Understanding that sickle cell disease has a character of depriving oxygen, is there any predicators that can tell if a child will have hypoxia after experiencing acute chest syndrome or pneumonia.

Improvement of health for persons with SCD.
Decreased hospitalizations and use of health resources.
Better understanding of the role of bronchospastic/inflammatory airway disease and hypoxemia as causes of acute chest syndrome and VOC.

Feasible but stumbling block could be enrollment of patients since many patients with SCD are not seen by asthma specialists. Study could be a multicenter study with two hospitals in one major city and in one center, patients with SCD receive usual care and at another center they receive aggressive treatment and monitoring of their lung disease.

AMI and heart failure continues to be a major cause of morbidity and mortality in the Western world.

Promising cardioprotective candidates are emerging. Additional pre-clinical and clinical research is needed to further investigate these new strategies, alone and in combination, to improve outcomes following AMI.
Numerous studies have implicated various pharmacological and interventional techniques (e.g., adenosine, cyclosporine, postconditioning, and remote ischemic per-conditioning) have been explored.

Understanding pathophysiology of coagulopathy in trauma patients due to these drugs may lead to innovations in management of coagulopathy and help increase our ability to predict/prognostic poor clinical outcomes in patients on these new anticoagulants, detect these drugs in a timely manner and develop antidotes/reversal agents. 

These are eminently feasible with adequate support from the NHLBI. Challenges will be finding collaborations or institutions that have enough clinical volume and adequate basic science/translational research infrastructure to look at these questions seriously.

Need more opportunities to put forth innovative diagnostic and therapeutic solutions than currently vetted through the CTSC process.
We have developed the Artery-on-a-chip (A-chip), currently in a research tool format, which accurately measures the extent of inflammatory monocyte activation in a whole blood sample by shearing it along a molecular sensor and enumerating monocyte capture.

Low tidal volume ventilation has been shown to significantly reduce mortality in ARDS patients (from 40% to 31% in the ARMA trial published in NEJM in 2000), but it is inconsistently adopted (frequently with rates <50% in both community and academic settings). Improving adherence has the potential to significantly improve mortality in patients with ARDS.

Given the rapid growth and interest in the field of implementation science over the past several years, addressing this question is now feasible.

Addressing this compelling question may lead to:

1. Improved therapy and outcomes for acute myocardial infarction
2. Reduction of acute morbidity/mortality following reperfusion
3. Prevention of heart failure

The progresses in basic science/signaling, preclinical models, imaging techniques, and invasive monitoring now provide the ideal setting to complete this research in a preclinical model or pilot exploratory clinical trials.