| Autor: |
Cooper, David K. C., Miller, Leslie W., Patterson, G. Alexander, Egan, T. M. |
| Zdroj: |
Transplantation & Replacement of Thoracic Organs; 1996, p565-571, 7p |
| Abstrakt: |
Cystic fibrosis (CF) is the most common lethal genetic disease of Caucasians. Although it is a multisystem disease it is estimated that 95% of patients with CF will succumb from end-stage pulmonary disease[1]. Up to 400 patients with CF die annually in the United States. The past decade has seen remarkable advances in understanding the pathophysiology of CF, including identification of a chloride channel abnormality 3. identification of the gene responsible for the chloride channel[4], and creation of a transgenic mouse with CF[5]. Even before the genetic defect was identified, it was apparent that the chloride channel epithelial abnormality present in CF, evidenced by an altered potential difference[3], was not manifested in the epithelium of heart-lung grafts in transplanted CF patients[6]. This provided assurance that the pulmonary abnormalities observed in CF patients were unlikely to recur following lung transplantation. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
