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Biomedical subjects

J W Finnie

Publications and source records attributed to J W Finnie.

64 records · Page 4Linked to original sources
PubMed1980

Acute and chronic canine parvovirus myocarditis following intrauterine inoculation.

Canine myocarditis virus was inoculated into puppies in utero 8 days before parturition. Puppies were clinically normal at birth. One puppy died 23 days after inoculation and a second puppy was comatose before euthanasia on day 27 post inoculation. Both had acute, non-suppurative myocarditis, and parvovirus was isolated from the heart of each pup. Two other puppies remained clinically normal until euthanasia at 87 and 131 days after inoculation. These latter puppies had extensive, focal fibrosis within the myocardium. Despite weekly monitoring, ECG changes were not recorded. The apparent predilection of canine parvovirus for cardiac myocytes is discussed.

Animals↗
PubMedDate not supplied

Effect of impact on different regions of the head of lambs.

The heads of anaesthetized lambs aged 4-5 weeks were subjected to impact (temporal, frontal or occipital) of constant strength with a humane stunner. Two hours later, the brains were perfusion-fixed with 4% paraformaldehyde and serial whole coronal slices processed by routine methods. Sections were stained with haematoxylin and eosin or labelled with a monoclonal antibody to amyloid precursor protein, a sensitive marker of axonal injury and neuronal reaction. Microscopical evaluation of axonal, neuronal and vascular damage was performed with a quantitative grid system. Frontal impact produced the greatest damage, followed by occipital then temporal impact. An unusual lesion found in the majority of lambs subjected to impact was multifocal necrosis of the cerebellar granular layer. The findings should assist clinicians in evaluating the probable outcome of traumatic head injury in domestic animals.

Amyloid beta-Protein Precursor↗
PubMedDate not supplied

Brain damage in sheep from penetrating captive bolt stunning.

OBJECTIVE: To determine the severity and distribution of structural changes in the brains of adult sheep stunned by penetrating captive bolt. PROCEDURE: The unconstrained heads of ten, anaesthetised, unhorned, 2-year-old Merino sheep were impacted at the summit of the head with a penetrating captive bolt pistol. Six sheep were ventilated and four received no respiratory support. Two hours after impact, brains from the six ventilated sheep were perfusion-fixed with 4% paraformaldehyde. Sixteen whole, serial coronal sections from each brain were stained with haematoxylin and eosin and immunohistochemically for amyloid precursor protein, a sensitive marker of axonal and neuronal reaction in the brain after trauma. Pathological changes in these brains were then quantified by morphometric analysis. RESULTS: Structural change in all impacted brains was a mixture of focal injury around the wound track and more widely distributed damage in the cerebral hemispheres, cerebellum and brainstem, but varied considerably in severity between individual sheep. All nonventilated sheep died rapidly following respiratory arrest. CONCLUSIONS: After penetrating captive bolt stunning, damage to the central reticular formation, axonal connections, and the cortical mantle is the likely reason for failure of respiratory control and traumatic loss of consciousness.

Animals↗
PubMedDate not supplied

Apoptosis in liver damage produced by tunicamycin.

OBJECTIVE: To determine whether apoptosis contributes to hepatocyte loss in tunicamycin poisoning. DESIGN: Groups of four guinea pigs were given 400 microg/kg of tunicamycin subcutaneously and killed at 24 h intervals up to 72 h post-injection. Livers were examined by routine histological methods and ancillary techniques (TUNEL staining, endonuclease activation, caspase activity, and electron microscopy) to ascertain whether any hepatocyte injury was apoptotic. RESULTS: Many hepatocytes exposed to tunicamycin showed evidence of apoptosis in the form of nuclear karyorrhexis with chromatin margination and crescent formation, TUNEL-positivity, DNA laddering, elevated caspase activity and apoptotic body formation. CONCLUSION: Tunicamycin caused the death of many hepatocytes in the livers of guinea pigs by apoptosis.

Animal Feed↗