Winter 2010
CF and Diabetes
Researcher Scott Blackman's search for modifier genes to tailor treatment.    

Spring 2009
Alternative Chloride Channels
CFTR isn’t the only kid on the block when it comes to chloride channels. ClC-2, pulmonologist Pam Zeitlin is finding, may provide a parallel pathway for chloride secretion.

Fall 2008
Coming Down the Pipeline
CFTR-targeted drugs lead a diverse pack of therapies to improve quality of life, extend survival and find a cure for CF patients.

Winter 2008
The Jigsaw Puzzle of CF Lung Disease Severity
What is it in the genes and environment that really makes a difference? Why does one cystic fibrosis patient have only mild lung disease while another patient with the same CFTR mutations-suffers sever lung disease? Are genes other CFTR responsible for these variations? Or is the environment the cause?

Summer 2007
Studying the Science of Resistance
Pseudomonas aeruginosa is a nasty bug, infecting nearly 80 percent of all CF patients. And its success lies in its ability to resist many common antibiotics thrown at it. In fact, although immediate treatment with antibiotics can clear the infection, in many cases the bacteria adapt and establish permanent colonies in the lungs, increasing sputum production and decreasing lung function.

Fall 2006
Advancing the Knowledge
A distinct advantage to being a patient of The Johns Hopkins Cystic Fibrosis Center is that the doctors you see regularly are contributing significantly to the understanding and management of cystic fibrosis worldwide.

January 2006
Raising the Bar on CF Care
Quality improvement sounds like a buzzword straight out of corporate America: how are we going to improve the quality of these widgets we’re building?

September 2005
Piloting the Enterprise
Master multi-taskers, research coordinators keep clinical trials running smoothly.

January 2005
Environment, More than Genes, Influences CF Lung Disease Severity
As scientists continue to learn more about the gene responsible for cystic fibrosis—CFTR—it is becoming clear that this genetic mutation alone does not determine why the severity of CF differs so much from person to person.