to day 28 . RESULTS The trial was stopped after the enrollment of 861 patients because  mortality was lower in the group treated with lower tidal volumes than in the group treated with traditional tidal volumes ( 31.0 percent vs. 39.8 percent , P=0.007 ) , and the number of days without ventilator use during the first 28 days after r and omization was greater in this group ( mean [ + /-SD ] , 12+/-11 vs. 10+/-11 ; P=0.007 ) . The mean tidal volumes on days 1 to 3 were 6.2+/-0.8 and 11.8+/-0.8 ml per kilogram of predicted body weight ( P<0.001 ) , respectively , and the mean plateau pressures were 25+/-6 and 33+/-8 cm of water ( P<0.001 ) , respectively . CONCLUSIONS In patients with acute lung injury and the acute respiratory distress syndrome , mechanical ventilation with a lower tidal volume than is traditionally used results in decreased mortality and increases the number of days without ventilator use AIMS The aim of this study was to assess the haemodynamic effects of tri-iodothyronine ( T3 ) and methylprednisolone in potential heart donors . METHODS AND RESULTS In a prospect i ve r and omized double-blind trial , 80 potential cardiac donors were allocated to receive T3 ( 0.8 microg kg(-1 ) bolus ; 0.113 microg kg(- 
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The remaining meta-analyses ( seven studies , 334 participants ) compared the effects of 10 min of ischaemic preconditioning on outcomes after liver transplantation and showed that ischaemic preconditioning improved short-term liver function , but not long-term transplant outcomes .
CONCLUSIONS There is currently insufficient evidence to conclude that any particular drug treatment or any intervention in the deceased donor improves long-term graft or patient survival after transplantation