The human papillomavirus type 16 (HPV-16) E6 and E7 oncogenes are thought to play a role in the development of most human cervical cancers. These E6 and E7 oncoproteins affect cell growth control at least in part through their association with and inactivation of the cellular tumor suppressor gene products, p53 and Rb. To study the biological activities of the HPV-16 E6 and E7 genes in epithelial cells in vivo, transgenic mice were generated in which expression of E6 and E7 was targeted to the ocular lens. Expression of the transgenes correlated with bilateral microphthalmia and cataracts (100%/ penetrance) resulting from an efficient impairment of lens fiber cell differentiation and coincident induction of cell proliferation. Lens tumors formed in 40% of adult mice from the mouse lineage with the highest level of E6 and E7 expression. Additionally, when lens cells from neonatal transgenic animals were placed in tissue culture, immortalized cell populations grew out and acquired a tumorigenic phenotype with continuous passage. These observations indicate that genetic changes in addition to the transgenes are likely necessary for tumor formation. These transgenic mice and cell lines provide the basis for further studies into the mechanism of action of E6 and E7 in eliciting the observed pathology and into the genetic alterations required for HPV-16-associated tumor progression.

Abstract. Nine horses with clinical and radiographic findings of cervical vertebral malformation that were necropsied and examined using frozen cervical spinal cord cross sections were reviewed. Only cases with actual distortion of the spinal cord due to compression were selected. The goal of the study was to determine the morphologic features responsible for narrowing of the spinal canal and compression of the spinal cord. In individual cases, bony changes are associated with osteochondrosis and osteomyelitis of the dorsal articular facets and osteosclerosis of the dorsal cervical lamina. Soft tissue pathology associated with spinal cord compression included ligamenturn flavum hypertrophy, joint capsule swelling and hypertrophy, and synovial cysts. In most cases, a combination of abnormalities was found in horses with spinal cord compression.Determination of the cause of ataxia secondary to neurologic impairment in horses based on physical and neurologic examinations is difficult.28 Impingement on the cervical spinal cord is the leading cause of ataxia in the horse. 26 Terms used to describe the syndrome that results in constant or intermittent impingement of the cervical spinal cord include wobblers, equine sensory ataxia, cervical vertebral instability, cervical stenotic myelopathy, and cervical vertebral malformation/malarticulation (CVM). 15,19,26,35,36 The signalment, history, and clinica1 15,19,26,35,36 and radiographic 17,21,22,25,37 signs of horses with CVM have been previously reported.The pathogenesis of CVM in horses remains unclear but appears to be multifactorial. Two general theories have evolved regarding the etiopathogenesis of CVM in horses. The first theory focuses on excessive and/or abnormal biomechanical forces, resulting in pathologic changes of the cervical vertebral canal that cause CVM. 24 The second theory describes a generalized dysmaturation of cartilage and bony development of the cervical vertebrae, leading to CVM.29 Lesions associated with equine CVM include osteosclerosis of the dorsal cervical lamina, 15,24 degenerative joint disease, l9,24 and osteochondrosis (OCD) 19,24,29 of the dorsal articular facets. Hypertrophy also occurs in the soft tissues surrounding the cervical vertebral canal, including the ligamenturn flavum, 24 joint capsule, 24 and synovial cyst formation. 8 The purpose of this report was to demonstrate by examination of frozen cross sections of cervical spinal intersegments the pathologic changes in horses with CVM that cause spinal cord compression. This technique allows the observer to record the extent of abnormality in both osseous and soft tissues that make up the spinal canal and to assess the relative importance of each component in the cause of spinal cord compression. Materials and methodsCriteria for selection of cases. Cases were selected for inclusion in this study if they were examined at necropsy using frozen cross sections of the cervical spine and if the frozen sections actually demonstrated distortion of the spinal cord as proof of compression....

Abstract. Thirty-nine percent of 1,448 working sheep dogs were affected with varying degrees of multifocal retinal disease on ophthalmoscopic examination. Lesions consisted of localized areas of hyperreflexia in the tapetal fundus, often associated with hyperpigmentation. Severely affected animals had widespread heperreflexia with retinal vascular attenuation. Only 6% of 125 New Zealand dogs raised in urban environment were similarly affected. Both eyes of 70 dogs from New Zealand were examined histologically. Forty-seven of 70 dogs had ocular inflammatory disease. Ten other dogs had noninflammatory eye disease, and 13 dogs had normal eyes. Histologically, eyes with inflammatory disease were divided into three categories: 1) Dogs 3 years of age or less with active inflammatory disease of the retina, uvea, and vitreous. Four dogs in this group had migrating nematode larvae identified morphologically as genus Toxocuru. 2) Diffuse retinitis and retinal atrophy in conjunction with localized retinal necrosis and choroidal fibrosis. Dogs in this category were severely, clinically affected. 3) Chronic, low-grade retinitis with variable retinal atrophy. Most dogs in this category were over 3 years of age, and many were visually functional. The existence of a definable spectrum of morphological changes associated with inflammation, suggests that Toxocuru sp. ocular larva migrans may be the cause of a highly prevalent, potentially blinding syndrome of working sheep dogs in New Zealand.Intraocular nematodiasis is a rare clinical disease in dogs. Aberrant localization of adult or larval Dirofiluriu immitis has been reported.I3 Four cases of ocular larva migrans associated with Toxocuru sp. were seen in association with inflammatory eye disease in one previous report. l4 This paper describes an unusually high incidence of inflammatory eye disease in New Zealand working sheep dogs and rural pet dogs. Evidence is presented that suggests a high incidence of ocular larva migrans caused by ocular migration of Toxocuru most likely T. cunis, in dogs less than 3 years of age. Materials and MethodsOphthalmic examinations were done using a hand-held direct ophthalmoscope in the course of routine veterinary practice in urban and rural areas of New Zealand. Most examinations were done to characterize the distribution and prevalence of multifocal retinitis. Large numbers of examinations of working sheep dogs were done on a volunteer basis at competitive trial events in New Zealand. Results were recorded and findings were compared over time when multiple examinations were done.Eyes were obtained for histologic examination only when animals died for other reasons or were unable to work due to visual impairment or, in some cases, when young dogs were purchased in order to study the ocular tissues. All eyes had been examined clinically prior to submission for histology. Eyes were fixed for 3 hours in Bouins solution and then in 70% ethanol solution. Standard sagittal sections were made of all eyes and were processed routinely for paraffin ...

Respiratory decompression sickness (RDCS, "the chokes") is a potentially lethal consequence of ambient pressure reduction. Lack of a clearly suitable animal model has impeded understanding of this condition. RDCS, unaccompanied by central nervous system signs, occurred in 17 of 18 unanesthetized sheep exposed to compressed air at 230 kPa (2.27 ATA) for 22 h, returned to normal pressure for approximately 40 min, and taken to simulated altitude (0.75 ATA, 570 Torr). Respiratory signs, including tachypnea, sporadic apnea, and labored breathing, were accompanied by precordial Doppler ultrasound evidence of marked venous bubble loading. Pulmonary arterial pressures exceeded 30 Torr in five catheterized sheep that died or became moribund. Hypoxemia (arterial Po2 less than 40 Torr), neutropenia, and thrombocytopenia were observed. Peribronchovascular edema was the most prominent necropsy finding. Chest radiography indicated interstitial edema in most affected sheep. High body weight and catheterization predisposed the sheep to severe RDCS. It appears that this protocol reliably provides a useful animal model for studies of RDCS and obstructive pulmonary hypertension, that the precipitating event is massive pulmonary embolization by bubbles, and that venous bubbles, detected by Doppler ultrasound, can signal impending RDCS.

A case of a malignant mesenchymoma with an unusual, vasoinvasive, metastatic behavior in a three-year-old, intact female basset hound is presented. Malignant mesenchymomas are rare neoplasms in humans and in dogs. No previous reports of a malignant mesenchymoma with vasoinvasive metastasis in the dog were found in the literature. The constituent neoplasms are discussed in relation to reports in the human and veterinary literature, and a potential etiology for this unique presentation is hypothesized.