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antidepressants
- Thread starter rvm1212
- Start date
lightNlife
New member
I read that the other day and wasn't particularly impressed. Here's my comments on the matter from another place online that I frequent:
<i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
I wasn't impressed by the article. It was too scant. *shrug*
Even so, I'll file it away and look into it more on my own later. </i>
<i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
I wasn't impressed by the article. It was too scant. *shrug*
Even so, I'll file it away and look into it more on my own later. </i>
lightNlife
New member
I read that the other day and wasn't particularly impressed. Here's my comments on the matter from another place online that I frequent:
<i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
I wasn't impressed by the article. It was too scant. *shrug*
Even so, I'll file it away and look into it more on my own later. </i>
<i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
I wasn't impressed by the article. It was too scant. *shrug*
Even so, I'll file it away and look into it more on my own later. </i>
lightNlife
New member
I read that the other day and wasn't particularly impressed. Here's my comments on the matter from another place online that I frequent:
<i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
I wasn't impressed by the article. It was too scant. *shrug*
Even so, I'll file it away and look into it more on my own later. </i>
<i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
I wasn't impressed by the article. It was too scant. *shrug*
Even so, I'll file it away and look into it more on my own later. </i>
lightNlife
New member
I read that the other day and wasn't particularly impressed. Here's my comments on the matter from another place online that I frequent:
<i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
I wasn't impressed by the article. It was too scant. *shrug*
Even so, I'll file it away and look into it more on my own later. </i>
<i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
I wasn't impressed by the article. It was too scant. *shrug*
Even so, I'll file it away and look into it more on my own later. </i>
lightNlife
New member
I read that the other day and wasn't particularly impressed. Here's my comments on the matter from another place online that I frequent:
<br />
<br /><i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
<br />
<br />I wasn't impressed by the article. It was too scant. *shrug*
<br />
<br />Even so, I'll file it away and look into it more on my own later. </i>
<br />
<br /><i>Kind of a weird article. I got the impression that the person who wrote it didn't do much background research on CF. The part about "CF is believed to cause mucus..." HUH? Haven't we already shown that faulty CFTR makes the mucus too sticky.
<br />
<br />I wasn't impressed by the article. It was too scant. *shrug*
<br />
<br />Even so, I'll file it away and look into it more on my own later. </i>
SaltyAndSweet
New member
Just remember it is a news article. No offense meant to the journalists here, but news articles always seem to twist the news a little because they don't usually fully understand the science in the scientific studies. I know this from personal experience where I did a TV report about the Targeted Genetics study and the news lady totally twisted my words. Supposedly she was even a doctor! It sounded like I knew NOTHING about CF in general, which was nuts! Made me sooo mad!
If anyone finds the actual scientific paper out there somewhere could you please post it here?
Thx!!
If anyone finds the actual scientific paper out there somewhere could you please post it here?
Thx!!
SaltyAndSweet
New member
Just remember it is a news article. No offense meant to the journalists here, but news articles always seem to twist the news a little because they don't usually fully understand the science in the scientific studies. I know this from personal experience where I did a TV report about the Targeted Genetics study and the news lady totally twisted my words. Supposedly she was even a doctor! It sounded like I knew NOTHING about CF in general, which was nuts! Made me sooo mad!
If anyone finds the actual scientific paper out there somewhere could you please post it here?
Thx!!
If anyone finds the actual scientific paper out there somewhere could you please post it here?
Thx!!
SaltyAndSweet
New member
Just remember it is a news article. No offense meant to the journalists here, but news articles always seem to twist the news a little because they don't usually fully understand the science in the scientific studies. I know this from personal experience where I did a TV report about the Targeted Genetics study and the news lady totally twisted my words. Supposedly she was even a doctor! It sounded like I knew NOTHING about CF in general, which was nuts! Made me sooo mad!
If anyone finds the actual scientific paper out there somewhere could you please post it here?
Thx!!
If anyone finds the actual scientific paper out there somewhere could you please post it here?
Thx!!
SaltyAndSweet
New member
Just remember it is a news article. No offense meant to the journalists here, but news articles always seem to twist the news a little because they don't usually fully understand the science in the scientific studies. I know this from personal experience where I did a TV report about the Targeted Genetics study and the news lady totally twisted my words. Supposedly she was even a doctor! It sounded like I knew NOTHING about CF in general, which was nuts! Made me sooo mad!
If anyone finds the actual scientific paper out there somewhere could you please post it here?
Thx!!
If anyone finds the actual scientific paper out there somewhere could you please post it here?
Thx!!
SaltyAndSweet
New member
Just remember it is a news article. No offense meant to the journalists here, but news articles always seem to twist the news a little because they don't usually fully understand the science in the scientific studies. I know this from personal experience where I did a TV report about the Targeted Genetics study and the news lady totally twisted my words. Supposedly she was even a doctor! It sounded like I knew NOTHING about CF in general, which was nuts! Made me sooo mad!
<br />
<br />If anyone finds the actual scientific paper out there somewhere could you please post it here?
<br />Thx!!
<br />
<br />If anyone finds the actual scientific paper out there somewhere could you please post it here?
<br />Thx!!
I could not access the full text of the article through my university library, the best I could get was the abstract. If anyone has a better research library that they can access, the info is: Nature Medicine; Apr2008, Vol. 14 Issue 4, p382-391, 10p and the lead researcher was Teichgräber, Volker1
<b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
<b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
I could not access the full text of the article through my university library, the best I could get was the abstract. If anyone has a better research library that they can access, the info is: Nature Medicine; Apr2008, Vol. 14 Issue 4, p382-391, 10p and the lead researcher was Teichgräber, Volker1
<b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
<b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
I could not access the full text of the article through my university library, the best I could get was the abstract. If anyone has a better research library that they can access, the info is: Nature Medicine; Apr2008, Vol. 14 Issue 4, p382-391, 10p and the lead researcher was Teichgräber, Volker1
<b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
<b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
I could not access the full text of the article through my university library, the best I could get was the abstract. If anyone has a better research library that they can access, the info is: Nature Medicine; Apr2008, Vol. 14 Issue 4, p382-391, 10p and the lead researcher was Teichgräber, Volker1
<b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
<b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
I could not access the full text of the article through my university library, the best I could get was the abstract. If anyone has a better research library that they can access, the info is: Nature Medicine; Apr2008, Vol. 14 Issue 4, p382-391, 10p and the lead researcher was Teichgräber, Volker1
<br />
<br />
<br /><b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
<br />
<br />
<br />Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]
<br />
<br />
<br /><b>Ceramide accumulation mediates inflammation, cell death and infection susceptibility in cystic fibrosis.</b>
<br />
<br />
<br />Microbial lung infections are the major cause of morbidity and mortality in the hereditary metabolic disorder cystic fibrosis, yet the molecular mechanisms leading from the mutation of cystic fibrosis transmembrane conductance regulator (CFTR) to lung infection are still unclear. Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells. This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide. The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections. Partial genetic deficiency of Asm in Cftr<sup>?/?</sup>Smpd1<sup>+/?</sup> mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection. These data suggest inhibition of Asm as a new treatment strategy for cystic fibrosis. [ABSTRACT FROM AUTHOR]