Lifetime effects of intratracheally instilled nickel subsulfide on B6C3F1 mice

A nickel subsulfide (Ni3S2) lung tumor model for the study of metal carcinogenesis was evaluated using intratracheally dosed B6C3F1 mice. A preliminary study of the survival of mice 14 days after a single intratracheal dose of Ni3S2 displayed an LD50 of 4 mg/kg. A lifetime study was then initiated using five graded doses of Ni3S2 or saline alone, administered once a week for 4 weeks. Animals which survived more than 60 days after the final dose were evaluated by histopathology. The study was terminated 27 months after initiation when ~50% of the control animals had died. There was no increase in neoplastic or non-neoplastic lesions observed in animals treated with Ni3S2 nor was there evidence of damage to the organs of the respiratory tract from this treatment. The lack of significant biological response appears to be the result of relatively low tolerated dose, efficient lung clearance, and repair of early lung lesions.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26090/1/0000166.pd

Comparison of the Host Ranges and Antigenicity of Cryptosporidium parvum and Cryptosporidium wrairi from Guinea Pigs

Oocysts of a Cryptosporidium isolate from guinea pigs were not infectious for adult mice, but were infectious for two of three newborn calves and for suckling mice. However, oocysts isolated from calves or mice infected with guinea pig Cryptosporidium were not infectious for guinea pigs. Four isolates of C. parvum from calves were incapable of infecting weanling guinea pigs. Microscopic examination of tissue from the colon and cecum of suckling guinea pigs inoculated with C. parvum revealed sparse infection of some pups. These host range studies and previously described differences in 125 I-labeled oocyst surface protein profiles between Cryptosporidium sp. from guinea pigs and C. parvum suggest they are distinct species. We propose the name Cryptosporidium wrairi be retained. Studies with monoclonal antibodies indicate that C. wrairi and C. parvum are antigenically related.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75184/1/j.1550-7408.1992.tb01471.x.pd

Effect of Vehicle on the Nasal Absorption of Epinephrine During Cardiopulmonary Resuscitation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90174/1/j.1875-9114.1996.tb03030.x.pd

Subcutaneous hemangiosarcomas in a rhesus macaque ( Macaca mulatta )

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71448/1/j.1600-0684.2001.300209.x.pd

Power Doppler evaluation of joint effusions: investigation in a rabbit model

Objective. To study the power Doppler findings of septic arthritis and noninfectious synovitis in an animal model. Materials and methods. The right knees of 10 rabbits were inoculated with an aqueous suspension of Staphylococcus aureus . The right knees of 5 rabbits were injected with talc suspension. The right knees of 5 rabbits were injected with saline. All 20 left knees were injected with saline. Serial power Doppler images were obtained using constant-imaging parameters. Images were reviewed by blinded observers who assessed for increased power Doppler signal. Results. All 10 knees inoculated with S. aureus developed septic arthritis. Each infected rabbit knee demonstrated increased signal on power Doppler on at least one examination, ranging from 1–6 days after inoculation. Only 23 of 45 examinations of infected knees were unequivocally positive by power Doppler on examinations performed 1 to 6 days after inoculation. No knee with talc synovitis demonstrated increased power Doppler signal. No control knee demonstrated increased power Doppler signal. Conclusion. Increased power Doppler signal may be seen with septic arthritis; however, its intensity and timing may vary from subject to subject. A normal power Doppler examination does not exclude septic arthritis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42050/1/247-29-8-617_90290617.pd

MRI evaluation of infectious and non-infectious synovitis: preliminary studies in a rabbit model

Background. Literature on magnetic resonance imaging (MR) evaluation of inflammatory joint effusions is sparse. Objective. To describe an animal model for studying infectious and non-infectious joint effusions with magnetic resonance imaging. Materials and methods. Ten rabbit knees with septic arthritis and four with talc synovitis were imaged with MR. Contralateral knees injected with saline served as controls. Fat saturation T2-weighted and gadolinium-enhanced T1-weighted images were assessed for joint effusion, and periarticular and adjacent intraosseous increased signal or enhancement. Each knee was cultured and underwent pathologic examination. Results. Both Staphylococcus aureus and talc produced effusions in all knees. The degree of periarticular signal and enhancement was greater in infected knees than talc-injected knees. No abnormal enhancement was seen within bone. Pathologic examination showed a greater degree of inflammation and joint destruction in the infected knees, but no evidence of osteomyelitis. Conclusion. A greater degree of abnormal signal and enhancement seen on MR suggests a more vigorous inflammatory process, as seen with septic arthritis. In spite of advanced septic arthritis, no enhancement was evident within bone, suggesting that enhancement within bone is not an expected finding in isolated septic arthritis and should raise concern for osteomyelitis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42049/1/247-29-5-367_90290367.pd

mnd2: A New Mouse Model of Inherited Motor Neuron Disease

The autosomal recessive mutation mnd2 results in early onset motor neuron disease with rapidly progressive paralysis, severe muscle wasting, regression of thymus and spleen, and death before 40 days of age. mnd2 has been mapped to mouse chromosome 6 with the gene order: centromere-Tcrb-Ly-2-Sftp-3-D6Mit4-mnd2-D6Mit6, D6Mit9-D6Rck132-Raf-1, D6Mit11-D6Mit12-D6Mit14. mnd2 is located within a conserved linkage group with homologs on human chromosome 2p12-p13. Spinal motor neurons of homozygous affected animals are swollen and stain weakly, and electromyography revealed spontaneous activity characteristic of muscle denervation. Myelin staining was normal throughout the neuraxis. The clinical observations are consistent with a primary abnormality of lower motor neuron function. This new animal model will be of value for identification of a genetic defect responsible for motor neuron disease and for evaluation of new therapies.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30778/1/0000429.pd