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At least 127 records · Page 7Linked to original sources
PubMed2001

Increased replication of respiratory syncytial virus (RSV) in pulmonary infiltrates is associated with enhanced histopathological disease in bonnet monkeys (Macaca radiata) pre-immunized with a formalin-inactivated RSV vaccine.

The pathology of respiratory syncytial virus (RSV) disease in bonnet monkeys parallels findings with human RSV disease. RSV-infected animals pre-immunized with a formalin-inactivated (FI) RSV vaccine develop inflammation in peribronchiolar, perivascular, interstitial and intra-alveolar sites with lung inflammation scores significantly higher than animals with a primary RSV infection and those pre-immunized with an FI-Vero cell control vaccine (P=0.05). Animals previously infected and re-exposed to RSV had significantly lower alveolar, interstitial and total lung inflammation scores than in primary infection (P=0.05). Immunization with two intra-muscular doses of 0.5 ml of the FI-RSV vaccine administered 21 days apart resulted in little serum-neutralizing and ELISA antibody, low levels of secretory IgA and a low lymphocyte proliferative response that was significantly lower than the response observed in animals that were previously infected with live RSV. Higher RSV virus titres were detected in the lungs and lung lavage fluid of monkeys immunized with the FI-RSV vaccine than in those with a primary infection (P=0.001). RSV was detected by in situ hybridization in pulmonary inflammatory infiltrates, where the single most abundant infiltrating cellular species was macrophages, so it may be these cells that support the enhanced virus replication that contributes to the enhanced pulmonary pathology of FI-RSV immunization.

Animals↗
PubMedDate not supplied

[Neurological anthropology among the Kamayura Indians of the Alto Xingu].

INTRODUCTION: The Kamayura tribe is made up of 300 persons living in the Alto Xingu in Mato Grosso, Brazil. Their traditional system of health care is based on the pajé, a witch doctor who uses plants and prayers for treatment. MATERIAL AND METHODS: Field work was done in the Kamayura village holding successive interviews with the chief and the pajé Takumá to obtain information regarding the neurological disorders found there, the indigenous beliefs regarding illness (natural or based on witch-craft), their classification and traditional treatment based on plants. The terms employed were translated from Kamayura into Portuguese. RESULTS: Illness in Indians is caused by the revenge of the spirit (mama'e) of the animal killed by the huntsman. Epilepsy (Teawurup) or armadillo disease is caused when a huntsman kills an armadillo. It is treated with two roots, tsimó and wewuru, kneaded, diluted in water and applied to the eyes. An infusion of enamum root is also used. Migraine or monkey disease causes a pulsatile headache and vertigo. Mental retardation and infantile cerebral palsy are included in the ant-bear disease. Depression is treated with the plant 'iputunú'; which is applied diluted in water to the face of the patient so that he no longer sees his dead relations and may be cured. Schizophrenia or apuayat (owl disease) also occurs, but not parkinsonism or stroke. CONCLUSION: The Kamayura pajes have established a system of health-care based on magic folklore, transmitted orally and making use of traditional plants.

Anthropology↗
PubMed1998

Endomysial antibody detection using human umbilical cord tissue as substrate: reactivity of cells in Wharton's jelly.

The measurement of immunoglobulin A (IgA) endomysial antibodies is now established as an important diagnostic test in gluten-sensitive disease. Monkey oesophagus is the commonly used tissue substrate, but it has been proposed that human umbilical cord tissue may be a suitable alternative for antibody detection. In this study, we report a modified method of examining endomysial antibody reactivity with cord tissue. This involves examination of antibody reactivity with cells in Wharton's jelly, and with umbilical cord blood vessel. A total of 370 patients being investigated for coeliac disease were studied and this diagnosis was established in 42. Endomysial antibodies were found in all 42 using umbilical cord tissue, and the test results were confirmed with monkey oesophagus substrate. In three of the remaining 328 non-coeliacs, a false-positive endomysial antibody test was noted and small intestine histology was normal in these patients. All positive sera were found to react with cells in Wharton's jelly, and reticular staining of blood vessels was also present. Examination for immunofluorescence in both Wharton's jelly and blood vessel components of cord tissue greatly simplified test interpretation.

Adolescent↗
PubMed2006

Fractalkine expression in the rhesus monkey brain during lentivirus infection and its control by 6-chloro-2',3'-dideoxyguanosine.

Existing data concerning the role of the delta-chemokine fractalkine (CX3CL1) and its receptor (CX3CR1) in lentivirus-induced encephalitis are limited and controversial. We explored, by quantitative in situ hybridization and immunohistochemistry, the cell-specific changes of CX3CL1 and CX3CR1 in rhesus macaque brain during simian immunodeficiency virus (SIV) infection and antiretroviral treatment. Neuronal expression of CX3CL1 was significantly reduced in cortex and striatum of AIDS-diseased monkeys as compared with uninfected and asymptomatic SIV-infected monkeys. CX3CL1 mRNA was increased in some endothelial cells and newly induced in astrocytes and macrophages focally in areas of SIV burden and inflammatory infiltrates. In most CX3CL1-positive astrocytes and macrophages, the transcription factor NF-kappaB was translocated to the nucleus. CX3CR1 was upregulated in scattered, nodule, and giant cell-forming microglia/macrophages and mononuclear infiltrates close to CX3CL1-induced cells in the brain. Treatment of AIDS monkeys with the central nervous system-permeant 6-chloro-2',3'-dideoxyguanosine fully reversed SIV burden, productive inflammation, nuclear NF-kappaB translocation as well as focal induction of CX3CL1 in astrocytes and macrophages and downregulation in neurons. In contrast, diffuse CX3CR1-positive microgliosis and GFAP-positive astrogliosis were partially reversed by 6-chloro-2',3'-dideoxyguanosine. Thus, focally induced CX3CL1 may be a target for therapeutic intervention to limit ongoing inflammatory infiltration into brain in lentivirus infection.

Active Transport, Cell Nucleus↗
PubMed2005

Interspecies transmission of chronic wasting disease prions to squirrel monkeys (Saimiri sciureus).

Chronic wasting disease (CWD) is an emerging prion disease of deer and elk. The risk of CWD transmission to humans following exposure to CWD-infected tissues is unknown. To assess the susceptibility of nonhuman primates to CWD, two squirrel monkeys were inoculated with brain tissue from a CWD-infected mule deer. The CWD-inoculated squirrel monkeys developed a progressive neurodegenerative disease and were euthanized at 31 and 34 months postinfection. Brain tissue from the CWD-infected squirrel monkeys contained the abnormal isoform of the prion protein, PrP-res, and displayed spongiform degeneration. This is the first reported transmission of CWD to primates.

Animals↗
PubMed1981

Renal disease in squirrel monkeys (Saimiri sciureus).

Renal lithiasis, pyelonephritis, and glomerulonephritis were common in our colony of Brazilian phenotype squirrel monkeys (Saimiri sciureus), with glomerulonephritis being a major cause of mortality in adult animals. Squirrel monkey glomerulonephritis was divided into four major classifications, based on light and electron microscopy, similar to those of man: focal sclerosing glomerulonephritis, membranoproliferative glomerulonephritis, membranous glomerulonephritis, and a combination of membranoproliferative and membranous glomerulonephritis.

Animals↗
PubMed2004

[Therapeutic study of autologous Schwann cells' bridge graft into the brain of hemiparkinsonian monkey].

OBJECTIVE: To evaluate the therapeutic effect of autologous transplantation of Schwann cells as "bridge" between the medial forebrain bundle (MFB) and caudate nucleus, into the brain of hemiparkinsonian monkey. METHODS: Six monkeys were used following 6-OHDA-induced hemiparkinsonism. Three of them were autologous transplanted using Schwann cells as "bridges" between MFB and caudate nucleus. The Schwann cells were pre-treated using Hoechst33342. The other three monkeys received sham operation as controls. All the monkeys received behavioral assessment. The metabolism of dopamine was measured by SPECT using (99)Tcm-TRODAT-1 and PET using 18F-FP-beta-CIT. After a 4-month follow-up, the monkeys' brain were removed from the skull, fixed in 4% paraformaldehyde and cut into serial sections. A fluorescence microscope examination and a tyroxine hydroxylase (TH) immunohistochemistry study were made on the sections. Cell types were determined by double staining. The level of TH protein around the needle track was determined by Western blotting. RESULTS: All three monkeys, which had undergone Schwann cells autologous bridge graft showed a decrease in the disability score and two of them had an increase in motor activity. The apomorphine evoked rotation was also decreased. The symptoms of the monkeys, which received sham operation, had not amelioration. In SPECT examination, the radioactivity count was greatly increased in the grafted monkeys. The dopamine levels were significantly increased in the caudate nucleus from 61% (before graft) to 79% (after graft) while there's no change in control group. In histological examination, autologous Schwann cells could survive and migrate in the brain. Around the Schwann cells "bridge", there were numerous TH positive short fibers in the MFB area. Around the whole length of the "bridge", there were a lot of TH positive reactive astrocytes, especially in thalamus. TH protein around the needle track of the graft group was 243% compared with that of control group. CONCLUSION: Autologous Schwann cells bridge graft is a feasible technique with therapeutic effects on parkinson disease monkeys. The Schwann cells play an important role in dopaminergic axonal elongation and in inducing the TH positive phenotype of reactive astroglia cell around it.

Animals↗
PubMed1981

Borna disease in rhesus monkeys as a models for uveo-cerebral symptoms.

Borna disease, a naturally occurring encephalomyelitis of horses and sheep, was induced in rhesus monkeys after intracerebral infection with virus containing rabbit brain suspension. The animals developed neurological disorders followed by a severe encephalomyelitis which was accompanied by a retinopathy. In all the analyzed brain and retina tissue pieces, virus-specific antigen could be demonstrated by immunoelectrophoretic techniques. Antibodies could be demonstrated by the intermediate gel technique as well as by the immunofluorescence test in the serum and the cerebrospinal fluid of all the monkeys. The histopathological findings in the brain and the eye might be comparable to certain types of encephalitis in man and to pathological changes in the eye of human patients, the etiologies of which are still obscure. An attempt was also made to study cell-mediated immunity by a chromium release assay in infected animals, the results of which might provide, together with the histopathological observations, strong evidence for the role of lymphocytes in the pathogenesis of BD infection in rhesus monkeys.

Animals↗
PubMed1995

Effects of nigrostriatal denervation and L-dopa therapy on the GABAergic neurons in the striatum in MPTP-treated monkeys and Parkinson's disease: an in situ hybridization study of GAD67 mRNA.

The effects of nigrostriatal denervation and L-dopa therapy on GABAergic neurons were analysed in patients with Parkinson's disease and in monkeys rendered parkinsonian by MPTP intoxication. The expression of the messenger RNA coding for the 67 kDa isoform of glutamic acid decarboxylase (GAD67 mRNA), studied by quantitative in situ hybridization, was used as an index of the GABAergic activity of the striatal neurons. A significant increase in GAD67 mRNA expression, generalized to all GABAergic neurons, was observed in MPTP-treated monkeys compared to control monkeys in the putamen and caudate nucleus (+44 and +67% respectively), but not in the ventral striatum. L-Dopa therapy significantly reduced GAD67 mRNA expression in the putamen and caudate nucleus to levels similar to those found in control monkeys. However, the return to normal of GAD67 mRNA expression was not homogeneous across all neurons since it was followed by an increase of labelling in one subpopulation of GABAergic neurons and a decrease in another. These data suggest that in MPTP-treated monkeys the degeneration of nigrostriatal dopaminergic neurons results in a generalized increase in GABAergic activity in all the GABAergic neurons of the striatum, which is partially reversed by L-dopa therapy. As the expression of GAD67 mRNA is less intense in the ventral than in the dorsal striatum, this increase in striatal GABAergic activity may be related to the severity of nigrostriatal denervation. In parkinsonian patients who had been chronically treated with L-dopa, GAD67 mRNA expression was significantly decreased in all GABAergic neurons, in the caudate nucleus (by 44%), putamen (by 43.5%) and ventral striatum (by 26%). The opposite variation of GAD67 mRNA in patients with Parkinson's disease, compared with MPTP-treated monkeys, might be explained by the combination of chronic nigrostriatal denervation and long-term L-dopa therapy.

Aged↗
PubMed1975

Alcoholic liver injury: experimental models in rats and baboons.

A model has been developed for the administration to rats and baboons of ethanol as part of a nutritionally adequate liquid diet. With this regimen, ethanol intake was much higher than with conventional procedures. All animals gained or maintained their body weight, and liver morphology was normal in the controls. Isocaloric substitution of carbohydrate by ethanol (36% of total calories in rats and 50% in baboons) resulted in the production of fatty liver in all animals, while the baboons also developed alcoholic hepatitis and cirrhosis with increased activities of serum glutamic oxaloacetic transaminase. Inebriation and manifestation of dependence upon withdrawal of the diet were observed in baboons and quantitated in the rat. Chemical alterations produced by ethanol at the fatty liver stage were characterized by hyperlipemia, striking triglyceride accumulation in the liver and enhanced activities of microsomal drug metabolizing enzymes, including the microsomal ethanol oxidizing system (MEOS). Ultrastructural changes of the mitochondria and the endoplasmic reticulum were already present at the fatty liver stage and persisted throughout the hepatitis and cirrhosis. The lesions were similar to those observed in alcoholics (including the inflammation and the central sclerosis), and differed strikingly from the alterations produced by other models of liver injury. In showing that all aspects of liver injury observed in alcoholics can be reproduced in animals by the feeding of pure ethanol with an adequate diet, this study incriminates ethanol itself as a cause for the hepatic complications. This new experimental model is proposed as a tool for the study of the pathogenesis and treatment of alcoholic liver injury and dependence.

Alcoholism↗
PubMed1996

The role of major histocompatibility complex polymorphisms on SIV infection in rhesus macaques.

To investigate whether Major Histocompatibility Complex (MHC) polymorphisms influence either susceptibility to SIV infection or progress to actual disease, rhesus monkeys were subjected to various forms of SIV infection and screened for allelic MHC heterogeneity by means of serological and biochemical methods. Animals that are protected against cell associated virus challenges were those that are SIV vaccinated and which shared a particular MHC class I allele (Mamu-A26) with the donor of the infected cells. Comparisons on the rate of infection to AIDS in SIVmac infected macaques showed that most Mamu-A26 positive animals belong to the group of long time survivors. In our outbred colony, about 25% of the rhesus macaques are positive for the Mamu-A26 serotype. Gel electrophoretic analyses demonstrated that isoelectric point (pI) differences of MHC class I heavy chains correlate with allotyping. In addition, the Mamu-A26 specificity was found to display heterogeneity. These results suggest that particular Mamu-A26 (associated) gene products may have the capacity or quality to induce antigen specific cytotoxic T lymphocyte responses that play a key role in controlling SIV infection or vaccine protection.

Animals↗