Maryse Picher is a successful medical research scientist, public speaker, author and editor. She is affiliated with the Cystic Fibrosis/Pulmonary Research and Treatment Center in North Carolina, and to Springer Publishing Co.

Her education combines a Ph.D. on cardiovascular enzymology, two post-graduate studies on pulmonary electrophysiology and pharmacology, and a decade of research and development on inhalation drug therapies for asthma, COPD and cystic fibrosis.

Dr. Picher is actively involved in the development of stringent drug screening assays to improve clinical trial success. This task is of critical importance to motivate venture capitalists to invest into the Biotech/Pharma industry in this economy.

This versatile communicator offers her expertise to the Cystic Fibrosis Community and welcomes questions by e-mail (; Profile on Linkedin).

 

Dr. Picher recently released a new book titled Purinergic Regulation of Respiratory Diseases, published by Springer-Verlagh on the therapeutic potential of a new class of drugs for chronic respiratory diseases (asthma, COPD, idiopathic pulmonary fibrosis and bronchiolitis obliterans) and acute complications (acute lung injury, lung transplant rejection, pulmonary edema and sepsis). The nine chapters review the underlying pharmacology, followed by a critical view on the past and current preclinical and clinical trials.

Here are some excerpts from the book:

 

“Respiratory insufficiency is considered among the most serious complications of patients with obstructive lung diseases…, the sporadic and intermittent low oxygen tension experienced by the epithelial surfaces could contribute to the aberrant airway purine concentrations...”

 

“Airway epithelia respond to pathogens and cytokines by a small oxidative burst to assist in bacterial killing, which is ended by scavengers and antioxidant enzymes [review: (79)]. Chronic conditions, like intermittent hypoxia, tilt the “reduction-oxidation” (redox) balance toward oxidants…,”

 

“Contrary to intranasal instillation, intramuscular injection of PEG-ADA suppresses early events in the development of lung inflammation, like leukocyte and dendritic cell migration (see Chapter 7 for details)...”

 

“…therapies aiming to suppress ADO production in chronic respiratory diseases could leave the patients vulnerable to hypoxia-induced pulmonary edema, and even aggravate lung inflammation, if the suppression of CD73 activity is not carefully optimized and restricted to the airways.”

 

“Acute lung injury reproduces the high airway ADO concentrations reported in asthmatic and COPD patients (43; 44)… These data suggest that a transient increase in airway ADO production is a defense mechanism to suppress acute lung injury…"

 

Click here to purchase Dr. Picher's book.