Goal 2: Reduce Human Disease

To extend our knowledge of the pathobiology of heart, lung, blood, and sleep disorders and enable clinical investigations that advance the prediction, prevention, preemption, treatment, and cures of human disease.
(@gcioffi)

Goal 2: Reduce Human Disease

Combination Iron Chelator Trials in Thalassemia and other transfusion-dependent anemias

Three chelators are presently available in the US and much of the world: parenteral deferoxamine, and oral deferasirox, as well as oral deferiprone. Monotherapy is unsuccessful in a significant minority of patients, due to side effects or inadequate response at tolerable doses. Taking a page from enormously successful strategies for combination oral therapy in hypertension, led by NHLBI and others over the past four ...more »

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(@nhlbiforumadministrator1)

Goal 2: Reduce Human Disease

Do we yet know all of the Resident Cellular Components of the Human Lung?

The DLD, NHLBI workshops conducted and published (Reference 1, 2, 3) had as their purpose to stimulate research that would identify still obscure or novel cellular components of the human lung to determine cell function in promoting respiratory tract development and in health that contributes to disease, so that better therapy might result. With robust technologies now available, especially genomic advances, how much ...more »

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8 up votes
13 down votes
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(@megcampbell)

Goal 2: Reduce Human Disease

What is the optimal process for terminal withdrawal of mechanical ventilation?

This palliative care process permits a natural death. The process is largely unstandardized and reflects local practice customs. In fact, the process may vary across ICUs and even within an ICU based on whose attending the patient. This process continues to be an under-investigated area of ICU care for terminally ill patients undergoing terminal ventilator withdrawal.

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(@ferrucciogalbiati)

Goal 2: Reduce Human Disease

Cellular senescence and age-related lung disease?

What is the role of cellular senescence in age-related lung disease? Do environmental factors, including smoking, contribute to the pathogenesis of lung disease through their ability to induce premature senescence? Does the accumulation of senescent cells in distal organs contribute to age-related lung disease through systemic inflammation?

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