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Simple Summary Abnormal, repetitive behaviors often pose a problem for dog owners. Such behaviors are considered undesirable if they pose a nuisance or a danger to humans. This study aimed to identify factors (breed, sex, origin, housing conditions) and situations that contribute to undesirable behaviors, such as aggression towards humans and other dogs/animals, separation anxiety, excessive vocalization, and oral and locomotion behaviors in the ancient dog breeds Akita, Alaskan Malamute, Basenji, Samoyed and Siberian husky. Undesirable behaviors were analyzed based on the results of a survey involving dog owners. Undesirable behaviors were most frequently reported in Akitas, Siberian huskies and Samoyeds, and they were more prevalent in males than in females and dogs living indoors with or without access to a backyard. Aggressive behaviors towards other dogs and animals, excessive vocalization and undesirable motor activities posed the greatest problems in ancient dog breeds. Abstract Abnormal repetitive behaviors often pose problems for dog owners. Such behaviors are considered undesirable if they pose a nuisance or a danger to humans. Ancient dog breeds are intelligent, sociable, active, boisterous and need regular outdoor exercise, but are also independent and reluctant to follow commands. This study aimed to identify factors (breed, sex, origin, housing conditions) and situations that contribute to undesirable behaviors, such as aggression towards humans and other dogs/animals, separation anxiety, excessive vocalization, and oral and locomotion behaviors in Akita, Alaskan Malamute, Basenji, Samoyed and Siberian husky. Undesirable behaviors in dogs were analyzed based on the results of 897 questionnaires. Breed influenced aggressive behavior towards other dogs/animals, aggression towards humans, undesirable oral and locomotion behaviors, and excessive vocalization. Aggressive behaviors were more prevalent in females than in males. Housing conditions were linked with aggression towards other dogs/animals, aggression at mealtime, and excessive vocalization. Undesirable behaviors were most frequently reported in Akitas, Siberian huskies and Samoyeds, and they were more prevalent in males than in females and dogs living indoors with or without access to a backyard. Aggressive behaviors towards other dogs and animals, excessive vocalization and undesirable motor activities posed the greatest problems in ancient dog breeds.

Mutations in the N-myc downstream-regulated gene 1 (NDRG1) cause degenerative polyneuropathy in ways that are poorly understood. We have investigated Alaskan Malamute dogs with neuropathy caused by a missense mutation in NDRG1. In affected animals, nerve levels of NDRG1 protein were reduced by more than 70% (p< 0.03). Nerve fibers were thinly myelinated, loss of large myelinated fibers was pronounced and teased fiber preparations showed both demyelination and remyelination. Inclusions of filamentous material containing actin were present in adaxonal Schwann cell cytoplasm and Schmidt-Lanterman clefts. This condition strongly resembles the human Charcot-Marie-Tooth type 4D. However, the focally folded myelin with adaxonal infoldings segregating the axon found in this study are ultrastructural changes not described in the human disease. Furthermore, lipidomic analysis revealed a profound loss of peripheral nerve lipids. Our data suggest that the low levels of mutant NDRG1 is insufficient to support Schwann cells in maintaining myelin homeostasis.

Peripheral nerves transmit signals between peripheral tissue and the central nervous system, essential for normal motor and sensory function. To enable this, the integrity of both the axon and Schwann cell is crucial. The Schwann cell forms a myelin sheath around large diameter axons, necessary for rapid nerve conduction and axonal survival. Neuropathies, diseases affecting peripheral nerves, have diverse etiologies and may cause severe clinical signs in both human and animals. Some neuropathies are caused by inherited deficiencies in proteins necessary for normal axonal function or formation/maintenance of the myelin sheath. In this work, we have investigated how deficiencies in NDRG1 or PrPC affect peripheral nerve myelin maintenance by using morphological studies in two unique, spontaneous animal models. The hereditary polyneuropathy of Alaskan Malamutes is associated with a mutation in N-myc downstream-regulated gene 1 (NDRG1). Other mutations in the same gene cause polyneuropathies in humans, rodent models and Greyhound show dogs. However, the function of NDRG1 in peripheral nerves is largely unknown and the pathomorphological changes described in NDRG1-associated neuropathies of different species diverge. Whereas the human disease, denominated Charcot-Marie-Tooth disease type 4D, is considered a primary demyelinating disease with secondary axonal loss, axonal degeneration dominated in the polyneuropathy of Greyhounds. A detailed mapping of NDRG1 in canine tissues and cells presented in this thesis revealed high NDRG1 expression in epithelia and myelinating Schwann cells. A phosphorylated isoform of the protein localized to the centrosomes and cleavage furrow in a primary canine Schwann cell culture. Phosphorylated NDRG1 was restricted to the abaxonal cytoplasm of myelinating Schwann cells in control dogs, but this signal was not observed in an affected Alaskan Malamute. Ultrastructural studies and teased fiber preparations of nerves from neuropathic Alaskan Malamutes uncovered a demyelinating neuropathy associated with accumulation of actin in the Schwann cell and prominent myelin infoldings. The latter ultimately segregated the axon into pockets with aggregates of organelles, suggestive of early axonal degeneration. We therefore suggest that impaired NDRG1 function in the myelinating Schwann cells of affected Alaskan Malamutes results in deranged myelin maintenance, demyelination and secondary axonal degeneration. The cellular prion protein (PrPC) has been studied extensively because of its role in the development of transmissible spongiform encephalopathies in several species, such as Creutzfeldt-Jakobs disease in humans, bovine spongiform encephalopathy (“mad cow disease”) in cattle and scrapie in small ruminants. In these diseases, a misfolded isoform of the protein, PrPSc, accumulates in the brain and ultimately results in neuronal death. The normal functions of PrPC are not fully understood. Some of the phenotypes reported from transgenic mice lacking PrPC have later been ascribed to other genes, but recent reports have suggested that PrPC is important in dampening pro-inflammatory signaling and in myelin maintenance. We have used a nontransgenic, spontaneous model to investigate the latter; a line of Norwegian dairy goats lacking PrPC. Morphological studies revealed a demyelinating neuropathy with infiltration of macrophages and lymphocytes, vacuolated fibers and paranodal myelin outfoldings. Peripheral nerve lipid composition of adult goats lacking PrPC was significantly different from controls, while no difference was observed in young goats, suggesting a progressive disease. In conclusion, this is the first report of a demyelinating polyneuropathy caused by loss of PrPC in a nontransgenic mammal, supporting that PrPC has a vital role in peripheral nerve myelin maintenance. Perifere nerver overfører nerveimpulser mellom perifert vev og sentralnervesystemet, og er derfor essensielle for normal motorisk og sensorisk funksjon. For opprettholdelse av denne funksjonen, er både aksonet og den Schwannske cellen viktige. Aksonet er en utløper fra nervecellen og sørger for overføring av nerveimpulser. Den Schwannske cellen danner en myelinskjede rundt større aksoner. Dette er nødvendig for rask nerveledningshastighet og aksonal overlevelse. Nevropatier, sykdommer i perifere nerver, har ulik etiologi og kan forårsake alvorlige kliniske tegn både hos mennesker og dyr. Noen nevropatier er forårsaket av arvelige forstyrrelser i proteiner som er nødvendig for normal aksonal funksjon eller dannelse/vedlikehold av myelinskjeden. I dette arbeidet har vi undersøkt hvordan mangel på NDRG1 eller PrPC påvirker myelinvedlikehold i perifere nerver ved å bruke morfologiske studier i to unike, spontane dyremodeller. Arvelig polynevropati hos alaskan malamute er assosiert med en mutasjon i N-myc downstream-regulated gene 1 (NDRG1). Andre mutasjoner i samme genet forårsaker polynevropatier hos menneske, gnagermodeller og utstillingslinjer av greyhound. Funksjonen til NDRG1 i perifere nerver er imidlertid ukjent, og de patomorfologiske forandringene ved NDRG1-assosierte nevropatier hos ulike arter divergerer. Mens den humane nevropatien, Charcot-Marie-Tooths sykdom type 4D, er ansett for å være en primær demyeliniserende sykdom med sekundært aksonalt tap, dominerte aksonal degenerasjon ved polynevropati hos greyhound. En detaljert kartlegging av NDRG1 i celler og vev fra hund presentert i denne avhandlingen viser høye nivåer av NDRG1 i epitel og myeliniserende Schwannske celler. En fosforylert isoform av proteinet ble lokalisert i centrosomer og kløyvingsfuren hos Schwannske celler isolert fra hund. Fosforylert NDRG1 var begrenset til abaksonale cytoplasma i myeliniserende Schwannske celler i kontrollhunder, men dette signalet ble ikke observert i en syk alaskan malamute. Ultrastrukturelle studier og teased nerve fibers av nerver fra affiserte alaskan malamuter avslørte en demyeliniserende nevropati assosiert med aktinaggregater i de myeliniserende Schwannske cellene og uttalte innfoldinger av myelin. Innfoldingene delte stedvis aksonene inn i atskilte lommer med aggregater av organeller, forenelig med tidlig aksonal degenerasjon. Resultatene tyder på at svekket NDRG1-funksjon i myeliniserende Schwannske celler hos affiserte alaskan malamuter fører til forstyrret vedlikehold av myelin, demyelinisering og sekundær aksonal degenerasjon. Det cellulære prionproteinet (PrPC) har blitt grundig studert på grunn av sin rolle i utvikling av overførbare spongiforme encefalopatier, eller prionsykdommer, hos flere arter, for eksempel Creutzfeldt-Jakobs sykdom hos menneske, bovin spongiform encefalopati («kugalskap») hos storfe og skrapesjuke hos små drøvtyggere. Ved disse sykdommene vil en misfoldet isoform av proteinet, PrPSc, akkumulere i hjernen og tilslutt resultere i nevronal celledød. Normalfunksjonen til PrPC er ikke fullstendig forstått, og forståelsen av denne kan være viktig for å belyse den molekylære patogenesen ved prionsykdommer. Noen fenotyper rapportert fra transgene mus uten PrPC ble senere vist å skyldes andre gener, men nylige rapporter foreslår at PrPC er viktig for å dempe proinflammatorisk signalering og myelinvedlikehold. Vi har brukt en ny, ikke-transgen, spontan modell - en linje av norske melkegeiter som mangler PrPC - til å undersøke om denne modellen kan bekrefte tidligere studier fra transgene mus som har vist myelinskader. Morfologiske studier hos geiter uten PrPC avslørte en demyeliniserende nevropati med infiltrasjon av makrofager og lymfocytter, vakuoliserte nervefibre og paranodale myelinutfoldinger. Lipidsammensetningen i perifere nerver hos voksne geiter uten PrPC var signifikant forskjellig fra kontrollene, mens ingen forskjell ble observert hos unge dyr, noe som tyder på en progredierende sykdom. Dette er den første rapporten av en demyeliniserende polynevropati forårsaket av PrPC-mangel hos et ikke-transgent pattedyr, og støtter at PrPC har en viktig rolle i myelinvedlikehold.

Cone degeneration (cd; day blindness) is one of the inherited retinal diseases of dogs. Its diagnosis is based on vision testing, fundoscopy, electroretinography (ERG) and, for some breeds, on genetic tests. Typical signs of the disease are day blindness and cone dysfunction during ERG while fundoscopy does not show any abnormalities. The aim of this study was to compare behavioural findings, fundoscopic lesions and electroretinographic alterations in 12 cd-affected dogs (Alaskan Malamute, Labrador Retriever, German Shepherd, Dachshund, Yorkshire Terrier, Shih Tzu, Siberian Husky and crossbreeds) examined at our clinic. None of the examined dogs had any fundoscopic lesions, and all of them had normal scotopic vision with strongly impaired or absent photopic vision. Light-adapted transient, cone-mediated and steady-state, 31-Hz cone flicker ERGs were much below the 5th percentile limits of normality or even unrecordable, while the rod-driven ERGs were within normal values. Vision test and ERG results corresponded to each other and, combined with the results of fundoscopy, were typical of cd. To date, our research is one of the few studies in the world presenting ERG alterations compared with vision test findings and fundoscopic results in the course of cd.

Primary ciliary dyskinesia (PCD) is a hereditary defect of motile cilia in humans and several domestic animal species. Typical clinical findings are chronic recurrent infections of the respiratory tract and fertility problems. We analyzed an Alaskan Malamute family, in which two out of six puppies were affected by PCD. The parents were unaffected suggesting autosomal recessive inheritance. Linkage and homozygosity mapping defined critical intervals comprising ~118 Mb. Whole genome sequencing of one case and comparison to 601 control genomes identified a disease associated frameshift variant, c.43delA, in the NME5 gene encoding a sparsely characterized protein associated with ciliary function. Nme5-/- knockout mice exhibit doming of the skull, hydrocephalus and sperm flagellar defects. The genotypes at NME5:c.43delA showed the expected co-segregation with the phenotype in the Alaskan Malamute family. An additional unrelated Alaskan Malamute with PCD and hydrocephalus that became available later in the study was also homozygous mutant at the NME5:c.43delA variant. The mutant allele was not present in more than 1000 control dogs from different breeds. Immunohistochemistry demonstrated absence of the NME5 protein from nasal epithelia of an affected dog. We therefore propose NME5:c.43delA as the most likely candidate causative variant for PCD in Alaskan Malamutes. These findings enable genetic testing to avoid the unintentional breeding of affected dogs in the future. Furthermore, the results of this study identify NME5 as a novel candidate gene for unsolved human PCD and/or hydrocephalus cases., Author summary Motile cilia are required for clearing mucous, infectious agents and inhaled dust from the airways. Primary ciliary dyskinesia (PCD) is a hereditary defect of motile cilia. Clinical findings may include recurrent airway infections, fertility problems, and sometimes hydrocephalus. We analyzed an Alaskan Malamute family, in which two out of six puppies were affected by an autosomal recessive form of PCD. Whole genome sequencing of an affected dog identified a one base pair deletion in the NME5 gene, c.43delA, leading to an early frame-shift and premature stop codon. Later in the study, we became aware of a previously published Alaskan Malamute with PCD involving respiratory infections and hydrocephalus. We observed perfect concordance of the NME5 genotypes with the PCD phenotype in all three affected Alaskan Malamutes and more than 1000 controls. The fact that the third case, which had no documented close relationship to the initial two cases, was homozygous for the same rare mutant NME5 allele, strongly supports our hypothesis that NME5:c.43delA causes the PCD phenotype. We confirmed absence of NME5 protein expression in nasal epithelium of an affected dog. Our results enable genetic testing in dogs and identify NME5 as novel candidate gene for unsolved human PCD cases.

Background Mutations in the N-myc downstream-regulated gene 1 (NDRG1) can cause degenerative polyneuropathy in humans, dogs, and rodents. In humans, this motor and sensory neuropathy is known as Charcot-Marie-Tooth disease type 4D, and it is assumed that analogous canine diseases can be used as models for this disease. NDRG1 is also regarded as a metastasis-suppressor in several malignancies. The tissue distribution of NDRG1 has been described in humans and rodents, but this has not been studied in the dog. Results By immunolabeling and Western blotting, we present a detailed mapping of NDRG1 in dog tissues and primary canine Schwann cell cultures, with particular emphasis on peripheral nerves. High levels of phosphorylated NDRG1 appear in distinct subcellular localizations of the Schwann cells, suggesting signaling-driven rerouting of the protein. In a nerve from an Alaskan malamute homozygous for the disease-causing Gly98Val mutation in NDRG1, this signal was absent. Furthermore, NDRG1 is present in canine epithelial cells, predominantly in the cytosolic compartment, often with basolateral localization. Constitutive expression also occurs in mesenchymal cells, including developing spermatids that are transiently positive for NDRG1. In some cells, NDRG1 localize to centrosomes. Conclusions Overall, canine NDRG1 shows a cell and context-dependent localization. Our data from peripheral nerves and primary Schwann cell cultures suggest that the subcellular localization of NDRG1 in Schwann cells is dynamically influenced by signaling events leading to reversible phosphorylation of the protein. We propose that disease-causing mutations in NDRG1 can disrupt signaling in myelinating Schwann cells, causing disturbance in myelin homeostasis and axonal-glial cross talk, thereby precipitating polyneuropathy.

Signalment: An 8-month-old female Alaskan malamute was presented for progressive cluster seizure disorder. Results: There were no abnormalities on neurological examination, survey radiographs, or blood analysis. Magnetic resonance (MR) imaging and computed tomography revealed extension of the olfactory bulb and frontal lobe into the nasal cavity. They also confirmed abnormal anatomy of the nasal turbinates within the rostral part of the nasal cavity and the absence of a cribriform plate. On T2-weighted and fluid-attenuated inversion recovery images, the herniated brain showed heterogeneous and hyperintense signals consistent with intraparenchymal edema. Transverse MR images showed brain herniation into the right frontal cavity and an asymmetrical lateral ventricle because of a left midline shift. On contrast-enhanced MR images, the protruding brain parenchyma was mildly enhanced. Ethmoidal encephalocele was suspected as the final diagnosis. Despite symptomatic treatment, the dog continued to exhibit seizures and was euthanized. Clinical relevance: Ethmoidal encephalocele is a rare disease in dogs. However, it could be considered as a cause of seizure in young dogs.

Background Malignant fibrous histiocytoma has been uncommonly described in dogs. Several extranasal neoplasias have been reported to result hypertensive epistaxis. There are, however, no published case reports of extranasal malignant fibrous histiocytoma with concurrent hypertension and epistaxis in dogs. Case presentation A 10-year-old dog presented with a spontaneous massive epistaxis persisting for 5 days. The dog exhibited unstable hypertension, which was considered as a cause of epistaxis. The complete blood count, prothrombin time, and activated partial thromboplastin time were within the reference limits, and other systemic examination showed no abnormalities except for a splenic mass occupying more than one third of the abdomen. Histologic examination of the resected spleen revealed the characteristic features of a malignant fibrous histiocytoma. One week after splenectomy, the hypertension and epistaxis resolved clinically and did not recur on the 5-month follow-up. Conclusions The dog’s blood pressure and epistaxis normalized after malignant fibrous histiocytoma resection suggesting that hypertensive epistaxis may be a rare manifestation of canine malignant fibrous histiocytoma.

Cartilaginous tumors of the larynx and trachea are uncommon in the dog. The authors describe 10 cases diagnosed between 1995 and 2014 and review 16 cases in the literature. Seven of our cases were tracheal and 3 were laryngeal. Two of the laryngeal tumors were chondromas, which have not been previously reported in this site. The third laryngeal tumor was a myxochondroma. Of the 7 tracheal tumors, 6 arose from the ventral tracheal wall, including 2 that were extraluminal. Tracheal tumor types included chondrosarcoma ( n = 3), chondroma ( n = 2), and osteochondroma ( n = 2). All of the laryngeal tumors and 5 of 7 of the tracheal tumors occurred in adult dogs (aged 5–11 years). The 2 tracheal osteochondromas were in young dogs (3–4 months) and were intrathoracic, while the remaining tracheal tumors were cervical. Surgical excision had a good outcome in most cases. Combining our 10 cases with the 16 previously reported cases showed that 6 (27%) of the affected dogs were Arctic breeds (Alaskan Malamute or Siberian Husky) suggesting a predisposition in this type of dog.

The aim of this study was to investigate the usefulness of hair to monitor the body content level of polonium activity, the utility of animals hair as a non-invasive indicator of exposure for natural 210Po. Among Polish dogs the highest 210Po concentrations were measured in 2 years old Shih Tzu and Bichon Maltese, small longhair males. Among Norwegian, 210Po concentrations were much higher and its highest values were measured in hair collected from 1 year old Greenland Dog and 3 years old Alaskan Malamute, also males. Mainly dogs’ gender and diet influenced the values of 210Po concentrations in analyzed samples.

Consciousness is the greatest enigma in human history. For centuries scientists and researchers have tried to describe it without coming to conclusions. In the last years with the neurosciences development, consciousness has become the common goal of numerous studies. But consciousness has always been studied only in humans, but after "Cambridge Declaration on Consciousness" in 2012, even non-human animalsthey feel possessed of the consciousness. According to "theory Orch-OR" of Hameroff and Penrose we have conducted a study on Alaskan malamute and German shepherd to analysed a triplet of platelet fatty acids (linoleic acid; palmitic acid; arachidonic acid). Through these analysis and the relative mapping of subjects within a SOM it was possible to make an assessment of the possible onset of mood disorders in the dogs. A critical analysis of the results obtained shows that animals have molecular analogies with humans compared to mood disorders. The German shepherd and Alaskan malamute, indeed, have, in the case of major depression, a bio-chemical profile, the most similar to man.

7-year-old, male Alaskan malamute was referred for a routine dental management. On the physical examination, the right hindlimb ataxia with a mild delay in proprioception was noted. On magnetic resonance images, an extradural ventral cystic structure compressing the spinal cord was found at the level between the first and second lumbar vertebra. The cyst showed hypointense on a T1-weighted image with rim enhancement and hyperintense on a T2-weighted image. The cystic lesion was removed through right-side hemilaminectomy. In the histopathological examination, evenly distributed fibroblasts and collagenous stroma with several cartilaginous materials were seen. The neurological signs of the right hindlimb were successfully recovered within a week in follow-up neurological examination and showed normal gait at 6 months after surgery.

An Alaskan Malamute underwent unilateral tibial tuberosity advancement (TTA) surgery to stabilise a stifle joint with a deficient cranial cruciate ligament. The dog made an excellent recovery with no postoperative complications, until 20 months post-surgery when he presented with acute onset ipsilateral pelvic limb lameness. Osteosarcoma (OSA) was diagnosed adjacent to the titanium implants. Currently, there is a paucity of information on the epidemiology of OSA adjacent to orthopaedic implants in canine patients. The clinical, radiological and pathological findings of this case of periprosthetic OSA, and a potential causal relationship between titanium implants and bone neoplasia, are discussed.

Summary Objective: To prove the hypothesis that a polyneuropathy in Alaskan Malamutes has a genetic background. Material and methods: Pedigrees of 131 related Alaskan Malamutes were included in the current study. Neurological examination, electrodiagnosis as well as muscle and nerve biopsies could be performed in 10 dogs. Information about the disease status of the other 121 Alaskan Malamutes were supplied by referring veterinarians, breeders and owners. Segregation analysis using four different models (monogenic, polygenic, mixed monogenicpolygenic and the phenotypic model) was performed on 71 dogs to test the different mechanisms of genetic transmission. Results: In seven clinically affected dogs abnormal electromyographic findings and reduced nerve conduction velocity were detected. Suspected diagnosis of polyneuropathy was confirmed by nerve biopsy results, characterized by axonal degeneration and hypomyelination. Muscle specimens revealed signs of neurogenic myopathy. Three related clinically normal Alaskan Malamutes also displayed moderate neuromuscular changes in histopathology. In the segregation analysis the polygenic model proved as best suitable to explain the observed segregation pattern among all other models tested. Conclusion: The current study could demonstrate that polyneuropathy in Alaskan Malamutes is a hereditary disease with variable phenotypic expression ranging from severely affected to subclinical forms, which has to be considered in future gene analysis studies.

Alaskan sled dogs are a genetically distinct population shaped by generations of selective interbreeding with purebred dogs to create a group of high-performance athletes. As a result of selective breeding strategies, sled dogs present a unique opportunity to employ admixture-mapping techniques to investigate how breed composition and trait selection impact genomic structure. We used admixture mapping to investigate genetic ancestry across the genomes of two classes of sled dogs, sprint and long-distance racers, and combined that with genome-wide association studies (GWAS) to identify regions that correlate with performance-enhancing traits. The sled dog genome is enhanced by differential contributions from four non-admixed breeds (Alaskan Malamute, Siberian Husky, German Shorthaired Pointer, and Borzoi). A principal components analysis (PCA) of 115,000 genome-wide SNPs clearly resolved the sprint and distance populations as distinct genetic groups, with longer blocks of linkage disequilibrium (LD) observed in the distance versus sprint dogs (7.5-10 and 2.5-3.75 kb, respectively). Furthermore, we identified eight regions with the genomic signal from either a selective sweep or an association analysis, corroborated by an excess of ancestry when comparing sprint and distance dogs. A comparison of elite and poor-performing sled dogs identified a single region significantly associated with heat tolerance. Within the region we identified seven SNPs within the myosin heavy chain 9 gene (MYH9) that were significantly associated with heat tolerance in sprint dogs, two of which correspond to conserved promoter and enhancer regions in the human ortholog.

Calcinose circunscrita ou calcinose tumoral é uma mineralização ectópica que apresenta-se na forma de depósito de cálcio em tecidos moles e pode manifestar-se em diversas espécies. Alguns autores recomendam usar o termo calcinose tumoral quando a deposição dos sais de cálcio ocorre no tecido periarticular e calcinose circunscrita quando localizada no tecido subcutâneo. Pode ocorrer na coluna vertebral e levar à compressão da medula espinhal. O quadro neurológico, quando se instala é progressivo e provoca distúrbios de leves a moderados. Com exceção da calcinose metastática, o tratamento indicado é a remoção cirúrgica, com baixo índice de recidiva da lesão e redução e/ou resolução das lesões neurológicas. O trabalho teve o objetivo de relatar um caso de compressão de medula espinhal cervical causada por uma calcinose tumoral entre o atlas e o axis em um cão Malamute do Alaska de oito meses de idade, o qual foi submetido a procedimento cirúrgico para remoção do tecido alterado. As alterações histológicas classificaram a massa como uma calcinose tumoral. Devido ao grau de compressão na medula, natureza progressiva da doença e prognóstico favorável, foi feita a opção pela remoção cirúrgica do tumor. Neste caso, a calcinose tumoral determinou compressão da medula espinhal com sinais neurológicos de dor e deficiência funcional leve, assimétrica, da locomoção e de reações posturais. Calcinosis circumscripta or tumoral calcinosis is an ectopic mineralization that presents itself in the form of calcium deposit in soft tissues and can be disclosed in many species. Some authors recommend to use the term tumoral calcinosis when deposition of calcium salts occur in the periarticular tissue and calcinosis circumscripta when it happens in the subcutaneous tissue. It can occur in the vertebral spine and lead to compression of the spinal cord. The neurological scene when it happens is progressive and provokes light to moderate riots. With exception of metastatic calcinosis, the indicated treatment is surgical removal, which has low relapse of the injury plus reduction and/or resolution of the neurological injuries. This report´s objective is to tell a case of compression of cervical spinal cord caused by a tumoral calcinosis between the atlas and the axis in an eight-year Alaska malamute dog which was submitted to surgical procedure for removal of modified tissue. The histologic alterations had classified the mass as a tumoral calcinosis one. Due to the cord compression degree, plus the desease progressive nature and positive prognosis, it was made the option for surgical tumoral mass removal. In this case, the tumoral calcinosis has determined spinal cord compression with neurological pain signals and subtle functional and antisymmetrical deficiency of locomotion and of position reaction.

By using a simple method of two-dimensional horizontal electrophoresis, phenotypes of an unidentified plasma protein (PA4) were determined in 967 dogs belonging to 43 different breeds. Two codominant, autosomal alleles (F and S) of PA4 were reported. While many of the breeds of middle and north-eastern Asia (akita inu, Alaskan malamute, chow chow, samoyed, Siberian husky and Tibetan terrier) showed a substantial frequency (0.1 to 0.6) of the S allele, a majority of the European breeds had only the F allele. Evidence was provided that the PA4 locus is closely linked to the plasma pretransferrin 1 locus (PRT1). No recombinant was observed in 45 informative offspring studied. In nearly all breeds, the PA4 S allele was almost always in coupling phase with the PRT1 F allele.