Re: Reduced expression of Ca2+-regulating proteins in the upper gastrointestinal tract of patients with

[Guest guest]

Thanks Notan for all your research.

Interesting articles including the chocolate. I use dark chocolate

sometimes but now will increase it.

You can spend all day looking at the references and trying to

understand them. I am very glad I have not had an operation, seems

like some combination of drugs will help, maybe even in my life time.

I am doing well as long as I keep on a routine using liquids,soup,

some pasta, Ensure and a lot of Coke. I walk to Mcs each

morning and get a drink of Coke off the fountian, drinking the CO2

off the top many times, then finally the Coke goes down. After this

at home I can have cerial with milk. Seems like the LES tightens at

night so must be opened in the morning.

I use Colchicine for my gout once in awhile, maybe it helps or caused

the problem.

This came from an article on Swallowing Disorders from eMedicine

Iatrogenic oropharyngeal dysphagia

Various medications, including the following, produce effects due to

a decrease in cognition or as a result of the development of drug-

induced myopathies:

CNS depressants

Antipsychotics

Corticosteroids

Lipid-lowering agents

Colchicine

Aminoglycosides

Anticholinergic drugs

rayme CA OC 78

>

> This is a couple years old. The researches found that the amount of

> proteins, calreticulin (CRT) and calsequestrin (CSQ), that store

calcium

> (Ca2+) and control the level of it are " significantly reduced " in

the

> LES of achalasia patients. This is interesting because calcium

plays a

> part in the contraction of smooth muscles, like the LES. It is by

> hindering this action of calcium that calcium channel blockers,

like

> nifedipine, work to lower LES pressure. One would think that

reducing

> proteins that store calcium may cause an increase in the amount of

free

> calcium and cause the opposite effect from that seen. The author

> discusses this and points out that in smooth muscle of the heart it

has

> been found that reducing the proteins that store calcium causes

> increased action of the muscle. More research needs to be done to

> confirm the findings and to find out if this points to a cause of

> achalasia or just another effect from the damage caused by

achalasia.

>

> I find this interesting because one of the theories for how neurons

> become damaged in achalasia is that over distention, or chronic

> distention, by food due to blockage at the LES causes it. But that

> raised the question of why would there be blockage at the LES if

the

> neurons were not already damaged. Kind of a chicken and egg

problem. If

> these proteins are the cause then there is no chicken or egg

problem,

> calcium would cause LES blockage and would lead to the damage of

the

> neurons and start the cycle. There are also other possible causes

of

> achalasia that get around the chicken and egg problem. Other

> researchers have found abnormal amounts of Interstitial cells of

Cajal

> (ICC) in the LES of achalasia patients. Again, it is not clear if

this

> change in ICCs is a cause or effect of other destruction in

achalasia.

>

>

> Reduced expression of Ca2+-regulating proteins in the upper

> gastrointestinal tract of patients with achalasia

> World J Gastroenterol 2006 October 7

> http://www.wjgnet.com/1007-9327/12/6002.asp

>

> Reduction of interstitial cells of Cajal (ICC) associated with

neuronal

> nitric oxide synthase (n-NOS) in patients with achalasia.

> http://www.ncbi.nlm.nih.gov/pubmed/18070236

>

> Alterations in the density of interstitial cells of Cajal in

achalasia.

> http://www.ncbi.nlm.nih.gov/pubmed/18030621

>

> notan

>

[Guest guest]

Interesting. Thanks for the list of meds that can cause the LES to tighten. For

the last 8 years because of Familial Hypercholesterolanemia I have to take

Simvastating 40mg every night and morning for the rest of my life. Food for

thought. I find that myself personally cannot drink anything fizzy as the gas

gets trapped and the pain is through the roof if you know what I mean but I do

eat peppermint chocolate to help me burp after eating, I find that it does help

me but each to his/her own. Yes I have had the ectomy but the pylorus valve is

now my new Les and therefore behaves in the same way as the oesophageal Les.

Experts told me this.

________________________________

From: me_rayme <ray_me_99@...>

achalasia

Sent: Tuesday, December 2, 2008 2:15:27 AM

Subject: Re: Reduced expression of Ca2+-regulating proteins in the

upper gastrointestinal tract of patients with achalasia

Thanks Notan for all your research.

Interesting articles including the chocolate. I use dark chocolate

sometimes but now will increase it.

You can spend all day looking at the references and trying to

understand them. I am very glad I have not had an operation, seems

like some combination of drugs will help, maybe even in my life time.

I am doing well as long as I keep on a routine using liquids,soup,

some pasta, Ensure and a lot of Coke. I walk to Mcs each

morning and get a drink of Coke off the fountian, drinking the CO2

off the top many times, then finally the Coke goes down. After this

at home I can have cerial with milk. Seems like the LES tightens at

night so must be opened in the morning.

I use Colchicine for my gout once in awhile, maybe it helps or caused

the problem.

This came from an article on Swallowing Disorders from eMedicine

Iatrogenic oropharyngeal dysphagia

Various medications, including the following, produce effects due to

a decrease in cognition or as a result of the development of drug-

induced myopathies:

CNS depressants

Antipsychotics

Corticosteroids

Lipid-lowering agents

Colchicine

Aminoglycosides

Anticholinergic drugs

rayme CA OC 78

>

> This is a couple years old. The researches found that the amount of

> proteins, calreticulin (CRT) and calsequestrin (CSQ), that store

calcium

> (Ca2+) and control the level of it are " significantly reduced " in

the

> LES of achalasia patients. This is interesting because calcium

plays a

> part in the contraction of smooth muscles, like the LES. It is by

> hindering this action of calcium that calcium channel blockers,

like

> nifedipine, work to lower LES pressure. One would think that

reducing

> proteins that store calcium may cause an increase in the amount of

free

> calcium and cause the opposite effect from that seen. The author

> discusses this and points out that in smooth muscle of the heart it

has

> been found that reducing the proteins that store calcium causes

> increased action of the muscle. More research needs to be done to

> confirm the findings and to find out if this points to a cause of

> achalasia or just another effect from the damage caused by

achalasia.

>

> I find this interesting because one of the theories for how neurons

> become damaged in achalasia is that over distention, or chronic

> distention, by food due to blockage at the LES causes it. But that

> raised the question of why would there be blockage at the LES if

the

> neurons were not already damaged. Kind of a chicken and egg

problem. If

> these proteins are the cause then there is no chicken or egg

problem,

> calcium would cause LES blockage and would lead to the damage of

the

> neurons and start the cycle. There are also other possible causes

of

> achalasia that get around the chicken and egg problem. Other

> researchers have found abnormal amounts of Interstitial cells of

Cajal

> (ICC) in the LES of achalasia patients. Again, it is not clear if

this

> change in ICCs is a cause or effect of other destruction in

achalasia.

>

>

> Reduced expression of Ca2+-regulating proteins in the upper

> gastrointestinal tract of patients with achalasia

> World J Gastroenterol 2006 October 7

> http://www.wjgnet. com/1007- 9327/12/6002. asp

>

> Reduction of interstitial cells of Cajal (ICC) associated with

neuronal

> nitric oxide synthase (n-NOS) in patients with achalasia.

> http://www.ncbi. nlm.nih.gov/ pubmed/18070236

>

> Alterations in the density of interstitial cells of Cajal in

achalasia.

> http://www.ncbi. nlm.nih.gov/ pubmed/18030621

>

> notan

>

[Guest guest]

Ray wrote:

> I use Colchicine for my gout once in awhile, maybe it helps or caused

> the problem.

>

Colchicine can cause muscle weakness. I don't know if the weakness could

be just in the esophagus. Maybe, but I don't know. One area it has

effect in some patients is respiratory muscle. But it makes muscles

weaker so while it may lead to weak peristalsis that doesn't explain

some of the spastic muscle action seen in achalasia or the aperistalsis.

It can irritate nerves though, so maybe that could add to whatever else

promotes the damage to nerves in achalasia.

> This came from an article on Swallowing Disorders from eMedicine

>

> Iatrogenic oropharyngeal dysphagia

>

Oropharyngeal is higher in the neck that the problems in achalasia.

> Various medications, including the following, produce effects due to

> a decrease in cognition or as a result of the development of drug-

> induced myopathies:

>

> CNS depressants

> Antipsychotics

> Corticosteroids

> Lipid-lowering agents

> Colchicine

> Aminoglycosides

> Anticholinergic drugs

>

All of these drugs can have effects to either nerves or muscles. Some of

these effect a person like alcohol does to a drunk. They make it hard to

control the body, even to swallow. The Lipid-lowing agents (think

statins) in rare cases can cause muscle damage. That damage is not

specific to the esophagus. BTW: some people will try to avoid using

statins by using red rice yeast, but it actually contains one of the

statin drugs, so if you take enough of it to have the health benefits

you also still have the same health risk you would have had with the

statin drug.

Of all the people that use these drugs very few get achalasia, or

achalasia would not be so rare. Also there are people that never use

they drugs but still get achalasia. I would think most of the youngsters

in this group have used very little if any of these drugs. There has to

be something more to why we have it. That does not mean our medication

couldn't have been a part of causing it, but there must be something

more. It is also possible that these drugs or other medication have

nothing to do with our achalasia.

notan

[Guest guest]

wrote:

> Interesting. Thanks for the list of meds that can cause the LES to tighten.

I saw a list of medications under the topic of " Iatrogenic oropharyngeal

dysphagia, " but I didn't see a list of medication that cause the LES to

tighten. Did I miss something?

> ... I have to take Simvastating 40mg every night and morning for the rest of

my life....

The main problem with statins is muscle damage not nerve damage, so I

doubt there is much of a connection to achalasia or the dysfunction of

other sphincters. You do need to keep an eye on muscle changes and pain

though.

notan

[Guest guest]

Hi Notan

I take 40mg of Omeprazole (Zoton)twice daily both morning and night and have

been taking them for the past 5-7 years now. I have Familial

Hypercholesterolanaemia so my level is 5.7 while taking medication. So I have

little choice unless I want to develop full blown heart disease. Tell me one

thing that baffles me a little Notan is Familial Hypercholesterolanaemia (high

levels of Cholesterol that run in families)heart disease???? I ask my GP and his

answer is always vague.

________________________________

From: notan ostrich <notan_ostrich@...>

achalasia

Sent: Wednesday, December 3, 2008 3:00:57 PM

Subject: Re: Re: Reduced expression of Ca2+-regulating proteins in

the upper gastrointestinal tract of patients with achalasia

Ray wrote:

> I use Colchicine for my gout once in awhile, maybe it helps or caused

> the problem.

>

Colchicine can cause muscle weakness. I don't know if the weakness could

be just in the esophagus. Maybe, but I don't know. One area it has

effect in some patients is respiratory muscle.. But it makes muscles

weaker so while it may lead to weak peristalsis that doesn't explain

some of the spastic muscle action seen in achalasia or the aperistalsis.

It can irritate nerves though, so maybe that could add to whatever else

promotes the damage to nerves in achalasia.

> This came from an article on Swallowing Disorders from eMedicine

>

> Iatrogenic oropharyngeal dysphagia

>

Oropharyngeal is higher in the neck that the problems in achalasia.

> Various medications, including the following, produce effects due to

> a decrease in cognition or as a result of the development of drug-

> induced myopathies:

>

> CNS depressants

> Antipsychotics

> Corticosteroids

> Lipid-lowering agents

> Colchicine

> Aminoglycosides

> Anticholinergic drugs

>

All of these drugs can have effects to either nerves or muscles. Some of

these effect a person like alcohol does to a drunk. They make it hard to

control the body, even to swallow. The Lipid-lowing agents (think

statins) in rare cases can cause muscle damage. That damage is not

specific to the esophagus. BTW: some people will try to avoid using

statins by using red rice yeast, but it actually contains one of the

statin drugs, so if you take enough of it to have the health benefits

you also still have the same health risk you would have had with the

statin drug.

Of all the people that use these drugs very few get achalasia, or

achalasia would not be so rare. Also there are people that never use

they drugs but still get achalasia. I would think most of the youngsters

in this group have used very little if any of these drugs. There has to

be something more to why we have it. That does not mean our medication

couldn't have been a part of causing it, but there must be something

more. It is also possible that these drugs or other medication have

nothing to do with our achalasia.

notan

[Guest guest]

wrote:

> ...is Familial Hypercholesterolanaemia (high levels of Cholesterol that run in

families)heart disease????

I only have a moment to answer this right now so I can't look anything

up, but from the word Hypercholesterolanaemia it only implies high

cholesterol. High cholesterol is a risk factor for heart disease but

does not guarantee you will get it. I don't know though if the

" Familial " type means anything more regarding HD.

notan

[Guest guest]

wrote:

> ... is Familial Hypercholesterolanaemia (high levels of Cholesterol that run

in families)heart disease????

Ok, I'm back. I did some checking, there are different types of heart

disease and the heart disease of FH is Coronary heart disease, or

Cardiovascular disease. Which are the types you would expect from high

cholesterol. Untreated FH would almost certainly lead to HD. With

treatment it is unclear how long you put off HD. It will depend on other

factors, such as, if you are heterozygous or homozygous (unlikely),

the age treatment is started and all the usual suspects for HD. It does

look like you have a very high risk for it if you don't have it.

I also have some wonderful genes. In my case they cause

hypertriglyceridemia. I once had my triglycerides at 1600. That and

diabetes and high blood pressure, I have some idea of what you are going

through. What are the chances that I won't die from a heart attack or

stroke? Well if my IgG falls lower as I age I suppose I could die from

some common infection first. I don't think this body was made for a long

haul. And there are no herbs or supplements that are going to change my

genes.

None of this is going to mess with today though. I am busy with life now.

notan

[Guest guest]

That's a rather generic assessment, indicting many classes of drugs

with few specifics.

One could also say, " Going to Mcs everyday and having a

'supersize diet' is going to do wonders for your health. " (most of

their food is puke-able. this aspect is very true.)

> >

> > This is a couple years old. The researches found that the amount of

> > proteins, calreticulin (CRT) and calsequestrin (CSQ), that store

> calcium

> > (Ca2+) and control the level of it are " significantly reduced " in

> the

> > LES of achalasia patients. This is interesting because calcium

> plays a

> > part in the contraction of smooth muscles, like the LES. It is by

> > hindering this action of calcium that calcium channel blockers,

> like

> > nifedipine, work to lower LES pressure. One would think that

> reducing

> > proteins that store calcium may cause an increase in the amount of

> free

> > calcium and cause the opposite effect from that seen. The author

> > discusses this and points out that in smooth muscle of the heart it

> has

> > been found that reducing the proteins that store calcium causes

> > increased action of the muscle. More research needs to be done to

> > confirm the findings and to find out if this points to a cause of

> > achalasia or just another effect from the damage caused by

> achalasia.

> >

> > I find this interesting because one of the theories for how neurons

> > become damaged in achalasia is that over distention, or chronic

> > distention, by food due to blockage at the LES causes it. But that

> > raised the question of why would there be blockage at the LES if

> the

> > neurons were not already damaged. Kind of a chicken and egg

> problem. If

> > these proteins are the cause then there is no chicken or egg

> problem,

> > calcium would cause LES blockage and would lead to the damage of

> the

> > neurons and start the cycle. There are also other possible causes

> of

> > achalasia that get around the chicken and egg problem. Other

> > researchers have found abnormal amounts of Interstitial cells of

> Cajal

> > (ICC) in the LES of achalasia patients. Again, it is not clear if

> this

> > change in ICCs is a cause or effect of other destruction in

> achalasia.

> >

> >

> > Reduced expression of Ca2+-regulating proteins in the upper

> > gastrointestinal tract of patients with achalasia

> > World J Gastroenterol 2006 October 7

> > http://www.wjgnet.com/1007-9327/12/6002.asp

> >

> > Reduction of interstitial cells of Cajal (ICC) associated with

> neuronal

> > nitric oxide synthase (n-NOS) in patients with achalasia.

> > http://www.ncbi.nlm.nih.gov/pubmed/18070236

> >

> > Alterations in the density of interstitial cells of Cajal in

> achalasia.

> > http://www.ncbi.nlm.nih.gov/pubmed/18030621

> >

> > notan

> >

>

[Guest guest]

Hi Notan

Familial as in Familial Hypercholesterolanaemia means high levels that run in

families i:e siblings, parents, their siblings and their parents.

________________________________

From: notan ostrich <notan_ostrich@...>

achalasia

Sent: Wednesday, December 3, 2008 4:52:29 PM

Subject: Re: Re: Reduced expression of Ca2+-regulating proteins in

the upper gastrointestinal tract of patients with achalasia

wrote:

> ...is Familial Hypercholesterolana emia (high levels of Cholesterol that run

in families)heart disease????

I only have a moment to answer this right now so I can't look anything

up, but from the word Hypercholesterolana emia it only implies high

cholesterol. High cholesterol is a risk factor for heart disease but

does not guarantee you will get it. I don't know though if the

" Familial " type means anything more regarding HD.

notan

[Guest guest]

Hi Notan

Yes part of the 5.7 reading for my Cholesterol is Triglyceraides.. Have spoken

to my father and some of his siblings (those that are still alive) and all have

high levels of Cholesterol, all suffer Angina and all suffer with Diabetes.

Bummer eh. Thanks as always for the info.

________________________________

From: notan ostrich <notan_ostrich@...>

achalasia

Sent: Wednesday, December 3, 2008 9:52:39 PM

Subject: Re: Re: Reduced expression of Ca2+-regulating proteins in

the upper gastrointestinal tract of patients with achalasia

wrote:

> ... is Familial Hypercholesterolana emia (high levels of Cholesterol that run

in families)heart disease????

Ok, I'm back. I did some checking, there are different types of heart

disease and the heart disease of FH is Coronary heart disease, or

Cardiovascular disease. Which are the types you would expect from high

cholesterol. Untreated FH would almost certainly lead to HD. With

treatment it is unclear how long you put off HD. It will depend on other

factors, such as, if you are heterozygous or homozygous (unlikely),

the age treatment is started and all the usual suspects for HD. It does

look like you have a very high risk for it if you don't have it.

I also have some wonderful genes. In my case they cause

hypertriglyceridemi a. I once had my triglycerides at 1600. That and

diabetes and high blood pressure, I have some idea of what you are going

through. What are the chances that I won't die from a heart attack or

stroke? Well if my IgG falls lower as I age I suppose I could die from

some common infection first. I don't think this body was made for a long

haul. And there are no herbs or supplements that are going to change my

genes.

None of this is going to mess with today though. I am busy with life now.

notan

[Guest guest]

wrote:

> Hi Notan

> Familial as in Familial Hypercholesterolanaemia means high levels that run in

families i:e siblings, parents, their siblings and their parents.

>

Yes. Sometimes things are more than the words in the name suggest. I

didn't know if it was limited to high cholesterol in the family, as the

name suggests, or if it was more of a syndrome. That was why I wanted

more time to look it up, which I did for the second message.

notan

[Guest guest]

Steve

Guess you are one of the ones biased against people like me who do

want an operation.

" One could also say, " Going to Mcs everyday and having a

'supersize diet' is going to do wonders for your health. " (most of

their food is puke-able. this aspect is very true.) "

Not sure what puke-able means. I go for the Coke ONLY ONLY it helps

me tremendously. Maybe you should try it!

It started last spring when after a quarter cup of coffee it came up,

then later the CO2 off the top of Coke made the LES shrink so I could

swallow. I have stopped eating at Mcs in 1996 when I had a

bypass.

Personally I used to like egg mcmuffins and still do.

rayme

> > >

> > > This is a couple years old. The researches found that the

amount of

> > > proteins, calreticulin (CRT) and calsequestrin (CSQ), that

store

> > calcium

> > > (Ca2+) and control the level of it are " significantly reduced "

in

> > the

> > > LES of achalasia patients. This is interesting because calcium

> > plays a

> > > part in the contraction of smooth muscles, like the LES. It is

by

> > > hindering this action of calcium that calcium channel blockers,

> > like

> > > nifedipine, work to lower LES pressure. One would think that

> > reducing

> > > proteins that store calcium may cause an increase in the amount

of

> > free

> > > calcium and cause the opposite effect from that seen. The

author

> > > discusses this and points out that in smooth muscle of the

heart it

> > has

> > > been found that reducing the proteins that store calcium causes

> > > increased action of the muscle. More research needs to be done

to

> > > confirm the findings and to find out if this points to a cause

of

> > > achalasia or just another effect from the damage caused by

> > achalasia.

> > >

> > > I find this interesting because one of the theories for how

neurons

> > > become damaged in achalasia is that over distention, or chronic

> > > distention, by food due to blockage at the LES causes it. But

that

> > > raised the question of why would there be blockage at the LES

if

> > the

> > > neurons were not already damaged. Kind of a chicken and egg

> > problem. If

> > > these proteins are the cause then there is no chicken or egg

> > problem,

> > > calcium would cause LES blockage and would lead to the damage

of

> > the

> > > neurons and start the cycle. There are also other possible

causes

> > of

> > > achalasia that get around the chicken and egg problem. Other

> > > researchers have found abnormal amounts of Interstitial cells

of

> > Cajal

> > > (ICC) in the LES of achalasia patients. Again, it is not clear

if

> > this

> > > change in ICCs is a cause or effect of other destruction in

> > achalasia.

> > >

> > >

> > > Reduced expression of Ca2+-regulating proteins in the upper

> > > gastrointestinal tract of patients with achalasia

> > > World J Gastroenterol 2006 October 7

> > > http://www.wjgnet.com/1007-9327/12/6002.asp

> > >

> > > Reduction of interstitial cells of Cajal (ICC) associated with

> > neuronal

> > > nitric oxide synthase (n-NOS) in patients with achalasia.

> > > http://www.ncbi.nlm.nih.gov/pubmed/18070236

> > >

> > > Alterations in the density of interstitial cells of Cajal in

> > achalasia.

> > > http://www.ncbi.nlm.nih.gov/pubmed/18030621

> > >

> > > notan

> > >

> >

>

[Guest guest]

I am NOT biased. You may have all the surgery you like. It's your

body, after all.

I've been sliced/diced/ripped-open and injected. I let the doctors

have their way with me, and the result is a TIGHTER LES, and MORE

pain, which can be treated MORE effectively and simply without surgery

or major side effects. Just guess what treatment that is? Then the

" bias " will REALLY start coming!

Why should I want some very invasive removal of my esophagus, an

operation that has a high probability for serious surgical risks?

That's not bias, but sound rational judgment.

Carbonated beverages containing (CO2) make burping and belching. Coke

sucks. In my experience CO2 has had NO effect on loosening of the LES

pressure.

and CA++ channel blockers and nifedine did absolutely nothing.

> > > >

> > > > This is a couple years old. The researches found that the

> amount of

> > > > proteins, calreticulin (CRT) and calsequestrin (CSQ), that

> store

> > > calcium

> > > > (Ca2+) and control the level of it are " significantly reduced "

> in

> > > the

> > > > LES of achalasia patients. This is interesting because calcium

> > > plays a

> > > > part in the contraction of smooth muscles, like the LES. It is

> by

> > > > hindering this action of calcium that calcium channel blockers,

> > > like

> > > > nifedipine, work to lower LES pressure. One would think that

> > > reducing

> > > > proteins that store calcium may cause an increase in the amount

> of

> > > free

> > > > calcium and cause the opposite effect from that seen. The

> author

> > > > discusses this and points out that in smooth muscle of the

> heart it

> > > has

> > > > been found that reducing the proteins that store calcium causes

> > > > increased action of the muscle. More research needs to be done

> to

> > > > confirm the findings and to find out if this points to a cause

> of

> > > > achalasia or just another effect from the damage caused by

> > > achalasia.

> > > >

> > > > I find this interesting because one of the theories for how

> neurons

> > > > become damaged in achalasia is that over distention, or chronic

> > > > distention, by food due to blockage at the LES causes it. But

> that

> > > > raised the question of why would there be blockage at the LES

> if

> > > the

> > > > neurons were not already damaged. Kind of a chicken and egg

> > > problem. If

> > > > these proteins are the cause then there is no chicken or egg

> > > problem,

> > > > calcium would cause LES blockage and would lead to the damage

> of

> > > the

> > > > neurons and start the cycle. There are also other possible

> causes

> > > of

> > > > achalasia that get around the chicken and egg problem. Other

> > > > researchers have found abnormal amounts of Interstitial cells

> of

> > > Cajal

> > > > (ICC) in the LES of achalasia patients. Again, it is not clear

> if

> > > this

> > > > change in ICCs is a cause or effect of other destruction in

> > > achalasia.

> > > >

> > > >

> > > > Reduced expression of Ca2+-regulating proteins in the upper

> > > > gastrointestinal tract of patients with achalasia

> > > > World J Gastroenterol 2006 October 7

> > > > http://www.wjgnet.com/1007-9327/12/6002.asp

> > > >

> > > > Reduction of interstitial cells of Cajal (ICC) associated with

> > > neuronal

> > > > nitric oxide synthase (n-NOS) in patients with achalasia.

> > > > http://www.ncbi.nlm.nih.gov/pubmed/18070236

> > > >

> > > > Alterations in the density of interstitial cells of Cajal in

> > > achalasia.

> > > > http://www.ncbi.nlm.nih.gov/pubmed/18030621

> > > >

> > > > notan

> > > >

> > >

> >

>