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Biomedical subjects

N M Duncan

Publications and source records attributed to N M Duncan.

8 recordsLinked to original sources
PubMed2005

Spinal spondylosis and acute intervertebral disc prolapse in a European brown bear (Ursus arctos arctos).

A 22-year-old male European brown bear (Ursus arctos arctos) was presented to the Onderstepoort Veterinary Academic Hospital after an acute onset of hind limb paralysis 4 days earlier. Previous radiographs revealed marked degenerative joint disease of the stifles, tarsi and digits. The clinical findings were consistent with acute disc prolapse. Lateral radiographs of the entire vertebral column were made as well as ventrodorsal pelvic radiographs. The latter were within normal limits. The vertebral column revealed multiple lesions consistent with chronic and acute disc herniations. Lateral compression of the caudal lumbar nerve roots could not be ruled out. Owing to multiple significant findings of the vertebral column and the poor prognosis for full recovery after surgery, the bear was euthanased. The diagnosis of an acute disc prolapse and multiple chronic disc herniations was confirmed on necropsy.

Animals↗
PubMed1999

Normal cochlear function in mdx and mdx(Cv3) Duchenne muscular dystrophy mouse models.

OBJECTIVES/HYPOTHESIS: Sensorineural hearing loss has been found in association with inherited muscular dystrophies in humans and in mouse models. An increased brainstem auditory evoked response threshold has been previously reported in the dystrophin-deficient mdx mouse model for Duchenne muscular dystrophy, suggesting that full-length dystrophin (Dp427) is involved in hearing. The objective of the present study was to confirm cochlear dysfunction with this gene defect and determine whether the shorter carboxyl terminus isoforms of dystrophin are also critical in maintaining normal hearing. STUDY DESIGN: Case controlled. Animal model. METHODS: Auditory brainstem response (ABR) audiometry to pure tones was used to evaluate cochlear function. Fourteen mdx, 4 mdx(Cv3), and 13 age-matched control (C57BL/6J and C57BL/10ScSn) male mice were tested at 5 weeks and 11 weeks of age. The ABR thresholds to tone-burst stimuli at 4, 8, 16, and 32 kHz were obtained for each ear and statistically compared (ANOVA) for potential group differences. RESULTS: Both mdx and mdx(Cv3) mice demonstrated normal ABR thresholds when compared with controls. CONCLUSIONS: Both mdx and mdx(Cv3) mouse models have normal hearing by ABR. The authors' data suggest that dystrophin and its carboxyl terminus isoforms do not play a critical role in hearing in the mouse. This was unexpected, as previous studies using the brainstem auditory evoked response method suggested that the mdx mouse has an increased threshold for hearing.

Animals↗
PubMed1998

Redefinition of dystrophin isoform distribution in mouse tissue by RT-PCR implies role in nonmuscle manifestations of duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is caused by a defect in a 427-kDa membrane-associated protein: dystrophin. The DMD gene also encodes several shorter isoforms which are believed to participate in nonmuscle manifestations of DMD, including abnormal retinal electrophysiology, dilated cardiomyopathy, mental retardation, and hearing defects. The purpose of this work was to determine the normal tissue expression of full-length dystrophin (Dp427) and the dystrophin isoforms Dp260, Dp140, Dp116, and Dp71, to aid in understanding what roles these isoforms might play in DMD nonmuscle manifestations. RT-PCR was performed on mRNA isolated from wild-type C57BL/6J mouse tissues, including brain, cardiac muscle, eye, intestine, kidney, liver, lung, skeletal muscle, spleen, stomach, testis, thymus, and uterus. RT-PCR amplification demonstrated that the isoforms were in a number of tissues which had not been revealed by previous Western and Northern blot analyses. Dp427 was expressed at equal levels in all tissues. Dp260 and Dp140 were present in all tissues tested, but the levels of expression varied. Dp116 was expressed in a subset of tissues and levels of expression varied. Dp71 was constitutively expressed in all tissues, suggesting that this isoform plays a basic role in normal tissue function. The expanded tissue distribution supports the hypothesis that dystrophin isoforms serve essential and unique functions, necessitating further investigation into their potential roles in DMD nonmuscle manifestations.

Actins↗
PubMed1995

Aortic thromboembolism associated with traumatic reticuloperitonitis in a downer cow.

A large thrombus was found at the ileal bifurcation on post mortem examination of a 6-year-old Jersey cow which presented clinically with a history of acute onset recumbency, hind limb paresis and skin necrosis over the sacral area. Other significant findings on post mortem were traumatic reticuloperitonitis accompanied by mural thrombosis of the left ventricle associated with a purulent sinus tract through the ventricular wall, fibrous adhesions between the pericardium, diaphragm and liver, and multiple infarcts in both kidneys.

Animals↗
PubMed1992

Possible vaccine-induced canine distemper in a South American bush dog (Speothos venaticus).

Suspected vaccine-induced canine distemper was diagnosed in a captive female bush dog (Speothos venaticus). Macroscopic lesions included mild congestion of the gastric mucosa and focal consolidation of the lung. Histopathological lesions included status spongiosis, gliosis, widespread eosinophilic, intranuclear and intracytoplasmic inclusion bodies in neurons, astrocytes and gitter cells of the cerebral, cerebellar and spinal white matter.

Animals↗
PubMed1991

Chylothorax in a kitten.

Chylothorax with collapse of the lungs was found on postmortem examination of a 2-week-old Siamese kitten. The chylothorax was probably due to a lack of continuity of the thoracic duct.

Animals↗
PubMedDate not supplied

Duchenne/Becker muscular dystrophy: correlation of phenotype by electroretinography with sites of dystrophin mutations.

The dark-adapted electroretinogram (ERG) of patients with Duchenne and Becker muscular dystrophy (DMD/BMD) shows a marked reduction in b-wave amplitude. Genotype-phenotype studies of mouse models for DMD show position-specific effects of the mutations upon the phenotype: mice with 5' defects of dystrophin have normal ERGs, those with defects in the central region have a normal b-wave amplitude associated with prolonged implicit times for both the b-wave and oscillatory potentials, and mice with 3' defects have a phenotype similar to that seen in DMD/BMD patients. The mouse studies suggest a key role for the carboxyl terminal dystrophin isoform, Dp260, in retinal electrophysiology. We have undertaken a systematic evaluation of DMD/BMD patients through clinical examination and review of the literature in order to determine whether the position-specific effects of mutations noted in the mouse are present in man. We have found that, in man, a wider variation of DMD defects correlate with reductions in the b-wave amplitude. Individuals with normal ERGs have mutations predominantly located 5' of the transcript initiation site of Dp260. Our results suggest that the most important determinant in the ERG b-wave phenotype is the mutation position, rather than muscle disease severity. Forty-six per cent of patients with mutations 5' of the Dp260 transcript start site have abnormal ERGs, as opposed to 94% with more distal mutations. The human genotype-phenotype correlations are consistent with a role for Dp260 in normal retinal electrophysiology and may also reflect the expression of other C-terminal dystrophin isoforms and their contributions to retinal signal transmission.

Dystrophin↗