Inherited Diseases Cystic Fibrosis Questions Regarding Cystic Fibrosis. See Details.?
Questions regarding Cystic Fibrosis. See details.? - inherited diseases cystic fibrosis
-What specific part of the cell or structure allows the mucus too thick and viscous fluid rather than (ie, a channel in the membrane, organelles, or something else)? Please be specific and describe step by step, the mechanism by which this new structure, a part of the cell produces secretions that contain less water.
Why does not Alvin shape of salt crystals on the skin? Explain the mechanism for this effect.
-What is the treatment for children with cystic fibrosis? Be sure to list at least three and explain why the work (ie what is) the purpose of the treatment.
List and explanation of the mechanism of at least two experimental treatments sought to help patients with cystic fibrosis.
-Give a brief description, such as gene therapy may help cure a hereditary genetic disease like cystic fibrosis.
Link to website containing further information (such as Alvin) is http://www.sciencecases.org/cf/cf.asp
If you do not answer all questions (a little) is better than nothing.
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3 comments:
I just discovered this new information that you want to check on this point. Much more to the question you have phlegm.
Abstract Most of the symptoms of cystic fibrosis are not explained by the existing mechanisms of disease. For this reason, the authors conducted an extensive literature and present a new model of the pathology of cystic fibrosis, which is the result of this search. Understand that the regulator of the cystic fibrosis transmembrane conductance regulator (CFTR) to glutathione (GSH) transport is responsible suspect the authors conclude that mutations in the CFTR gene, which create abnormal GSH transport will result in aberrations of two levels of intracellular GSH and extracellular medium. These modifications of the normal levels of cellular GSH redox status in the cell, the intracellular stress protein, metallothionein concerns. The authors describe how to avoid these changes in oxidation-reduction by excess cellular GSH, of course, occur to the delivery of zinc as a cofactor in various enzymatic processes, and how this disorder may experience a worsening of the normal redox Resulthumoral and cell-mediated. In addition, the symptom is a thick, sticky mucus in these patients by the observation that mucus oversulfation a direct consequence of increased cellular GSH and cysteine are explained. Hyperinflammation, changes in pH and the imbalance of fatty acids, which are treated with typical cystic fibrosis, all of which may also apply to changes in GSH homeostasis is possible. In addition, this new model of the disease is cystic fibrosis, the exact relationship between the CFTR protein and multidrug resistance and the lack of cellular immunity in the prediction of substrate proteins of a glutathione adduct of thiocyanate. Finally, a new therapeutic strategy with isothiocyanates, to redress the imbalance of the GSH and proposed the restoration of the immune system for the treatment of patients with cystic fibrosis. See here for more http://www.sharktank.org/
The situation of salt in the other room is an issue dealt with the nature of the body salt. Sodium chloride (salt) is divided into one part, each corresponding element (sodium --and chloride). Sodium is in the cell, while the chloride is absorbed by the cells passed Cirtain, sold, and later combined with the sodium. The problem is that CF cells are to divorce "chloride, chloride is not shed. Therefore, the excretion of salt mucosa, sweat glands and other organs, an imbalance of sodium and chloride may have (high and low sodium chloride). The memory of my school chemistry lessons Sodium is a bit unstable (reactive), without (its counterpart, the most common, iodine or chlorine) for the obligations of responsibility. Therefore, the sweat of CF patients with more salty tastes different. Questions and experimental gene-specific mechanism, which, to my Try understanding of what they do not try to answer it wants to expand. the search function on PubMed with the terms "hamster cystic fibrosis in your search. Many of the genetic information exists. http://www. ncbi.nlm.nih.gov / sites / entrez
Hope this helps you?
Best regards
Edric Záruba
I just discovered this new information that you want to check on this point. Much more to the question you have phlegm.
Abstract Most of the symptoms of cystic fibrosis are not explained by the existing mechanisms of disease. For this reason, the authors conducted an extensive literature and present a new model of the pathology of cystic fibrosis, which is the result of this search. Understand that the regulator of the cystic fibrosis transmembrane conductance regulator (CFTR) to glutathione (GSH) transport is responsible suspect the authors conclude that mutations in the CFTR gene, which create abnormal GSH transport will result in aberrations of two levels of intracellular GSH and extracellular medium. These modifications of the normal levels of cellular GSH redox status in the cell, the intracellular stress protein, metallothionein concerns. The authors describe how to avoid these changes in oxidation-reduction by excess cellular GSH, of course, occur to the delivery of zinc as a cofactor in various enzymatic processes, and how this disorder may experience a worsening of the normal redox Resulthumoral and cell-mediated. In addition, the symptom is a thick, sticky mucus in these patients by the observation that mucus oversulfation a direct consequence of increased cellular GSH and cysteine are explained. Hyperinflammation, changes in pH and the imbalance of fatty acids, which are treated with typical cystic fibrosis, all of which may also apply to changes in GSH homeostasis is possible. In addition, this new model of the disease is cystic fibrosis, the exact relationship between the CFTR protein and multidrug resistance and the lack of cellular immunity in the prediction of substrate proteins of a glutathione adduct of thiocyanate. Finally, a new therapeutic strategy with isothiocyanates, to redress the imbalance of the GSH and proposed the restoration of the immune system for the treatment of patients with cystic fibrosis. See here for more http://www.sharktank.org/
The situation of salt in the other room is an issue dealt with the nature of the body salt. Sodium chloride (salt) is divided into one part, each corresponding element (sodium --and chloride). Sodium is in the cell, while the chloride is absorbed by the cells passed Cirtain, sold, and later combined with the sodium. The problem is that CF cells are to divorce "chloride, chloride is not shed. Therefore, the excretion of salt mucosa, sweat glands and other organs, an imbalance of sodium and chloride may have (high and low sodium chloride). The memory of my school chemistry lessons Sodium is a bit unstable (reactive), without (its counterpart, the most common, iodine or chlorine) for the obligations of responsibility. Therefore, the sweat of CF patients with more salty tastes different. Questions and experimental gene-specific mechanism, which, to my Try understanding of what they do not try to answer it wants to expand. the search function on PubMed with the terms "hamster cystic fibrosis in your search. Many of the genetic information exists. http://www. ncbi.nlm.nih.gov / sites / entrez
Hope this helps you?
Best regards
Edric Záruba
can be here, and if you do not add it anyway. Spread the word. Find a cure
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