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At least 325 records · Page 18Linked to original sources
PubMed1962

Anthrax toxin: causative agent in the death of rhesus monkeys.

Anthrax toxin was present in the blood obtained from rhesus monkeys at the terminal stage of anthrax and was also present in increasing amounts in the lymph as death approached. When sterile toxin produced in vitro was injected in sufficient amounts, monkeys died unless they were injected with specific antiserum. Death with symptoms of toxemia occurred within 2 hours after injection of 10(11) spores, whereas 10(10) spores or less required 20 or more hours of growth in vivo to cause death.

Animals↗
PubMed2004

Molecular analysis of SV-40-CAL, a new slow growing SV-40 strain from the kidney of a caged New World monkey with fatal renal disease.

A decline of the Callimico goeldii population in American zoos is presently occurring due to glomerulonephritis of unknown etiology. We hypothesized that this emerging idiopathic fatal renal disease (IFRD) was caused by a virus. We therefore attempted to isolate virus from the kidneys three C. goeldi in Illinois that had IFRD. Along with other viruses, Simian virus 40 (SV-40) strain CAL was isolated. SV-40-CAL is currently the slowest-growing natural isolate of SV-40 in CV-1 cells. Inefficient SV-40-CAL growth in CV-1 cells stems from two features: a suboptimal protoarchetypal regulatory region, and a Large tumor antigen gene sequence like that of SV-40 strain T302, previously considered the slow-growing natural isolate of SV-40. To our knowledge, this is the first documented isolation of SV-40 from a New World monkey outside of a laboratory setting. Though SV-40 is renaltropic, the role of SV-40-CAL in IFRD is uncertain. Transmission of SV-40 to C. goeldii through anthropogenic activity is suspected.

Animals↗
PubMed1997

[Behaviour after transplantation of brain cells into monkey models of Parkinson's disease].

OBJECTIVE: To observe the improved degree of pathogenic behaviour in monkey models of Parkinson's disease after transplantation of substantia nigra cells of human fetus. METHOD: 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to prepare monkey models of hemiparkinson's disease, i.e., early substantia nigra cells of human fetus were stereotaxically transplanted into PD monkey's behaviour for six months, using immuno-electromicroscopy to prove the transplanted survived neuron. RESULTS: After transplantation, the model monkey's motion slow and muscle hypertonia was apparently improved. Limb tremor almost disappeared, Right spontaneous rotation behavior relieved. Rotating frequency caused by APO became less than before transplanytation, and its effect could last a year. Under the immunoelectromicroscope, we observed that transplanted tyrosine hydroxylase positive neuron was connected with the host brain cells in synapse. CONCLUSION: Substantia nigra neuron transplanted into the PD monkey brain can establish synaptic connection with the host nervous cells. Pathogenic symptoms are improved and the effect may remain for a longer time.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

The effects of a topically-active non-steroidal anti-inflammatory drug on ligature-induced periodontal disease in the squirrel monkey.

Prostaglandins are believed to be important mediators of periodontal inflammation and bone resorption. The purpose of the present blind study was to quantify clinically and histologically the effects of a topically applied nonsteroidal prostaglandin synthetase inhibitor, namely a substituted oxazolopyridine derivative (SOPD), on ligature-induced periodontal disease in the squirrel monkey. For a period of 14 days, one group of ligated animals received 2 daily topical applications of the SOPD. A group receiving systemically administered indomethacin served as a positive control while a group receiving only topically applied vehicle served as a negative control. Results indicate that throughout the 14-day period of the study, the SOPD significantly inhibited gingival inflammation and loss of attachment as compared to either the placebo or indomethacin groups. Both indomethacin and the SOPD significantly inhibited bone resorption.

Administration, Topical↗
PubMed1995

Chronic lyme disease in the rhesus monkey.

BACKGROUND: We have previously reported the clinical, pathologic, and immunologic features of "early" Borrelia burgdorferi infection in rhesus monkeys (3). We have now evaluated these features during the chronic phase of Lyme disease in this animal model. EXPERIMENTAL DESIGN: Clinical signs, and pathologic changes at the gross and microscopic levels, were investigated 6 months post-infection in several organ systems of five rhesus macaques (Macaca mulatta), which were infected with Borrelia burgdorferi by allowing infected Ixodes scapularis nymphal ticks to feed on them. A sixth animal was used as an uninfected control. Borrelia antigens recognized by serum antibody were identified longitudinally by Western blot analysis, and C1q-binding immune complexes were quantified. Localization of the spirochete in the tissues was achieved by immunohistochemistry and in vitro culture. The species of spirocheta cultured was confirmed by the polymerase chain reaction. RESULTS: Chronic arthritis was observed in five out of five animals. The knee and elbow joints were the most consistently affected. Articular cartilage necrosis and/or degenerative arthropathy were the most severe joint structural changes. Synovial cell hyperplasia and a mononuclear/lymphocyte infiltrate were commonly seen. Nerve lesions were also observed, including nerve sheath fibrosis and focal demyelinization of the spinal cord. Peripheral neuropathy was observed in five out of five animals and could be correlated in the most severely affected monkey with the presence of higher levels of circulating immune complexes. Differences in disease severity did not correlate with differences in the antigens recognized on Western blot analysis. CONCLUSIONS: B. burgdorferi infection in rhesus macaques mirrors several aspects of both the early and chronic phases of the disease in humans. This animal model will facilitate the study of the pathogenesis of Lyme arthritis and neuroborreliosis.

Animals↗
PubMed1992

Clinical features and predictive markers of disease progression in cynomolgus monkeys experimentally infected with simian immunodeficiency virus.

OBJECTIVE: To study the pathogenicity of simian immunodeficiency virus (SIVsm) in cynomolgus monkeys in order to establish an animal model for human AIDS. METHODS: Thirty-three cynomolgus monkeys were monitored for more than 2 years following experimental infection with SIVsm. RESULTS: All the macaques became SIV-infected, as demonstrated by virus recovery from peripheral blood lymphocytes and by the appearance of viral antibodies. SIVsm was found to be pathogenic, killing 29 out of the 33 monkeys (88%) within 26 months. Clinically, infected monkeys developed lymphadenopathy, splenomegaly, diarrhoea, weight loss, neurological symptoms and a remarkably high incidence (39%) of malignant lymphomas. All lymphomas were high-grade malignant and of B-cell origin. Disease progression was associated with low CD4+ lymphocyte count, involution of initially hyperplastic follicular B-cell areas in lymph nodes, reappearance of viral antigen in serum, loss of anti-Gag antibodies and development of systemic giant cell disease in 55% of the monkeys. CONCLUSIONS: There are many similarities between SIVsm-induced AIDS in cynomolgus monkeys and human AIDS with regard to clinical, virological, immunological and pathological manifestations.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Sequence of inflammatory cell migration into lung during recovery from hyaline membrane disease in premature newborn monkeys.

The appearance of polymorphonuclear leukocytes (PMN) and macrophages (MAC) in lung during the development of hyaline membrane disease (HMD) may be important in lung injury and repair. These inflammatory cells may cause additional lung injury during recovery from HMD and contribute to the development of bronchopulmonary dysplasia (BPD). By morphometric methods, we compared the proportion of PMN and MAC in lung tissue of premature M. nemestrina monkeys with HMD to the proportion of these cells in the lungs of healthy control animals of a similar postnatal age and to fetuses of the same gestational age. Expressed as a fraction of all lung cells, healthy premature control monkeys have the same %PMN and %MAC in lung tissue as fetal animals. However, during the development of acute HMD, there is an increase in %PMN (p less than 0.05), but not in %MAC, compared to fetal animals. During recovery, there is a greater than 10-fold increase in %MAC (p less than 0.02), but no significant additional increase in %PMN compared to animals with acute HMD. We conclude that the sequence of inflammatory cell migration into the premature lung injured during HMD is first a polymorphonuclear one, followed by entry of macrophages. Control of this inflammatory response during recovery from HMD may play a role in the pathogenesis of BPD.

Animals↗