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1.
Congenital cataracts and microphthalmia in the Miniature Schnauzer were inherited as an autosomal recessive trait. Eighteen matings of affected X affected Miniature Schnauzers resulted in 87 offspring with congenital cataracts and microphthalmia (49 males/38 females). Two matings of congenital cataractous and microphthalmic Miniature Schnauzers (2 females) X a normal Miniature Schnauzer (1 male) yielded 11 clinically normal Miniature Schnauzers (7 males/4 females). Eighteen matings of congenital cataractous and microphthalmic Miniature Schnauzers (6 males) X carrier Miniature Schnauzers (9 females) produced 81 offspring; 39 exhibited congenital cataracts and microphthalmia (20 males/19 females) and 42 had clinically normal eyes (17 males/25 females).  相似文献   

2.
Myotonia is a clinical sign characterized by the delay of skeletal muscle relaxation following the cessation of a voluntary activity or the termination of an electrical or mechanical stimulus. Recently, Miniature Schnauzers with myotonia congenita associated with defective chloride ion conductance across the skeletal muscle membrane were identified. Congenital myotonia in these dogs appears to follow an autosomal recessive mode of inheritance. Craniofacial and dental findings of eight Miniature Schnauzer dogs with myotonia congenita are described in the present paper. These findings include: delayed dental eruption of both deciduous and permanent dentition: persistent deciduous dentition; unerupted or partially erupted permanent teeth: crowding and rotation of premolar and or incisor teeth: missing teeth: increased interproximal space between the maxillary fourth premolar and first molar teeth: decreased interproximal space between the maxillary canine and lateral incisor teeth: inability to fully close the mouth due to malocclusion: distoclusion: and, decreased mandibular range of motion. A long narrow skull with a flattened zygomatic arch and greater mandibular body curvature were also consistent findings in the affected dogs. The small number of dogs studied prevents conclusive statements about the origin of these abnormalities, however it is interesting that only 1 of 45 unaffected Miniature Schnauzer dogs showed similar traits.  相似文献   

3.
Multifocal retinal dysplasia was detected in 96 American Cocker Spaniels. Affected dogs were part of approximately 500 American Cocker Spaniels examined from 1972 to 1976 in statewide survey clinics for inherited cataracts and progressive retinal atrophy. The dysplastic retina was observable ophthalmoscopically in dogs as young as 3 to 4 weeks and as old as 7 years. Ophthalmoscopic features varied, depending on whether the dysplastic foci were in the tapetal or non-tapetal portion of the fundus. Over the tapetum, dysplastic foci appeared as multiple small irregularities of diminished and altered tapetal reflectivity. In the non-tapetal fundus, dysplasia appeared as areas of decreased pigmentation. Blindness or other apparent visual deficits were not observed in affected dogs. Histologic examination of affected eyes revealed focal dysplasia limited to the retina and optic nerve. Abnormalities included localized areas of retinal folding, rosettes, and retinal pigment epithelium hypertrophy and hyperplasia. Pedigree analysis demonstrated that 71 of the 96 affected dogs were related and could be identified in an extended pedigree. A recessive mode of inheritance was suggested, because in 5 litters (born to 10 affected parents), all 23 progeny that lived were affected. A dominant or polygenic mode of inheritance could not be ruled out.  相似文献   

4.
OBJECTIVES: To identify the prevalence of Borzoi chorioretinopathy in western Canada, characterize lesions with fluorescein angiography, determine if lesions were progressive, clarify the association of progressive retinal atrophy and investigate the etiology. MATERIALS AND METHODS: Serial ophthalmic examination, fundus photography, electroretinography, and fluorescein angiography were used to evaluate Borzoi dogs with lesions of Borzoi chorioretinopathy. Pedigree analysis and test breeding of two affected dogs were completed to determine the heritability of Borzoi chorioretinopathy. RESULTS: One hundred three Borzoi dogs were examined between 1998 and 2003. Focal, peripheral, tapetal, hyper-reflective and pigmented areas consistent with focal retinal degeneration and RPE pigmentation were identified in 12 dogs between 7 months and 7 years of age. Seven males and five female dogs were affected. Ophthalmoscopy and fundus photography over 5 years revealed individual lesions that did not progress or coalesce in 12 affected dogs. Electroretinography of affected and normal Borzoi dogs confirmed that retinal function was similar in normal and affected dogs up to 7 years of age. Fluorescein angiography was performed in three affected dogs and confirmed intact blood-ocular barriers, focal retinal pigment epithelium hypertrophy, and focal absence of choroiocapillaris corresponding to chronic, focal lesions. Pedigree analysis precluded simple dominant, X-linked dominant, or X-linked recessive inheritance. One male dog from the test-bred litter developed bilateral lesions at 14 months of age. Simple recessive, polygenetic, and acquired etiologies of these lesions cannot be ruled out at this time. CONCLUSIONS: Borzoi chorioretinopathy is an acquired condition that initially manifests as focal retinal edema and loss of choriocapillaris and tapetum. With time the retina degenerates becoming hyper-reflective and with RPE hyper-pigmentation and clumping within the borders of the tapetal lesions. Choriocapillaris remains hypofluorescent on fluorescein angiography. Progressive retinal atrophy was excluded as an etiology of multifocal chorioretinopathy in Borzois dogs. This condition is not inherited by simple autosomal dominant or sex-linked modes of inheritance.  相似文献   

5.
Prevalence of calcium oxalate uroliths in miniature schnauzers.   总被引：2，自引：0，他引：2  
Epidemiologic data were evaluated from all dogs admitted to the University of Minnesota, Veterinary Teaching Hospital (UMVTH) between June 1981 and November 1989. Of 69,890 admissions, 2,077 were Miniature Schnauzers. Uroliths were retrieved from 63 of the 2,077 Miniature Schnauzers admitted. In 20 of the 63 urolith episodes, calcium oxalate was the predominant mineral identified. By comparison, calcium oxalate uroliths were identified in only 56 of the remaining 67,813 non-Miniature Schnauzer canine admissions. The odds that uroliths from Miniature Schnauzers were composed of calcium oxalate was 11.8 times greater than for other canine breeds evaluated at the UMVTH (95% confidence interval = 6.8 to 20.1). Data also were evaluated from files of uroliths retrieved from dogs and submitted to the Minnesota Urolith Center for quantitative mineral analysis, between June 1981 and November 1989. Of 3,930 uroliths analyzed, 615 (15.6%) uroliths were obtained from Miniature Schnauzers. of the 615 uroliths, 175 (28.4%) were calcium oxalate. By comparison, only 550 (16.6%) of the remaining 3,315 from dogs of breeds other than Miniature Schnauzers were calcium oxalate. The odds that uroliths submitted for analysis were composed of calcium oxalate was 2 times greater for Miniature Schnauzers than for dogs of other breeds (95% confidence interval = 1.6 to 2.4). Calcium oxalate uroliths were retrieved more frequently in males than females. The risk for males developing calcium oxalate uroliths was greater than 3 times the risk for females in both groups of data evaluated. The mean age of all Miniature Schnauzers admitted to the UMVTH with calcium oxalate uroliths was 9 years. Calcium oxalate uroliths were not detected in Miniature Schnauzers younger than 1.7 years.  相似文献   

6.
Persistent Müllerian duct syndrome (PMDS) is a sex‐limited disorder in which males develop portions of the female reproductive tract. Important consequences of PMDS are cryptorchidism and its sequelae of infertility and increased risk of testicular cancer. Anti‐Müllerian hormone (AMH) and its receptor (AMHR2) induce the regression of the Müllerian ducts in male embryos. In Miniature Schnauzer dogs, the genetic basis has been identified as an autosomal recessive nonsense mutation in AMHR2, but the allele frequency of the mutation is unknown. Thus, the primary objective of this study was to estimate the prevalence of the AMHR2 mutation in North American Miniature Schnauzers, in order to ascertain the value of genetic testing in this breed. An additional objective was to determine whether mutations in AMH or AMHR2 were responsible for PMDS in a Belgian Malinois; this would aid development of a genetic test for the Belgian Malinois breed. Genomic DNA from 216 Miniature Schnauzers (including one known PMDS case) was genotyped for the AMHR2 mutation, and DNA from a single PMDS‐affected Belgian Malinois was sequenced for all coding exons of AMH and AMHR2. The Miniature Schnauzer cohort had an AMHR2 mutation allele frequency of 0.16 and a carrier genotypic frequency of 0.27. The genetic basis for PMDS in the Belgian Malinois was not determined, as no coding or splicing mutations were identified in either AMH or AMHR2. These findings support a benefit to AMHR2 mutation testing Miniature Schnauzers used for breeding or with cryptorchidism.  相似文献   

7.
OBJECTIVE: To develop a molecular genetic test to detect the mutant skeletal muscle chloride channel (CIC-1) allele that causes myotonia congenita in Miniature Schnauzers and to analyze the relationship of affected and carrier dogs. ANIMALS: 372 Miniature Schnauzers from the United States, Canada, Australia, and Europe that were tested between March 2000 and October 2001. PROCEDURE: The sequence surrounding the mutation in the CIC-1 allele was amplified by use of a unique pair of primers. Polymerase chain reaction (PCR) products were digested with the restriction enzyme Hpy CH4 III and separated on a 6% polyacrylamide gel. Pedigrees from all available carrier and affected dogs were analyzed, and a composite pedigree was established. RESULTS: Enzyme digestion of PCR products of the normal CIC-1 allele resulted in 3 fragments of 175, 135, and 30 bp, whereas PCR products of the mutant allele resulted in fragments of only 175 and 165 bp. Of the 372 Miniature Schnauzers, 292 (78.5%) were normal, 76 (20.4%) were carriers, and 4 (1.1%) were affected (myotonic) dogs. Frequency of the mutant allele was 0.113. Pedigree analysis revealed that a popular sire, documented to be a carrier, was a common ancestor of all carriers and affected dogs. CONCLUSIONS AND CLINICAL RELEVANCE: A PCR-based enzyme digestion DNA test was developed. The mutant allele for this disease is frequent in Miniature Schnauzers that are related to a common carrier ancestor. Breeding dogs should be tested by this specific DNA test to help limit the spread of this deleterious mutation.  相似文献   

8.
Congenital total blindness in three related litters of Dobermann puppies is reported. The relationship of the parents indicates an autosomal recessive mode of inheritance. The blindness resulted from a range of ocular lesions that included bilateral microphthalmia, aphakia, retinal dysplasia and detachment.  相似文献   

9.
Three eight-week-old Golden Retriever puppy littermates were evaluated because of left basilar systolic murmurs and were diagnosed with primary infundibular stenosis. Pedigree analysis in this line was also performed to identify a mode of inheritance. All dogs were asymptomatic at the time of diagnosis; two of the three had congenital lesions in addition to primary infundibular stenosis. Two additional affected dogs were identified in the line, and pedigree analysis suggested an autosomal recessive mode of inheritance. Another, unrelated golden retriever was also identified with isolated infundibular stenosis in the record database. Primary infundibular stenosis should be considered in the differential diagnoses for golden retriever dogs with a left basilar systolic murmur, and is often associated with complex congenital cardiac disease. Primary infundibular stenosis may worsen in severity with time, and in this line of dogs an autosomal recessive pattern of inheritance is likely.  相似文献   

10.
Background: Familial juvenile glomerulonephropathy (JGN) is reported in several breeds of dogs. The mode of inheritance and spectrum of pathological lesions vary among breeds. A progressive JGN was detected in a pedigree of French Mastiff (FM) dogs. Objectives: To describe clinical, laboratory, and histopathologic findings in related FM dogs suffering from progressive JGN and to determine the mode of inheritance of this condition. Animals: Sixteen affected and 35 healthy related FM dogs Methods: FM dogs <24 months of age and diagnosed with chronic kidney disease with evidence of proteinuria entered the study. Clinical, laboratory, histopathologic findings, and pedigree data were recorded. Results: Clinical signs were typical of progressive glomerulopathy with resultant renal failure. Increased blood urea nitrogen, creatinine and total cholesterol concentrations, and proteinuria were found in all patients. Affected dogs had abnormal kidney structure on abdominal ultrasound examination. Histopathologic examination revealed extensive cystic glomerular atrophy, glomerular hypercellularity, and capillary wall thickening without immune complex deposition when tested with immunohistochemistry or immunofluorescence. Electron microscopy did not disclose specific primary glomerular lesions. Mean age at death was 20 months and mean length of survival after diagnosis was 6 months. Both males and females from healthy parents were affected. An autosomal recessive mode of transmission is suspected, but a more complex mode of inheritance cannot be excluded. Conclusions and Clinical Importance: Progressive familial JGN occurs in FM dogs. Characterization of the pathogenesis and mode of inheritance of this disease warrants additional study.  相似文献   

11.
A breeding colony was established to investigate the inheritance of associated ocular and skeletal dysplasia in Labrador Retrievers; 124 pups were produced. These pups were evaluated for the presence of ocular lesions, including cataracts, vitreous strands, persistent hyaloid remnants, retinal folds, retinal dysplasia, peripapillary hyperreflectivity, and rhegmatogenous retinal detachments, and skeletal abnormality, which was recognized by shorter than normal forelimbs and an abnormal morphologic appearance of the radius and ulna. Analysis of the distribution of lesions in pups indicated that the syndrome is caused by one abnormal gene, which has recessive effects on the skeleton and incompletely dominant effects on the eye. This would suggest that suspect carrier dogs could be identified by test matings with a known homozygote.  相似文献   

12.
Background: C‐reactive protein (CRP) is a sensitive marker for inflammation in people and dogs. In people, an association between CRP concentration and atherosclerosis has been reported. Atherosclerosis is rare in dogs, but the Miniature Schnauzer breed may be at increased risk for developing this vascular disease. It is not known if CRP concentrations in Miniature Schnauzer dogs differ from those in other dog breeds. Objectives: Our objectives were to validate an automated human CRP assay for measuring CRP in dogs and compare CRP concentrations in healthy Miniature Schnauzer dogs with those in non‐Miniature Schnauzer breeds. Methods: Sera from 37 non‐Miniature Schnauzer dogs with inflammatory disease were pooled and used to validate a human CRP immunoturbidimetric assay for measuring canine CRP. Blood was collected from 20 healthy Miniature Schnauzer dogs and 41 healthy dogs of other breeds. Median serum CRP concentration of healthy Miniature Schnauzer dogs was compared with that of healthy non‐Miniature Schnauzer dogs. Results: The human CRP assay measured CRP reliably with linearity between 0 and 20 mg/L. CRP concentration for healthy Miniature Schnauzer dogs (median 4.0 mg/L, minimum–maximum 0–18.2 mg/L) was significantly higher than for the healthy non‐Miniature Schnauzer dogs (median 0.1 mg/L, minimum–maximum 0–10.7 mg/L); 17 of the 20 Miniature Schnauzer dogs had values that overlapped with those of the non‐Miniature Schnauzer dogs. Conclusions: Median CRP concentration of Miniature Schnauzer dogs was slightly higher than that of other breeds of dogs. A relationship between higher CRP concentration in Miniature Schnauzer dogs and idiopathic hyperlipidemia, pancreatitis, and possible increased risk for atherosclerosis remains to be determined.  相似文献   

13.
Background: The association between hypertriglyceridemia and pancreatitis remains obscure in dogs. A possible role of hypertriglyceridemia as a cause of pancreatitis in Miniature Schnauzers has been suspected. Hypothesis/Objectives: To compare serum triglyceride concentrations between Miniature Schnauzers with and without a recent history of pancreatitis. Animals: Seventeen Miniature Schnauzers with a history of pancreatitis (group 1) and 34 age‐matched Miniature Schnauzers without a history of pancreatitis (group 2) were prospectively enrolled. Methods: Prospective case‐control study. Two samples were collected from each of the 17 Miniature Schnauzers with pancreatitis: 1 during pancreatitis and 1 after clinical and biochemical resolution of pancreatitis. Serum triglyceride and cholesterol concentrations were compared between group 1 (after resolution of pancreatitis) and group 2. Results: Miniature Schnauzers in group 1 were significantly more likely to have hypertriglyceridemia (>108 mg/dL) (71%) after resolution of pancreatitis than Miniature Schnauzers in group 2 (33%; odds ratio = 5.02; 95% confidence interval = 1.4–17.8; P= .0163). Serum triglyceride concentrations were significantly higher in dogs of group 1 (median: 605.0 mg/dL) after resolution of pancreatitis than in dogs of group 2 (median: 73.5 mg/dL; P= .002). Conclusions and Clinical Importance: Miniature Schnauzers with a history of pancreatitis were 5 times more likely to have hypertriglyceridemia than controls. Hypertriglyceridemia might be associated with the development of pancreatitis in some dogs of this breed. Additional studies are needed to further clarify the role of hypertriglyceridemia in the development of pancreatitis in Miniature Schnauzers as well as other dog breeds.  相似文献   

14.
A study was conducted to define the mode of inheritance of lateral luxation of the superficial digital flexor (SDF) tendon in different lines of Shetland sheepdogs by examination of pedigree data. This pedigree analysis included affected and unaffected dams, sires, and offspring; common clinical signs; and age at onset. The clinical, histopathologic, and radiographic features of the disease were also studied. Of the 14 offspring from five matings of an affected sire to unrelated affected females, 100% were affected with lateral luxation of the SDF tendon. Of the 59 offspring from the same affected sire to unrelated, unaffected females, 44% were affected. The mating between normal parents produced 61% unaffected and 39% affected offspring. Application of the phenotypic findings in this study to a Mendelian genetic model of inheritance suggests that lateral luxation of the superficial digital tendon in Shetland sheepdogs is inherited as a simple autosomal recessive trait.  相似文献   

15.
To better characterize the idiopathic hyperlipoproteinemia of Miniature Schnauzer dogs, the plasma lipoproteins of 20 Miniature Schnauzers (MS) and 11 dogs of other breeds (DOB) were evaluated by ultracentrifugation, electrophoresis, and biochemical tests. Seventeen MS were healthy; 3 had diabetes mellitus. Plasma from 6 of 17 healthy and all 3 diabetic MS was visibly lipemic. Lipemia was slight to marked in healthy lipemic MS, and marked in diabetic ones. All DOB had clear plasma; 8 were healthy and 3 had diabetes. All healthy lipemic MS and diabetic lipemic MS had hypertriglyceridemia associated with excess very low density lipoproteins. Chylomicronemia was present in 4 of 6 healthy lipemic MS and all 3 diabetic lipemic MS. Lipoproteins with ultracentrifugal and electrophoretic characteristics of normal low density lipoprotein were lacking in 4 of 6 healthy lipemic MS. The lipoprotein patterns of 4 of 11 healthy nonlipemic MS were characterized by mild hypertriglyceridemia associated with increased very low density lipoproteins and a lack of lipoproteins with characteristics of normal low density lipoproteins. Lipoprotein patterns of diabetic DOB closely resembled those of healthy DOB; those of diabetic lipemic MS resembled those of markedly lipemic healthy lipemic MS. In conclusion, the hyperlipoproteinemia of Miniature Schnauzers is characterized by increased very low density lipoproteins with or without accompanying chylomicronemia; some affected dogs may have decreased low density lipoproteins. (Journal of Veterinary Internal Medicine 1993; 7:253–260. Copyright © 1993 by the American College of Veterinary Internal Medicine.)  相似文献   

16.
Hereditary cataract in the dog is described as it occurs in the Boston Terrier, the Staffordshire Bull Terrier, the Miniature Schnauzer, the Golden Retriever, the Labrador Retriever, the American Cocker Spaniel, the Afghan Hound, and the Old English Sheepdog. The mode of inheritance in each breed is also discussed and includes both dominant and recessive patterns.  相似文献   

17.
To evaluate underlying causes of calcium oxalate urolithiasis, 24-hour excretion of urine metabolites was measured in 6 Miniature Schnauzers that formed calcium oxalate (CaOx) uroliths during periods when they were fed a standard diet and during periods when food was withheld. Serum concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D also were evaluated. Serum calcium concentrations were normal in all 6 affected Miniature Schnauzers; however, during diet consumption, mean 24-hour urinary excretion of calcium was significantly (P = 0.025) higher than calcium excretion when food was withheld. In 1 dog, urinary calcium excretion was lower during the period of food consumption, compared with the period when food was withheld. Compared with clinically normal Beagles, Miniature Schnauzers that formed CaOx uroliths excreted significantly greater quantities of calcium when food was consumed (P = 0.0004) and when food was withheld (P = 0.001). Miniature Schnauzers that formed CaOx uroliths excreted significantly less oxalate than clinically normal Beagles during fed (P = 0.028) and nonfed (P = 0.004) conditions. Affected Miniature Schnauzers also excreted abnormally high quantities of uric acid. Excretion of citrate was not different between Miniature Schnauzers with CaOx urolithiasis and clinically normal Beagles. In 5 of 6 Miniature Schnauzers with CaOx urolithiasis, concentrations of serum parathyroid hormone were similar to values from age- and gender-matched Miniature Schnauzers without uroliths. The concentration of serum parathyroid hormone in 1 dog was greater than 4 times the mean concentration of clinically normal Miniature Schnauzers. Mean serum concentrations of 1,25-dihydroxyvitamin D in Miniature Schnauzers with calcium oxalate urolithiasis were similar to concentrations of clinically normal Miniature Schnauzers.  相似文献   

18.
Objective To retrospectively review ophthalmologic findings in German Pinschers in Finland. Animals studied One hundred and twenty‐two German Pinschers that had ophthalmologic examination performed according to the Finnish Kennel Club’s Eye Scheme before June 15, 1999. Procedures A total of 154 eye examination reports of 122 dogs were analysed and all described findings were reported. Results Persistent hyperplastic tunica vasculosa lentis (PHTVL) was diagnosed in 8.4% of all cases, and hereditary cataract (HC) in 6.5%. Even higher numbers of similar changes were reported by ophthalmologists; some of the dogs, however, were officially diagnosed as ‘free of symptoms’ of inherited ocular diseases. A relatively high number (4.5%) of dogs had reported changes in Y sutures. A pedigree analysis suggests recessive inheritance for both diseases. Because of missing information about many dogs in the pedigree, an autosomal incomplete inheritance pattern cannot be ruled out in either case. Conclusions Both HC and PHTVL are inherited diseases in German Pinschers. Further studies are needed to determine the importance of the changes found in Y sutures. Discrepancies between the official diagnosis and described changes are probably partially due to the lack of familiarity with the published literature concerning this breed. Further studies are needed to ascertain the inheritance pattern for both diseases. So far breeding with affected animals should be avoided.  相似文献   

19.
OBJECTIVE: To determine whether hypertriglyceridemia in healthy Miniature Schnauzers is associated with high serum liver enzyme activities. DESIGN: Cross-sectional study. ANIMALS: 65 Miniature Schnauzers with serum triglyceride concentrations within the reference range (group 1), 20 Miniature Schnauzers with slightly high serum triglyceride concentrations (group 2), and 20 Miniature Schnauzers with moderately to severely high serum triglyceride concentrations (group 3). PROCEDURES: Questionnaires regarding each dog's medical history were completed, and serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and G-glutamyltransferase (GGT) activities were measured. RESULTS: Median serum ALP activity was significantly higher in group 3 than in group 1 or 2 dogs, but was not significantly higher in group 2 than in group 1 dogs. Median serum ALT activity was significantly higher in group 3 than in group 1 dogs, but was not significantly different between any of the other groups. Compared with group 1 dogs, group 2 and 3 dogs were significantly more likely to have high serum ALP activity (odds ratio, 26.2 and 192.6, respectively). Group 3 dogs also were significantly more likely to have high serum ALT activity (odds ratio, 8.0), serum AST activity (odds ratio, 3.7), and serum GGT activity (odds ratio, 11.3), compared with group 1 dogs. Group 3 dogs were significantly more likely (odds ratio, 31.0) to have > or = 2 high serum liver enzyme activities than were group 1 dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that moderate to severe hypertriglyceridemia was associated with high serum liver enzyme activities in Miniature Schnauzers.  相似文献   

20.
O bjectives : To study forms of congenital heart disease present in a family of beagle dogs with a strong prevalence of ventricular septal defect and to document the pathological findings associated with the ventricular septal defects and investigate the mode of transmission.
M ethods : The animals were investigated by physical examination, radiography, electrocardiography and ultrasonography to diagnose the presence of congenital heart disease. Some animals were diagnosed at post-mortem examination and the dead animals underwent post-mortem examination to verify the presence of ventricular septal defect. An analysis of pedigree was undertaken and two of the affected animals were mated to investigate the mode of transmission.
R esults : Among the 28 dogs evaluated clinically or by post-mortem examination, 14 cases of ventricular septal defect were identified. The post-mortem examination showed some abnormalities of the ventricular outflow region associated with malformation of conotruncal septum development. When two affected dogs were bred, congenital heart disease was present in all of the offspring.
C linical S ignificance : The congenital heart disease identified in this beagle family can be classified as conotruncal malformation, and an autosomal recessive mode of inheritance was suggested by pedigree analysis.  相似文献   

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