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Our Dogs Correspondence July/August 2017

2/9/2017

2 Comments

 
Our Dogs Breed Notes 21.07.17 by Tim Hutchings
I think we can all be pleased that our puppy classes are so much better filled these days than they have been in recent years. If you want my personal opinion, I think that a lot of the 'bounce back' can be attributed to the fact that most breeders now taking a very sensible and pragmatic approach to the challenges of Juvenile Kidney Disease. I am certain that we went through a period when breeders were either too scared to breed at all, or when outcrossing at all cost appeared to be taking over. Bearing in mind how much hysteria was whipped up over the issue by folk who, quite frankly, should have known better, I'm not surprised that breeders responded in the way they did. However, my current take on it is that the vast majority of breeders now share the same view, that JKD is definitely something which we need to be mindful of but we should not completely over-react to it. There is absolutely no doubt that it has been with us since the breed was created and, dare I say, in the pre-internet age I'm sure that cases were conveniently swept under the carpet.
However, I do honestly believe that the incidence remains low and there are definitely other conditions which are far more detrimental to breed health as the last KC Breed Health Survey proved. I have said it before, and I will say it again, breeding dogs is like spinning plates. There are many variables that you need to be keeping an eye on and the knack is to balance out all of the competing issues when planning your matings. Unlike some folk who seem to spot dark ulterior motives everywhere (what kind of sad, paranoid world do they live in?).
I absolutely believe that the vast majority of Boxer breeders in this country are genuinely trying to breed the healthiest and most typey Boxers that they can. No breeder in their right mind wants their phone ringing with problems from past litters which could have been avoided and I find it hugely insulting when anyone suggests differently. However, very pleasingly, I see that the more hysterical internet contributions on the topic of JKD attract very little attention or comment these days. Boxer breeders in the UK are a down to earth group and they are certainly sensible enough to spot (and ignore) any troublemakers. Thankfully, there are very few (if any) troublemakers in the current population of exhibitors who are still actively involved in showing and breeding their Boxers in this country. I don't think any of us who are still living with the daily challenges of showing and breeding take very kindly to be lectured, hectored and sometimes abused by people who gave it up years ago. I know I don't.
In reply - published in Our Dogs Letters
​I write at the request of the small international group of Boxer people (boxerjkd.com) who have dedicated much of their time over the last few years trying to understand and find a way through the inherited kidney disease problem that has come to attention in the breed. They are appalled by the disgraceful and demeaning comments directed at them by the Breed Notes correspondent who has also consistently sought to diminish and discredit the evidence on JKD from the start. We feel that a rebuttal that will put the whole problem into perspective is needed.
Nearly 40 years ago at a London and Home Counties Boxer Chatter event, a veterinary neurologist, Ian Griffiths, and I were describing an inherited progressive axonopathy (PA) that had emerged in Boxers when ago one famous Boxer breeder of the day stood up urging that PA was not so important and did not merit the attention it was being given. She was shouted down by the rest of the audience. This was at just one of a series of the open meetings on the subject organised by all the breed clubs around the country, not only to describe the disease and its inheritance but also to show explicit film of the affected dogs. Everyone was very hot on the subject. Ultimately a very tough breeding control scheme was adopted with extensive breeder input; it was a total success. We no longer have PA. This action started a movement to deal with other Boxer health issues that came to the fore. This took us through the heart conditions aortic stenosis (AS) and cardiomyopathy (CM or ARVC) with these also being reduced or eliminated from the show section of the breed. But here we are now with an inherited lethal kidney disease and the spirit of that breeder of 40 years ago rises again. How is it in the new era, when everyone is aware of genetics and inherited disease in dogs, there is still such a lack of understanding?
We are told all we need to do is be mindful of the situation. What on earth does this mean? The health committee and, I am afraid, Breed Council have advocated the pedigrees of affected cases should not be made public. So how is any one to be mindful? Were it not for the boxerjkd.com publication of JKD pedigrees, Boxer breeders would have had to rely on treacherous ringside gossip and the like. I think boxerjkd .com has done very well by the breed both in this country and overseas.
And then there is criticism of hysteria about JKD on Facebook. There was no Facebook 40 years ago but with PA there were masses of very upset people. But they were mainly show breeders, because the non-show section did not follow the dog papers or club news and so would barely have heard of the disease and they had no way of discussing it either. Odd cases of PA would have remained odd cases. Whether these folk knew it or not their fate was in the hands of show breeders and this was to prove well-placed. But now we have a turn around with non-show people having the larger voice, on Facebook, and once the kidney disease was mentioned there, everybody was aware. New cases were reported in this medium, and so the movement for action took off with some show people leading the way. And, through Facebook, which is the only medium that is not tightly controlled, JKD quickly became recognised as a major international problem despite the lack of concern expressed in the dog press and the absence of any open meetings. Was this hysteria? It was real. We could not wish it away. Something had to be done and the only group to take it up were the boxerjkd.com members, greatly aided by this public support and also by many concerned show breeders. Cases were reported and pedigrees published along with carefully-assessed breeding guidelines. But do we have support from the Breed Notes correspondent? No, we are considered merely as trouble makers. Are we now back to the ignorance and poor thinking of 40 years ago?
But why the turn-around in thinking about inherited disease? My answer, based on genetical issues rather than political, is that with PA there was a neat recessive inheritance where on average 25% of puppies in affected litters suffered the disease. Everyone could understand this. But now with JKD, as also also with ARVC, there is the problem that only a small proportion of the genetically affected cases actually develop the disease and this leads to disbelief in the severity of the problem. So is JKD really a major breed problem? Is it worth bothering about? Yes it is, because it is not just the incidence of affected pups that we have to think about, horrible as the disease is (photos) but the far greater incidence of carriers and undetectably affected dogs. These will greatly increase in frequency if we continue to breed from JKD-producing animals. This is how JKD is to be found everywhere in the world; it is an international problem for the breed. I suggest the lack of perception of JKD in earlier days was not necessarily a hide-it-under-the-carpet thing’; the kidney disease was simply not recognised as inherited – until mass inbreeding in the UK and over-use of certain dogs brought it to light.
So the bottom line is that the only means at our disposal for dealing with JKD is NOT to breed further from animals that have produced it (and widen the stud dog options). To do otherwise only propagates the disease gene. Such selective breeding is aided by the JKD pedigrees published by boxerjkd.com, but probably limited by the withholding of other pedigrees by the Health Committee.
The breeding recommendation was made by boxerjkd.com, and do not forget that members of the group have successful breeding and showing experience with Boxers here or abroad, and have many years’ experience on health committees. Moreover, three of us are professional research geneticists. And, for my part and blowing my own trumpet, I have probably worked with more new mutations and totally novel inheritances than anyone else on the planet. Furthermore, none of us is linked to any breeder group that could be deemed to risk personal bias, and indeed I felt I had to drop all Boxer breeding to deal with what I saw as the emerging huge JKD problem.
There is, as everyone knows a last ditch effort to find the location of the gene for JKD. This attempt uses a very different approach from all other methods and has had enormous backing from Boxer breeders around the world. It is funded by the former Council of Docked Breeds and notably also by The Kennel Club. I pray that it has success, but believe me, if it does there could then be serious panic notably in the UK where I expect the incidence of carriers in UK populations might be frighteningly high. So, again, it would be wise to apply some simple selective breeding now to reduce the incidence of carriers as much as possible before any gene test comes into play.
What is needed in effect is an end to all this opposition and unwarranted criticism but instead full support from all, including our Breed Council, both for the efforts of boxerjkd.com to help breeders, and the research to find the location of the gene.
Bruce Cattanach
Tim then replied in the the Breed Notes 
When I gave some opinions on JKD in a recent column I almost ended my remarks by saying that I fully expected to be immediately pilloried and screamed at as a result. I see that, entirely predictably, this has now happened yet again. It really does bother me that we have some folk in our midst who simply cannot abide anything other than complete, unquestioned agreement with their theories on this topic. In the latest outburst I even see that some poor un-named person from 40 years ago is still being attacked for holding a different opinion on a previous health issue. With the topic being made so toxic, it is hardly surprising that very few people are actually prepared to express their own views on JKD since they know that they will be immediately attacked for doing so. I also find it very depressing that the very vocal actions of a tiny minority make it seem to the outside world that Boxer people are at war. I don't think anything could be further from the truth. My experience is that the overwhelming majority of Boxer exhibitors in this country actually rub along with each other pretty well and very sociably. The atmosphere at shows is really good and there is usually a good exchange of views, conducted in a civilised manner at the ringside. We don't all agree with each other but we can respect each other's opinions. The keyboard warriors don't ever take part in that since we seldom, if ever, actually see them at shows. Having now 'dangerously' expressed some more opinions (which I think I am perfectly entitled to do after more than 30 years in this breed) I shall now set my watch and wait for the next onslaught but in the meantime I will continue to enjoy the shows and the many friendships that are an integral part of that enjoyment.

​BoxerJKD in reply 
It seems that our attempts have failed to convince the Boxer Breed Notes correspondent that a few hundred Boxer deaths from Juvenile Kidney Disease (JKD) do mean something. He would still deny us opportunity to present the scientific evidence simply because it does not agree with his preferred opinions and beliefs, these based on his lack of understanding of the genetics and development of the disease. This should not really matter but for his almost total control over the UK Boxer media and the influence that this has. So let us try again.
The main issue seems to be the low incidence of the disease relative to what might be expected with a recessive gene inheritance. He does not seem to understand that the kidney damage is variable and there has to be almost total kidney failure before the symptoms appear. A low incidence of dogs affected with this disease is therefore to be expected, but this does not mean the disease is not inherited. Perhaps also part of the problem is that some of the JKD pedigrees that we (boxerjkd.com) have published don’t show enough information to illustrate the inheritance fully. So let us a try a mini-step further with an example of an annotated pedigree giving more information on the disease transmission. The pedigree shown is a real pedigree, if without dogs’ names, but it indicates more forcefully the capacity of key dogs to transmit the gene. The transmission criterion used is three or more progeny that ‘have produced affected cases to different partners’, whether or not the key dogs have produced cases themselves. Parents that have produced JKD are routinely shown in blue. The previously empty pedigree is now filled with evidence of JKD. This can be done for all the published pedigrees.
Boxerjkdf.com is not peddling myths and beliefs to be debated, but presents actual genetic evidence, and we continue this with the new molecular studies. The Cambridge work, funded by the Council for Docked Breeds and The Kennel Club has received the support of Boxer breeders and owners around the world with the result that:
- over 1000 swabs for making DNA have been obtained;
- a survey of microsatellite markers (anonymous bits of DNA) has shown many to be highly variable, with numbers of different forms, which makes them ideal for gene screens ;
- the very first screen has indicated one particular chromosome as the location of the gene for JKD. Two markers on this chromosome appear to be significantly co-inherited with the disease phenotype, this incidentally supporting the inheritance of the disease;
- consistent with this, a dog suspected of being homozygous for JKD (two doses of the gene) was found to be homozygous for the marker (two doses of the same microsatellite form);
- it has further been found that Boxers of different national origins can have different forms of the microsatellite marker associated with JKD. The co-inheritance is therefore loose. Better/closer markers are therefore being sought.
So, as of now, everything fits perfectly and in a single step we have got as far attained with the heart disease cardiomyopathy (ARVC) with its loosely co-inherited striatin marker; we know the chromosome on which the gene for JKD is located. As with ARVC we have still to identify the gene itself; but with JKD there are several candidate genes in the region. Finding the actual gene will be the hardest part of this work, and everything to date has to be checked and double-checked, but these findings represent a major step forward in understanding and resolving the very real JKD problem of Boxers.
Bruce Cattanach, on behalf of boxerjkd.com
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2 Comments

Publication in Vet Times

2/6/2016

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Addition of a new publication in the Vet Timesunder the Publications section
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Norwegian case is added 

29/12/2015

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Norway 8 has been added. Sire is the same as Sweden 43
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New Pedigrees added to Denmark and Norway

10/12/2015

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Another two pedigrees have been added to the website. The first from Denmark - Case 2 and then another from Norway - Case 7 
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New cases added to UK and Norwegian lists

2/12/2015

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Two more pedigrees of confirmed Boxer JKD cases were added to the website today - one from Norway (Norway 6) and another from the UK (UK 174). The Norwegian case was confirmed by diagnostic tests, Imaging and also a Post Mortem. The UK case was confirmed by diagnostic tests and Imaging. Both pedigrees contain a number of carriers in their pedigrees. The Norwegian case has both continental and UK families. Both of the newly published cases also contain siblings to known carriers in their pedigrees. Both these new cases strongly support a recessive inheritance pattern
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The Confusing Picture of Boxer JKD - Bruce Cattanach

7/11/2015

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The following article was written a few weeks ago for the American Boxer magazine, Boxer Daily, and should appear in the December 2015 edition.  It is printed here ahead of time with the permission of the Boxer Daily editor.
 
It is clear from anecdotal evidence that kidney disease has existed in Boxers for many years but the frequency has always been low, diagnosis has been uncertain, and there has been only dubious evidence that it might be inherited.  It has ‘appeared’ and ‘disappeared’ in several Boxer groups such that with the knowledge that kidney failure can be caused by external agents, it is hardly surprising that many breeders have been sceptical about the disease having a genetic basis.  Even as evidence is currently accumulating, uncertainty and confusion dominates thinking.
Here I summarise this background history as I have seen it, leading on to the more definite evidence that we have today.
Background
I have been made aware of kidney disease in Boxers a number of times over the past 30 or so years but up until about 5 years ago I too was not truly convinced it was inherited.  I first met a kidney disease in Boxers at the time of progressive axonopathy (PA) in the early 80s.  That delightful lady, Leslie Boyle, came to me seeking advice over a couple of litters that contained show age puppies that were suffering from kidney failure.  The two litters were related; both were inbred on one of Leslie’s major dogs.  The evidence for the condition being inherited was there, but limited, and only loosely suggested that a recessive gene might be involved.  However, Leslie accepted that there was a risk that should be avoided and took it seriously enough to close the line.  Sadly, she died a few years back and never learned that she had made the right decision.
No more cases appeared and I thought that this might be the end of the matter but early in the 2000s I learned that Sweden had been picking up kidney failures in Boxers, with the Swedish Kennel Club immediately banning parents from further breeding.  Some of these dogs were British-bred.  On enquiry, I was supplied with the pedigrees, but they showed a mixture of lines and nothing to indicate to me that the condition was really inherited.  I was even less convinced when I learned that Sweden was recording kidney problems in a number of breeds at the same time.  This did not sound like a genetic problem.
Not long after I was notified that a small group of American Boxers were suffering kidney problems.  Obtaining the pedigrees I saw that some showed inbreeding on one notable stud dog of the day, but seeming outcrosses had also produced the disease.  Again, a genetic effect seemed possible but a bit dubious, yet there was enough concern among owners that blood samples were collected and sent to Dr Lindblad-Toh at the Broad Institute to instigate a scan to find the gene; and funding was obtained in the name of one unfortunate dog, Suky – the Suky story.  The amount of material was admittedly limited but no indications of a responsible gene were detected.  This event brought some further hints of kidney disease in the UK to my attention, but again a genetic effect could not be seen.  However, kidney disease was clearly around as internal medicine specialist Marge Chandler of Edinburgh University was able to collect some 30 cases within a short period of time.  She published a detailed paper in 2008, but, as before, the pedigree evidence did not stretch to establishing a genetic cause.  Shortly after, Sheila Cartwright of Tyegarth Boxers, reported early observations of Boxers suffering a range of kidney problems to Breed Council, but nothing came of this.
But finally, when a general practice vet asked me to speak to one of his clients, Sharon McCurdy, who was experiencing numbers of kidney cases in her breeding, I found I was faced with indisputable indications that the condition was indeed inherited. The evidence that gradually accumulated was as follows:
Genetics and breeding
  • The first pedigrees provided by Sharon McCurdy showed close inbreeding on one dog, immediately suggesting an inherited basis with a recessive gene likely to be involved.
  • This conclusion was then supported by further pedigrees presented by other breeders.  All showed the same inbreeding on the same dog.  A family group was evident.
  • But cases were found involving the key dog’s ancestors and relatives.  Inbreeding on them was producing the disease.  The family group was thus much larger and it seemed that the main core of British breeding was involved.
  • Cases were then detected in outcrosses to foreign dogs, seemingly disputing a recessive gene inheritance.
  • But, as already indicated, kidney disease had been found in Boxers elsewhere in the world and when all the pedigrees internationally were considered together one found that the foreign dogs that had produced the kidney disease in the UK came from families that in their own countries had produced the disease.
  • In all cases that could be studied there was therefore either inbreeding or a doubling up on the disease from both sides of pedigrees.  The pedigree evidence therefore fully supported the recessive gene inheritance and further indicated that the same gene was responsible for kidney disease in Boxers world-wide.
  • There were several problems with this conclusion though.  With a recessive gene, 25% of puppies in affected litters should be affected, and while we have as yet little evidence on the actual frequency, it is abundantly clear that the incidence must be very much lower.  For example, extensively-used males often produce no more than a single affected pup.  There was also the finding that far more bitches are affected than dogs, and that age of onset is not a crucial factor for diagnosis.  Further understanding of the disease itself was needed.
The disease
  • The kidney disease has most typically been seen in young, juvenile Boxers (less than 3 years of age).  Hence the inclusion of the term ‘juvenile’ in naming the disease.
  • For diagnosis in Sweden and America detailed histo-pathology has been the absolute requirement to define what is known as ‘renal dysplasia’. Hence the name they use, juvenile renal dysplasia (JRD), or renal dysplasia (RD).
  • Other names for the disease, such as progressive nephropathy, chronic renal failure, Ask-Upmark syndrome, polycystic kidney disease and others have also been applied simply to describe what was found on pathology.
  • In the UK, diagnosis has been based simply on symptoms and standard blood and urine analyses, but with the critical rider that there must be family evidence of the disease being inherited.  Hence, application of the broad, non-specific name, juvenile kidney disease (JKD) to denote the inherited kidney disease we find in Boxers.
  • With seemingly different diagnoses, it has not been clear to researchers in the past whether there were several different kidney diseases within the breed or only one with different expressions or effects.
  • However, as all these conditions appear to be occurring within the same family groups, an important conclusion from the pedigree studies is that most, whatever their diagnostic names, are merely manifestations of the single kidney disease we here call JKD.
Different disease manifestations
  • JKD is found far more frequently in bitches than in dogs, the difference possibly being as great as 10 : 1.  How could this be?  JKD commonly leads to urinary tract infections (UTIs) such that UTIs commonly signal developing JKD.   The urinary tract is much shorter in bitches and therefore more prone to infection than in dogs.  The incidence of detected kidney disease is therefore expected to be higher in bitches than in dogs.
  • Limited studies have suggested that the age of onset of JKD may actually be much earlier in dogs than bitches and may also be more severe, such that affected individuals may be ‘lost’ as fading puppies.  The cause of death of such dying pups is seldom investigated but several dying MALE pups of suckling age have been found, with subsequent kidney pathology showing damaged kidneys.  JKD may therefore be responsible for some fading puppies.  If males are more likely to die early (and be missed as fading puppies), it follows that most later-occurring cases (juvenile or older), which are the actual diagnosed cases, will be bitches.
  • JKD has also been detected following stress, notably in bitches during pregnancy or following caesareans, when deaths attributable to JKD have been diagnosed.  Again, as with UTIs, this enhances JKD detection in this sex.
  • JKD has tended to be defined by its early, juvenile age of onset.  The consequence has been that later onsets of kidney failure (at 5 or more years of age) have been attributed to other causes and old age itself, rather JKD.  However, JKD has recently been convincingly diagnosed by pathology in older Boxers showing indications of kidney failure.  There is therefore the possibility, or even expectation, that some individuals with mild degrees of JKD may go through their full lives without disease detection. 
  • All of the above occurrences will contribute to the observed shortage of affected cases relative to the 25% expected, but a major factor is the structure and function of the kidney itself; it has spare capacity such that damage cannot easily be detected.  In fact over 70% of the capacity of the kidney must be knocked out before any symptoms of kidney failure appear.  This immediately suggests that if JKD damage is not substantial, affected dogs will not experience the actual disease.  In total therefore, a first effect may occur in fading puppies, notably in males; a variable degree may occur in juveniles; but at later ages the disease may only occur when triggered by UTIs or other stress events, or even old age; and it is almost certain that severe damage is never reached in many dogs, such that those with minor levels of effect may be symptom-free and live outwardly normal lives until dying from other causes.  It is therefore essentially expected that the frequency of JKD cases will be less than the 25% expected with a recessive gene.  Genetically affected but outwardly healthy dogs will exist in our breeding populations.
 
Summation
It is clear from the above that JKD has been with us for years but has been largely unnoticed because of its partially hidden nature.  Here, I have addressed only the biological reasons on how JKD is largely missed, focussing on the difficulties of recognising and understanding the disease and its expression.  Much of the background evidence is limited; there is a need for research upon the disease itself.  And to this end a UK specialist in internal medicine has agreed to help the breed with this difficult disease.  The aim is to seek hard evidence that some fading puppies may have JKD and also older, post-juvenile dogs.  Both aspects will require UK breeder cooperation in providing the needed material, and to this end appeals have already been placed in the media requesting the help of breed clubs and individuals.  The results will not only aid a better understanding of the disease but provide essential information for the operation of valid scans to find the responsible gene that are running In Norway, Sweden and America.  Here is the chance to for breeders to obtain answers for the many problems they see with JKD.
Information source
All available pedigrees are to be found on the www.boxerjkd.com website together with breeding guidelines based on currently available information.  The pedigrees are being updated as released by owners.  References and links to published work are also provided, as also basic information on the disease, its diagnosis and treatment.
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Updated Diet information page

26/10/2015

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The page on diet has been updated - there is still work to do and would love some input from owners who have tried various diets for their Boxers that have been diagnosed with JKD
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Claudio Brovida - Research thesis

25/10/2015

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Addition of the Research Thesis of the Italian researcher Claudio Brovida - there is an abstract in English but the thesis is published in Italian. We have provided a translation of the thesis obtained by the use of Google Translate
Abstract
Renal dysplasia is defined as a disorganized development of the renal parenchyma, consequent to an anomalous differentiation of the nephron’s various segments. The final diagnosis is based on the correct histopathology evaluation of the kidney and the finding of the typical structural anomalies. In Boxer dogs, renal dysplasia, also defined juvenile nephropathy, has been described, however the published material on this topics is still limited and different theories about the development of this disease are proposed. The author, starting from the evaluation of a group of cases of juvenile nephropathy, that he diagnosed, by kidney biopsy, in a period of five years, planned a prospective study, on a population of young Boxers, aging a mean of 12 months, which have been evaluated during one year of time. Starting from a group of 120 investigated Boxers, he included in the study 84 dogs on which basic haematology, biochemistry and urinalysis tests have been performed. The consequent data, statistically evaluated, have been analysed to envisage elements that could help to define an early detection of signs of renal damage, that may be associated to a juvenile nephropathy, in these Boxer dogs. 

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Frequently Asked Questions

21/10/2015

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Added a FAQ section - please ask your questions through this Blog and we will attempt to answer them as soon as possible
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Research Proposal

17/10/2015

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Updated website with a plea to breeders to support a research project with a UK Vet School. This research requires the submission of post mortem and fading puppy tissues. 
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