Fedor Del Nasi - his and his lines influence on the breed

Unread postby Weinberge » Thu Aug 19, 2010 6:29 pm

Insomnia

I inform you than Baksal already go in holiday.
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Unread postby jotunheim » Thu Aug 19, 2010 6:35 pm

BasKal wrote:I will not write here anymore - if someone wants something, (even to call me names), he is welcomed to sent me a message through this forum.
BB.


Could you please have the curticy to answer my questions - the more information, the better choices can be made.

Thank's

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Unread postby Weinberge » Thu Aug 19, 2010 6:37 pm

Bitten...Baksal already enter in holiday ....
And I will go soon.

Pause !
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Unread postby Ronindobe » Fri Aug 20, 2010 6:02 am

Hello good people. I have been pretty busy milling puppies [joke ok?]. Keep hashing at it...you guys are the good ones. You are really on the same side.

Here's my short input. I think regardless of the issues with Fedor, his ped and his massive use, here is a general issue. The ruling bodies, FCI, DV,IDC, kennel and breed clubs at the national and regional levels need to install some parameters for uber producers most especially. First, DNA must be filed, for legitamacy issues and health research, current and future. Second, dogs with huge statistical impact must be followed. Date of death, cause, and certified necropsy should be required for the breeder and owner to remain in good standing in the community. Complete health testing should be an absolute requirement at prescribed interval [test dependent]. Third, progeny of mass producers should be followed closely and outcomes certified. Personally I feel that any animal producing more than 3 litters should come under this ideal.

My main issue with ped research, and I am completely for it at the Bitten level of 13gen, are the holes in the data and the anecdotal outcomes. How am I to make proper conclusions based on rumor, opinions based on suspicsions or the conclusions on medical outcomings from non professional sources? If it was not for a few people here and my encyclopedia of dog/line info in the first person, Bitten, I would be totally reliant on the "subjective" prose of jouralists and the owners themselves.

Again my friends, we are on the same side. We are for the better future for our breed, the Dobermann. Peace to you all and success in this quest!

8)
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Unread postby Weinberge » Fri Aug 20, 2010 6:48 am

Ronindobe wrote:. Date of death, cause, and certified necropsy should be required for the breeder and owner to remain in good standing in the community. Complete health testing should be an absolute requirement at prescribed interval [test dependent]. Third, progeny of mass producers should be followed closely and outcomes certified. Personally I feel that any animal producing more than 3 litters should come under this ideal.


:smt023
All the data regarding shows, working and health /age /death must be writed on REPRODUCTIVE REGISTER and in puppys pedigree REGISTER EXTRAS (like the Italian model but completed with health and death functions) !

Declaration of dogs death (like on humans deaths)and the reasons must be OBLIGATORY for any Breeder which like to have acces on REGISTER . Oterwise , the puppys of undeclared parent will have the pedigree STAMPED and ZERO on AVERAGE AGE calculation regarding undeclared parent.

Without a minimal criterias respected and without a NATIVE ZTP BYE BYE IDC TITLE ! Ups !

I said NATIVE ZTP because really is a jeering how Big Breeders train their dogs for ZTP in K99 schools . The Trainers are for performance , for IPO onworking field , not for ZTP - the breeding natural test.
ZTP must become a normal think pased by any normal dobermann , leaded by any normal , old or young owner .

THAT SAID MR.PALMER- FURSTENFELD KENNEL , THAT WILL ALWAYS TELL ANY TRUE FURSTENFELD BREEDER.

But I have doubt that will happend till the dobermann world is leaded by humans which bring race in this point and the shows will decide who will live and who will died .

But ..the stupidity of brains and irony of fate, they destroy exactly their longevity chance :lol:
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Unread postby Weinberge » Fri Aug 20, 2010 7:14 am

Baksal, where are you ? In one the exotic island ?
You leave me alone....my unfaithful friend !

I hope you will send to me a postal card with exotic places and womans!
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Unread postby BasKal » Fri Aug 20, 2010 2:30 pm

Hi, I am not here for discussion and I will not answer to anything, but, I think that I had to do this.

Here are parts from the -IMHO- most important study about the connection of Titin gene with DCM in dobermanns (because the whole study - which I put it in this forum in 2006- may is tiresome for most people, I preferred to put here only the Abstract and the Discussion - also, IMHO, a test for the presense of the "protective" form of the Titin gene, must be developed as soon as possible :

Genetic epidemiological studies of DCM in the
Dobermann dog point to a crucial role of titin in DCM
susceptibility

Polona Stabej, Peter A.J. Leegwater, Sandra Imholz, Manon
Loohuis, Paul J.J. Mandigers, Arnold A. Stokhof, Aleksandra
Domanjko-Petrič, Bernard A. van Oost

ABSTRACT
Dilated cardiomyopathy (DCM) is a disease of the myocardium associated
with dilatation and impaired contraction of the ventricles. In the dog, it primarily
affects large and giant breeds with the Dobermann being one of the most
frequently affected. The high prevalence of DCM in specific breeds suggests a
genetic background, but causal mutations have not yet been identified in dogs.
The gene encoding the giant myofilament protein titin (TTN) was one of the
candidate genes that we evaluated as part of our study of the genetic aetiology of
DCM in Dobermanns. The diagnosis of DCM was based on clinical and/or
radiographic symptoms of congestive heart failure (CHF) and was confirmed in
each case by two-dimensional echocardiography. Genotyping of TTN marker
REN252E18 revealed a strong partition of TTN alleles between the DCM and
DCM non-affected groups. The main difference between DCM and DCM nonaffected
Dobermanns is the enrichment for one allele in the DCM non-affected
group. The same applies to the haplotypes defined by genotypes of three TTN
markers. This result suggests that the titin allele over represented in the DCM
non-affected group, is either the allele that is not linked to a pathological mutation
or confers protection against DCM in the presence of a mutation elsewhere in the
genome. Hypotheses explaining the possible role of TTN in the DCM in the
Dobermann dogs will be discussed.


DISCUSSION

GENOTYPES OF THE TITIN GENE MARKERS IN THE DCM AND DCM-FREE
DOBERMANNS
Typing of TTN microsatellite marker REN252E18 in the Dobermanns
showed a sharp partition of genotypes between the DCM and DCM non-affected
Dobermanns. The difference is enrichment of the 260 allele in the DCM-free
group and enrichment of all other alleles (especially allele 256) in the DCM group.

The haplotype analysis of two small deletions and one
nucleotide substitution showed a similar partition between DCM and DCM-free
dogs. The most striking finding of the haplotype analysis was the variance of
haplotypes in the group of DCM Dobermanns as opposed to the relative
uniformity of the DCM-free group . While individual TTN marker alleles
showed association with the DCM phenotype, they did not combine to a
single haplotype that was predominant in the DCM group. Next to
haplotype 2, which was shared between 12 out of 26 DCM dogs, we defined a
total of four different haplotypes in the DCM group. The
divergent haplotypes in the DCM group and the high frequency of haplotype 1 in
the non-affected group and the random group form the basis for the hypotheses
that will be discussed. In statistical terms, the two alternative explanations are:

1. All titin alleles other than 260 (or haplotype 1) cause DCM or
2. The 260 allele (haplotype 1) confers protection against DCM.

For the first explanation it has to be assumed that the DCM-causing mutation
is either very old, so the linkage phase has been lost, even for intragenic markers,
or that a DCM-causing mutation has occurred multiple times in the Doberman
breed. For the second possibility, it has to be assumed that there is a DCMcausing
gene elsewhere in the genome. In favour of the second possibility is the
condition that it requires the least number of mutational events. Our data do not
allow us to conclude as yet whether the DCM-causing mutation is in a gene
different from the titin gene or that the first and the second explanation are not
mutually exclusive.
There were 2 dogs in the DCM group that were homozygous for the 260
allele and 3 dogshomozygous for haplotype 1. In the DCM-free group, there were
five dogs that were not homozygous for the 260 allele or haplotype 1 .
There are several explanations possible for these exceptions. In the DCM group, it
is possible that dogs had developed DCM due to a secondary cause. Conversely,
dogs that were classified as healthy may still develop DCM at an age older than 9
years. Another explanation (under the protective allele hypothesis) for the five
non-affected dogs that are not 260 (haplotype 1) homozygous is that they are
DCM non-affected due to the absence of the pathological mutation.
In the DCM and DCM non-affected dogs described in this study, several
markers for DCM candidate genes and the DLA markers (mentioned below) have
previously been typed (Stabej et al. 2004; Stabej et al. 2005a; Stabej et al. 2005b)
and showed no association with one or the other phenotype, making it unlikely
that the partition of the REN252E18 is due to a selection bias different from the
DCM status.

SELECTIVE SWEEP – A LOCAL REDUCTION OF GENETIC VARIATION

The consecutive polymorphic sites in linkage disequilibrium (LD) in
haplotype 1 could represent a signature of a recent, local reduction of genetic
variation, commonly called “selective sweep” (Kim and Nielsen 2004). The high
frequency of haplotype 1 in the DCM non-affected group is suggestive of a recent
positive selection for this haplotype in the European Dobermann population. In
the light of our results, this would mean that haplotype 1 confers some kind of
protection against development of the prevalent DCM phenotype. Dobermann
breeders, recognizing the severity of DCM and sudden death, could have
enhanced the positive selection pressure on haplotype 1.
An example of a recent variant of a gene that has been subjected to positive
selection in a human population is the protective effect of the hemoglobin E
variant (HbE; β26Glu→Lys) against Plasmodium falciparum malaria (Ohashi et
al. 2004). Similar to the relative long region with LD of haplotype 1 in the
Dobermann, an extended LD surrounding the protective variant of hemoglobin E
was found (Ohashi et al. 2004).
Based on the current knowledge of the properties of titin and DCM, we
developed two working hypotheses explaining the emergence of a protective TTN
haplotype in the Dobermann breed. In the first hypothesis, DCM would be the
result of an autoimmune reaction against titin. In human DCM, a number of
observations suggest that autoimmune reactions underlie at least a subset of cases.
Ericksson et al. (2003) and Okazaki et al. (2003) demonstrated that an acute
immunological reaction to a viral infection can lead to the development of an
autoimmune reaction targeted against cardiac antigens. Although cardiotropic
viruses are considered to be the most common causative agent, in the majority of
cases it has not been possible to isolate a viral genome from the myocardium as
proof for this pathway of etiology in natural cases (Feldman and McNamara
2000). Taylor et al. (2004) discovered the crucial role of the HLA system in
autoimmune DCM. They demonstrated that transgenic mice expressing thehuman DLA-DQ8 molecule developed DCM spontaneously, in the absence of an
inflammatory or infective trigger.
Titin is already known to be involved in an autoimmune disease of human
and dog, myasthenia gravis. Myasthenia gravis (MG) occurs spontaneously and is
associated with autoantibodies against the nicotinic acetylcholine receptor
(AChR). Some of the MG patients (human and dog) also develop antibodies
against the titin (Shelton et al. 2001). The functional significance of the titin
antibodies is not yet known (Gautel et al. 1993; Shelton et al. 2001). To explore
the possibility of Dobermann DCM being an autoimmune disease, we typed the
DLA region (DQA1, DQB1 and DRB1) in the Dobermanns. We found no
differences in the haplotype frequencies between the DCM and the healthy group.
In fact, there was very little variation of alleles of the three genes in the breed;
88.7% of Dobermanns shared one haplotype, 8.75% the other most common
haplotype and 1.25% (2 dogs) had an additional two haplotypes (data not
presented). In addition, in collaboration with Dr. Skeie (Haukeland University
Hospital, Bergen) the sera of seven of our DCM Dobermanns were tested for the
presence of antibodies against the main immunogenic region of titin using
purified titin antigen MGT-30 (Gautel et al. 1993) and detected no antibodies.
The same MGT-30 antigen successfully detected the titin antibodies in dogs with
myasthenia gravis (Shelton et al. 2001). Therefore, we suggest that the sera of
DCM Dobermanns do not contain the antibodies against the main titin
immunogenic region, but we cannot rule out that antibodies against other parts of
the giant titin protein are involved. Since there was little variation in DLA
haplotypes and no antibodies against the MGT-30 titin antigen in the sera of
DCM dogs, we consider the autoimmune hypothesis of Dobermann DCM
unlikely.
In the second hypothesis, the protective form of TTN would compensate for a
DCM causing mutation in another gene. Ventricular premature contractions are
often detected prior to the development of DCM and ventricular tachycardia and
subsequent sudden death are characteristics of DCM also seen frequently in the
Dobermann. These observations suggest that disturbed calcium trafficking in the
cardiomyocyt is a possible primary cause of DCM in the breed. In human, genes
causing disturbed calcium trafficking (coding for mutated troponin T, titin,
SCN5A and ABCC9) were identified as a cause of DCM with heart rhythm
disturbances (Chapter 1, Table 1).
An interesting experiment supporting a protective role of titin was performed
with transgenic mice that develop severe DCM due to cardiac-specific overexpression
of the calsequestrin gene (CSQ). A strong mouse strain dependance of
the DCM phenotype was observed in mice over-expressing CSQ. Calsequestrin is
a sarcoplasmic reticulum Ca2+-binding protein, which sequesters the dependent pool of Ca2+. A genome wide scan in progeny from two mouse strains
that showed distinctly different DCM phenotypes identified two loci that were
significantly linked to cardiac function and survival (Suzuki et al. 2002). The titin
gene maps to the exact same region on chromosome 2 that showed strong linkage
to survival. Future studies will determine whether DNA sequence alterations in
the titin gene are responsible for the observed differences in the heart failure
phenotype (Suzuki et al. 2002).
Titin has a pivotal role in the physiology of the heart. In the heart, passive
tension primarily developed by the titin is a restorative force that acts in
opposition to external stretching forces that lengthen the sarcomere. The force of
the titin is also important in stretch sensing and modulation of the actomyosin
interaction (Cazorla et al. 2001; Labeit et al. 2003; Miller et al. 2004). Several
titin isoforms with different structural and mechanical properties are generated by
differential splicing of the exons coding for the I-band region. In the heart, two
principal isoforms have been described, a shorter (stiffer) N2B isoform and a
longer (more compliant) N2BA isoform (Freiburg et al. 2000). In heart failure
patients with DCM, the upregulation of N2BA isoform has been noted. It was
suggested that increased N2BA expression negatively impacts systolic function
but improves diastolic function by increased chamber compliance (Nagueh et al.
2004). It has also been proven that calcium affects passive myocardial tension in a
titin isoform-dependent manner. While calcium significantly increased passive
tension during and after stretch in the heart muscle that contained the N2BA titin
isoform, passive tension developed by the N2B isoform was calcium insensitive
(Fujita et al. 2004). Titin has therefore been proven to have a prominent role not
only in the healthy heart, but also in the diseased heart.
The association of the titin gene with DCM in the Dobermann described in
this article serves as a basis for further studies of DCM in dogs. Firstly, the
genotyping of TTN markers presented here in breeds with high incidence of DCM
other than the Dobermann will reveal the potential role of TTN in these breeds.
Titin gene DNA sequence analysis and studies of physiological properties of the
titin variants observed in the Dobermanns using the functional genomics tools,
will shed light on the question whether mutations in titin cause DCM or protect
against DCM.

Whole PDF here (they are many studies included, most without a positive result, but interesting - the Titin related study is no 7 :

igitur-archive.library.uu.nl/dissertations/2005-0415-200010/full.pdf
Last edited by BasKal on Fri Aug 20, 2010 2:52 pm, edited 2 times in total.
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Unread postby BasKal » Fri Aug 20, 2010 2:33 pm

Byeee Alin!!! :lol:
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Unread postby jotunheim » Fri Aug 20, 2010 2:48 pm

Thank's for the information Baskal - have already read those findings and more ...

I still would appreciate an answer to the questions I previously made.

Thank YOU ...

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Unread postby Weinberge » Fri Aug 20, 2010 4:43 pm

BasKal wrote:Byeee Alin!!! :lol:



before to go in your exotic island , you broken my nervs again with your TITIN gene, with your 260 aleles or your REN252E18454518541214484187 JDSHJSJDHJDD GENE.

Any normal man will nothing understand from that Doctor Doctorandum theory and suppositions when now, nobody know exactly the genetic of this ill.
In reality that ills was multiplied by 20 years day by day and still are multiplied every day with a large international participation.
All these years was destroyed, losted and infected the unique antidot =healtly lines.

The rest are theory, false excuses (always ills and DCM was all around ) and ipotheses which NOTHING WILL SOLVE! Because theory nothing solve and in first DR page result clear, all the breeders keep walking on their way like till now.

Show me ONLY ONE show breeder mating with a not soo beautiful stud but healtly and longevive in pedigree 3 generations !

ONLY ONE ! :lol: :lol:

I think if God help me I will be the first. But I am not a breeder.

Happy holidays in your exotical island !
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Unread postby AnneStruvePhotography » Fri Aug 20, 2010 5:03 pm

BasKal wrote:My friend - if she is alive due to thyroxin then she havent the typical dobermann DCM. A dog cannot be diagnosed with DCM and live above 6 months even with advanced cardiological medication. Thyroxin only helps in her lacking of the correct quantity in thyroid hormones. It is a very cheap and commom drug, but it never leghten the life of a real DCM case. This case doesnt look a typical case.
The presense of a thyroid problem clouds this case - if she had a clear DCM condition it would be more interesting.
I think that the only way to really help dobs is to raise funds for genetic research - and the developement of a genetic test. Also we must have a clearing of the mode of inheritance. This will solve the problem for good.
Till now I had found only one study that pointed to a particular possible gene. But no test was developed and nothing was heard from them.


@BasKal
you doubt that my dog has DCM ????

I am the owner of Esyndia v Bismark. http://www.working-dog.eu/dogs-details/ ... 0Bismarck/
ONLY and only because of Esyndia´s pedigree ( inbreeding del Citone) we flew to Munich to the DCM Doberman Study http://www.tierkardiologie.lmu.de/besit ... ojekt.html

After the first minutes - on the 5 min. ECG, I was asked by three different cardiologist, how old my dog is. At this time her ECG has shown a lot VES. We were really shocked.
The first heart examination result has knocked us KO. We felt as if we fell into a deep hole. It was so sad for us. Esyndia was only 24 month old. Munich gave us not much hope for her

http://www.annestruve.com/ekg_esyndia_v_bismark__1.html

After ca 3 month the heart sonography examination showed the first abnormalities - and now 9103 VES!
In 3 month from 6289 VES straight up to 9103 VES!
http://www.vom-bayrischen-loewen.de/cms ... 6/EKG2.jpg
Munich gave us no hope! The cardiologist gave us 2 different heart medications for her.
We have tried to set her on these heart drugs. But every time she was not well after taking it, so we have discontinued the medications.

We were so sad. We had to explain to our son (at the time 12 years old) that his beloved dog could suddenly die any time..........This was a very hard time for all of us.....

The last blood test result ( Munich) showed that her thyroid level T4 was very low, but still low in the reference value.
The cardio-vets in Munich said, there everything is OK with her thyroid level, but we don´t believe them.
We looked on the I-net for more information about hypothyroidism and heart. We found Jean Dodds informations about hypothyroidism.

Dec 2006 we set her on thyroid medication - Thyroxin.

After 3 month we went again to Munich with the following holter result
The VES went down in 3 month http://www.annestruve.com/ekg_esyndia_v_bismark_.html

Munich were very surprised about the result. They said there is no medical context between heart and hypothyroidism. We have spoken with so many cardiology vets, they think contrary, -there is an medical context between heart and hypothyroidism.
In the human medicine is it known for so many years.

Esyndia is living since 4 years only with thyroxine and is doing very very well. She is not taking any heart drugs!! Her heart is beating normally and regularly.

The fly to Munich is a really big stress for her, so we have decided not to fly with her any more only for the check up. We are here in Spain for the regular heart check


To all the breeders here. Please take a dog with is regularly heart tested result,- with a long-lived ancestors in the pedigree to breed with. Don´t runs all always to the next IDC winner.

Please pay attention to the selection of your breeding dogs. Short life x short life = short life
Only one known DCM dog in the pedigree gives many short - lived dogs.
There are too many broken hearts worldwide.........
Last edited by AnneStruvePhotography on Fri Aug 20, 2010 5:08 pm, edited 1 time in total.
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Unread postby AnneStruvePhotography » Fri Aug 20, 2010 5:03 pm

BasKal wrote:My friend - if she is alive due to thyroxin then she havent the typical dobermann DCM. A dog cannot be diagnosed with DCM and live above 6 months even with advanced cardiological medication. Thyroxin only helps in her lacking of the correct quantity in thyroid hormones. It is a very cheap and commom drug, but it never leghten the life of a real DCM case. This case doesnt look a typical case.
The presense of a thyroid problem clouds this case - if she had a clear DCM condition it would be more interesting.
I think that the only way to really help dobs is to raise funds for genetic research - and the developement of a genetic test. Also we must have a clearing of the mode of inheritance. This will solve the problem for good.
Till now I had found only one study that pointed to a particular possible gene. But no test was developed and nothing was heard from them.


@BasKal
you doubt that my dog has DCM ????

I am the owner of Esyndia v Bismark. http://www.working-dog.eu/dogs-details/ ... 0Bismarck/
ONLY and only because of Esyndia´s pedigree ( inbreeding del Citone) we flew to Munich to the DCM Doberman Study http://www.tierkardiologie.lmu.de/besit ... ojekt.html

After the first minutes - on the 5 min. ECG, I was asked by three different cardiologist, how old my dog is. At this time her ECG has shown a lot VES. We were really shocked.
The first heart examination result has knocked us KO. We felt as if we fell into a deep hole. It was so sad for us. Esyndia was only 24 month old. Munich gave us not much hope for her

http://www.annestruve.com/ekg_esyndia_v_bismark__1.html

After ca 3 month the heart sonography examination showed the first abnormalities - and now 9103 VES!
In 3 month from 6289 VES straight up to 9103 VES!
http://www.vom-bayrischen-loewen.de/cms ... 6/EKG2.jpg
Munich gave us no hope! The cardiologist gave us 2 different heart medications for her.
We have tried to set her on these heart drugs. But every time she was not well after taking it, so we have discontinued the medications.

We were so sad. We had to explain to our son (at the time 12 years old) that his beloved dog could suddenly die any time..........This was a very hard time for all of us.....

The last blood test result ( Munich) showed that her thyroid level T4 was very low, but still low in the reference value.
The cardio-vets in Munich said, there everything is OK with her thyroid level, but we don´t believe them.
We looked on the I-net for more information about hypothyroidism and heart. We found Jean Dodds informations about hypothyroidism.

Dec 2006 we set her on thyroid medication - Thyroxin.

After 3 month we went again to Munich with the following holter result
The VES went down in 3 month http://www.annestruve.com/ekg_esyndia_v_bismark_.html

Munich were very surprised about the result. They said there is no medical context between heart and hypothyroidism. We have spoken with so many cardiology vets, they think contrary, -there is an medical context between heart and hypothyroidism.
In the human medicine is it known for so many years.

Esyndia is living since 4 years only with thyroxine and is doing very very well. She is not taking any heart drugs!! Her heart is beating normally and regularly.

The fly to Munich is a really big stress for her, so we have decided not to fly with her any more only for the check up. We are here in Spain for the regular heart check


To all the breeders here. Please take a dog with is regularly heart tested result,- with a long-lived ancestors in the pedigree to breed with. Don´t runs all always to the next IDC winner.

Please pay attention to the selection of your breeding dogs. Short life x short life = short life
Only one known DCM dog in the pedigree gives many short - lived dogs.
There are too many broken hearts worldwide.........
AnneStruvePhotography
 

Unread postby BasKal » Fri Aug 20, 2010 5:38 pm

Well, noone can have a vacation with peace....

No, I dont doubt that your dog has a condition which is similar to DCM (an enlarged not fuctional heart).
I tried to investigate the genetic source - nothing else.
I also said that the condition was atypical - I think that is the same your doctors said...

"Munich were very surprised about the result. They said there is no medical context between heart and hypothyroidism. We have spoken with so many cardiology vets, they think contrary, -there is an medical context between heart and hypothyroidism.
In the human medicine is it known for so many years.

Esyndia is living since 4 years only with thyroxine and is doing very very well. She is not taking any heart drugs!! Her heart is beating normally and regularly."

The fly to Munich is a really big stress for her, so we have decided not to fly with her any more only for the check up. We are here in Spain for the regular heart check "

And... is she alive?
This is higly atypical for DCM.
Offcourse hypothyroidism is a genetic disease too - one which all we must have under consideration...

End of storry.
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Unread postby Ferdinand » Fri Aug 20, 2010 6:21 pm

Adlercrest Hessian was diagnosed with DCM at only 18 month of age and he lived without medication up to 7 years. Hessian was out of Danzig v. Adlercrest and Kira v. Norden Stamm. He was breed 2-2 to Ebo vd Groote Maat.
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Unread postby jotunheim » Fri Aug 20, 2010 6:42 pm

Baskal

-->
1. I know the pedigrees ...I am a pedigree freak in reality.

but that doesn't explain HOW - which dogs are you looking at etc.

3. CAYA Cirrus is from Nike, Bitten - a younger brother of Alabama.

Didn't understand that it was CAYA Cirrus you were refering to

4. My female produced one dog who died early (7) to another male unrelated to Nike, so she could be a DCM gene heterozygous carrier considering her family history - at least a brother with DCM, her father lived to 11 and his offspring was generally long lived. But her maternal grandsire died at 8 - sudden death.
Her Nike offspring doesnt have DCM and they are allready seniors.
I think that Nike helped the situation.

have you had them tested ?

Why is she a carrier - Why isn't Nike a carrier ? In Regard to Nike, as far as I can see/understand his pedigree, he has several ancestors on both parents sides that died prematurly

<--

Please have the curticy to answer the above questions - Thank You
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