The effects of chitin/chitosan and their oligomers/monomers on the migrations of mouse peritoneal macrophage (PEM) and the rat macrophage cell line (rMp) were evaluated in vitro. In direct migratory assay using the blind well chamber method, the migratory activity of PEM was enhanced significantly by chitin and chitosan oligomers (NACOS and COS, respectively), but reduced by chitin, chitosan, and the chitosan monomer (GlcN). The migratory activity of rMp was increased significantly by chitin, chitosan, and the polymers, NACOS and GlcN.

ABSTRACT. A 2-year-old castrated miniature Dachshund dog was presented to the Rakuno Gakuen Veterinary Teaching Hospital for diagnosis of progressive hindlimb paresis and ataxia. There was no thoracolumbar intervertebral disk hernia and magnetic resonance imaging revealed an intramedullary spinal cord lesion at the ninth and tenth thoracic vertebrae. Following surgical excision of the neoplasm, there was minor amelioration of neurological signs, but forelimb function was not recovered. The extracted tumor was histopathlogically diagnosed as spinal nephroblastoma. KEY WORDS: canine, magnetic resonance imaging (MRI), spinal nephroblastoma.J. Vet. Med. Sci. 68(12): 1383-1385, 2006 Nephroblastoma of the spinal cord is a rare neoplasm in young dogs. Myelography for diagnosis of spinal neoplasm has been described [3,4,11], but more recently, there have been some case reports on the magnetic resonance imaging (MRI) features of nephroblastoma in dogs [5,8]. This paper describes the MRI, surgical treatment and histopathology of canine spinal cord nephroblastoma with progressive hindlimb paresis and ataxia.A 2-year-old castrated miniature Dachshund dog was referred to the Rakuno Gakuen Veterinary Teaching Hospital for diagnosis of progressive hindlimb paresis and ataxia. The dog had sudden onset of left hindlimb lameness 3 weeks earlier. He was treated with oral prednisolone and intravenous methyrprednisolone, but there was no improvement for three weeks.Right hindlimb paresis appeared during the fourth week, indicating that the bilateral hindlimb paresis and ataxia were progressive. Neurological examination revealed proprioceptive, hopping and placing deficits of the left and right hindlimbs. Patellar and pedal reflexes were normal or slightly asthenic. The forelimb was normal and the hindlimb was positive for upper motor neuron sign. Based on clinical neurologic examination, an upper motor neuron third thoracic to third lumbar spinal cord lesion was suspected.Survey radiographs of the entire spine were normal. The dog was anesthetized and imaged in dorsal recumbency using a 0.2-Tesla MR scanner (Signa Profile Open Sprit, GE Yokogawa Medical Systems, Tokyo, Japan) with a surfacearray human extremity coil. T2-weighted and T1-weighted images were obtained in the transvervse and sagittal planes at slice thicknesses of 2.7 and 3.5 mm.T2-weighted, midline sagittal slices revealed an abnormal region in the spinal cord at the ninth and tenth thoracic vertebrae (Fig. 1). The spinal cord lesion was isointense relative to normal spinal cord on T1-weighted MRI (Fig. 2). On enhanced T1-weighted midline sagittal images after intravenous administration of the meglumine gadopentetate (Gd; Magnebisto Nihon Shering Inc., Osaka. 0.1 mmol/kg body weight), the lesion was enhanced and observed at the ninth and tenth thoracic vertebrae. The enhanced lesion was 27 mm in length (Fig. 3). On transverse images, the mass occu-