Vet check question, during a vet visit should the vet pull a 3 month pups legs back to check hips - Page 3

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Hundmutter

by Hundmutter on 30 May 2016 - 19:05

Susie: absolutely agree. Don't know about the genetics
professors who taught Bubba, but Willis had absolutely
no reason NOT to update his work, if there had been good
grounds. Also with him it really wasn't about ego, as I
suspect it may have been with some others; he cared so
much for our breed, and about HD in ALL affected breeds
(and many of the large breeds' communities held him in
the same degree of esteem that we did in Shepherds), that
he genuinely wanted to do anything he could to help reduce
it.

Of course, as far as Bubba and America is concerned, one
could ask questions about why OFA took the route it has,
with the gradings it has, when it could have had a scheme
which sat easier with other countries' way of reckoning hip
status and made it less difficult to work out the comparisons.

by Swarnendu on 30 May 2016 - 22:05

First, to answer OP's query:

I wouldn't let my THREE MONTH OLD pup to go through that experience because, whether or not the procedure would tear a ligament or dislocate a joint, that rather scary (in the pup's opinion) incidence can cause a lasting, even unrecoverable psychological damage to a pup of that particular age group.

Now, a layman's view on the genetic war:

It is a fact that X-RAY, done at the right age, is still the best option for diagnosing HD, but it's also a fact that neither it can assure non-occurance of future HD, nor it can assure non-occuranc in the descendants.

Now, inspite of the b/s (as per Bubbabooboo) theory of Polygenentics & Dominant, Intermediate, Recessive genes and their pairings or the b/s (because that also doesn't help to determine the genes) theory of Incomplete Inheritance, no person in a sane mind would want to breed from a parent with bad hips OR a parent with excellent hips but a history of abundance of HD in the progeny. So, availability of a reliable database is extremely important.

And, though two Wongs would never be able to make a White even in Scandinavia, I am, not even in my dreams, suggesting that there is no environmental influence on HD OR smoking doesn't cause lung cancer, but.......

A survey done a decade ago in my country had shown that around 70% of people with lung cancer were either passively or activity exposed to smoking.

Another completely unrelated survey said 70% of the total population, either passively or activity, were exposed to smoking.

Now do your maths...

Here's another hypothetical survey. In a country where smoking is not allowed, a survey would state that 100% of the people affected with lung cancer were never exposed to smoking.

And, then the ban will be lifted !!! 😉😉

bubbabooboo

by bubbabooboo on 31 May 2016 - 00:05

Then there is the SV, OFA and all of the phoney baloney experts looking at x-rays which are simply a hard to observe phenotypic trait and do not reflect underlying genetics at all since we don't have a clue what if any genetic factors influence HD, DM, or a host of other maladies in the GSD that were created by doing exactly the same thing .. judging quality, health, and vigor based on appearance. The more likely scenario is what is typical in nature .. the outcome of an individual and how healthy they will be is 10% genetics, 40% genetics X environment and 50% pure environment. Even with simple recessive and single gene traits there will be some who should be affected that won't become ill and some that do not have the genes at all that will get the disease as a result of random mutations or environmental effects. That is why identical twins raised in the same home will often have different diseases and medical conditions late in life when environment has had time to change there genetic expression. Genetic expression is not locked ... it changes and adapts to environment to accomplish the one important goal of every species .. survival. Soon after fertilization the egg starts being altered by environment and in some cases the genetic alterations began before the mother was even born. All the SV and OFA with their hip scoring and phenotypic selection are doing is trying to select away from one problem with a ridiculous system while unwittingly selecting toward other problems using a flawed and simplistic approach. The SV and OFA are still trying to get on the Mendelian genetics boat long after that ship sailed and fell off the edge of the earth.

Hundmutter

by Hundmutter on 31 May 2016 - 07:05

Whoa, pull back hard on your first sentence ... when an X ray is taken of hips and presented to a Panel for assessment, (whichever Scheme is in use), they see what WE see if an X ray is put up on here. Enny fule no that in really bad hips the heads and sockets will proclaim that they are 'out of joint' long & loud, the panel of experts has the advantage of understanding the grades of luxation of the various angles etc, but they are NOT "looking at X rays which are simply a hard to observe phenotypic trait" because you don't 'look' for genes like that ! In reading X rays, you are looking for the degree of expression of the genetic make-up, which is different.  Nothing to do, in yer individual (X rayed) dog, with how heritability works.

You can call it 'post-Mendalian' or something if you like,

but the underlying principle doesn't change:  the collection

and comparison of statistics in HD as in many other genetic and polygenic conditions either shows a GREATER LIKELIHOOD that the trait / disease  will be inherited, and

at (maybe roughly) what rates, or it won't.  It may not be a precise measurement, but using it makes more sense than

'throwing the baby out with the bath water'.


jdiaz1791

by jdiaz1791 on 31 May 2016 - 12:05

Many veterinarians are such especial people!!! Until we all start filing complains, they will not stop; they had done this to 2 of my pups,as far as i know, very incompetent, unprofessional.

bubbabooboo

by bubbabooboo on 31 May 2016 - 16:05

There are a lot of harmful lies being told to pet owners by veterinarians, the SV, OFA, vaccine makers, drug companies, company front organizations ( American Heartworm Society, AAFCO, etc. ) and pet food corporations ... they all involve money and enriching all of the businesses previously mentioned at the expense of our pet's health. They create a story based on little or no science ( 12 month a year Heartworm poisons ) and then beat the drums and scare the uninformed (or just too lazy to find out the truth) pet owners into spending billions on products that harm and slowly kill our pets. Wise up and don't let these businesses ( and a veterinarian runs a business ) harm or kill your pet.  Follow the money!!!


Les The Kiwi Pauling

by Les The Kiwi Pauling on 02 June 2016 - 09:06

[Hundmutter] 27.5.2016 - 16:05 ● "Good posts Les" With me, flattery gets you nowhere - what counts are the BRIBES plus the quality of the gorgeous hygienic teenaged Titian-tops who deliver them! (An old geezer can dream, can't he?) ● "but please don't blame UK breeders for the KC's intractability over hip scoring - gawd knows we've asked for this often enough down the years, from Malcolm Willis individually - to various Breed Clubs - to breeders - to the Breed Council - without success." It was far from Malcolm alone, although Malcolm DID get kicked out of The KC for speaking openly of some of its many flaws. The first USEFUL HD scheme was developed by BIF (the Breed Improvement Foundation formed in 1975, chaired by Malcolm, the ONLY judge to dump my Lorelei German Graffiti - Graff had previously been VP.1 Baby, Best Dog Puppy, Best Baby In Show under Walter Martin, then VP.3 Minor under Rolf Fauser, but Malcolm could not forgive that Graff was one P1 short at 9 months. Graff never produced that P1 - blame Jonny Rheinhalle & 2 distant lines to Vondaun Belisima of Brinton - so went to Singapore as a security dog. The BIF's other people were: Percy Eliott, breeder of the dam of my first registered GSD, also the only judge to keep my Lorelei Peter Proust "off the pegs" - he kept pulling me to the centre of the ring, gazed soulfully at Peter's bitchy head, then again sent me back to my 1-off position; Clarissa & Roy Allan, breeders of the bitch that put my senior mentor on the map (her stock 3 times won BIS at our equivalent of Crufts & Westminster); Barbara Lines, breeder of my first import; Harold Teal, breeder of one of your bitches; and May Tidbold, whose stock I AVOIDED!). Its biggest triumph was getting radiology Prof Latham (I might misremember that L-- name) to create the BIF-scoring scheme for hips, later adopted by the BVA and The KC (which for at least 3 years refused to accept it for breeds other than GSDs), plus by Australia’s & NZ’s canine people (but NZ's current veterinary osteopathy prof persuaded the NZVA to switch to the cheaper-to-operate PennHIP scheme a couple of years ago, damn him. Never mind - we Kiwi fans of GSDs can use the GSDCAustralia's scheme). ● "Maybe one day they will move on it, after all they've just about agreed about eye tests now ..." A scheme of negligible value to DownUnder GSDs. The only eye problem I ca recollect causing a problem here was "night blindness" (Juvenile Retinal Dysplasia) which was quickly identified as stemming from a German stud imported to Australia from the UK. His stock was discontinued, end of problem. [bubbabooboo] 27.5.2016 - 17:05 ● "If any of you know which genes are involved in HD or hip and joint formation please educate all of us. The last time I researched HD in dogs or GSD there was little to no indication that any scientist know which genes ( likely many ) are involved in promoting or resisting HD and joint problems in dogs or the GSD." Obviously you haven't "researched" in the last 6 years (a LONG time in modern genetics!): │ 2008: On 31 March the Hannover Veterinary University (Stiftung Tierärztliche Hochschule Hannover) │ claims to have identified the main gene for HD. There have been promotional updates since then, but nothing definite about the initial locus and whichever other loci they were investigating. There are, of course SEVERAL obvious candidates - the ones whose proteins chemically control: #1 the efficiency of the digestive system at supplying the necessary minerals and vitamins; #2 the density of the bone; #3 the growth rate of the various bones that form the hip-ball and its socket; #4 the pH (acidity) & density of the lubricating fluid inside the hip-joint; #5 the length & width and angle of the pelvis; #6 the attachment points and tightness & elasticity of the tendons. Most of those ARE, of course, susceptible to environmental factors, just as our adult height is "set" by our genes but our actual adult height can be limited by poor nutrition etc. Last I heard from Dr Mark Neff he intended to get stuck into researching the DNA of HD, but I've heard nothing from or about him since he left Davis California. ● "Any talk about dominant and recessive alleles is pure BS if we have no idea how the joint problems are inherited." Illogical RUBBISH! As an example, the locus & alleles of the modifier controlling how much of the coat displays eumelanin (black or its degrades - liver, blue, Isabella) versus displays phaeomelanin (tans) have not yet been identified, nor has the gene been named (except by those debating what it does and how it produces its effect - and they have used many terms to "describe" the gene), but sheer NUMBERS of dogs displaying the neffect if its alleles make it obvious that ▫1 the dominant turns wolf-sables into gold-sables, tan-points into saddle-backs; ▫3 the recessive turns wolf-sables into "black"-sables, tan-points into bi-colours. Until the gene & its alleles ARE DNA identified I cannot rule out that there are 2 co-dominant alleles of that gene, but the rarity of the ▫3 pattern convinces me that there is an intermediate allele, giving ▫2 the intermediate turns wolf-sables into grey sables, tan-points into blanket-backs. To see a genuine "black"-sable join https://groups.yahoo.com/neo/groups/The_GSD_Source/info then click https://groups.yahoo.com/neo/groups/The_GSD_Source/photos/albums/1844587168 and look at Jake as he developed - his darkness as an adult altered from a "summer"-coat to a "winter"-coat each year. ● "The more likely scenario is what geneticist call an incomplete inheritance or presentation which is geneticist speak for we don't know or environmental influences play a huge role in the outcome regardless of genetics." I gather you didn't pass that genetics course. I believe that the term you forgot is "limited penetrance" or "limited penetration". Personally, I dismiss the validity of the concept - if a dominant's effect is variable I want to know what modifier at a DIFFERENT locus has altered the effect of that "variable" dominant, whether by epistasis (blocking its production), or by reinforcement (adding more of the dominant's chemical production). Either way, it is not the dominant allele that is "variable", it is the combined polygenic EFFECT that varies - exactly as happens with HD and many other disorders. Perhaps you also fail to recognise that the total genome of each individual IS a crucial part of its "environment", even though you later recognise that the mitochondria ARE part of an individual's "personal environment". And the articles you referenced in a later post point out that the viruses and bacteria are ALSO part of each individual's "personal environment". Not to forget the toxins that enter us, and the atomic particles that pass through us, "knocking spots off" various genes as they go.... ● "Multiple allele with incomplete dominance is the normal way the world works for most diseases" Maybe, maybe not - my father wanted me to be a doctor, but I DIDN'T want to be, so he had to make do with my junior sister and VERY junior brother becoming registered nurses. IF your claim is true, I imagine it will be because disorders caused by or linked to autosomal dominants are easy to avoid and so are soon eliminated by people who are more intelligent than to prefer the damaging dominants for such as Merle. But I very much doubt the factuality of your claim. And I dismiss it for HD - I accept HD's inheritance mode as being polygenic recessives, with environment worsening the effects of the genes. [bubbabooboo] 30.5.2016 - 11:05 ● "In the case of HD and most conditions correlation does not prove causation ... polygenetic is correlation speak ... everything is either polygenetic or it is not and science uses polygenetic to explain the unknown. If some disease or trait is very simple and only involves a few genes with some predictability it is not polygenetic otherwise it is polygenetic using the simplistic Mendelian genetics" Do YOU understand your theory, the way that you wrote it there? You show total ignorance of the language roots of "polygenetic" and my preferred "polygenic", and so wrote total nonsense with "If (...it...) only involves a few genes with some predictability it is not polygenetic". Your "The simple facts are that environment, environment X genetics, and non-genetic factors play a bigger role in HD than genetics alone. Otherwise HD would not be called polygenetic at present." similarly fails to use the term "polygenetic" correctly, so is incorrect nonsense. LEARN that "polygenetic" simply means "the effect of more than one gene". So HD is definitely polygenic, unless you foolishly jump back to the outdated "autosomal dominant with limited penetrance" theory from almost 60 years ago. As for "This is why the OFA strategy of breeding out HD based on hip scores will never succeed. OFA hip scores can only predict what is but not what can be." 1: It will never succeed because (a) at present oit has to operate on PHENOTYPE, not genotype, and xrays cannot detect solo recessives - but they CAN detect the influence of paired recessives, a fact recognised by Dr Willis's reporting and continued by the GSDCAustralia, (b) it uses a too-blunt 7-categories scale (only the SV's 5-categories 'a'-stamp is more primitive - I ignore the 'a'-6 because it means only that the dog's hips been Passed somewhere outside Germany), (c) its reports tell breeders NOTHING of value until the pooch is categorised as one of the Fails, by which time it is too late for details to help, (d) it allows owners to NOT display their Fails, plus (e) there are a HELLUVA lot of massively arrogant+ignorant so-called "breeders" in the USA who place their desires as superior to whatever evidence doesn't suit their wishes, and (f) there is NO requirement from the AKC for pooches to have provided official hip (& elbows) scores before they can have a litter registered. 2: OFA's users not only do not get to see the important WORST "scores" produced by a pooch they are considering incorporating into their kennel-line, they also DON'T appear to have any responsible breed-club websites displaying the current results for each stud's (& brood's) progeny. A Willis-type report based on OFA's categories might report for "Slobbo of Dis Tillery" might show │ Pups║ Ex. │ Gd. │ Fr. │ B-L │ F1. │ F2. │ F3. │ │ 567 ║ 15% │ 17% │ 29% │ 6% │ 3% │ 19% │ 11% │ You night regard him as a good stud for hips, as 61% of the offspring gained Passes. But Aussies would regard him as a DREADFULLY DANGEROUS stud, as ONE THIRD of his offspring failed, with most of the Fails being in the worst 2 categories. That means that, on average, 2 to 3 pups PER LITTER are doomed to a miserable old age and probably an uncomfortable middle-age, too. The BIF scale having numerical scores from 0 to 106, it also reports the best & worst actual score and the average of the whole 567 scores (but OFA's reports aren't suitable to that sort of analysis. On PennHIP's reports, only the laxity DI is suitable), plus how many different broods the stud has scored progeny from. [melba] 30.5.2016 - 13:05 ● "Had a vet do this and cause damage to one hip, resulting in a failing OFA grade later on that oNE hip." Your assessment might be correct, but I doubt that any Court would accept it. Did you do an analysis of the hip-categories of her parents, the other offspring of each parent, the categories of her grandparents and of the other offspring of each grandparent, and then for the greatgrandparents? But the only "twisting" necessary when diagnosing HD is to keep the legs straight & the hocks vertical - NOT to rotate the leg. Despite claims to the contrary, expert breeders can NOT detect HD in its early stages. Norm, a friend of mine, showed his dog under my nation's only SV-ticket judge. After choosing the dog as BOB, the judge asked Norm to do a solo lap, during which the judge lauded about how smoothly the dog accelerated. What the judge DIDN'T know was that the dog had badly Failed his xrays, and the reason his acceleration was so smooth was that the dog declined to thrust HARD to get quick acceleration. Norm never allowed him to have a litter. From which you might sensibly deem that dogs that move smoothly have lousy hips, and so be attracted to dogs that delight in leaping and accelerating. I once banned a Czech vet from touching any of my dogs - he had stitched up Rella without any anaesthetic after she had escaped from her pen while only my wife was home. Rella attacked daughter Hetze, and had been thoroughly beaten up before Jeannie could get Hetze into a pen. In hindsight, I was wrong - see, Rella was SO badly wounded that Jeannie had to massage her to keep reminding her to breathe, and so even a local anaesthetic would probably have killed Rella. [bubbabooboo] 30.5.2016 - 14:05 ● "there was a concern about stairs and puppies using them such that many owners would not let their puppies use the stairs and would carry the puppy up and down the stairs." Thus making them more likely to have dysplasia, from lack of exercise. From 4½ weeks onwards, in suitable weather my pups start on the top terrace (the dog part of my property has 4 "levels"). As curiosity overrides the unfamiliarity of the territory, they explore, chase, push one another off the edge - and the ones that had to scrabble as they slid down the creepers complain that they can't yet get up the steps to rejoin the litter. Gradually they built up fitness, and explored all 4 levels - there was then no sensible way I could prevent them from, as soon as I opened the door, leaping from level 3 to grassy level 2 which was 2 concrete blocks lower, and from there leaping to the concrete of level 1 which was 3 concrete blocks lower. No, once we had BIF-scoring in NZ the only case of HD I know of was a 1983 pup from a very clever Ciwa who was suddenly 6 weeks pregnant - obviously she'd sneakily taken her son to the top of the property & taught him the "facts of life" before I knew she was on-heat. That litter had 3:2 inbreeding on a gorgeous BS.Cl.1 bitch whose hips were borderline. But LORDY that dysplastic pup was OBESE! [Hundmutter] 30.5.2016 - 16:05 ● "Bubba, Malcolm Willis ... I have no recollection that he recanted anything !" Actually, he admitted that he'd made a mistake by printing that http://www.pedigreedatabase.com/german_shepherd_dog/dog.html?id=191-vello-zu-den-siebenfaulen (greatgrandsire of my obedience bitch, Jena http://lesp90.wix.com/lorelei-gsd-kennels ) was KKl. His argument as to why the allele for bi-colour and the allele for self-black could NOT BOTH be in the Agouti Pattern locus was impeccable. Unfortunately he stuck his neck out and guessed that bi-colour was IN and recessive self-black was OUT. But whether he bothered to correct it after DNA revealed the truth I don't know. When I last had an e-mail from him he was assembling his 3rd GSD book - but he died before finishing it. He also made an error in the Colour locus and, I think, the Extension locus. [bubbabooboo] 30.5.2016 - 17:05 ● "I took an animal breeding genetics class in 1976 ... This was during the time that Mendelian genetics was thought to be all there was. I asked some probing questions and the professors told me that science knew "everything" about genetic inheritance and there was no room for discussion." Maybe in YOUR area - there are some VERY dogmatic Yanks! But I doubt that the whole world believed that in 1976. ● "In the 40 years hence the old science of Mendelian genetics has been replaced and amended with more complex non-Mendelian and epigenetic science." Replaced? NEVER! Certainly what can now be analysed is more complex than was possible before the current VERY fast computer chips were available. But before breeders can START to understand post-Mendelian genetics they MUST have a very full understanding of the modes that Gregor Mendel worked out without even a pocket calculator. HE knew that his modes didn't cover EVERYTHING when he ran into a mechanism that involved alleles of TWO genes - I forget which plant it was. As the term "Epigenetics" was coined by Waddington in 1942, deriving it from the 333± years old "epigenesis", you can be sure that Dr Willis knew about it, even if your lecturers didn't. [Your] 30.5.2016 - 18:05 message is not worth arguing against - it demonstrates that your grasp of #1: The way polygenic recessives operate and contribute to one another's damage probably doesn't extend to being able to see how mating an A^ a^, B^ b^, C^ c^, D^ d^, E^ e^ pooch to an A^ a^, B^ b^, C^ c^, D^ d^, E^ e^ pooch (I'm inventing codes for genes in which the the dominants contribute to perfect hips, the recessives contribute to dysplastic hips) - both pooches having PERFECT hips under any xray scheme - can produce a range from pups with perfect hips to pups with the worst-possible hips without any environmental influences being needed. The randomisation that occurs twice - one during the production of the gametes, the other during the process of fertilisation - provides enough variety to explain the variations. Of course, overweight, poor nutrition or over-feeding will HASTEN the moment at which the joint's development becomes too damaged for the sufferer to compensate for by such as shifting its weight onto the fore-hand and moving VERY smoothly. But whether those ENVIRONMENTAL factors will produce dysplasia in individuals without ANY pairs of the undesirable recessives remains to be tested - we can't test it until all the genes & alleles involved are DNA-identified. But https://www.avma.org/News/Journals/Collections/Documents/javma_217_11_1678.pdf proves that "on-demand feeding" aka "free-feeding" produces both MORE cases of HD and WORSE dysplasia than does controlled feeding. The "worse" aspect was totally expected, and - to me - demonstrates that the gene pools of those litters included the genetic factors for HD. Therefore the "more cases" aspect could be explained by the extra weight having caused the damage to become obvious in pooches who might normally have not shown noticeable indications for another year or more. #2: You aren't aware of "susceptibility" and "threshholds". As a type2 diabetic with a type2 diabetic sister and a type2 diabetic father whose mother was a type2 diabetic but HER mother was far from diabetic (I don't know enough about that greatgrandfather) I recognise that, so far as SOME OF "the change in diseases and health problems reflects this change", but I dispute the "not a genetic causation" part. Using type2 diabetes as the tool to help you see WHY: In my greatgrandparents' time sugar was scarce in most of the world, and so few people consumed enough sugar (fructose, glucose, lactose, maltose, sucrose, whatever) to trigger their genetic susceptibility to type2 diabetes - and medical capability couldn't save the babies born with type1 diabetes. (An early death is a useful way of slowing the spread of defective genes!) But nowadays the "rich" countries have sugars galore - whether as alcohols, carbohydrates, cordials, "energy drinks", fats, "health drinks", KFC-etc, "soft drinks", and the biscuits & cakes & chocolates galore - so that many of us have our children then slow down and develop the type2 diabetes that was latent in us - I was in my late 40s before I felt "slow" enough to seek a diagnosis. It might well be that the poor survive, the rich die early! [susie] 30.5.2016 - 18:05 Google was good enough to translate the headings as Hip Joint Dysplasia in German Shepherd Dogs Influence of Parents on the HD Level of Offspring but I wish you had informed us as to what the numbers from 1 up to 2 at the left signify. Und nein, mein Liebchen ßuzie - ich nicht sprechen sie Deutsche. But in the days when computers ran on DOS I programmed a database to produce a near-enough translation of Körscheinen or whatever the plural of Körschein is. [Hundmutter] 30.5.2016 - 19:05 ● "Of course, as far as Bubba and America is concerned, one could ask questions about why OFA took the route it has, with the gradings it has, when it could have had a scheme which sat easier with other countries' way of reckoning hip status and made it less difficult to work out the comparisons." The main reason is that they are USAmericans, and in 1935 the American veterinarian G.B. Schnelle discovered hip dysplasia in dogs - but it attracted little attention until, in 1956, the American Aninvale Kennels publicised that their dogs are affected. Followed by the 1958 Swedish study, the Swedish KC setting up an HD scheme for just GSDs in 1959, and THEN, in autumn 1964 John M Olin gathered a group of individuals - representatives of the Golden Retriever Club of America, German Shepherd Dog Club of America and the veterinary community - to discuss means of limiting hip dysplasia. This led to the formation of the Orthopedic Foundation for Animals (OFA), incorporated as a non-profit corporation by the state of Illinois on July 7, 1966. So OFA was second into the field, first of the English-speaking nations (if one can accept Cajun, Cornish, Gaelic, Glaswegian, Irish, Welsh, Yanklish as English...). The KC (UK) began its first scheme in 1965. The SV started "investigating" in 1966 but didn't set up the 'a'-stamps until 1967. My nation's veterinary university began its study in 1967 but the NZVA didn't make the scheme nationwide until 1972. ALL of those schemes - including the FCI's - are blunt "category" schemes. The Breed Information Foundation's system was the first (and so far ONLY, unless you count PennHIP's single 0-to-100 scale) scheme to use actual MEASUREMENTS instead of "trained eyes", to report on EACH of the 18 aspects, and to introduce a fine scale - BIF-scoring gives numbers from 0 to 106, which makes mathematical analysis MUCH easier. And being able to see the aspect scores of all 18 aspects warns THINKING breeders as to which possible mates are getting close to "POOR" on the same aspects as each other. [bubbabooboo] 31.5.2016 - 00:05 ● "Then there is the SV, OFA and all of the phoney baloney experts looking at x-rays which are simply a hard to observe phenotypic trait and do not reflect underlying genetics at all since we don't have a clue what if any genetic factors influence HD, DM" You ARE determined to slander experts and exaggerate outrageously! YOU apparently "don't have a clue what if any genetic factors influence HD, DM" - but almost anyone who can be bothered can work out both the logical genetic MODE and logical environmental factors producing HD. IDENTIFYING the actual alleles is taking longer - but have you bothered to find out how many genes and how many alleles there are in the canine genotype? Without starting to count the mDNA? IDENTIFICATION WILL TAKE TIME. As for DM: Dr Roger Clemens thought he knew, with the Jack Flash Test (named for Marjorie's sufferer). Now there are perhaps 476,000 labs around the world claiming to be able to identify the alleles for non-DM versus DM. That OFA admits "Among the hundreds of dogs studied so far at the University of Missouri, only two dogs with test results of N/N (Normal) have been confirmed to have DM" is a little bit unfortunate, but not enough to totally discredit the test - maybe time will prove that DM is polygenic. I've had my bitch tested - N P, damnit! - and so her breeders have tested her relatives and found that the sire and every one of his offspring is a carrier. And gossip-line "research" found that both of Bea's dam's grandsires were either producers of or died of DM. IF I can get Bea pregnant to an N N stud I am going to have to test every pup in the first 3 weeks (the Australian lab is VERY slow getting results back), and endorse the registrations of the carriers that they are NOT to be bred from unless their owner can produce an adult N N certificate (quite possible: As Bea's milk includes her own DNA, and so milk in a pup's mouth could produce a false Positive from swabbing while the pups are still suckling - and no, I am NOT going to starve my pups and wash their mouths out. Nor am I going to hold the whole litter back until they are well & truly no longer attempting to suckle). But again, this is Off Topic to the hip-check thread, although relevant to your rants.... As for your ● "That is why identical twins raised in the same home will often have different diseases and medical conditions late in life when environment has had time to change there genetic expression" - you DO insist in using language so loosely that you end up stating untruths. Sadly, many vets with USA web-sites ALSO misuse words. To make your thoughts CLEAR you must use words pedantically. ☆ DISEASES are "caught" from the environment - whether bacteria, "germs", parasites, poisons, pollutants, snake-bites, toxins, viruses, or whatever other infectious agents you care to name. ☆ Genes produce DEFECTS, DISORDERS or SUSCEPTIBILITIES (as with type2 diabetes). And fuckin' HELL - as soon as I posted that at 06:46 on Thursday morning (NZTime), the pdb declared that "something was left behind at the vet's". So I am having to try a THIRD time to paste & format & post this - will I manage before midnight Thursday? The damned thing failed again at 9.45pm.

 

'll try to reformat thjis spaced version later.


Sunsilver

by Sunsilver on 02 June 2016 - 12:06

Les, I'll have to go back and read this when I'm not trying to get ready for work (and still have to shower, make a lunch, and get at least one of my dogs out for a walk and a bit of training!) WOW! You wrote quite the book there! :D

If you enable the editor BEFORE you type your post, the paragraph spacing will show up as you intended it to.

Les The Kiwi Pauling

by Les The Kiwi Pauling on 02 June 2016 - 12:06

[Sunsilver] wrote:


"Les, I'll have to go back and read this when I'm not trying to get ready for work"

They let females WORK in your country?? Don't they know that a woman's place is chained to the stove, sink, laundry and bed?
But take your time. I'm going to have to split it into at least TWO posts. And my eyes are already sore....



"If you enable the editor BEFORE you type your post, the paragraph spacing will show up as you intended it to."
Hey - so does the "ink-colour"! But my fontface and text size vanish.

UPDATE: But the colour ALSO vanishes as soon as I save the message.


I don't TYPE into web-forms. I compose in a flexible word processor then paste into the clumsy bloody web-form.
The problem seems to be that there are so MANY formatting codes in my message that it has overloaded the memory limit that the programmer set. Just the plain ASCII text almost fills that limit. So I'll need to split & format it as TWO messages. I cannot find any
Delete, so I hope that when I save an empty "message" that that will remove the plain ASCII I saved so that there would be a copy of bits I had amended from my personal copy.


Les The Kiwi Pauling

by Les The Kiwi Pauling on 02 June 2016 - 14:06

[Hundmutter] 27.5.2016 - 16:05

"Good posts Les"
With me, flattery gets you nowhere - what counts are the BRIBES plus the quality of the gorgeous hygienic teenaged Titian-tops who deliver them!
(An old geezer can dream, can't he?)

"but please don't blame UK breeders for the KC's intractability over hip scoring - gawd knows we've asked for this often enough down the years, from Malcolm Willis individually - to various Breed Clubs - to breeders - to the Breed Council - without success."
It was far from Malcolm alone, although Malcolm DID get kicked out of The KC for speaking openly of some of its many flaws. The first USEFUL HD scheme was developed by BIF
(the Breed Improvement Foundation formed in 1975, chaired by Malcolm, the ONLY judge to dump my Lorelei German Graffiti - Graff had previously been VP.1 Baby, Best Dog Puppy, Best Baby In Show under Walter Martin, then VP.3 Minor under Rolf Fauser, but Malcolm could not forgive that Graff was one P1 short at 9 months. Graff never produced that P1 - blame Jonny Rheinhalle & 2 distant lines to Vondaun Belisima of Brinton - so went to Singapore as a security dog. The BIF's other people were: Percy Eliott, breeder of the dam of my first registered GSD, also the only judge to keep my Lorelei Peter Proust "off the pegs" - he kept pulling me to the centre of the ring, gazed soulfully at Peter's bitchy head, then again sent me back to my 1-off position; Clarissa & Roy Allan, breeders of the bitch that put my senior mentor on the map (her stock 3 times won BIS at our equivalent of Crufts & Westminster); Barbara Lines, breeder of my first import; Harold Teal, breeder of one of your bitches; and May Tidbold, whose stock I AVOIDED!). Its biggest triumph was getting radiology Prof Latham (I might have misremembered that L-- name) to create the BIF-scoring scheme for hips, later adopted by the BVA and The KC (which for at least 3 years refused to accept it for breeds other than GSDs), plus by Australia’s & NZ’s canine people (but NZ's current veterinary osteopathy prof persuaded the NZVA to switch to the cheaper-to-operate PennHIP scheme a couple of years ago, damn him. Never mind - we Kiwi fans of GSDs can use the GSDCAustralia's scheme).

"Maybe one day they will move on it, after all they've just about agreed about eye tests now ..."
A scheme of negligible value to DownUnder GSDs. The only eye problem I can recollect causing a problem here was "night blindness"
(Juvenile Retinal Dysplasia) which was quickly identified as stemming from a German stud imported to Australia from the UK. His stock was discontinued, end of problem.


[bubbabooboo] 27.5.2016 - 17:05

"If any of you know which genes are involved in HD or hip and joint formation please educate all of us. The last time I researched HD in dogs or GSD there was little to no indication that any scientist know which genes ( likely many ) are involved in promoting or resisting HD and joint problems in dogs or the GSD."
Obviously you haven't "
researched" in the last 6 years
(a LONG time in modern genetics!):
│ 2008:     On 31 March the Hannover Veterinary University
(Stiftung Tierärztliche

Hochschule Hannover) claims to have identified the main gene for HD.
There have been promotional updates since then, but nothing definite about the initial locus and whichever other loci they were investigating. There are, of course SEVERAL obvious candidates - the ones whose proteins chemically control:
#
1 the efficiency of the digestive system at supplying the necessary minerals and vitamins;
#
2 the density of the bone;
#
3 the growth rate of the various bones that form the hip-ball and its socket;
#
4 the pH
(acidity) & density of the lubricating fluid inside the hip-joint;
#
5 the length & width and angle of the pelvis;
#
6 the attachment points and tightness & elasticity of the tendons.
Most of those ARE, of course, susceptible to environmental factors, just as our adult height is "set" by our genes but our actual adult height can be limited by poor nutrition etc.
Last I heard from Dr Mark Neff he intended to get stuck into researching the DNA of HD, but I've heard nothing from or about him since he left Davis California.


"Any talk about dominant and recessive alleles is pure BS if we have no idea how the joint problems are inherited."
RUBBISH! As an example, the locus & alleles of the modifier controlling how much of the coat displays eumelanin
(black or its degrades - liver, blue, Isabella) versus displays phaeomelanin (tans) have not yet been identified, nor has the gene been named (except by those debating what it does and how it produces its effect - and they have used many terms to "describe" the gene), but sheer NUMBERS of dogs displayig the neffect of its alleles make it obvious that
▫1 the dominant turns wolf-sables into gold-sables, tan-points into saddle-backs;
▫3 the recessive turns wolf-sables into "black"-sables, tan-points into bi-colours.
Until the gene & its alleles ARE DNA identified I cannot rule out that there are 2 co-dominant alleles of that gene, but the rarity of the ▫3 pattern convinces me that there is an intermediate allele, giving

▫2 the intermediate turns wolf-sables into grey sables, tan-points into blanket-backs.
To see a genuine "black"-sable join

https://groups.yahoo.com/neo/groups/The_GSD_Source/info
then click
https://groups.yahoo.com/neo/groups/The_GSD_Source/photos/albums/1844587168
and look at Jake as he developed - his darkness as an adult altered from a "summer"-coat to a "winter"-coat each year.


"The more likely scenario is what geneticist call an incomplete inheritance or presentation which is geneticist speak for we don't know or environmental influences play a huge role in the outcome regardless of genetics."
I gather that you didn't pass that genetics course. I believe that the term you forgot is "
limited penetrance" or "limited penetration". Personally, I dismiss the validity of the concept - if a dominant's effect is variable I want to know what modifier at a DIFFERENT locus has altered the effect of that "variable" dominant, whether by epistasis
(blocking its production), or by reinforcement (adding more of the dominant's chemical production). Either way, it is not the dominant allele that is "variable", it is the combined polygenic EFFECT that varies - exactly as happens with HD and many other disorders.
Perhaps you also fail to recognise that the total genome of each individual IS a crucial part of its "
environment", even though you later recognise that the mitochondria ARE part of an individual's "personal environment". And the articles you referenced in a later post point out that the viruses and bacteria are ALSO part of each individual's "personal environment". Not to forget the toxins that enter us, and the atomic particles that pass through us, "knocking spots off" various genes as they go....


"Multiple allele with incomplete dominance is the normal way the world works for most diseases"
Maybe, maybe not - my father wanted me to be a doctor, but I DIDN'T want to be, so he had to make do with my junior sister and VERY junior brother becoming registered nurses.

IF your claim is true, I imagine it will be because disorders caused by or linked to autosomal dominants are easy to avoid and so are soon eliminated by people who are more intelligent than to prefer the damaging dominants for such as Merle. But I very much doubt the factuality of your claim. And I dismiss it for HD - I accept HD's inheritance as being polygenic recessives, with environment worsening the effects of the genes.


[bubbabooboo] 30.5.2016 - 11:05

"In the case of HD and most conditions correlation does not prove causation ... polygenetic is correlation speak ... everything is either polygenetic or it is not and science uses polygenetic to explain the unknown. If some disease or trait is very simple and only involves a few genes with some predictability it is not polygenetic otherwise it is polygenetic using the simplistic Mendelian genetics"
Do YOU understand your theory, the way that you wrote it there?
You show total ignorance of the language roots of "
polygenetic" and my preferred "polygenic", and so wrote total nonsense with "If (...it...) only involves a few genes with some predictability it is not polygenetic".
Your
"
The simple facts are that environment, environment X genetics, and non-genetic factors play a bigger role in HD than genetics alone. Otherwise HD would not be called polygenetic at present."
similarly fails to use the term "
polygenetic" correctly, so is incorrect nonsense.
LEARN that "
polygenetic" simply means "the effect of more than one gene". So HD is definitely polygenic, unless you foolishly jump back to the outdated "autosomal dominant with limited penetrance" theory from almost 60 years ago.
As for
"
This is why the OFA strategy of breeding out HD based on hip scores will never succeed. OFA hip scores can only predict what is but not what can be."
1: It will never succeed because (a) it operates on PHENOTYPE, not genotype, and xrays cannot detect solo recessives - but they CAN detect the influence of paired recessives, a fact recognised by Dr Willis's reporting and continued by the GSDCAustralia, (b) it uses a too-blunt 7-categories scale
(only the SV's 5-categories 'a'-stamp is more primitive - I ignore the "a"-6 because it means only that the dog's hips been Passed somewhere outside Germany), (c) its reports tell breeders NOTHING of value until the pooch is categorised as one of the Fails, by which time it is tool late, (d) it allows owners to NOT display their Fails, plus (e) there are a HELLUVA lot of massively arrogant+ignorant so-called "breeders" in the USA who place their desires as superior to whatever evidence doesn't suit their wishes, and (f) there is NO requirement from the AKC for pooches to have provided official hip (& elbows) scores before they can have a litter registered.
2: OFA's users not only do not get to see the important WORST "scores" produced by a pooch they are considering incorporating into their kennel-line, they also DON'T appear to have any responsible breed-club websites displaying the current results for each stud's
(& brood's) progeny. A Willis-type report based on OFA's categories might report for

Slobbo of Dis Tillery
│ Pups║ Ex. │ Gd. │ Fr. │ B-L │ F1. │ F2. │ F3. │
│ 567 ║ 15% │ 17% │ 29% │  6% │  3% │ 19% │ 11% │

You night regard him as a good stud for hips, as 61% of the offspring gained Passes. But Aussies would regard him as a DREADFULLY DANGEROUS stud, as ONE THIRD of his offspring failed, with most of the Fails being in the worst 2 categories. That means that, on average, 2 to 3 pups PER LITTER are doomed to a miserable old age and probably an uncomfortable middle-age, too. The BIF scale having numerical scores from 0 to 106, it also reports the best & worst actual score and the average of the whole 567 scores
(but OFA's reports aren't suitable to that sort of analysis. On PennHIP's reports, only the laxity DI is suitable), plus how many different broods the stud has scored progeny from.


[melba] 30.5.2016 - 13:05

"Had a vet do this and cause damage to one hip, resulting in a failing OFA grade later on that oNE hip."
Your assessment might be correct, but I doubt that any Court would accept it.
Did you do an analysis of the hip categories of her parents, the other offspring of each parent, the categories of her grandparents and of the other offspring of each grandparent, and then for the greatgrandparents?

But the only "
twisting" necessary when diagnosing HD is to keep the legs straight & the hocks vertical - NOT to rotate the leg.

Despite claims to the contrary, expert breeders can NOT detect HD in its early stages. Norm, a friend of mine, showed his dog under my nation's only SV-ticket judge. After choosing the dog as BOB, the judge asked Norm to do a solo lap, during which the judge lauded about how smoothly the dog accelerated. What the judge DIDN'T know was that the dog had badly Failed his xrays, and the reason his acceleration was so smooth was that the dog declined to thrust HARD to get quick acceleration. Norm never allowed him to have a litter.
From which you might sensibly deem that dogs that move smoothly have lousy hips, and so be attracted to dogs that delight in leaping and accelerating.

I once banned a Czech vet from touching any of my dogs - he had stitched up Rella without any anaesthetic after she had escaped from her pen while only my wife was home. Rella attacked daughter Hetze, and had been thoroughly beaten up before Jeannie could get Hetze into a pen. In hindsight, I was wrong - see, Rella was SO badly wounded that Jeannie had to massage her to keep reminding her to breathe, and so even a local anaesthetic would probably have killed Rella.



[bubbabooboo] 30.5.2016 - 14:05

"there was a concern about stairs and puppies using them such that many owners would not let their puppies use the stairs and would carry the puppy up and down the stairs."
Thus making them more likely to have dysplasia, from lack of exercise.
From 4½ weeks onwards, in suitable weather my pups start on the top terrace
(the dog part of my property has 4 "levels"). As curiosity overrides the unfamiliarity of the territory, they explore, chase, push one another off the edge - and the ones that had to scrabble as they slid down the creepers complain that they can't yet get up the steps to rejoin the litter. Gradually they built up fitness, and explored all 4 levels - there was then no sensible way I could prevent them from, as soon as I opened the door, leaping from level 3 to grassy level 2 which was 2 concrete blocks lower, and from there leaping to the concrete of level 1 which was 3 concrete blocks lower.
No, once we had BIF-scoring in NZ the only case of HD I know of was a 1983 pup from a very clever Ciwa who was suddenly 6 weeks pregnant - obviously she'd sneakily taken her son to the top of the property & taught him the "facts of life" before I knew she was on-heat. That litter had 3:2 inbreeding on a gorgeous BS.Cl.1 bitch whose hips were borderline, so she was allowed only 2 litters - one for me, one for her owner.

But LORDY that dysplastic pup was OBESE!






 


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