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At least 1,351 records · Page 75Linked to original sources
PubMed1997

Entacapone enhances levodopa-induced reversal of motor disability in MPTP-treated common marmosets.

Oral administration of levodopa (L-dopa) (2.5-25.0 mg/kg) plus carbidopa (12.5 mg/kg p.o.) to MPTP-treated common marmosets produced a dose-related increase in locomotor activity and a corresponding decrease in motor disability. Pretreatment with the peripheral COMT inhibitor entacapone (12.5 mg/kg p.o.) enhanced the intensity and duration of the increase in locomotor activity and the reversal of motor disability produced by a threshold dose of L-dopa (2.5 mg/kg p.o.) plus carbidopa. By contrast, entacapone pretreatment did not potentiate the increased locomotor activity or reversal of motor disability produced by a near-maximal dose of L-dopa (12.5 mg/kg p.o.) plus carbidopa. The effects of entacapone (5.0-25.0 mg/kg p.o.) were dose related, with doses of > 12.5 mg/kg tending to produce less potentiation of L-dopa's effects compared to lower doses. Pretreatment with entacapone (12.5 mg/kg p.o.) without carbidopa caused a short-lasting enhancement of L-dopa's (12.5 mg/kg p.o.) action, whereas pretreatment with carbidopa (12.5 mg/kg p.o.) alone had a more dramatic effect. However, pretreatment with both carbidopa and entacapone produced the greatest overall motor response. In conclusion, entacapone enhances the motor response produced by a low-threshold dose of L-dopa plus carbidopa. However, optimization of both the dose of L-dopa and entacapone appears necessary to obtain the maximal therapeutic response.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1998

De novo administration of ropinirole and bromocriptine induces less dyskinesia than L-dopa in the MPTP-treated marmoset.

In contrast to levodopa (L-dopa), de novo administration of the D2-like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2-like selective dopamine agonist ropinirole with that of bromocriptine and L-dopa to induce dyskinesia in MPTP-treated common marmosets. MPTP-treated common marmosets were treated with placebo, L-dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L-dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L-dopa-treated group (p < 0.05). However, in a separate group of marmosets previously primed with L-dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L-dopa in a dose-dependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L-dopa to produce dyskinesia while similarly improving motor performance in drug-naive MPTP-treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L-dopa priming has occurred. These results predict a similar response to ropinirole and other long-acting dopamine agonists in L-dopa-naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2002

Theory of nonexponential NMR signal decay in liver with iron overload or superparamagnetic iron oxide particles.

A quantitative theory is proposed for the nonexponential NMR proton signal decay observed in liver with iron overload or superparamagnetic iron oxide particles. This effect occurs for Carr-Purcell-Meiboom-Gill (CPMG) sequences and is argued to be a direct consequence of the strong magnetic field inhomogeneities generated by the iron, rather than being due to tissue compartments. An approximate mathematical form is given for the signal decay, which is fit to experimental data for samples of rat liver with iron oxide particles, for samples of marmoset liver with hemosiderosis, and for in vivo human liver with hereditary hemochromatosis. The fitting parameters obtained are consistent with the pattern of iron deposition determined from histology. For the case of hereditary hemochromatosis, a good correlation is found between a parameter characterizing the nonexponential decay and the iron concentration. Implications for practical MR quantification of hepatic iron are discussed.

Animals↗
PubMed2004

Mimicking liver iron overload using liposomal ferritin preparations.

Close monitoring of liver iron content is necessary to prevent iron overload in transfusion-dependent anemias. Liver biopsy remains the gold standard; however, MRI potentially offers a noninvasive alternative. Iron metabolism and storage is complicated and tissue/disease-specific. This report demonstrates that iron distribution may be more important than iron speciation with respect to MRI signal changes. Simple synthetic analogs of hepatic lysosomes were constructed from noncovalent attachment of horse-spleen ferritin to 0.4 microm diameter phospholipid liposomes suspended in agarose. Graded iron loading was achieved by varying ferritin burden per liposome as well as liposomal volume fraction. T1 and T2 relaxation times were measured on a 60 MHz NMR spectrometer and compared to simple ferritin-gel combinations. Liposomal-ferritin had 6-fold stronger T2 relaxivity than unaggregated ferritin but identical T1 relaxivity. Liposomal-ferritin T2 relaxivity also more closely matched published results from hemosiderotic marmoset liver, suggesting a potential role as an iron-calibration phantom.

Animals↗
PubMed1997

Hepatic hemosiderosis in non-human primates: quantification of liver iron using different field strengths.

Using a non-human primate model of idiopathic hemochromatosis, hemosiderin-induced T2 shortening of the liver was assessed at nine different field strengths over a range of 0.05 to 1.5 Tesla. The 1/T2 values increased linearly with field strength, with all specimens having approximately the same zero-field intercept. The slope of the field increase, termed "field-dependent T2 proton relaxation enhancement (PRE)", appeared to be proportional to the chemically determined tissue iron content, viz. 10.8 s-1T-1(mg Fe/g wet tissue)-1. The correlation between iron content and field-dependent T2 PRE (r = 0.94) was better than the correlation between iron content and 1/T2 values obtained at single field strengths. For livers containing > or = 2 mg Fe/g wet weight, biexponential T2 relaxation behavior emerged at higher field strengths, with the short T2 component (intracellular water) exhibiting a linear dependence of 1/T2 on field, while T2 of the long component (extracellular/sinusoidal water) was nearly field-independent. After maceration of the specimens, all T2 relaxation curves became monoexponential, including those for high iron content at high field strengths. The present data suggest that the use of double-field MR imaging to assess the field-dependent T2 PRE has potential for specific quantification of (liver) tissue iron stores.

Animals↗
PubMed2007

Quantitative MRI-pathology correlations of brain white matter lesions developing in a non-human primate model of multiple sclerosis.

Experimental autoimmune encephalomyelitis (EAE) induced with recombinant human myelin/oligodendrocyte glycoprotein in the common marmoset is a useful preclinical model of multiple sclerosis in which white matter lesions can be well visualized with MRI. In this study we characterized lesion progression with quantitative in vivo MRI (4.7 T; T(1) relaxation time +/- Gd-DTPA; T(2) relaxation time; magnetization transfer ratio, MTR, imaging) and correlated end stage MRI presentation with quantitative ex vivo MRI (formaldehyde fixed brains; T(1) and T(2) relaxation times; MTR) and histology. The histopathological characterization included axonal density measurements and the numeric quantification of infiltrated macrophages expressing markers for early active [luxol fast blue (LFB) or migration inhibition factor-related protein-14 positive] or late active/inactive [periodic acid Schiff (PAS) positive] demyelinating lesion. MRI experiments were done every two weeks until the monkeys were sacrificed with severe EAE-related motor deficits. Compared with the normal appearing white matter, lesions showed an initial increase in T(1) relaxation times, leakage of Gd-DTPA and decrease in MTR values. The progressive enlargement of lesions was associated with stabilized T(1) values, while T(2) initially increased and stabilized thereafter and MTR remained decreased. Gd-DTPA leakage was highly variable throughout the experiment. MRI characteristics of the cortex and (normal appearing) white matter did not change during the experiment. We observed that in vivo MTR values correlated positively with the number of early active (LFB+) and negatively with late active (PAS+) macrophages. Ex vivo MTR and relaxation times correlated positively with the number of PAS-positive macrophages. None of the investigated MRI parameters correlated with axonal density.

Animals↗
PubMed1983

Histopathology of experimental Legionnaires' disease in guinea pigs, rhesus monkeys and marmosets.

Guinea pigs, rhesus monkeys and marmosets were infected with L. pneumophila in small particle aerosols. Fever and acute fibrinopurulent pneumonia resulted. The lesions involved distal lung tissue only, spreading from terminal and respiratory bronchioles and producing heavy infiltration of alveoli by polymorphs and macrophages and widespread exudation of oedema fluid and fibrin. Lesions were not found in extra-pulmonary sites.

Animals↗
PubMed1983

Ultrastructure of pulmonary alveoli and macrophages in experimental Legionnaires' disease.

Guinea pigs, rhesus monkeys and marmosets infected with Legionella pneumophila in small particle aerosols developed an acute fibrinopurulent bronchopneumonia. Changes from 24 hr included exudation into alveoli of protein-rich, often fibrinous fluid and many polymorphonuclear leucocytes (PMN) and macrophages. Damage to alveolar capillary endothelium consisted of widespread cytoplasmic swelling and vesiculation, but necrosis of endothelium and the associated alveolar epithelium was focal and less common. Phagocytosis of L. pneumophila organisms was predominantly by macrophages, but the bacteria were also seen in PMN. Free organisms were present in alveoli and capillary lumina at all stages of the infection but were not observed in lung parenchymal cells. Some infected macrophages and PMN became necrotic and lysed to release intact bacteria. In all species of experimental animal, intracytoplasmic aggregations of granular material, believed to be glycogen, were seen frequently in macrophages and PMN which had phagocytosed L. pneumophila. These deposits of glycogen may reflect either an increased energy demand by the host cell or an interference with its carbohydrate metabolism.

Animals↗
PubMed2004

Detailed distribution of neuropeptide FF receptors (NPFF1 and NPFF2) in the rat, mouse, octodon, rabbit, guinea pig, and marmoset monkey brains: a comparative autoradiographic study.

The distribution of neuropeptide FF receptors (NPFF(1) and NPFF(2)) was analyzed throughout the central nervous system of rodents (rat, mouse, Octodon degus, and guinea pig), rabbit, and marmoset monkey brains, representing three orders of mammals. Quantitative in vitro receptor autoradiography with [(125)I]EYF ([(125)I]EYWSLAAPQRF-NH(2)) and [(125)I]YVP ([(125)I]YVPNLPQRF-NH(2)) as specific radioligands for NPFF(2) and NPFF(1) receptors, respectively, was used. The NPFF(2) receptor is predominantly expressed in all species, except in the central nervous system of Octodon degus, in which it is undetectable. The density of the NPFF(1) subtype is low in rat and mice, moderate in octodon, rabbit, and monkey, and relatively high in the guinea pig. The present study reveals prominent species differences in the NPFF receptors expression in the brain. The distribution pattern of NPFF(2) receptors in the diencephalon and the superficial layers of the spinal cord is consistent with a hypothesized potential role for NPFF in the modulation of sensory input and opioid analgesia. In contrast, the constant presence of NPFF(1) receptors in the septum, the nucleus of the tractus solitarius, and the hypothalamus suggest its participation in neuroendocrine functions.

Animals↗
PubMed2005

Ductus venosus shunting in marmoset and baboon fetuses.

OBJECTIVES: The increased shunting of blood through the ductus venosus (DV) during stress situations is an important mechanism that ensures fetal survival. Although primate fetuses may serve to study the function of this important venous shunt, the rate of DV shunting has not been determined in non-human primates under normal conditions. METHODS: DV shunting was measured in 11 marmoset (eight mothers) and eight singleton baboon fetuses in mid and late gestation using Doppler ultrasound. RESULTS: DV shunting in marmosets was 39 +/- 20% (mean +/- SD) and 28 +/- 8% in baboon fetuses. Umbilical vein (UV) blood volume rate increased significantly in baboons with gestational age (GA) (UV flow volume = -111.8 + 1.6*GA; r = 0.94, P < 0.05) and slightly in marmosets (UV flow volume = -10.37 + 0.13*GA; r = 0.42, P > 0.05). Both UV diameter (r = 0.84) and the time-averaged mean UV flow velocity in baboons depended on GA (r = 0.8, P < 0.05). Distinct pulsation was found in marmoset fetuses in the UV (pulsatility index (PI) = 1.3 +/- 0.9) and the DV (PI = 1.9 +/- 1.2) with zero blood flow velocity during atrial contraction. CONCLUSIONS: A high level of pulsation is observed in the UV in marmoset fetuses. DV shunting in marmosets is higher than in baboon fetuses.

Animals↗
PubMed1997

Marmoset liver cytochrome P450s: study for expression and molecular cloning of their cDNAs.

Northern blot and immunoblot analyses indicated that considerable levels of CYP2B, CYP2C, CYP2D, CYP2E, and CYP3A were expressed in the liver of untreated marmosets. CYP1A was also expressed but to lesser extents. CYP3A mRNA was also detectable in the small intestine of untreated marmoset; the amount was increased by treatment with polychlorinated biphenyl. From a liver cDNA library, two cDNA clones coding for CYP2D19 and CYP3A21 (clones CM2D-1 and CM3A-10, respectively) were isolated. CM2D-1 and CM3A-10 contained an entire coding region for polypeptide 497 and 503 amino acid residues, respectively. The deduced amino acid sequences of CYP2D19 and CYP3A21 showed 90% identities to human CYP2D6 and CYP3A4, respectively. The value of CYP3A21 was 3% lower than that of cynomolgus monkey CYP3A8. On the other hand, these values were 11 to 23% higher than those of the other experimental animals, including dogs, rabbits, guinea pigs, rats, mice, and hamsters. These results indicate that the marmoset stands at a midpoint between human and nonprimate experimental animals.

Amino Acid Sequence↗
PubMed1999

Molecular cloning, expression, and characterization of CYP2D17 from cynomolgus monkey liver.

The cynomolgus monkey is a species used in drug-safety evaluation and biotransformation studies by the pharmaceutical industry. Relatively little is known, however, about the catalytic activities and specificities of cytochromes P450 (CYP) in this species. As a first step in characterizing monkey CYPs, a cDNA was cloned by reverse-transcriptase PCR from cynomolgus monkey liver mRNA using oligonucleotide primers based on the human CYP2D6 sequence. The full-length cDNA (called CYP2D17) encoded a 497-amino-acid protein that is 93% identical to human CYP2D6 and 90% identical to marmoset CYP2D19. The CYP2D17 cDNA was cloned into a baculovirus expression vector, and microsomes prepared from CYP2D17-infected insect cells were used to determine the catalytic properties of the recombinant enzyme. The recombinant CYP2D17 results were compared to data generated with monkey liver microsomes, human liver microsomes, and recombinant CYP2D6 and demonstrated catalytic similarity using probe substrates and inhibitors. Recombinant CYP2D17 catalyzed the oxidation of bufuralol to 1'-hydroxybufuralol and dextromethorphan to dextrorphan, reactions shown to be mediated by CYP2D6 in humans; the apparent K(m) values for bufuralol and dextromethorphan were 1 and 0.8 microM, respectively. Moreover, both of these reactions were more strongly inhibited by quinidine than by quinine. A more complete understanding of the substrate specificities and activities of monkey CYPs will be advantageous in delineating species differences in metabolite profiles and metabolic activation of new chemical entities in the pharmaceutical industry.

Amino Acid Sequence↗
PubMed1993

Increased heterogeneity of tyrosine hydroxylase in humans.

Humans produce four different forms of tyrosine hydroxylase (TH) mRNA via alternative splicing of the gene. Here we demonstrate that New- and Old-World monkeys and the gorilla produce only two of the TH isoforms. Comparison among the genomic DNA sequences of various primates revealed that mutations that had accumulated in the genomic DNA created a new exon, resulting in the appearance of two new TH isoforms in man. These findings offer new insight into the sequence of events leading to the evolution of the higher primates into separate species. They also represent what may be the first evidence of a genetic difference between man and primates with respect to a specific brain function.

Animals↗
PubMed1995

Polymorphic tandem repeats in dopamine D4 receptor are spread over primate species.

The human dopamine D4 receptor has polymorphic tandem repeats in the third cytoplasmic loop. However, these repeats are not present in the rat counterpart. To determine whether the tandem repeats are specific to humans or not, we analyzed genomic DNA sequences for the D4 receptor of six primate species (human, chimpanzee, gorilla, orangutan, macaque, marmoset). Sequencing data revealed that all primates have the 48-bp tandem repeats in the D4 receptor gene. This finding suggests that these repeats originated before the separation of the New World monkey lineage from the Old World monkey and ape-human lineages.

Amino Acid Sequence↗
PubMed1995

Molecular genetic analysis of the duplication of human inducible nitric oxide synthase (NOS2) sequences.

In previous studies, we found multiple copies of inducible nitric oxide synthase gene (NOS2)-like sequences in the human genome and mapped them to the pericentric region of chromosome 17. Here, we describe the cloning and sequencing of exon22 regions from three of these NOS2-like sequences. We have also mapped another NOS2-like sequence to human chromosome 14. Since there are multiple NOS2-like sequences present in the human genome, we have also carried out Zoo Blot hybridisation analysis using a NOS2 cDNA probe. Our data suggest that duplication of NOS2-like sequences occurred very recently in primate evolution.

Amino Acid Oxidoreductases↗
PubMed1996

Functional reconstitution of oxidase activity in X-linked chronic granulomatous disease by retrovirus-mediated gene transfer.

The feasibility of correction of the disease phenotype by gene gene transfer was investigated in cells of four patients with X-linked chronic granulomatous disease. These patients carry point mutations of the gp91-phox gene, encoding for the large subunit of the catalytic core of the phagocytic cell NADPH oxidase. A retroviral vector expressing the gp91-phox protein was constructed and used to transduce lymphoblastoid cell lines established from the patients. Several transduced lymphoblastoid cell clones were investigated for mRNA and protein expression, and for functional reconstitution of oxidase activity. Although extensive quantitative variability was detected among different clones, functional reconstitution of O2- production was obtained in most cases, with oxidase function within the same range as in B cell lines derived from normal individuals. The same vector was also used for transduction of hematopoietic precursors from bone marrow or peripheral blood either with or without enrichment for CD34+ cells. A comprehensive analysis was performed on differentiated myeloid colonies, to evaluate the efficiency of transduction, the levels of gp91-phox expression, and the extent of functional reconstitution of oxidase activity. A high efficiency of transduction was obtained in most experiments, with 60-100% of colonies containing proviral DNA. Among the transduced colonies, an extensive variability in the levels of expression of the transduced gene and of functional restoration of NADPH oxidase activity was observed. These results represent a step toward the development of a gene therapy protocol for these patients.

3T3 Cells↗
PubMed1999

Functional benefit from clomethiazole treatment after focal cerebral ischemia in a nonhuman primate species.

Clomethiazole (CMZ) (Zendra) is neuroprotective in rodents following focal and global ischemia. However, its neuroprotective effects in other species, particularly on functional outcome, have not been reported. We have therefore examined the ability of CMZ to ameliorate the functional deficits produced by a focal cerebral ischemic lesion in the marmoset, a New World primate. Six monkeys received permanent middle cerebral artery occlusion (pMCAO); six further monkeys received pMCAO with administration of CMZ, 5 min after the arterial occlusion, by intraperitoneal bolus injection and by subcutaneous implantation of an osmotic minipump, which released CMZ for 24 h. The monkeys were trained and tested preoperatively on a number of behavioral tasks which were repeated 3 and 9 weeks after surgery. CMZ-treated monkeys were better than non-drug-treated monkeys at using the disabled arm contralateral to the lesion and also showed a reduction in contralateral spatial hemineglect. Postmortem histopathological analysis at several stereotaxic levels showed a significant reduction in the area of ischemic damage in CMZ-treated monkeys compared to that in untreated animals. CMZ treatment reduced the overall volume of damage by 31.8% (MCA group, 370.8 +/- 37.4 mm3 of damage; CMZ group, 253.0 +/- 38.0 mm3 of damage). This study demonstrates that CMZ is neuroprotective in a nonhuman primate species and is able to ameliorate the level of functional disability and reduce the size of infarct produced by focal cerebral ischemia.

Animals↗