INT103842
From wiki-pain
|
|
|
|
|
Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The expression of the cystic fibrosis transmembrane conductance regulator (CFTR), as assessed by Northern blotting, was unchanged. cAMP levels in isolated colonocytes were markedly reduced by inflammation. | |||||||||||||||
| |||||||||||||||
|
The expression of the cystic fibrosis transmembrane conductance regulator (CFTR), as assessed by Northern blotting, was unchanged. cAMP levels in isolated colonocytes were markedly reduced by inflammation. | |||||||||||||||
| |||||||||||||||
|
CFTR expression has not been documented in osteoblasts or osteoclasts. | |||||||||||||||
| |||||||||||||||
|
The expression profiles of trypsinogen, pancreas-specific trypsin inhibitor, cholecystokinin A receptor, cystic fibrosis transmembrane conductance regulator (CFTR), carbonic anhydrase, and Muc1 and Muc4 mucins transcripts were analyzed by RNA slot blot analysis. | |||||||||||||||
| |||||||||||||||
|
The expression of carbonic anhydrase and CFTR remained unaltered when inflammatory signs were not detected in histological examinations. | |||||||||||||||
| |||||||||||||||
|
The expression profiles of trypsinogen, pancreas-specific trypsin inhibitor, cholecystokinin A receptor, cystic fibrosis transmembrane conductance regulator (CFTR), carbonic anhydrase, and Muc1 and Muc4 mucins transcripts were analyzed by RNA slot blot analysis. | |||||||||||||||
| |||||||||||||||
|
CFTR(inh)-172 acutely produces CFTR dysfunction in rodents for up to 24 h. | |||||||||||||||
| |||||||||||||||
|
CFTR(inh)-172 acutely produces CFTR dysfunction in rodents for up to 24 h. | |||||||||||||||
| |||||||||||||||
|
It is clear from these atypical presentations of CFTR dysfunction that it is the vas deferens, pancreas, and sinuses that are the tissues most sensitive to decreases in CFTR function. | |||||||||||||||
| |||||||||||||||
|
Furthermore, greater attention to 'adult' CF has also led us to identify, with increased frequency, atypical presentations of dysfunction of cystic fibrosis transmembrane conductance regulator (CFTR): chronic pancreatitis, congenital bilateral absence of the vas deferens (CBAVD), chronic sinusitis, and allergic bronchopulmonary aspergillosis. | |||||||||||||||
| |||||||||||||||
|
A prime example of an area in which this question should be asked is the role of CFTR dysfunction in increasing the risk for malignancy. | |||||||||||||||
| |||||||||||||||
|
This has occurred in particular in isolated presentations of CFTR-related diseases such as CBAVD, chronic pancreatitis, and chronic sinusitis with nasal polyposis. | |||||||||||||||
| |||||||||||||||
|
Do these unique presentations and chronic complications of adult CF teach us anything about the function of CFTR?
| |||||||||||||||
| |||||||||||||||
|
The manifestation of CFTR dysfunction in the pancreas is determined by the degree of decrease in CFTR levels, with a decrease to 10% of normal leading to an increased risk for pancreatitis, and a decrease to levels less than 1% leading invariably to exocrine pancreatic insufficiency. | |||||||||||||||
| |||||||||||||||
|
When deciding whether the complications of adult CF provide us with insight into CFTR function, the key question to ask is: do these complications suggest previously unrecognized functions for CFTR, or are they due to the long-term absence of already recognized CFTR functions? | |||||||||||||||
| |||||||||||||||
|
Furthermore, greater attention to 'adult' CF has also led us to identify, with increased frequency, atypical presentations of dysfunction of cystic fibrosis transmembrane conductance regulator (CFTR): chronic pancreatitis, congenital bilateral absence of the vas deferens (CBAVD), chronic sinusitis, and allergic bronchopulmonary aspergillosis. | |||||||||||||||
| |||||||||||||||
|
DNA analyses of the cystic fibrosis transmembrane conductance regulator (CFTR) gene in Japanese patients with idiopathic chronic pancreatitis (ICP) were performed to determine the relationship between the CFTR mutation and ICP. | |||||||||||||||
| |||||||||||||||
|
A rigorous search was conducted for other mutations in patients with one CFTR mutation, and CFTR function in nasal epithelia was assessed in vivo in patients with ICP [17]. | |||||||||||||||
| |||||||||||||||
|
The airway epithelial cell, which normally expresses the cystic fibrosis transmembrane conductance regulator (CFTR), directs the inflammatory response. | |||||||||||||||
| |||||||||||||||
|
The airway epithelial cell, which normally expresses the cystic fibrosis transmembrane conductance regulator (CFTR), directs the inflammatory response. | |||||||||||||||
| |||||||||||||||
|
General Comments
This test has worked.