- ICH GCP
- US Clinical Trials Registry
- Clinical Trial NCT04696523
Effect of Xenon on Brain Injury After Aneurysmal Subarachnoid Hemorrhage (Xe-SAH)
Effect of Xenon on Brain Injury, Neurological Outcome and Survival in Patients After Aneurysmal Subarachnoid Hemorrhage
An investigator-initiated clinical drug study
Main Objective:
To explore neuroprotective properties of xenon in patients after aneurysmal subarachnoid hemorrhage (SAH).
Primary endpoint: Global fractional anisotropy of white matter of diffusion tensor imaging (DTI). Hypothesis: White matter damage is less severe in xenon treated patients, i.e. global fractional anisotropy is significantly higher in the xenon group than in the control group as assessed with the 1st magnetic resonance imaging (MRI).
After confirmation of aSAH and obtaining a signed assent subjects will be randomized to the following groups:
Control group: Standard of Care (SOC) group: Air/oxygen and Normothermia 36.5-37.5°C; Xenon group: Normothermia 36.5-37.5°C +Xenon inhalation in air/oxygen for 24 hours. Brain magnetic resonance imaging techniques will be undertaken to evaluate the effects of the intervention on white and grey matter damage and neuronal loss. Neurological outcome will be evaluated at 3, 12 and 24 months after onset of aSAH symptoms Investigational drug/treatment, dose and mode of administration: 50±2 % end tidal concentration of inhaled xenon in oxygen/air.
Comparative drug(s)/placebo/treatment, dose and mode of administration: Standard of care treatment according to local and international consensus reports.
Duration of treatment: 24 hours
Assessments:
Baseline data Information that characterizes the participant's condition prior to initiation of experimental treatment is obtained as soon as is clinically reasonable. These include participant demographics, medical history, vital signs, oxygen saturation, and concentration of oxygen administered.
Acute data The collected information will contain quantitative and qualitative data of aSAH patients, as recommended by recent recommendations of the working group on subject characteristics, and including all relevant Common Data Elements (CDE) can be applied. Specific definitions, measurements tools, and references regarding each SAH CDE can be found on the weblink here: https://www.commondataelements.ninds.nih.gov/SAH.aspx#tab=Data_Standards.
Study Overview
Status
Conditions
Intervention / Treatment
Detailed Description
Assessments of efficacy:
- A brain Computer tomography angiography (CTA) and / or 3 D Digital subtraction angiography (DSA) (whenever possible instead of 2D DSA) will be performed at hospital arrival and whenever clinically indicated.
- 1st 3 Tesla MRI 72 ± 24 hours after onset of aSAH symptoms; 2nd 3 Tesla MRI 42 ± 4 days after onset of aSAH symptoms.
- 3D DSA: Computational fluid dynamic simulations (CFD), artificial intelligence and machine learning.
- Brain Positron emission tomography (PET): The 1st 4 ± 1 weeks and the 2nd at 3 months after onset of aSAH symptoms.
- Biochemical assessment: A blood samples of 20 ml for determination of plasma catecholamines, plasma metabolomics (see details of metabolomics in section 18.4.7), cardiac enzyme release (P-hs-troponin-T and heart fatty-acid binding protein), selected biomarkers will be analysed at intensive crae unit (ICU) arrival and at 24h, at 48h and at 72h after onset of SAH symptoms. In addition, a sample of spinal fluid will be collected through external ventricular drainage (EVD) at ICU arrival or as soon as it is in place and at 24h, at 48h and at 72h after onset of SAH symptoms for assessment of metabolomics
- Electrocardiograph (ECG) at ICU arrival and at 24h, at 48h and at 72h after onset of aSAH symptoms.
- Neurological evaluation: at 3, 12 and at 24 months after aSAH with GOSe, Modified ranking score (mRS).
Statistical methods: 1) Basic statistical tests (t-tests, Mann-Whitney, Chi square, etc); 2) Survival analysis methods; 3) An analysis of variance for repeated measurements; 4) A sample size of 100 is estimated on the basis of a recent studies in SAH patients to provide 80% power with a 2-sided α level of 0.05 to detect a mean difference of 0.02 (SD 0.035) in the global fractional anisotropy of white matter between the xenon group and the control group (98). Accordingly, this mean difference is estimated to have a predictive value for DCI and poor neurological outcome (i.e. mRS 3-6).Significance level of 0.05 and an estimation of 95 % confidence intervals will be used in the statistical analyses.
Study Type
Enrollment (Anticipated)
Phase
- Phase 2
Contacts and Locations
Study Contact
- Name: Timo T Laitio, MD, PhD
- Phone Number: +358504653201
- Email: timo.laitio@tyks.fi
Study Locations
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Helsinki, Finland
- Aalto University School of Science
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Contact:
- Timo Roine, PhD
- Email: timo.roine@gmail.com
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Kuopio, Finland
- Kuopio University Hospital
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Contact:
- Stepani Bendel
- Email: stepani.bendel@kuh.fi
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Tampere, Finland
- Tampere University Hospital
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Contact:
- Sari Karlsson, MD, PhD
- Email: sari.karlsson@pshp.fi
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Turku, Finland, 20521
- Turku University Hospital
-
Contact:
- Timo T Laitio, MD, PhD
- Phone Number: +358504653201
- Email: timo.laitio@tyks.fi
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Turku, Finland, 20810
- Elomatic
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Contact:
- Juha Tanttari, MSc
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Turku, Finland
- University of Turku, Turku Bioscience, Analysis of the metabolomics
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Contact:
- Matej Orešič, PhD
- Email: matej.oresic@utu.fi
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Contact:
- Alex Dickens, PhD
- Email: alex.dickens@utu.fi
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Örebro, Sweden
- Örebro University
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Contact:
- Tuulia Hyötyläinen, PhD
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Participation Criteria
Eligibility Criteria
Ages Eligible for Study
Accepts Healthy Volunteers
Description
Inclusion Criteria:
To be considered eligible to participate in this study, a SAH subject must meet the inclusion criteria listed below:
- Informed consent obtained from the next of kin or legal representative
- Aneurysmal subarachnoid hemorrhage visible on CTA or DSA.
- Deterioration of consciousness to Hunt-Hess 3-5
- Age of ≥ 18 years
- Intubated.
- GCS 3-12 obtained off neuromuscular blocking agents
- Xenon treatment can be started within 6 hours after onset of SAH symptoms
Exclusion Criteria:
An aSAH subject may not be enrolled in the trial if he/she meets any one of the exclusion criteria below:
- Acute or chronic traumatic brain injury
- Maximum diameter of intracerebral hemorrhage > 2.5 cm
- Pneumothorax or pneumomediastinum,
- Acute lung injury requiring ≥ 60% FIO2 (fraction of inspired oxygen).
- Systolic arterial pressure < 80 mmHg or mean arterial pressure < 60 mmHg for over 30 min period
- Bilaterally fixed and dilated pupils
- Positive pregnancy test, known pregnancy, or current breast-feeding
- Neurological deficiency due to traumatic brain injury or other neurological illness
- Imminent death or current life-threatening disease
- Current enrollment in another interventional study
- The subject is known to have clinically significant laboratory abnormality, medical condition (such as decompensated liver disease or severe chronic obstructive pulmonary disease), or social circumstance that, in the investigator's opinion, makes it inappropriate for the subject to participate in this clinical trial.
- Presence of implants or foreign bodies which are not known to be MRI safe
Study Plan
How is the study designed?
Design Details
- Primary Purpose: Treatment
- Allocation: Randomized
- Interventional Model: Parallel Assignment
- Masking: Double
Arms and Interventions
Participant Group / Arm |
Intervention / Treatment |
---|---|
Active Comparator: Air/Oxygen
Control arm: air/oxygen with standard of care
|
Control group will be treated with air/oxygen
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Experimental: xenon
Xenon arm: xenon inhalation in air/oxygen with standard of care
|
Xenon arm will be treated with xenon inhalation with endtidal concentration of 50 % in air/oxygen and with standard of care
|
What is the study measuring?
Primary Outcome Measures
Outcome Measure |
Measure Description |
Time Frame |
---|---|---|
Fractional anisotropy of the white matter
Time Frame: 48-96 hours after start of aSAH symptoms
|
Global fractional anisotropy of white matter of diffusion tensor imaging (DTI).
Hypothesis: White matter damage is less severe in xenon treated patients, i.e. global fractional anisotropy is significantly higher in the xenon group than in the control group as assessed with the 1st MRI.
|
48-96 hours after start of aSAH symptoms
|
Secondary Outcome Measures
Outcome Measure |
Measure Description |
Time Frame |
---|---|---|
Fractional anisotropy of white matter at cerebellum and/or at corpus callosum as assessed with the 1st MRI.
Time Frame: 48-96 hours after start of aSAH symptoms
|
Fractional anisotropy of white matter at cerebellum and/or at corpus callosum as assessed with the 1st MRI.
|
48-96 hours after start of aSAH symptoms
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Safety and tolerability of xenon
Time Frame: during the follow-up of one year
|
Safety and tolerability of xenon as assessed with a ratio of adverse events, serious adverse events and suspected unexpected serious adverse reactions (SUSARs) during the follow-up of one year between the xenon group and the control group.
|
during the follow-up of one year
|
Composite of radiological early brain injury (EBI) and delayed cerebral ischemia (DCI)
Time Frame: EBI: within first 72 hours after start of aSAH symptoms; mRS at 3 months and at 1 year and at 2 years after onset of aSAH symptoms
|
Composite of radiological EBI (within 72 hours after start of SAH symptoms) and DCI (Criterion of DCI: 1. a new focal neurological deficit (such as hemiparesis, aphasia, apraxia, hemianopia, or neglect) /decrease in level of consciousness (i.e.
decrease of at least 2 points on the Glasgow Coma Scale; either on the total score or on one of its individual components, such as eye, motor on either side, or verbal).
This should last for at least 1 hour and not is due to other causes (e.g.
hydrocephalus, seizures, metabolic derangement, infection, sedation) and is not apparent immediately after aneurysm occlusion, and cannot be attributed to other causes by means of clinical assessment, CT or MRI scanning of the brain, and appropriate laboratory studies, 2. a new infarct on follow-up imaging (i.e. in any of the following: 2nd MRI, CT, CTA, DSA and perfusion CT) after 4 days post-SAH, or 3. both 1 and 2), and poor outcome at 3-months (good: mRS 0-2; poor: mRS 3-6) at 3-months and at 1 year
|
EBI: within first 72 hours after start of aSAH symptoms; mRS at 3 months and at 1 year and at 2 years after onset of aSAH symptoms
|
Neurogenic Stress Cardiomyopathy and Stunned Myocardium
Time Frame: follow-up of 1 year
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Neurogenic Stress Cardiomyopathy and Stunned Myocardium (i.e.
myocardial injury caused by sympathetic storm and autonomic dysregulation with hs-troponin elevation, left ventricular dysfunction or ECG changes)
|
follow-up of 1 year
|
Intracerebral pressure (ICP)
Time Frame: during ICU stay up to 14 days after onset of aSAH symptoms
|
ICP level Duration of therapy for ICP control/monitoring |
during ICU stay up to 14 days after onset of aSAH symptoms
|
Intracerebral pressure (ICP)
Time Frame: during ICU stay up to 14 days after onset of aSAH symptoms
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Need for ICP therapies (hypothermia, decompressive craniotomy)
|
during ICU stay up to 14 days after onset of aSAH symptoms
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Intracerebral pressure (ICP)
Time Frame: during ICU stay up to 14 days after onset of aSAH symptoms
|
Duration of therapy for ICP control/monitoring
|
during ICU stay up to 14 days after onset of aSAH symptoms
|
Plasma catecholamine level
Time Frame: within 3 hours of ICU arrival, at 24h, 48h and 72 h after onset of aSAH symptoms
|
Plasma level of noradrenaline , adrenaline, and dopamine
|
within 3 hours of ICU arrival, at 24h, 48h and 72 h after onset of aSAH symptoms
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Selected biomarkers
Time Frame: within 3 hours of ICU arrival and at 24h, at 48h and at 72h after onset of aSAH symptoms
|
Selected biomarkers of brain injury: neurofilament light (NF-L), glial fibrillary acidic protein (GFAP), calcium binding protein S100B (S100B), ubiquitin carboxyterminal hydrolase L1 (UCH-L1), total tau, cytokines (tumour necrosis factor alpha, interleukins 6 and 10)
|
within 3 hours of ICU arrival and at 24h, at 48h and at 72h after onset of aSAH symptoms
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Development of prognostication models
Time Frame: long-term outcome at 3 months, at 1 and at 2 years after onset of aSAH symptoms
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Development of prognostication models with a selected combination of brain imaging, clinical data, biomarkers and metabolomics by applying artificial intelligence and machine learning for long-term outcome after aSAH
|
long-term outcome at 3 months, at 1 and at 2 years after onset of aSAH symptoms
|
Development of prognostication models
Time Frame: between day 4 and 6 weeks after onset of aSAH symtoms
|
Development of prognostication models with a selected combination of brain imaging, clinical data, biomarkers and metabolomics by applying artificial intelligence and machine learning for DCI after aSAH
|
between day 4 and 6 weeks after onset of aSAH symtoms
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Development of prognostication models
Time Frame: within 21 days after onset of aSAH symptoms
|
Development of prognostication models with a selected combination of brain imaging, clinical data, biomarkers and metabolomics by applying artificial intelligence and machine learning for vasospasm after aSAH
|
within 21 days after onset of aSAH symptoms
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Development of prognostication models
Time Frame: within 72 hours after onset of aSAH symtoms
|
Development of prognostication models with a selected combination of brain imaging, clinical data, biomarkers and metabolomics by applying artificial intelligence and machine learning for EBI after aSAH
|
within 72 hours after onset of aSAH symtoms
|
Difference of MRI parameters between xenon and control group
Time Frame: within 72 hours after onset of aSAH symptoms
|
Difference of MRI parameters (fractional anisotropy, axial diffucivity, radial diffucivity of diffusion tensor imaging, DTI) between xenon and control group and in predicting risk for EBI
|
within 72 hours after onset of aSAH symptoms
|
Difference of MRI parameters between xenon and control group
Time Frame: within 21 days after onset of aSAH symptoms
|
Difference of MRI parameters (fractional anisotropy, axial diffucivity, radial diffucivity of DTI) between xenon and control group and in predicting risk for vasospasm
|
within 21 days after onset of aSAH symptoms
|
Difference of MRI parameters between xenon and control group
Time Frame: between day 4 and 6 weeks after onset of aSAH symptoms
|
Difference of MRI parameters (fractional anisotropy, axial diffucivity, radial diffucivity of DTI) between xenon and control group and in predicting risk for DCI
|
between day 4 and 6 weeks after onset of aSAH symptoms
|
Difference of MRI parameters between xenon and control group
Time Frame: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Difference of MRI parameters (fractional anisotropy, axial diffucivity, radial diffucivity of DTI) between xenon and control group and in predicting risk for good/poor neurological outcome at 3 moths, at 1 year and at 2 years after onset of aSAH symptoms (mRS 0-2/mRS 3-6).
|
at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Difference of CTA findings
Time Frame: within 72 hours after onset of aSAH symptoms
|
Difference of CTA ischemic findings between xenon and control group and in predicting risk for EBI
|
within 72 hours after onset of aSAH symptoms
|
Difference of CTA findings
Time Frame: within 21 days after onset of aSAH symptoms
|
Difference of ischemic findings in CTA between xenon and control group and in predicting risk for vasospasm
|
within 21 days after onset of aSAH symptoms
|
Difference of CTA findings
Time Frame: between day 4 and 6 weeks after onset of aSAH symptoms
|
Difference of ischemic findings in CTA between xenon and control group and in predicting risk for DCI
|
between day 4 and 6 weeks after onset of aSAH symptoms
|
Difference of CTA findings between xenon and control group
Time Frame: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Difference of ischemic findings in CTA between xenon and control group and in predicting risk for good/poor neurological outcome at 3 moths, at 1 year and at 2 years after onset of aSAH symptoms (mRS 0-2/mRS 3-6).
|
at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Difference of DSA findings between xenon and control group
Time Frame: within 72 hours after onset of aSAH symptoms
|
Difference of DSA findings indicating ischemic pattern of perfusion between xenon and control group and in predicting risk for EBI
|
within 72 hours after onset of aSAH symptoms
|
Difference of DSA findings between xenon and control group
Time Frame: within 21 days after onset of aSAH symptoms
|
Difference of DSA findings indicating ischemic pattern of perfusion between xenon and control group and in predicting risk for vasospasm
|
within 21 days after onset of aSAH symptoms
|
Difference of DSA findings between xenon and control group
Time Frame: between day 4 and 6 weeks after onset of aSAH symptoms
|
Difference of DSA findings indicating ischemic pattern of perfusion between xenon and control group and in predicting risk for DCI
|
between day 4 and 6 weeks after onset of aSAH symptoms
|
Difference of DSA findings between xenon and control group
Time Frame: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Difference of DSA findings indicating ischemic pattern of perfusion between xenon and control group and in predicting risk for good/poor neurological outcome at 3 moths, at 1 year and at 2 years after onset of aSAH symptoms (mRS 0-2/mRS 3-6).
|
at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Activity of microglia cells assessed with PET
Time Frame: DCI between day 4 and 6 weeks after onset of aSAH symptoms; The 1st PETscan 4 ±1 weeks after onset of aSAH symptoms and the 2nd scan at 3 months after onset of SAH symptoms.
|
It will be explored whether [11C](R)-PK11195 can be used to test the hypothesis of neuroprotective effect of xenon and to explore the role of inflammatory process for DCI after SAH.
This could be demonstrated by showing less microglial activation in xenon group than in the reference therapy group and in the patients with good outcome, i.e. no DCI; Difference of activity of microglia cells between xenon and control group and in predicting risk for DCI
|
DCI between day 4 and 6 weeks after onset of aSAH symptoms; The 1st PETscan 4 ±1 weeks after onset of aSAH symptoms and the 2nd scan at 3 months after onset of SAH symptoms.
|
Activity of microglia cells assessed with PET
Time Frame: The 1st scan at 4 ±1 weeks after and the 2nd scan at 3 months after onset of SAH symptoms. Outcome: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
It will be explored whether [11C](R)-PK11195 can be used to test the hypothesis of neuroprotective effect of xenon and to explore the role of inflammatory process for neurological outcome after SAH.
This could be demonstrated by showing less microglial activation in xenon group than in the reference therapy group and in the patients with good outcome, i.e. mRS 0-2;
|
The 1st scan at 4 ±1 weeks after and the 2nd scan at 3 months after onset of SAH symptoms. Outcome: at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Cerebral fluid dynamics
Time Frame: Measures performed within 72 hours of ICU arrival
|
Predictive value of CFD simulations assessed with 3 dimensional DSA within 4 days of ICU arrival in predicting risk for EBI within 72 hours after onset of aSAH symptoms
|
Measures performed within 72 hours of ICU arrival
|
Cerebral fluid dynamics
Time Frame: Measures performed within 21 days of ICU arrival; outcome at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Predictive value of CFD simulations assessed with 3 dimensional DSA within 21 days of ICU arrival in predicting risk for neurological outcome at 3 months, at 1 year and at 2 years after SAH (mRS 0-2)
|
Measures performed within 21 days of ICU arrival; outcome at 3 months, at 1 year and at 2 years after onset of aSAH symptoms
|
Cerebral fluid dynamics
Time Frame: Measures performed within 21 days of ICU arrival; DCI within 6 weeks after onset of aSAH symptoms
|
Predictive value of CFD simulations assessed with 3 dimensional DSA within 21 days of ICU arrival in predicting risk for DCI within 6 weeks after onset of aSAH symptoms
|
Measures performed within 21 days of ICU arrival; DCI within 6 weeks after onset of aSAH symptoms
|
Collaborators and Investigators
Sponsor
Collaborators
Publications and helpful links
General Publications
- Laitio R, Hynninen M, Arola O, Virtanen S, Parkkola R, Saunavaara J, Roine RO, Gronlund J, Ylikoski E, Wennervirta J, Backlund M, Silvasti P, Nukarinen E, Tiainen M, Saraste A, Pietila M, Airaksinen J, Valanne L, Martola J, Silvennoinen H, Scheinin H, Harjola VP, Niiranen J, Korpi K, Varpula M, Inkinen O, Olkkola KT, Maze M, Vahlberg T, Laitio T. Effect of Inhaled Xenon on Cerebral White Matter Damage in Comatose Survivors of Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial. JAMA. 2016 Mar 15;315(11):1120-8. doi: 10.1001/jama.2016.1933.
- Arola O, Saraste A, Laitio R, Airaksinen J, Hynninen M, Backlund M, Ylikoski E, Wennervirta J, Pietila M, Roine RO, Harjola VP, Niiranen J, Korpi K, Varpula M, Scheinin H, Maze M, Vahlberg T, Laitio T; Xe-HYPOTHECA Study Group. Inhaled Xenon Attenuates Myocardial Damage in Comatose Survivors of Out-of-Hospital Cardiac Arrest: The Xe-Hypotheca Trial. J Am Coll Cardiol. 2017 Nov 28;70(21):2652-2660. doi: 10.1016/j.jacc.2017.09.1088.
Study record dates
Study Major Dates
Study Start (Anticipated)
Primary Completion (Anticipated)
Study Completion (Anticipated)
Study Registration Dates
First Submitted
First Submitted That Met QC Criteria
First Posted (Actual)
Study Record Updates
Last Update Posted (Actual)
Last Update Submitted That Met QC Criteria
Last Verified
More Information
Terms related to this study
Additional Relevant MeSH Terms
- Pathologic Processes
- Necrosis
- Heart Diseases
- Cardiovascular Diseases
- Vascular Diseases
- Cerebrovascular Disorders
- Brain Diseases
- Central Nervous System Diseases
- Nervous System Diseases
- Craniocerebral Trauma
- Trauma, Nervous System
- Stroke
- Brain Infarction
- Intracranial Hemorrhages
- Infarction
- Heart Failure
- Brain Ischemia
- Ischemia
- Brain Injuries
- Wounds and Injuries
- Hemorrhage
- Cerebral Infarction
- Subarachnoid Hemorrhage
- Physiological Effects of Drugs
- Central Nervous System Depressants
- Anesthetics, General
- Anesthetics
- Anesthetics, Inhalation
- Xenon
Other Study ID Numbers
- 109/2019 Xe-SAH
- 2019-001542-17 (EudraCT Number)
Plan for Individual participant data (IPD)
Plan to Share Individual Participant Data (IPD)?
IPD Plan Description
IPD Sharing Time Frame
IPD Sharing Access Criteria
IPD Sharing Supporting Information Type
- STUDY_PROTOCOL
- SAP
- CSR
Drug and device information, study documents
Studies a U.S. FDA-regulated drug product
Studies a U.S. FDA-regulated device product
This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.
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