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The remaining clinical signs at presentation were fly catching and panic attacks, focal seizures, aggression toward people, urinary incontinence as a result of loss of house training, poor vision or blindness, fecal incontinence, or dementia. Non-pathogenic polyglucosan bodies occur as an aging-related change in many species including cats, dogs and man. Further prospective study is needed to further characterize the canine disease and to allow more specific therapeutic strategies and to tailor therapy as the disease progresses. Visualization, Hyperphosphorylation of glucosyl C6 carbons and altered structure of glycogen in the neurodegenerative epilepsy Lafora disease. The mean age of onset of clinical signs was 6.94 years which correlated with the median age of onset of 7 years. Glycogen synthase is the only enzyme that catalyzes formation of 14 interglucosidic linkages that generate glycogen (or polyglucosan) strands. Other presenting signs included hypnic myoclonus (51.9%) and generalized seizures (40.7%). Both are mutation positive for LD. As the disease progresses clinical signs become more intense and often dogs may be euthanized due to their severity. Ahonen S, Grossman TP, Wang P, Turnbull J, Zhao X, Minassian BA. by using low carbohydrate diets such as the ketogenic diet. Dachshund Breed Council, Wrington, North Somerset, United Kingdom, Roles Writing review & editing, Affiliation The signalment results are illustrated in Table 1. PLoS ONE 12(8): Key G. Progression Survey 2013 [cited 2016 16th April]. Owners described the (presumed) panic attacks as particularly distressing and from the description [24] we hypothesize that the dogs may be experiencing frightening visual hallucinations as the dogs behavior suggested fear and an escape response. Which proteins are the precise target(s) of malin remains unknown, but absence of malins function, like absence of laforin, leads to poorly branched and insoluble glycogen (polyglucosans), which accumulate in neuronal somatodendritic compartments into Lafora bodies (polyglucosan bodies), over time driving the neurodegeneration and progressive myoclonic epilepsy[28] (Fig 3). Neuronal somatodendritic polyglucosan bodies in young animals or humans are essentially pathognomonic of LD. Bar equals 50m. 8600 Rockville Pike The myoclonus in particular becomes more severe and more refractory to treatment. 62.5% of the cohort was female. Clinical trials require detailed description of the clinical disease and its natural progression. This is an open access article distributed under the terms of the, GUID:91CCEE6A-E4E6-492F-970D-A1123748117C, GUID:38134FE2-03B5-4D29-98C8-6993CDA64541, GUID:34F21679-30E8-4ED1-A9F0-FBA8C9044A71. The range of the onset of clinical signs was wide at 3.5 to 12 years. There was also open questions to allow participants to enter other clinical signs and other comments. The Southern blot based approach (Fig 2) is presently the only approved test but is expensive for the dog owner and is performed intermittently on batched samples which limits the number of dogs tested. This is likely a reflection that they are euthanatized before this stage but also because of their longevity. An official website of the United States government. Current therapy for LD is aimed at limiting clinical signs of the disease. Investigation, The mean age of onset of clinical signs was 6.94 years which correlated with the median age of onset of 7 years. In particular, clinically affected dogs presented to veterinary surgeons are less likely to be tested. This retrospective study was based on the analysis of responses to a confidential online survey which did not collect personal data and no aspect comes under the auspices of Animals (Scientific Procedures) Act 1986. Methodology, Roles Yamanami S, Ishihara T, Takahashi M, Uchino F. Comparative study of intraneuronal polyglucosan bodies in brains from patients with Lafora disease and aged dogs, Zonisamide for progressive myoclonus epilepsy: long-term observations in seven patients. GK is a member of the Lafora disease Subcommittee which is part of the Dachshund Breed Council affiliated with the UK Kennel Club. Signs that developed later in the disease include dementia (51.9%), blindness (48.1%), aggression to people (25.9%) and dogs (33.3%), deafness (29.6%) and fecal (29.6%) and urinary (37.0%) incontinence as a result of loss of house training (disinhibited type behavior). Received 2016 Dec 15; Accepted 2017 Jul 11. The confidential online survey ran between January 2013 and January 2014. Epileptic disorders: international epilepsy journal with videotape. Similar syndromes occur in other species including dogs [30] cats [31], and the grey-head flying fox [32]. official website and that any information you provide is encrypted All these clinical signs appear, and then increase over time, in all dogs (S1 Movie). Mice (our unpublished observation) and humans [41] in whom this has been tried maintain physiological blood glucose levels and generate just as profuse LB as with normal diet. Yes Inhibiting glycogen synthesis prevents Lafora disease in a mouse model. Lafora disease (LD) is an autosomal recessive late onset, progressive myoclonic epilepsy with a high prevalence in the miniature Wirehaired Dachshund. (b) Transverse T2W at the level of temporal lobes demonstrating cortical atrophy with widening of the subarachnoid space (green arrow) and enlargement of the lateral ventricle (orange arrow). It is possible that the dogs do not develop more severe signs because they would die of natural causes first [1]. Finally there was a question about possible comorbidities including previous diagnosis of intervertebral disease. No, PLOS is a nonprofit 501(c)(3) corporation, #C2354500, based in San Francisco, California, US, Corrections, Expressions of Concern, and Retractions, https://doi.org/10.1371/journal.pone.0182024, http://laforadogs.org/surveys/interim-survey-results-autumn-2012, https://sites.google.com/site/ukdachshundhealthreport/dachshund-health-resources/lafora-disease, http://www.thekennelclub.org.uk/health/breeding-for-health/dna-screening-schemes-and-results/dna-screening-for-breeds-c-g/dachshund-(miniature-wire-haired)-dna-screening/. This phosphate appears to be critical to ensuring the sphericity of glycogen, which is essential to its solubility. Program in Genetics and Genome Biology, The Hospital for Sick Children, Toronto, Canada, 4 As the disease progresses the severity, frequency and refractoriness of the seizures increase. This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials. Distribution of clinical signs in the LD affected and suspected dogs at presentation, In the gene test-positive group the most frequent new clinical sign that developed over the first 13 years following presentation was poor vision /blindness which was reported in over one third of the dogs. In humans, LD is arguably the severest adolescence-onset epilepsy [4]. Webb AA, McMillan C, Cullen CL, Boston SE, Turnbull J, Minassian BA. Recent breed-wide testing suggests that the carrier plus affected rate may be as high as 20%. In human or canine LD, polyglcuosan bodies are also seen in various tissues outside the brain, such as muscle, heart and liver, but in these organs, they appear to be clinically neutral, usually the patient succumbing to the neurological disease without ever having developed clinical signs of hepatic, cardiac or skeletal muscle disease. The genetic test is the definitive test in confirming the disease and the percentage for mutation positive dogs has decreased since breed wide testing has been implemented. 2016. p. 15. http://laforadogs.org/surveys/interim-survey-results-autumn-2012, https://sites.google.com/site/ukdachshundhealthreport/dachshund-health-resources/lafora-disease, http://www.thekennelclub.org.uk/health/breeding-for-health/dna-screening-schemes-and-results/dna-screening-for-breeds-c-g/dachshund-(miniature-wire-haired)-dna-screening/. There was also open questions to allow participants to enter other clinical signs and other comments. It must be emphasized that dogs with LD, even in the MWHD breed alone, outnumber all known cases of human LD. This is not possible to achieve merely through dietary restriction, e.g. Yes This is likely a reflection that they are euthanatized before this stage but also because of their longevity. The genetic test is the definitive test in confirming the disease and the percentage for mutation positive dogs has decreased since breed wide testing has been implemented. This retrospective study was based on the analysis of responses to a confidential online survey which did not collect personal data and no aspect comes under the auspices of Animals (Scientific Procedures) Act 1986. The survey participant was asked to enter the dogs age that they first noticed the clinical signs or never if this sign was not noticed. There were more specific questions about urinary incontinence to enable assessment as to whether incontinence occurred as a result of loss of house training (i.e. Click through the PLOS taxonomy to find articles in your field. Ianzano L, Zhang J, Chan EM, Zhao XC, Lohi H, Scherer SW, et al. Department of Pediatrics (Neurology), The Hospital for Sick Children, University of Toronto, Toronto, Canada, 6 International Veterinary Epilepsy Task Force's current understanding of idiopathic epilepsy of genetic or suspected genetic origin in purebred dogs, Polyglucosan storage disease in a dog resembling Lafora's disease, Journal of veterinary internal medicine / American College of Veterinary Internal Medicine. Common signs of disease were identified: myoclonic jerks (spontaneous and reflex, most commonly induced by light, sound or sudden movement in the visual field), hypnic myoclonus (twitch as falling asleep), seizures (both focal and tonic-clonic), ataxia, poor vision/blindness, deafness, dementia (defined as a behavior change suggesting disorientation and memory loss with or without altered sleep wake cycle and anxiety), aggression (toward people and other dogs), incontinence due to loss of house training i.e. All affected dogs to date, from all breeds, have the same expansion mutation in the Epm2b dodecamer repeat unique to the canid orthologue of the gene. Other presenting signs included hypnic myoclonus (51.9%) and generalized seizures (40.7%). Epm2b, the gene commonly mutated in dogs, encodes an ubiquitin E3 ligase (malin). Average age of onset of clinical signs was 6.94 years (3.512). For more information about PLOS Subject Areas, click Discover a faster, simpler path to publishing in a high-quality journal. The Dachshund Breed Council coordinated fundraising to contribute towards the cost of genetic testing. No, Is the Subject Area "Mutation" applicable to this article? Fitzpatrick Referrals Ltd, provided support in the form of salaries and materials for authors LS, AT and CR. Polyglucosan bodies can also be associated with other neurological syndromes often referred to in humans as polyglucosan body disease [29]. Needle electromyography (EMG) has been reported to show abnormal spontaneous activity of the muscles with positive sharp waves and fibrillation potential [8]. However, all treatment is anecdotal as no research has been performed to assess the efficacy of individual therapies. This mutation consists of a massive expansion of a dodecamer repeat sequence present exclusively in the canine (and generally canid) Epm2b gene, leading to near-absent expression and loss of function of the gene [1, 12]. LD, in this sense, can be regarded as a canine genome particular disease, and is likely to continue to be seen in different purebred breeds with each recurrence of the expansion mutation. The authors are grateful to the Dachshund Breed Council, the Wire Haired Dachshund club and Lafora Subcommittee for enabling this project. These are usually present not in neurons but in glia, and in the human literature are termed corpora amylacea. These are usually present not in neurons but in glia, and in the human literature are termed corpora amylacea. It is most frequent in Miniature Wirehaired Dachshunds (MWHD) [1, 8, 9], Bassett Hounds [1, 10] and Beagles [11, 12], and single cases have been reported in the Miniature and Standard Poodle [13], Pointer [14], and a Corgi [15]. School of Veterinary Medicine, Faculty of Health & Medical Sciences, University of Surrey, Guildford, Surrey, United Kingdom. Data Availability: All relevant data are within the paper and its Supporting Information files. Distribution of clinical signs in the LD affected and suspected dogs after 3 years of disease. No, Is the Subject Area "Glycogens" applicable to this article? disinhibited behavior (both fecal and urinary), jaw smacking and fly catching however the survey did not include data on how this disease progressed. As such a larger amount of DNA is required than can be obtained from cheek swabs, and generally a blood sample is used. In the untested group the most common developing late clinical signs were those of aggression towards other dogs and urinary and fecal incontinence as a result of loss of house training (disinhibited). The cardinal features of the disease are: spontaneous myoclonus, reflex myoclonus (myoclonus in response to light, sounds and / or movement in visual field), hypnic jerks (jerking as falling asleep), generalized seizures, focal seizures, anxiety, impaired vision, and later cognitive decline to dementia, ataxia, deafness, and fecal and urinary incontinence as a result of loss of house training (disinhibited behavior). Roles None of the authors have personal or financial relationships with other people or organizations that might inappropriately influence or bias the content of the paper. Ataxia and emotional disturbances develop, followed by spasticity and dementia. In particular, clinically affected dogs presented to veterinary surgeons are less likely to be tested. (2017) Lafora disease in miniature Wirehaired Dachshunds. The untested group had slightly different development of clinical signs, the most frequent being dementia, which was reported in two thirds of the cases, followed by focal seizures. LD has also been reported in other species including a Fennec fox [16], cows [17] and possibly a parakeet [18]. The B. Electron micrograph of a LB in the terminal cytoplasm of a dendrite. Owners of affected dogs stated that they were unable to walk the dog off the leash because if it occurred then the affected dog could run off uncharacteristically. Fourteen dogs were immediately excluded from the study as they were not showing clinical signs at the time of the study; four of these dogs had tested positive for the LD disease mutation but did not yet show clinical signs (all these dogs were younger than the age of onset of canine LD). Signalment and age of onset of first clinical signs in a cohort of data for 27 MWHD with confirmed and suspected LD. Visualization, Is the Subject Area "Dogs" applicable to this article? (c) Transverse T2W at level of occipital lobes demonstrating cortical atrophy with widening of the subarachnoid space (green arrow) and enlargement of the lateral ventricle (orange arrow). Genetic testing is not routinely available because the massive dodecamer repeat expansion mutation makes PCR-based sequencing options unreliable for detecting the carrier state and consequently only a southern blot based test is offered by the University of Toronto and is an official DNA screening test recommended by the UK Kennel Club (Fig 2). No, Is the Subject Area "Myoclonus" applicable to this article? What is clear is that the former encodes a phosphatase (laforin) that regulates a small but important amount of phosphate covalently bound to glycogen. A characteristic feature of the disease is spontaneous and reflex myoclonus; however clinical signs and disease progression are not well described. To date, a single mutation has been found in canine LD, in all three of three breeds (MWHD, Bassett Hounds and Beagles) in which mutation testing has been performed [1, 12]. Fitzpatrick Referrals Orthopedics and Neurology, Halfway Lane, Eashing, Godalming, Surrey, United Kingdom, Roles Notwithstanding, a shortcut to therapy was recently suggested. The new PMC design is here! Participants gave their written consent for the clinical data to be used for research purposes and the raw data from the survey (S1 Table) was subsequently passed to this group with a request for analysis to provide information on disease progression and further knowledge of the disease. Magnetic resonance imaging (MRI) may reveal generalized cortical atrophy with ventriculomegaly (Fig 1) [1, 9]. In humans, LD is arguably the severest adolescence-onset epilepsy [4]. Mice (our unpublished observation) and humans [41] in whom this has been tried maintain physiological blood glucose levels and generate just as profuse LB as with normal diet. Funding: The Kennel Club Charitable Trust registered charity (No. Precisely how the laforin-malin partner enzymes regulate glycogen structure remains unclear [19, 20]. Inclusion criteria for the analysis was a UK bred MWHD that had either positive genetic testing for LD or had showed pathognomonic signs of LD including reflex myoclonic jerks, had medical history available for review and died before genetic testing was available. Late onset clinical signs (those developing 3 years or more after initial presentation) in the mutation-positive group were dementia followed by panic attacks, urinary incontinence, and deafness (Table 4). The precise roles of the Epm2a and Epm2b genes remain unknown. The Dachshund Breed Council coordinated fundraising to contribute towards the cost of genetic testing. HHS Vulnerability Disclosure, Help The most common initial presenting sign was reflex and spontaneous myoclonus (77.8%). Investigation, The .gov means its official. The myoclonus in particular becomes more severe and more refractory to treatment. Rusbridge C, Fitzmaurice SN, Lohi H, Young EJ, Minassian BA. With the development of the genetic database it should become easier to identify the risk to each individual animal and eventually eliminate LD from the UK MWHD population. To more comprehensively and definitively determine the natural progression and treatment of canine LD a prospective study looking at multiple animals with genetically confirmed disease should be completed. As the disease progresses the severity, frequency and refractoriness of the seizures increase. Similar syndromes occur in other species including dogs [30] cats [31], and the grey-head flying fox [32]. The range of the onset of clinical signs was wide at 3.5 to 12 years. A characteristic feature of the disease is spontaneous and reflex myoclonus; however clinical signs and disease progression are not well described. Federal government websites often end in .gov or .mil. No, Is the Subject Area "Aggression" applicable to this article? The Southern blot based approach (Fig 2) is presently the only approved test but is expensive for the dog owner and is performed intermittently on batched samples which limits the number of dogs tested. Accessibility Bethesda, MD 20894, Web Policies broad scope, and wide readership a perfect fit for your research every time. Project administration, Clinical signs are similar to those of the human disease, including spontaneous and reflex myoclonus, hypnic jerks and generalized tonic clonic seizures [1]. The Dachshund Breed Council is affiliated with the UK Kennel Club and represents the interests of sixteen UK Dachshund Breed Clubs and appoints Health and Welfare Sub-committees to develop policies and coordinate plans for Dachshund breed health improvement. Daisy a 13 year old female spayed MWHD together with her 10 year male neutered son Bertie. https://doi.org/10.1371/journal.pone.0182024.t001. The DraIII-EcoR fragment of EPM2B gene in wild-type animal is 980 base pairs (bp), while the same fragment of EPM2B mutation allele in affected or Carrier animals is around 1200 bp. Department of Pathology and Laboratory Medicine, The Hospital for Sick Children, University of Toronto, Toronto, Canada, Roles In the untested group the most common developing late clinical signs were those of aggression towards other dogs and urinary and fecal incontinence as a result of loss of house training (disinhibited). Before Bar equals 50m. by using low carbohydrate diets such as the ketogenic diet. Current therapy for LD is aimed at limiting clinical signs of the disease. Late onset clinical signs (those developing 3 years or more after initial presentation) in the mutation-positive group were dementia followed by panic attacks, urinary incontinence, and deafness (Table 4). Both dogs have spontaneous and reflex myoclonic jerks with an intention tremor. Less frequent signs were jaw smacking, fly catching, focal seizures, aggression toward other dogs, fecal incontinence as a result of loss of house training, and deafness. Our study showed that LD in the MWHD is a progressive myoclonic epilepsy similar to the disease process in humans. Based on data published by the UK Kennel Club the frequency of carriers (34%) and genetically affected dogs (6%) is high [27] although this figure does not include hereditary clear dogs and the estimated carrier and affected rate may be closer to 20% (Ian Seath, personal communication). As an older dog Daisy is more severely affected and is nearly blind and has a high stepping hypermetric gait particularly of the pelvic limbs with a pelvic limb tremor. Animals suffering from generalized seizures have received licensed anti-epileptic drugs such as phenobarbital at standard doses and unlicensed second or third generation anti-epilepsy drugs such as leviteracetam or zonisamide [9, 40]. It is most frequent in Miniature Wirehaired Dachshunds (MWHD) [1, 8, 9], Bassett Hounds [1, 10] and Beagles [11, 12], and single cases have been reported in the Miniature and Standard Poodle [13], Pointer [14], and a Corgi [15]. Antisense oligonucleotide therapy for the fatal epilepsy Lafora disease. Myoclonus, in particular, becomes progressively more severe although anecdotally there is an initial response to levetiracetum. LD has also been reported in other species including a Fennec fox [16], cows [17] and possibly a parakeet [18]. All these clinical signs appear, and then increase over time, in all dogs (S1 Movie). Participants were also asked their opinion on the impact of LD on daily living. Work is very much underway to identify small molecule or other glycogen synthesis inhibitors to achieve 50% reduction in brain glycogen synthesis. Much smaller LBs are located throughout (small arrows). The most common sign for both were reflex and spontaneous myoclonus, hypnic myoclonus, generalized seizures, and jaw smacking. All relevant data are within the paper and its Supporting Information files. e0182024. As demonstrated by our study, LD is a significant inherited condition in MWHD, and as such knowledge of the disease is pertinent in early detection and diagnosis. Genetic testing is not routinely available because the massive dodecamer repeat expansion mutation makes PCR-based sequencing options unreliable for detecting the carrier state and consequently only a southern blot based test is offered by the University of Toronto and is an official DNA screening test recommended by the UK Kennel Club (Fig 2). It is possible that the dogs do not develop more severe signs because they would die of natural causes first [1]. With the development of the genetic database it should become easier to identify the risk to each individual animal and eventually eliminate LD from the UK MWHD population. The genetic test is Southern blotting based [12], because PCR-based sequencing options through the massive dodecamer repeat expansion mutation have so far proven inadequately reliable. Owners of affected dogs stated that they were unable to walk the dog off the leash because if it occurred then the affected dog could run off uncharacteristically. In dogs, LD is also inherited as an autosomal recessive condition and is one of the most common recognized structural-metabolic epilepsies [7]. All dogs that tested negative for LD were also excluded. Recent breed-wide testing suggests that the carrier plus affected rate may be as high as 20%. Table 2 illustrates the distribution of fourteen common clinical signs at presentation in LD for both mutation-positive and untested cases. In human or canine LD, polyglcuosan bodies are also seen in various tissues outside the brain, such as muscle, heart and liver, but in these organs, they appear to be clinically neutral, usually the patient succumbing to the neurological disease without ever having developed clinical signs of hepatic, cardiac or skeletal muscle disease. A vegetative state in constant myoclonus precedes death, which occurs in status epilepticus approximately 10 years after onset [3, 5]. Lafora disease (progressive myoclonic epilepsy) in the Bassett houndpossibility of early diagnosis using muscle biopsy? Progressive myoclonus epilepsy in a beagle. Glycogen accumulation underlies neurodegeneration and autophagy impairment in Lafora disease. SA, PW, CA and BM are employed by the Hospital for Sick Children, University of Toronto. Precisely how the laforin-malin partner enzymes regulate glycogen structure remains unclear [19, 20]. A detailed canine natural progression study will allow organization of clinical trials also in dogs. One of these is the LD Subcommittee which constructed an online survey in 2012 with the aim of assessing the clinical signs and impact of LD [24, 25]. The DraIII-EcoR fragment of EPM2B gene in wild-type animal is 980 base pairs (bp), while the same fragment of EPM2B mutation allele in affected or Carrier animals is around 1200 bp. All these clinical signs may appear, and then increase in frequency and intensity over time. Non-pathogenic polyglucosan bodies occur as an aging-related change in many species including cats, dogs and man. Less frequent clinical signs are illustrated in Table 3, https://doi.org/10.1371/journal.pone.0182024.t003. Turnbull J, Epp JR, Goldsmith D, Zhao X, Pencea N, Wang P, et al. Seath I, Holt S. Lafora Disease: Dachshund Breed Council 2014 [cited 2016 April 16th]. Conceptualization, Achieving reduced brain glycogen synthesis as a therapy for LD will therefore require approaches that directly downregulate glycogen synthesizing enzymes. Conceptualization, Myoclonus, in particular, becomes progressively more severe although anecdotally there is an initial response to levetiracetum. Electroencephalographic (EEG) measurements reveal bilateral synchronous polyspike-wave paroxysms and erratic myoclonus without EEG correlation [11]. In particular we would like to thank Ian Seath, Nora Price, Susan Holt and Roger Sainsbury for their considerable support. PTG depletion removes Lafora bodies and rescues the fatal epilepsy of Lafora disease. Ethics committee approval for this project was not sought because the decision to create and run the survey was made by the Lafora disease subcommittee (part of the Dachshund Breed Council) and ethics approval cannot be made retrospectively. Less frequent signs were jaw smacking, fly catching, focal seizures, aggression toward other dogs, fecal incontinence as a result of loss of house training, and deafness. The disease is late onset with an average age of approximately 7 years at presentation. Its early signs are myoclonus and generalized tonic-clonic seizures, along with transient blindness, visual hallucinations (often with frightening content) or photoconvulsions. PLOS ONE promises fair, rigorous peer review, Gradual precipitation, aggregation, and accumulation of polyglucosans results in massive neurotoxic inclusions (Lafora bodies; LB), which drive the neurodegenerative epilepsy [3] (Fig 3). Survey responses were excluded if the dogs were not UK bred MWHD or were mutation positive and not yet showing clinical signs. Competing interests: AT and CR are and LS was employed by Fitzpatrick Referrals Ltd, Surrey, GU7 2QQ. To improve survey accuracy technical terms were explained within the survey for example generalized seizures were explained as also known as grand mal or tonic clonic and characterized by initial stiffening of the limbs followed by jerking of the limbs and face. Clinical signs are similar to those of the human disease, including spontaneous and reflex myoclonus, hypnic jerks and generalized tonic clonic seizures [1]. Glycogen synthase is the only enzyme that catalyzes formation of 14 interglucosidic linkages that generate glycogen (or polyglucosan) strands. Neuronal somatodendritic polyglucosan bodies in young animals or humans are essentially pathognomonic of LD. In work recently published in abstract form, antisense oligonucleotides targeting glycogen synthase eliminated Lafora bodies in LD mouse models, establishing proof of principle for this strategy [43].
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