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At least 253 records · Page 14Linked to original sources
PubMed2004

Epidemiology of Helicobacter infection in wild rodents in the Xinjiang-Uygur autonomous region of China.

Helicobacter species were detected in the feces of wild rodents captured in Qiemo and Ruoqiang in the Xinjiang-Uygur autonomous region of China by polymerase chain reaction and 16S rRNA partial sequence analysis. Forty-four wild rodents, including one Przewalski's gerbil (Brachiones przewalskii), three Northern three-toed jerboas (Dipus sagitta), one long-eared jerboa (Euchoreutes naso), 34 midday gerbils (Meriones meridianus), two short-tailed bandicoot rats (Nesokia indica) and three great gerbils (Rhombomys opimus), were examined. Epidemiological studies indicated that Helicobacter spp. were detected in all genera tested; that H. hepaticus, H. apodemus, H. canadensis, and H. winghamensis were widespread in wild rodents; and that the dominant Helicobacter species in rodents differed depending not only on the order or genus of the animal but also on the animal's habitat. H. bilis, H. pylori, H. rodentium and " H. suncus" were not detected in any animals. It appears that the wild rodents tested in this study are not a reservoir of H. pylori infection.

Animals↗
PubMed2003

Marine resources subsidize insular rodent populations in the Gulf of California, Mexico.

Inputs of energy and nutrients from one ecosystem may subsidize consumers in adjacent ones, with significant consequences for local communities and food webs. We used stable isotope and faecal pellet analysis to quantify use of ocean-derived resources by small mammals on islands in the Gulf of California, Mexico. Rodents were live-trapped on grids originating near shore and extending 125-200 m inland to evaluate the extent to which rodents transport marine nutrients inland, and to determine whether marine foods subsidize island populations, permitting higher densities than would be possible based on terrestrial resources alone. Both faeces and stable carbon and nitrogen isotopes revealed that omnivorous mice (Peromyscus maniculatus) consume ocean-derived prey, including littoral and supralittoral invertebrates, and that their diets differed markedly from those of granivorous rodents (Chaetodipus rudinoris). On a small, seabird roosting island, marine prey were important in the diet of mice regardless of their proximity to shore, underscoring the pervasive influence of the ocean on small islands with relatively large coastline area. On a large island, however, consumption of marine foods declined sharply > or =50 m from shore, which suggests that mice are poor conduits of inland movement of energy and nutrients from the sea. Marine resources seemed to act as subsidies for omnivorous rodents: more P. maniculatus were captured near shore than farther inland and there was an inverse relationship between island area and rodent abundance, suggesting that small islands with large amounts of marine inputs support the highest population densities. Patterns of local and island-wide abundance of P. maniculatus are likely the result of several interacting factors, including frustrated dispersal, competition with C. rudinoris, and the absence of predators. We speculate, however, that the availability of marine resources allows P. maniculatus to reach high densities and to persist on small islands in the Gulf despite low and unpredictable terrestrial productivity. Spatial trophic subsidies thus provide a possible mechanistic explanation for the widely reported inverse relationship between population density and island or habitat area.

Animals↗
PubMed2005

Sheep grazing and rodent populations: evidence of negative interactions from a landscape scale experiment.

Inter-specific competition, facilitation and predation influence herbivore assemblages, but no study has experimentally explored the interactions between large ungulates and small rodents. In a fully replicated, landscape scale experiment, we manipulated densities of domestic sheep in mountain pastures in Norway. We then determined population growth and densities of rodents by live trapping in each of the areas with different sheep densities. We found that the (summer) population growth rate and autumn density of the field vole (Microtus agrestis) was lower at high sheep density. This provides the first experimental evidence of negative interactions between an ungulate and small rodent species. There was no effect on the bank vole (Clethrionomys glareolus), whose diet differs from sheep. Sheep density, therefore, potentially alters the pattern of inter-specific population synchrony amongst voles. Our study shows that negative interactions between large ungulates and small rodents may be species-specific and negative population consequences for the rodent population appear above threshold ungulate densities.

Animals↗
PubMed2005

Two-phase seed dispersal: linking the effects of frugivorous birds and seed-caching rodents.

Frugivorous birds disperse the seeds of many fruit-bearing plants, but the fate of seeds after defecation or regurgitation is often unknown. Some rodents gather and scatter hoard seeds, and some of these may be overlooked, germinate, and establish plants. We show that these two disparate modes of seed dispersal are linked in some plants. Rodents removed large (>25 mg) seeds from simulated bird feces (pseudofeces) at rates of 8-50%/day and scatter hoarded them in soil. Ants (Formica sibylla) also harvested some seeds and carried them to their nests. Rodents carried seeds 2.5+/-3.2 m to cache sites (maximum 12 m) and buried seeds at 8+/-7 mm depth. Enclosure studies suggest that yellow pine chipmunks (Tamias amoenus) and deer mice (Peromyscus maniculatus) made the caches. In spring, some seeds germinated from rodent caches and established seedlings, but no seedlings established directly from pseudofeces. This form of two-phase seed dispersal is important because each phase offers different benefits to plants. Frugivory by birds permits relatively long-range dispersal and potential colonization of new sites, whereas rodent caching moves seeds from exposed, low-quality sites (bird feces on the ground surface) to a soil environment that may help maintain seed viability and promote successful seedling establishment.

Animals↗
PubMed2006

Mathematical models for hantavirus infection in rodents.

Hantavirus pulmonary syndrome is an emerging disease of humans that is carried by wild rodents. Humans are usually exposed to the virus through geographically isolated outbreaks. The driving forces behind these outbreaks is poorly understood. Certainly, one key driver of the emergence of these viruses is the virus population dynamics within the rodent population. Two new mathematical models for hantavirus infection in rodents are formulated and studied. The new models include the dynamics of susceptible, exposed, infective, and recovered male and female rodents. The first model is a system of ordinary differential equations while the second model is a system of stochastic differential equations. These new models capture some of the realistic dynamics of the male/female rodent hantavirus interaction: higher seroprevalence in males and variability in seroprevalence levels.

Algorithms↗
PubMed1996

Species-specific differences in taxol transport and cytotoxicity against human and rodent tumor cells. Evidence for an alternate transport system.

The efficacy of taxol against a wide range of sensitive and refractory solid tumors has prompted extensive investigation into the factors that influence its cytotoxicity. Our preliminary observations indicated that taxol had a superior antitumor effect against human cells (Daudi, K562, 2008, 2008/C13*, 2780 and C70) compared with its effect against rodent cells (WS, WR, NIH3T3, and CHO). Although verapamil, an inhibitor of P-glycoprotein function, markedly increased the efficacy of taxol against the rodent cells (WS, WR, and CHO), the expression of P-glycoprotein was found only at low levels in the WR cells. In addition, levels of the multidrug resistance-associated protein (MRP), as assessed by reverse transcriptase-polymerase chain reaction analysis, were found to be higher in the human than in the rodent cells, although MRP mRNA was not detected by northern blotting. Transport studies indicated that the reduced sensitivity of the rodent cells to taxol was due to decreased intracellular taxol levels and reduced intracellular binding. However, no correlation was found between the intracellular binding of taxol and the intracellular levels of alpha- and beta-tubulin, or the intracellular concentration of polymerized tubulin. These studies were extended further by assessing the binding of taxol to semi-purified microtubule proteins from WS, CHO and 2008/C13* cells in vitro. The microtubule protein preparations from WS, CHO and 2008/C13* cells, which have a 50-fold difference in their sensitivity to taxol, were found to bind equal amounts of radiolabeled taxol, and this binding was inhibited (80%) in the presence of unlabeled taxol. These results lead us to propose the presence in the rodent cells of an alternative taxol transport system that is distinct from the P-glycoprotein and MRP systems.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Melatonin binding sites in sciurid and hystricomorph rodents: studies on ground squirrels and guinea pigs.

Little is known about the distribution of binding sites for the pineal hormone melatonin in non-myomorph rodents. We used 2-[125I]iodomelatonin (IMEL) to analyze the distribution, affinity, and specificity of binding sites in the golden-mantled ground squirrel, a sciurid rodent that reportedly lacks IMEL binding sites in the brain. Specific binding was found not only in the pars tuberalis, but also in several telencephalic and diencephalic areas including the hypothalamic suprachiasmatic region. The affinity and specificity of IMEL binding are comparable to those reported in other rodents. IMEL binding studies in a hystricomorph rodent, the guinea pig, revealed high concentrations of receptor in the nucleus accumbens and dorsolateral thalamus. Central melatonin binding sites have now been demonstrated in species of all three rodent families. The heterogeneous distribution of melatonin receptors appears similar in the species studied, and no evidence is found to link IMEL binding sites at any particular locus to photoperiodic, circannual, or non-seasonal breeding patterns.

Animals↗
PubMed1985

Differences in the metabolism of MPTP in the rodent and primate parallel differences in sensitivity to its neurotoxic effects.

Primates and rodents show marked differences in sensitivity to the neurotoxic effects of MPTP. We and others have previously shown that the toxic effects of MPTP on nigrostriatal cells are dependent on the oxidative metabolism of MPTP to the quaternary species MPP+. We have therefore compared the distribution and metabolism of MPTP in the monkey and several rodent species. Three major differences have been identified: 1) the primate, but not the rodents, showed a persistently high concentration of MPTP metabolites in the caudate nucleus compared to other brain regions; 2) the rodent brains cleared MPTP and its metabolites much more rapidly than did the monkey, and; 3) the predominant metabolite retained by the monkey brain was MPP+, while MPP+ cannot be detected in rodent brains for more than a few hours after injection. The persistence of MPP+ in the primate brain may explain the heightened toxicity of MPTP in this species.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1995

Chemicals for evaluating the sensitivity and specificity of reduced/transgenic rodent cancer bioassay protocols.

The standard two-species/two-gender lifetime carcinogenicity bioassay protocol is not practical when assessing the possible carcinogenicity of a large number of chemicals. This has led to consideration of reduced cancer bioassay protocols (e.g., male rat/female mouse), or to the use of genetically altered rodents that succumb to chemically induced cancer in a fraction of their lifespans. Two uncertainties accompany these endeavours. First, that use of reduced protocols may lead to the non-detection of some weak or tissue-specific carcinogens. Second, that genetically altered rodents may be so sensitive to chemical disturbance of homoeostasis that their carcinogen specificity may be low. Such uncertainties lead to the requirement that the modified test protocols should be validated using appropriate carcinogens and non-carcinogens. Given that several such studies may take place over the coming years it seems appropriate that a common pool of chemicals should be agreed upon for this purpose. To this end a selection of human carcinogens, and rodent carcinogens/non-carcinogens defined by the US National Toxicology Program (NTP), have been collected together. Six categories of chemicals are listed: (1) representative human carcinogens; (2) representative trans-species genotoxic carcinogens; (3) all two-species non-carcinogens reported to be negative in the Salmonella mutation assay and lacking structural alerts to electrophilicity; (4) representative single-species/presumed non-genotoxic carcinogens; (5) all two-species non-carcinogens that are mutagens in the Salmonella mutation assay and which are structurally alerting; (6) all chemicals possessing equivocal evidence of carcinogenicity and which are both structurally alerting and mutagenic to Salmonella. Chemicals in the first four groups provide robust calibrants for determining the sensitivity and specificity of reduced/accelerated rodent carcinogenicity bioassay protocols. Chemicals in the last two groups may be of value when studying the interface between the sensitivity and the specificity of modified rodent carcinogenicity bioassay protocols.

Animals↗
PubMed1995

Rodent models for studying steroids and hypertension: from fetal development to cells in culture.

We have used several different approaches to study the role of steroids in hypertension, including rodent in vivo models, transgenic animals, and cell culture systems. Using the developing rodent fetus as a model for the ontogeny of regulation of glucocorticoid and mineralocorticoid synthesis, we found that in the developing rodent fetus, expression of both P450scc (cholesterol side chain cleavage) and P450c11 beta (11 beta-hydroxylase) mRNAs occur early, before there is complete organization of the fetal adrenal. Even after the zones of the adrenal are evident, the fetal adrenal still does not express the glomerulosa-specific P450c11AS (aldosterone synthase) mRNA. Stimulating maternal adrenal mineralocorticoid or glucocorticoid synthesis does not affect accumulation of fetal adrenal steroidogenic mRNAs, suggesting that the rodent fetal adrenal may be somewhat transcriptionally quiescent in vivo. We also used two different transgenic rodent systems to study the roles of steroids in hypertension. Using promoter-directed tumorigenesis in transgenic mice, we created transgenic mice that expressed SV40 T antigen under control of the P450scc promoter. Massive adrenal tumors, but not gonadal tumors, developed in all transgenic mice, and cells from these tumors were easily cultured. Using a novel selection tactic, we obtained several adrenocortical cell lines which have distinct characteristics, suggesting they were locked into various stages of differentiation; both expression of steroidogenic mRNAs and the steroids synthesized differ among the lines. Regulation of steroid synthesis and mRNA abundance also varies among cell lines. Several cell lines also express mouse renin, and its synthesis, secretion, and mRNA abundance is also hormonally regulated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1987

The dopamine and serotonin systems during aging in human and rodent brain. A brief review.

During nonpathological aging, quantitative changes occur in the pre- and post-synaptic elements of both the dopamine and serotonin systems. The level of dopamine in the human striatum declines up to 50% with age, while smaller and more variable changes are found in rodent brain (0-30%). Postsynaptically, the density of D-2 dopamine receptors also declines by 25-50% in both human and rodent striata. Conversely, D-1 receptors have been reported to increase with age in human, and to remain stable in rodent brain. In the serotonin system, the concentration of serotonin remains stable during nonpathological aging in both rodents and humans. The density of S-2 serotonin receptors declines 20-50% with age in human frontal cortex and hippocampus, and by 30% in mouse cortex. The density of S-1 serotonin receptors is unchanged throughout the mouse lifespan, but declines by 30-50% in human frontal cortex. In rodents, the up-regulation of D-2 receptors in response to antagonist (neuroleptic) treatment is impaired in old animals. Conversely, the down-regulation of D-2 receptors in response to chronic agonist (bromocriptine) treatment is equivalent at all ages. Similarly, the down-regulation of S-2 receptors to antidepressant (amitriptyline) treatment in mice is constant over the lifespan. Attempts to up-regulate serotonin receptors with antagonists have, thus far, been unsuccessful.

Aging↗
PubMed1991

The response of human and rodent cells to hyperthermia.

Inherent cellular radiosensitivity in vitro has been shown to be a good predictor of human tumor response in vivo. In contrast, the importance of the intrinsic thermosensitivity of normal and neoplastic human cells as a factor in the responsiveness of human tumors to adjuvant hyperthermia has never been analyzed systematically. A comparison of thermal sensitivity and thermo-radiosensitization in four rodent and eight human-derived cell lines was made in vitro. Arrhenius plots indicated that the rodent cells were more sensitive to heat killing than the human, and the break-point was 0.5 degrees C higher for the human than rodent cells. The relationship between thermal sensitivity and the interaction of heat with X rays at low doses was documented by thermal enhancement ratios (TER's). Cells received either a 1 hr exposure to 43 degrees C or a 20 minute treatment at 45 degrees C before exposure to 300 kVp X rays. Thermal enhancement ratios ranged from 1.0 to 2.7 for human cells heated at 43 degrees C and from 2.1 to 5.3 for heat exposures at 45 degrees C. Thermal enhancement ratios for rodent cells were generally 2 to 3 times higher than for human cells, because of the fact that the greater thermosensitivity of rodent cells results in a greater enhancement of radiation damage. Intrinsic thermosensitivity of human cells has relevance to the concept of thermal dose; intrinsic thermo-radiosensitization of a range of different tumor cells is useful in documenting the interactive effects of radiation combined with heat.

Animals↗
PubMed1992

Higher rates of amino acid substitution in rodents than in humans.

An analysis of 54 protein sequences from humans and rodents (mice or rats), with the chicken as an outgroup, indicates that, from the common ancestor of primates and rodents, 35 of the proteins have evolved faster in the lineage to mouse or rat (rodent lineage) whereas only 12 proteins have evolved faster in the lineage to humans (human lineage). The average rate of amino acid substitution is significantly faster in the rodent lineage than in the human lineage. In addition, the average rate of insertion/deletion is also faster in rodents than in humans and there is a positive correlation between the rate of amino acid substitution and the rate of insertion/deletion in a protein sequence.

Animals↗
PubMed1987

Liver tumors in rodents: extrapolation to man.

Man is a poor model for the prediction of agents that are hepatocarcinogenic for laboratory rodents. Relatively few agents are known to cause any form of primary liver cancer in man. The most important is hepatitis B virus, for which there is possibly a model in the woodchuck but not one in rats or mice. The only other agents known to cause primary liver cancer in man are certain steroid hormones, vinyl chloride, and thorium dioxide. There are animal models for the first two of these and a reasonable expectation that thorium dioxide would produce liver tumors in animals if the appropriate experiments were done. Aflatoxin, a potent hepatocarcinogen in rats and other species but not mice, is strongly suspected of being an important human hepatocarcinogen in certain geographical areas of the world, but the evidence is circumstantial. There is no more than a weak association between the nutritional type of cirrhosis secondary to excessive intake of alcohol and increased primary liver cancer in man, and no evidence at all that ethanol per se causes liver tumors in mice, rats, hamsters, or mastomys. By contrast, a very large number of chemicals to which people in the West have been exposed for many decades have been found to be hepatocarcinogens in laboratory rodents. In most cases the levels of exposure required to produce liver tumors in rodents far exceed those to which man is normally exposed. The problem is to guess whether low-level exposure to such rodent hepatocarcinogens poses any real liver cancer threat to man?The mortality from primary liver cancer is very low in countries such as England and Wales where there is widespread exposure to low doses of both natural and synthetic agents which, in high dosage, cause liver tumors in rodents. This suggests that, if there is any risk, it can only be very small. Death rate data collected in England and Wales by the Registrar General are consistent with there having been a small increase in the incidence of primary liver cancer in England and Wales during the past 20 years, but the apparent increase might well be a consequence of revisions in the International Classification of Diseases system and not real. During the first half of the present century the age-standardized incidence of primary liver cancer in England and Wales was falling.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Thiol compounds metabolism in mice, rats and humans: comparative study and potential explanation of rodents protection against vascular diseases.

BACKGROUND: Rodents are often used as animal models to dissect mechanisms underlying hyperhomocysteinemia atherogenicity in humans. However, neither wild-type rodents nor cystathionine beta-synthase deficient mice develop spontaneous atherosclerosis. We investigated whether species-specific differences in thiols metabolism may explain the respective sensitivity of rodents and humans to hyperhomocysteinemia. METHODS: Thiols and vitamins B levels were determined in normohomocysteinemic humans and rodents, and in hyperhomocysteinemic mice. RESULTS: In basal status, although plasma homocysteine, cysteine and cysteinylglycine levels were lower, glutathione levels were higher in mice than in humans (4.0+/-1.6 vs. 7.9+/-2.2, P<0.0005; 147.4+/-40.3 vs. 278.5+/-50.0, P<0.0001; 2.3+/-0.7 vs. 36.6+/-7.3, P<0.0001; and 70.9+/-20.1 vs. 4.6+/-1.6, P<0.0001). Serum vitamin B12 and folate levels were 2.5- and 7.7-fold higher in rats than in humans. In wild-type mice, the increase in plasma Hcy levels induced by methionine-enriched diet was accompanied by a proportional increase in GSH levels. CONCLUSION: GSH levels are enough to modulate Hcy effects in normo- and hyperhomocysteinemic mice but not in humans. This rodents characteristic, likely supported by species differences in the relative contribution of remethylation and transsulfuration pathways, may partly explain their protection against atherosclerosis.

Animals↗
PubMed2005

Antidepressant treatment and rodent aggressive behaviour.

This review examines two 'ethologically relevant' rodent models, the resident-intruder and social hierarchy paradigms, that are sensitive to chronic antidepressant treatment (including repeated electroconvulsive shock). These models of rodent social and agonistic behaviour demonstrate that acute and chronic treatment with antidepressant drugs (regardless of their acute pharmacological activity) induce diametrically opposite changes in rodent aggressive behaviour. The common ability of chronic antidepressant treatment to increase rodent aggression (which in turn results in increased hierarchical status in closed social groups) most likely reflects the increased assertiveness and associated externalization of emotions (indicative of increased extrapunitive aggression) expressed during recovery from depressive illness. Finally, findings that relate observed behavioural changes to underlying neurochemical changes are briefly reviewed in terms of adaptive mechanisms in the rodent central nervous system induced by antidepressants, and also with respect to suicide ideation and panicogenic responses observed in some patients at the onset of treatment with selective serotonin reuptake inhibitors for affective disorders.

Aggression↗
PubMed2004

Perchlorate in water, soil, vegetation, and rodents collected from the Las Vegas Wash, Nevada, USA.

Water, soil, vegetation, and rodents were collected from three areas along the Las Vegas Wash, a watershed heavily contaminated with perchlorate. Perchlorate was detected at elevated concentrations in water, soil, and vegetation, but was not frequently detected in rodent liver or kidney tissues. Broadleaf weeds contained the highest concentrations of perchlorate among all plant types examined. Perchlorate in rodent tissues and vegetation was correlated with perchlorate concentrations in soil as expected, however rodent residues were not highly correlated with plant perchlorate concentrations. This indicates that soil may be a greater source, or a more constant source of perchlorate exposure in rodents than vegetation.

Animals↗
PubMed2006

Effects of latanoprost on rodent intraocular pressure.

The aim of the present study was to evaluate the effects of the prostaglandin F2 alpha analog, latanoprost, on the intraocular pressure (IOP) in rodent eyes. Rodents have been increasingly used in glaucoma research; however, conflicting results regarding the actions of prostaglandins on rodent IOP have been published. In Wistar rats, a single dose of latanoprost (60 ng) produced a biphasic change in IOP: an initial rise in pressure (2.1+/-0.7 mmHg) peaking at 2 h, followed by a prolonged hypotension with a peak reduction in IOP (5.2+/-0.7 mmHg) at 5 h. Both the hyper and hypotensive actions of latanoprost were dose-related with ED50 values of 108 and 5.2 ng, respectively. These responses were antagonized by pretreatment with 4% pilocarpine. In Brown Norway rats and C57BL/6 mice, a single dose of latanoprost also produced a biphasic response in IOP with an initial rise in pressure peaking between 1 and 2 h, followed by prolonged hypotension from 4 to 8 h. These results demonstrate that in rodents the IOP response to topical latanoprost is characterized by an initial hypertension followed by a prolonged hypotension. This prolonged hypotension is similar to that measured in monkeys and humans. Taken together, these results support the idea that rodents can serve as in vivo models to study the actions of ocular hypotensive agents, such as prostaglandins.

Animals↗