Psoriasis Doctor

Question:

> This is a real long shot: I had pyloric stenosis as a baby.  This is > thought to be genetic, but there was a cluster of cases in the Hudson > Valley around the early 60s, which included my daughter.  I had exzema > as a kid, "grew out of" that at about age 30-35, and now have had P for > several years – since my 50s.  I know pyloric stenosis is extremely > rare, but maybe we’re talking about the same bug…  Maybe I’ll try mastic. > Paul M.

Hi Paul, I rounded up a few links that have a couple of keywords to follow up on: This first one is so get the general area involved. http://www.pedisurg.com/PtEduc/Pyloric_Stenosis.htm The area afflicted is far from the colon, were you breast fed? And received some huge amount of antibiotics for this procedure? A shortage of NOS may be implicated for PS. http://groups.google.com/groups?q=pyloric+stenosis+gene&hl=en&lr=&ie=… Here is a little gene info, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=OMIM&do… This may be congenital or caused by a lack of folate during fetal development. A heavy load of antibiotics would seem to be the offender as far as p is concerned, but, you were OK for a length of time prior to your P onset? So, i’m guessing you were breast fed and your late P onset were due to factors that go along with it. Please, see your doctor before doing anything more then chewing on a few sticks of mastic gum. And i think you can buy the gum thru the www.lef.org people. Good luck and please let us know anything that happens positive or negative. I for one am interested in your gut feelings on this one. randall – Hide quoted text — Show quoted text ->>Hi, >>or, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=OMIM&do… >>or, http://www.ncbi.nlm.nih.gov/htbin-post/Omim/getmap?l177900 > I love these. Like looking at the makers maP. > What does in the proper digestion of fats and influences DNA and > lives in the gut and has been mentioned here and is ubiquitious > enough to be a p suspect? Just another culPrit in the > P basket case of maladies? Can chewing some gum helP? > Don’t worry there are some real Medical options here also. > Ferret them out. > http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=H.+Pylori+m… > Once again a S Harris post lights the way. > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… > Methylation due to a H. Pylori critter in the gut. > Possible DNA monkey bizness from a gut denizen? > This one just keeps poping uP in my little grey cells > as a result of crusiers emails. Thanks for the stimulation. > Do you want to chew on this one some? > Does Pylori indirectly mediate fatty acid metabolism? > randall… balsam gum to the gut rescue of P?

Response:

- Hide quoted text — Show quoted text -> I’m looking for how the LPS gets into us in the > first place. That fact that it does is established. > The xoma pdf on endotoxins put that one in perspective. > Wouldn’t it be nice if we only needed to stop gut > permeability to a few lipids(A) or proteins > from one or two ubiquitous bugs? Can you think > of any other more likely candidates? > Here is a lead, > A protein that opens a little hole in the gut > and does something that lets LPS in? Toss in > some iNOS for inflammation etc. > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… > Of mice and men and gut things. NO and ONOO(-)!!!

That swedish P gene revelation is still stuck in my brain. So, i found some links to LPS, liver (kupffer cells) and that chloride channel and found these, Recently, it was demonstrated that liver injury and TNF-alpha production as a result of endotoxin (lipopolysaccharide, LPS) were attenuated by feeding animals a diet enriched with glycine. This phenomenon was shown to be a result of, at least in part, activation of a chloride channel in Kupffer cells by glycine, which hyperpolarizes the cell membrane and blunts increases in intracellular calcium concentrations ([Ca(2+)](i)) http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… Recent studies have demonstrated that glycine blunts the response of Kupffer cells to endotoxin http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… Next, figuring out the co-transporter chloride gene overlap with PSOR5 susceptibility gene may give an understanding of why we don’t clear the LPS toxins from the liver fully. I wonder what the function of glycine and chloride to each other in the liver are? And how they affect P. Seems like we may have a shortage of glycine as far as p goes. With everything else going on, i wonder what some low amount of glycine will do? If it stops the LPS from bypassing the liver and is cleared by the kupffer cells in a nice orderly fashion then we’re in the money. Whoops, can’t forget glutamine. (next) randall… i bow my thinking cap to all with P that desire less P > P guts are either the same or almost the same > as any others in the population at large. > It has to be something right under our noses > that is evading the radar. IRVCOMM had antibiotics > for every combo of bug that they could find. > As i recall he had over 500 pathogenic bugs? > Or just plain bad gut bugs (aka- bad flora) > Did they learn anything decimating his gut flora?

Like, glutamine will help gut mucosa to recover. > If that Swedish study has found the genetic link > to a protein that is primary or secondary to P, > then it seems like a short hoP or jumP to dealing with it. > And what the heck is a chloride cotransporter have to do > with it?

H’mmmm. Got that one figured out, above. > I also posted an abstract that showed AA (arachidonic acid) > out of place in the lower part of the epidermis for P. > What does it take to start the cascade of inflammation? > Some NO with leaky cell membranes or apoptosis to spill > the mess? We have dendritic cells in the skin, gut and lymph. > If they’re reacting to LPS then why in the odd areas that > p develops in?

Take the knees or elbows? Why here and not in the scalp as much? > Think of your system like your car. Something is cloging > up the oil filter and the goop is causing friction in > the engine which shunts it out into your paint job that > is now rusting faster then normal cars rust. > That stuff gets in from the oil pan and disables > the filter and backs up the kidneys which throw > out nitric oxide (NO) to keep some homeostasis as a result > of the back pressure. Whoops, this example is going south > faster then your P. OK, your not your car. Your skin is > acting in concert to maintain pH balence and red is > a better color then white in the winter. Now the primer > coat… darn it.

Seems like the oil filter needs to have defined, how the chlorides work to lesson the damage from the LPS and stop it from getting around the filter, period. – Hide quoted text — Show quoted text -> You are your car and the antigens are sticking to > the paint and the adhesion proteins from the cytokines > are now joining the union and want higher wages. > So vote for me and i’ll clean up the air and water. > And protect the forests. > That clears things uP? > I feel like a blind man trying to explain what > an elephant looks like from touching its trunk. > Or in the case of P. Having a hundred blind men with DS (down’s) > feeling uP the critter and reporting it all back. > In their case the baby elephant eats the mothers poop to > establish good bacteria in its Gi tract! > And if someone feeds him to many banana’s > he get’s gas and not P. > Your not your car but you still need a new paint job.

And a new immune system and better oil filters etc. – Hide quoted text — Show quoted text –

Response:

This is a real long shot: I had pyloric stenosis as a baby.  This is thought to be genetic, but there was a cluster of cases in the Hudson Valley around the early 60s, which included my daughter.  I had exzema as a kid, "grew out of" that at about age 30-35, and now have had P for several years – since my 50s.  I know pyloric stenosis is extremely rare, but maybe we’re talking about the same bug…  Maybe I’ll try mastic. Paul M. – Hide quoted text — Show quoted text ->Hi, >or, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=OMIM&do… >or, http://www.ncbi.nlm.nih.gov/htbin-post/Omim/getmap?l177900 > I love these. Like looking at the makers maP. > What does in the proper digestion of fats and influences DNA and > lives in the gut and has been mentioned here and is ubiquitious > enough to be a p suspect? Just another culPrit in the > P basket case of maladies? Can chewing some gum helP? > Don’t worry there are some real Medical options here also. > Ferret them out. > http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=H.+Pylori+m… > Once again a S Harris post lights the way. > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… > Methylation due to a H. Pylori critter in the gut. > Possible DNA monkey bizness from a gut denizen? > This one just keeps poping uP in my little grey cells > as a result of crusiers emails. Thanks for the stimulation. > Do you want to chew on this one some? > Does Pylori indirectly mediate fatty acid metabolism? > randall… balsam gum to the gut rescue of P?

Response:

- Hide quoted text — Show quoted text -> >I love these. Like looking at the makers maP. > >What does in the proper digestion of fats and influences DNA and > >lives in the gut and has been mentioned here and is ubiquitous > >enough to be a p suspect? Just another culPrit in the > >P basket case of maladies? Can chewing some gum helP? > Whatever role gut stuff has in psoriasis, it still seems to have a > genetic/hereditary aspect as well.  Lots of folks can have terribly > upset guts without their skin going nutz. > J. > Dear J, > I agree. Yes, for sure. Right on. Cool. > I’m looking for how the LPS gets into us in the > first place. That fact that it does is established. > The xoma pdf on endotoxins put that one in perspective. > Wouldn’t it be nice if we only needed to stop gut > permeability to a few lipids(A) or proteins > from one or two ubiquitous bugs? Can you think > of any other more likely candidates?

Here is a hint, A protein that opens a little hole in the gut and does something that lets LPS in? Toss in some iNOS for inflammation etc. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… Of mice and men and gut things. NO and ONOO(-)!!! Lions and tigers and bears, OH MY. Bacteria, proteins and antigens, OH MY P! > P guts are either the same or almost the same > as any others in the population at large. > It has to be something right under our noses > that is evading the radar. IRVCOMM had antibiotics > for every combo of bug that they could find.

As i recall he had over 500 pathogenic bugs? Or just plain bad gut bugs (aka- bad flora) > Did they learn anything decimating his gut flora? > If that Swedish study has found the genetic link > to a protein that is primary or secondary to P, > then it seems like a short hoP or jumP to dealing with it.

And what the heck is a chloride cotransporter have to do with it? – Hide quoted text — Show quoted text -> I also posted an abstract that showed AA (arachidonic acid) > out of place in the lower part of the epidermis for P. > What does it take to start the cascade of inflammation? > Some NO with leaky cell membranes or apoptosis to spill > the mess? We have dendritic cells in the skin, gut and lymph. > If they’re reacting to LPS then why in the odd areas that > p develops in? > Think of your system like your car. Something is cloging > up the oil filter and the goop is causing friction in > the engine which shunts it out into your paint job that > is now rusting faster then normal cars rust. > That stuff gets in from the oil pan and disables > the filter and backs up the kidneys which throw > out nitric oxide (NO) to keep some homeostasis as a result > of the back pressure. Whoops, this example is going south > faster then your P. OK, your not your car. Your skin is > acting in concert to maintain pH balence and red is > a better color then white in the winter. Now the primer > coat… darn it. > You are your car and the antigens are sticking to > the paint and the adhesion proteins from the cytokines > are now joining the union and want higher wages. > So vote for me and i’ll clean up the air and water. > And protect the forests. > That clears things uP? > I feel like a blind man trying to explain what > an elephant looks like from touching its trunk.

Or in the case of P. Having a hundred blind men with DS feeling uP the critter and reporting it all back. – Hide quoted text — Show quoted text -> In their case the baby eats the mothers poop to > establish good bacteria in its Gi tract! > And if someone feeds him to many banana’s > he get’s gas and not P. > Your not your car but you still need a new paint job. > randall… are you haPPy NOw J?

Response:

> > Whatever role gut stuff has in psoriasis, it still seems to have a > genetic/hereditary aspect as well.  Lots of folks can have terribly > upset guts without their skin going nutz. > These new findings on eczema may lend some weight to this. The > peptides missing in the skin cause bacteria overgrowth and dermatitis. > Everyone that has a bad diet and lives in cities does not lose their > skin peptides, so those that do have a genetic disposition ? The next > question is : are atopics born without peptides, and then the whole > environment argument becomes difficult. The same may apply with the > gut dysbiosis.

The argument for P is different then for seb on the surface of the skin. How the two get to that point may be mechanically the same. Yet, without the proteins the point is moot. I’ll get some info on both. http://gnn.tigr.org/articles/07_02/stomach.shtml What is the mechanism that these proteins use to gain entry in the gut? By blocking their entry can we stop all LPS with a similar method? At this point seb and P would benefit from less LPS that mucks uP the system. Now, this is the point we part company; "Background The innate immune system of human skin contains antimicrobial peptides known as cathelicidins (LL-37) and -defensins.In normal skin these peptides are negligible, but they accumulate in skin affected by inflammatory diseases such as psoriasis." So, P people don’t need honey. We have to much antibiotics from our own natural pharma’s. You do mean to slather the honey topically? Or are you proposing an enema with it? > BTW Honey effectively inhibits H Pylori.

Oh, for the days of milk and honey. > Dig Dis Sci 1999 Mar;44(3):462-4 Related Articles, Links   > Osmotic effect of honey on growth and viability of Helicobacter > pylori. > Osato MS, Reddy SG, Graham DY. > Baylor College of Medicine and the Veterans Affairs Medical Center, > Department of Medicine, Houston, Texas 77030, USA > Honey solutions, with or without catalase, inhibited 24/28 isolates at > a concentration of 10%, and 28/28 isolates at a concentration of 15%.

This is all fine and good, but how do P’s benefit from it? As a part time caveman i try to avoid any extra sugars. And yet i’ve heard that honey from your local environs contains anti allergy stuff in it. Maybe during ragweed season. Nah. randall

Response:

>I love these. Like looking at the makers maP. >What does in the proper digestion of fats and influences DNA and >lives in the gut and has been mentioned here and is ubiquitious >enough to be a p suspect? Just another culPrit in the >P basket case of maladies? Can chewing some gum helP?

Whatever role gut stuff has in psoriasis, it still seems to have a genetic/hereditary aspect as well.  Lots of folks can have terribly upset guts without their skin going nutz. J.

Response:

> Whatever role gut stuff has in psoriasis, it still seems to have a > genetic/hereditary aspect as well.  Lots of folks can have terribly > upset guts without their skin going nutz.

These new findings on eczema may lend some weight to this. The peptides missing in the skin cause bacteria overgrowth and dermatitis. Everyone that has a bad diet and lives in cities does not lose their skin peptides, so those that do have a genetic disposition ? The next question is : are atopics born without peptides, and then the whole environment argument becomes difficult. The same may apply with the gut dysbiosis. BTW Honey effectively inhibits H Pylori. Dig Dis Sci 1999 Mar;44(3):462-4 Related Articles, Links   Osmotic effect of honey on growth and viability of Helicobacter pylori. Osato MS, Reddy SG, Graham DY. Baylor College of Medicine and the Veterans Affairs Medical Center, Department of Medicine, Houston, Texas 77030, USA Honey solutions, with or without catalase, inhibited 24/28 isolates at a concentration of 10%, and 28/28 isolates at a concentration of 15%.

Response:

- Hide quoted text — Show quoted text -> Hi, > or, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=OMIM&do… > or, http://www.ncbi.nlm.nih.gov/htbin-post/Omim/getmap?l177900 > What happens to the proper digestion of fats and influences DNA and > lives in the gut and has been mentioned here and is ubiquitious > enough to be a p suspect? Just another culPrit in the > P basket case of maladies? Can chewing some gum helP?

I wonder if taking H. Pylori out of the equation will help? (Reuters Health) – Scientists may be one step closer to developing a vaccine against the ulcer-causing stomach bug Helicobacter pylori. Infection with H. pylori bacteria is extremely common, with 70% of people worldwide estimated to carry the bug–although most will not develop ulcers or stomach cancer, another H. pylori-linked condition. Now researchers are putting together the secret behind the bacteria’s amazing staying power in the human stomach–in findings they say could lead to a vaccine or better treatments for H. pylori infection. The international research team has identified a so-called adhesin protein on the H. pylori bacterial surface that allows it to get a strong grip on cells lining the stomach. This protein, dubbed SabA, along with a similar H. pylori protein the researchers discovered several years ago (called BabA), could form the basis of an H. pylori vaccine. "BabA and SabA are proteins that are absolutely unique [to] H. pylori," the study’s lead author, Dr. Thomas Boren of Umea University in Sweden, told Reuters Health. "These proteins," he said, "are prime candidates for a vaccine that would be specific for Helicobacter and would not affect any other bacteria." Such specificity, Boren noted, is particularly important in the gastrointestinal tract, where many beneficial bacteria dwell. He and his colleagues report their study results in the July 26th issue of Science. Their findings also highlight how sly H. pylori must be to maintain such a foothold in the stomach. Both of its "attachment" proteins, BabA and SabA, bind to sugar molecules that are displayed on the surface of stomach cells in order to alert immune cells to an infection. So H. pylori actually uses these molecular distress signals for even stronger binding to stomach cells, Boren explained. This tactic is thought to allow at least some H. pylori bacteria in the stomach to evade the immune system. But if a vaccine can train the immune system to specifically recognize BabA and SabA, Boren said, "the H. pylori bacteria will then have a hard time in the stomach defending themselves against the activated and targeted immune response." He noted that his team has already tested a BabA-based vaccine in mice, and will now try adding the SabA protein to the mix. Even if these experiments are successful, though, Boren said it would be 6 to 8 years until an H. pylori vaccine is available. Science 2002;297:573-578.   Where in Sweden did we hear of two proteins recently? > Don’t worry there are some real Medical options here also. > Ferret them out. > http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=H.+Pylori+m… > Once again a S Harris post lights the way. > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… > Methylation due to a H. Pylori critter in the gut. > Possible DNA monkey bizness from a gut denizen?

A pubmed abstract shows a 50% reduction in H. Pylori from mastic gum. Someone of us should chew a few packs. I don’t want to wait eight years for anything. Unless i’m in prison and have no other choice. I guess that what p is all about? – Hide quoted text — Show quoted text -> Do you want to chew on this one some? > Does Pylori indirectly mediate fatty acid metabolism? > randall… balsam gum to the gut rescue of P?

Response:

> >I love these. Like looking at the makers maP. >What does in the proper digestion of fats and influences DNA and >lives in the gut and has been mentioned here and is ubiquitous >enough to be a p suspect? Just another culPrit in the >P basket case of maladies? Can chewing some gum helP? > Whatever role gut stuff has in psoriasis, it still seems to have a > genetic/hereditary aspect as well.  Lots of folks can have terribly > upset guts without their skin going nutz. > J.

Dear J, I agree. Yes, for sure. Right on. Cool. I’m looking for how the LPS gets into us in the first place. That fact that it does is established. The xoma pdf on endotoxins put that one in perspective. Wouldn’t it be nice if we only needed to stop gut permeability to a few lipids(A) or proteins from one or two ubiquitous bugs? Can you think of any other more likely candidates? P guts are either the same or almost the same as any others in the population at large. It has to be something right under our noses that is evading the radar. IRVCOMM had antibiotics for every combo of bug that they could find. Did they learn anything decimating his gut flora? If that Swedish study has found the genetic link to a protein that is primary or secondary to P, then it seems like a short hoP or jumP dealing with it. I also posted an abstract that showed AA (arachidonic acid) out of place in the lower part of the epidermis for P. What does it take to start the cascade of inflammation? Some NO with leaky cell membranes or apoptosis to spill the mess? We have dendritic cells in the skin, gut and lymph. If they’re reacting to LPS then why in the odd areas that p develops in? Think of your system like your car. Something is cloging up the oil filter and the goop is causing friction in the engine which shunts it out into your paint job that is now rusting faster then normal cars rust. That stuff gets in from the oil pan and disables the filter and backs up the kidneys which throw out nitric oxide (NO) to keep some homeostasis as a result of the back pressure. Whoops, this example is going south faster then your P. OK, your not your car. Your skin is acting in concert to maintain pH balence and red is a better color then white in the winter. Now the primer coat… darn it. You are your car and the antigens are sticking to the paint and the adhesion proteins from the cytokines are now joining the union and want higher wages. So vote for me and i’ll clean up the air and water. And protect the forests. That clears things uP? I feel like a blind man trying to explain what an elephant looks like from touching its trunk. In their case the baby eats the mothers poop to establish good bacteria in its Gi tract! And if someone feeds him to many banana’s he get’s gas and not P. Your not your car but you still need a new paint job. randall… are you haPPy NOw J?

Response:

> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=OMIM&do… > Hi, > I went into the OMIM to check this SLC12A8 out and > found it in the protein directory and also pubmed > abstract.

The Swedish researchers found something on gene 3 in their discovery announced on October 4, 2002 or thereabouts. Did the British find the same thing? > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… > To check it out click the box on the left and click protein > and enter SLC12A8.

The PSOR5 susceptibility gene is on 3q21 (604316) > The only other thing that stands out with SCL12A is > reading the above abstract this P suspect gene has something to do > with cation-chloride cotransporters? Am i wrong? > There are about 40 hits on pubmed. I list two here. > The diuretic-sensitive cotransport of cations with chloride is > mediated by the cation-chloride cotransporters, a large gene family > encompassing a total of seven Na-Cl, Na-K-2Cl, and K-Cl > cotransporters, in addition to two related transporters of unknown > function

(so what do they do?) Flood the extracellular fluid and and cause apoptosis? Didn’t the swedish news release say something to that effect for the discovered P gene? > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… > The electroneutral cotransport of potassium and chloride is mediated > by potassium-chloride transporters, which are encoded by members of > the gene family of cation-chloride cotransporters > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&…

Did the Swedes find what one of the two proteins does, is related to P? > Whoops can’t recall this one. It’s here now. > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&…

OK? What? If LPS/? causes back pressure in the kidneys it raises NO levels and that may account for FAS in the wrong levels of the skin? I know its a stretch. Cytoprotective effects of nitrates in a cellular model of hydronephrosis. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… So the basket case of p maladies could be explained partially by the effects of inflammation working to protect organs (kidneys) with the use of NO (nitric oxide). A closer look at the mechanical pathways involved may explain more. Or explain why this hypothesis doesn’t work. – Hide quoted text — Show quoted text -> randall…

Response:

- Hide quoted text — Show quoted text -> >I wonder what this one means. In relationship to the other seven > >P genes, anyway. > >You suppose those scientist will go on finding p genes forever? > The article says expression was increased, not that it was unique to > psoriasis. > Maybe six or so of these genes is just involved in the inflammatory > process rather than being directly causative. > J. > Hi, > I couldn’t wait or i may have forgotten this. > I found 1600 hits on gene transcriptions & fatty acids. > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&… > Selective cooperation between fatty acid binding proteins and > peroxisome proliferator-activated receptors in regulating > transcription > Now we are back to the PPAR thread! Holy cow, how much > CoQ10 is in that meat?

OK! Here is a conclusion from a link posted to the PPAR gene thread. [...] The discovery of PPARs and identification of fatty acids and their derivatives as ligands, a few years ago, have uncovered an unexpected and fascinating regulatory mode of action of lipids as direct modulators of gene expression. Since then, the excitement has not weakened while compelling evidence has accumulated that PPAR and PPAR act at crucial nodes of the regulatory network that achieve energy homeostasis in the organism. More specifically, an emerging picture is that of a dual and complementary role of PPAR and – isotypes in the regulation of the catabolic and anabolic aspects of lipid metabolism, respectively. Stimulating findings also include the discovery that lipid mediators, such as some eicosanoids (leukotrienes and prostaglandins), are natural PPAR ligands, opening new perspectives for investigating possible novel determinants of energy balance, as well as novel functions for PPARs, with links to glucose homeostasis, cell cycle control, inflammation, and immune response. As a corollary, PPARs are promising targets for therapeutic intervention, through the development of agonists but also antagonists, in disorders such as obesity and diabetes, atherosclerosis, chronic inflammatory diseases, and tumorigenesis. However, one characteristic of the PPARs is that their activation can occur through a broad spectrum of ligands with rather low affinity. This implies that particular care must be taken when assessing the PPAR dependence of a given signaling pathway. More interestingly, some signals might be transduced by different ways, as exemplified by the subtle interplay between the membrane and nuclear receptors, introducing new levels of complexity in PPAR biology as determinants of the fine tuning of interconnected metabolic processes. The above being the conclusion from this 1999 abstract on PPAR’s http://edrv.endojournals.org/cgi/content/full/20/5/649 The best way to update yourself from 99 to the present is simply enter PPAR into the pubmed site and read em chronologically to the present. – Hide quoted text — Show quoted text -> randall

Response:

>>Who KNEW that the seb derms had the same genes but not >the two proteins that make defensins and cathelcidins? >Wait a minute, if they had 100% the same genes, we *presume* we would >all have the same proteins.

… plus or minus exogenous factors, eg exposure to disease. J.

Response:

> Selective cooperation between fatty acid binding proteins and > peroxisome proliferator-activated receptors in regulating > transcription > Now we are back to the PPAR thread! Holy cow, how much > CoQ10 is in that meat? > randall

LOL ! Want to resurrect the diabetes-insulin-ppar-psoriasis blowtorch wars ?! Seriously, this stuff is starting to show more links than ever. IMO.

Response:

> >I hope anyway. I loved to eat a few things with impunity. > I prefer Grey Poupon.

Does it have chinese mustard in it? >Who KNEW that the seb derms had the same genes but not >the two proteins that make defensins and cathelcidins? > Wait a minute, if they had 100% the same genes, we *presume* we would > all have the same proteins.

We’ve left the seb vs P thread, so i’ll grab up some info from them to refresh the conversation. >And as evetsm has said concerning the similarities and differences we >all share the small differences are huge yet all clues.

Yep. (J said) >We, you and i, do differ on omega6/egg yolks/borage oil/EPO? >Do we NOT? (randall said)

Dunno. (J said) Maybe the benefits I see from eggs and EPO are all benefits to secondary problems that I have and you don’t, even while they actually aggravate the underlying primary psoriasis. (J said) J. Post number 11 in this thread is a PPAR and fatty acid thing for regulating gene transcription. And the above foods all have fatty acids in them. LA, LNA, EFA’s and more then i can list. N-3’s and N-6’s needing close attention plus the interaction of refined sugars with Tnf and iNOS. Here is the abstract on the two proteins, Background The innate immune system of human skin contains antimicrobial peptides known as cathelicidins (LL-37) and -defensins. In normal skin these peptides are negligible, but they accumulate in skin affected by inflammatory diseases such as psoriasis. We compared the levels of expression of LL-37 and human -defensin 2 (HBD-2) in inflamed skin from patients with atopic dermatitis and from those with psoriasis. Methods The expression of LL-37 and HBD-2 protein in skin-biopsy specimens from patients with psoriasis, patients with atopic dermatitis, and normal subjects was determined by immunohistochemical analysis. The amount of antimicrobial peptides in extracts of skin samples was also analyzed by immunodot blot analysis (for LL-37) and Western blot analysis (for HBD-2). Quantitative, real-time reverse-transcriptase