.
Question, s
If this defective gene (Below) is still defective after stem cell treatment then wouldn't the disease continue decline ? Wouldn't any progress fall to the same defects if smoking caused the gene mutations.
Wouldn't stem cell treatment have to be combined with gene treatment for effective correction ?
Just my thoughts !
US-based researchers Alireza Sadeghnejad, Jill Ohar, Eugene Bleecker and colleagues from the Wake Forest School of Medicine and Saint Louis University, looked at a disintegrin and metalloprotease (ADAM) gene known as ADAM33 in 880 long-term heavy smokers. Located on chromosome 20, ADAM33 has been linked with asthma in previous studies. This new study is unique in comparing long-term smokers with COPD versus a control group of long-term smokers without COPD.
The researchers found five single nucleotide polymorphisms (SNPs) – human DNA sequence variations - in ADAM33 that were more frequent in the COPD group than in the group of smokers without COPD. One SNP, known as S1, had a particularly strong link to lung abnormalities. "Functional studies will be needed to evaluate the biologic significance of these polymorphisms in the pathogenesis of COPD," according to the authors.
COPD is characterized by progressive decline in lung function, and encompasses chronic bronchitis and emphysema. Almost 90% of COPD is caused by long-term cigarette smoking, yet only 25% of chronic tobacco smokers will go on to develop COPD.
Question, s
If this defective gene (Below) is still defective after stem cell treatment then wouldn't the disease continue decline ? Wouldn't any progress fall to the same defects if smoking caused the gene mutations.
Wouldn't stem cell treatment have to be combined with gene treatment for effective correction ?
Just my thoughts !
US-based researchers Alireza Sadeghnejad, Jill Ohar, Eugene Bleecker and colleagues from the Wake Forest School of Medicine and Saint Louis University, looked at a disintegrin and metalloprotease (ADAM) gene known as ADAM33 in 880 long-term heavy smokers. Located on chromosome 20, ADAM33 has been linked with asthma in previous studies. This new study is unique in comparing long-term smokers with COPD versus a control group of long-term smokers without COPD.
The researchers found five single nucleotide polymorphisms (SNPs) – human DNA sequence variations - in ADAM33 that were more frequent in the COPD group than in the group of smokers without COPD. One SNP, known as S1, had a particularly strong link to lung abnormalities. "Functional studies will be needed to evaluate the biologic significance of these polymorphisms in the pathogenesis of COPD," according to the authors.
COPD is characterized by progressive decline in lung function, and encompasses chronic bronchitis and emphysema. Almost 90% of COPD is caused by long-term cigarette smoking, yet only 25% of chronic tobacco smokers will go on to develop COPD.