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PubMed1973

Prospects of chemosterilant and genetic control of rodents.

This paper discusses some requirements of an ideal rodent chemosterilant, analyses the advantages of chemosterilants over other control methods, and compares the potential values of chemosterilants that affect females, males, and both sexes. Examples are given of specific situations where chemosterilants will be valuable in rodent control, together with suggested methods of applying them. The theory and practicability of using genetics in rodent control are also discussed. Neither the chemosterilant nor the genetic method is expected to become a panacea, but their eventual application will be a significant advance in rodent-control technology. Since both approaches are based on sound biological principles and are relatively safe, they should be helpful in regulating rodent populations in the future.

Animals↗
PubMed1983

[Populations of harmful rodents on commercial swine-breeding farms and their effect on the technology of swine feeding].

The effect was studied of the swine-feeding technology in five industrial complexes on the population density of the harmful rodents in them. This made it necessary to estimate the population density of the rodents in each productional section of the swine-breeding complexes, and to work out their technologic characteristic on the nutrition principle. It was established that the population density of rodents correlated positively with their access to feeds. In sections where rated, mechanical, and protected feeding was prectised the number of rodents were considerably lower than in sections with unrated feeding of pigs. It is believed that the rat invasion of the buildings in the industrial swine-breeding complexes is a factor that contributes to the rise of populations of harmful rodents, while the vast access to feeds is of greater importance chiefly for their further development.

Animal Feed↗
PubMed1996

Rodent parvovirus infections.

Parvoviruses are among the most common infectious agents of laboratory rodents and major impediments to rodent-based research. The original prototypic rodent parvoviruses-minute virus of mice, rat virus, and H-1 virus-have recently been joined by biologically and antigenically distinct parvoviruses in mice, rats, and hamsters. Recognition of the increased diversity of rodent parvoviruses presents new challenges for determining the impact of parvovirus infection on research and for detecting, preventing, and eliminating infection. This review summarizes current knowledge about rodent parvoviruses and parvovirus infections, highlighting recent research on newly isolated virus strains.

Animals↗
PubMed1997

Community structure and prevalence of hantavirus infection in rodents: a geographic division of the enzootic area in far eastern Russia.

The results of an extensive rodent trapping effort throughout the southern part of far eastern Russia and hantavirus antigen screening of tissues were used to develop a multifaceted approach for the geographic division of the enzootic territory of hantavirus. Four species of rodents (Apodemus agrarius, Apodemus peninsulae, Microtus fortis, and Clethrionomys rufocanus) comprised 88.5 percent of 10,595 captured rodents and 94.1 percent of 996 antigen-positive animals. Rodent fauna and the prevalence and distribution of hantavirus antigen-positive animals were compared among major biotic communities in the region. The species composition of the rodent communities and the predominant hantavirus reservoir species were used as criteria to define zones with similar enzootic characteristics.

Animals↗
PubMed1999

Concurrent deregulation of gelsolin and cyclin D1 in the majority of human and rodent breast cancers.

Decreased gelsolin and increased cyclin D1 are among the most common defects found in human and rodent breast cancers. Our purpose was to determine the frequency of concurrence of these 2 alterations in this malignancy. Our results demonstrate that gelsolin protein and mRNA were significantly reduced in 80-100% of rodent mammary carcinomas that developed spontaneously, following oncogene introduction, or after treatment with viral, chemical or hormonal agents. The reduction in gelsolin most likely occurs during the transition from preneoplasia to carcinoma because hyperplasias had normal levels of gelsolin whereas microtumors had reduced expression. Southern analysis revealed no major mutations in the gelsolin gene of tumors with low expression. Cyclin D1 mRNA was increased in 50-100% of these rodent mammary tumors, although the cyclin D1 gene was not amplified. By nuclear runon assay, downregulation of gelsolin in both human and mouse mammary cancer cells involved diminished transcription and, conversely, human breast cancer cells expressing high levels of cyclin D1 had increased initiation of cyclin D1 transcription compared with cyclin D1 low expressors. Thus, alteration in the rate of transcription appears to be an important factor underlying the dysfunction of these genes. According to our data, concurrent deregulation of gelsolin and cyclin D1 is highly prevalent among breast cancers of humans and rodents, with both defects present in 89% of the neoplasms analyzed in this study. In fact, most tumors in every rodent model of mammary tumorigenesis examined had the 2 alterations.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1977

The comparative fine structure of the interhemal membrane of chorioallantoic placentas from six genera of myomorph rodents.

In order to extend the cytological information available on the structure of the interhemal membrane in cricetid rodents, in particular, and myomorph rodents, in general, we have examined the fine structure of the placental labyrinth in five genera of cricetid rodents (Lemmus, Dicrostonyx, Clethrionomys, Microtus and Peromyscus) and one genus of murid rodent (Acomys). Small pieces of labyrinth from near-term placentas were fixed in glutaraldehyde and osmium tetroxide and processed for electron microscopy. The interhemal membranes of all the species examined were hemotrichorial. The outermost layer of trophoblast, bordering the maternal blood spaces, was cellular and often contained some patent fenestrae, whereas the middle and linner trophoblastic layers were apparently syncytial. The outermost trophoblastic layer of all the species contained abundant granular endoplasmic reticulum. The intercellular space between the outer and middle layers was variable in width, primarily due to the complex folding of the surface of the middle layer. The surfaces of the middle and inner layers were closely apposed. The middle trophoblastic layer in several species contained filamentous "glomerular bodies" and the innermost layer, particularly of Peromyscus, contained smooth membranous whorls. A basal lamina separated the innermost trophoblastic layer from the fetal capillary endothelium. The endothelial cells in most of the species contained fenestrated regions. These observations are compared to those on other hemochorial placentas, and common features of cricetid (and myomorph) rodent placental find structure are emphasized.

Animals↗
PubMed1980

The ultrastructural histochemistry and stereoscanning electron microscopy of the rodent and amphibian surfactant systems.

Ultrastructural histochemical precedures were employed to determine the carbohydrate components and their contributions to the rodent and amphibian surfactant systems. Zirconium stained the rodent (rat) cytoplasm surrounding the multilamellar bodies, the Golgi, and was associated with the membrane structures of the compact lamellae of alveolar multilamellar bodies. In the rodent and amphibian (Rana pipiens), ruthenium red stain was observed within all tubular myelin surfactant matricies. The "gutters," tubular myelin surfactant matrix, and intratubular myelin surfactant matrix materials all demonstrated a positive reaction product. The periodic acid-chromic acid-silver procedure revealed irregular channels extending from the multilamellar bodies to the surface of the rodent great alveolar pneumocyte. The extra-pulmonary and respiratory surfaces in both species were additionally studied by stereoscanning electron microscopy. The respiratory anatomy of the rodent was corroborated. The amphibian lung demonstrated three orders of septa, and in the expired state, tertiary septal pits. The amphibian primary septa were hollow, blind tubules containing respiratory surfaces.

Animals↗
PubMed2006

Diffusion tensor imaging (DTI) of rodent brains in vivo using a 1.5T clinical MR scanner.

PURPOSE: To evaluate the feasibility of using a clinical 1.5T MR scanner to perform magnetic resonance (MR) diffusion tensor imaging (DTI) on in vivo rodent brains and to trace major rodent neuronal bundles with anatomical correlation. MATERIALS AND METHODS: Two normal adult Sprague Dawley (SD) rats were anesthetized and imaged in a 1.5T MR scanner with a microscopic coil. DTI was performed at a resolution of 0.94 mm x 0.94 mm x 0.5 mm (reconstructed to 0.47 mm x 0.47 mm x 0.5 mm, with b-factors of 600 seconds/mm2 and 1000 seconds/mm2) and a higher resolution of 0.63 mm x 0.63 mm x 0.5 mm (reconstructed to 0.235 mm x 0.235 mm x 0.5 mm, with a b-factor of 1500 seconds/mm2). The fiber-tracking results were correlated with corresponding anatomical sections stained to visualize neuronal fibers. The apparent diffusion coefficient (ADC) and fractional anisotropy (FA) of the neuronal fibers were measured and compared with results in published reports. RESULTS: Several major neuronal fiber tracts, including the corticospinal cord, corpus callosum, and anterior commissure, were identified in all DTI data sets. Stained anatomical sections obtained from the rats confirmed the location of these fibers. The ADC values (0.6-0.8 +/- 10(-3) mm2/second) of the fibers were similar to published figures. However, the FA values (0.3-0.35) were lower than those obtained in previous studies of white matter in rodent spinal cord. CONCLUSION: We have demonstrated the feasibility of using a 1.5T clinical MR scanner for neuronal fiber tracking in rodent brains. The technique will be useful in rodent neuroanatomy studies. Further investigation is encouraged to verify the FA values generated by DTI with such techniques.

Animals↗
PubMed1995

Analysis of multiple gap junction gene products in the rodent and human mammary gland.

The expression and localization of three different connexins (alpha 1, Cx43; beta 1, Cx32; and beta 2, Cx26) were analyzed in human, mouse, and rat mammary glands by PCR analysis of reverse-transcribed RNA (RT-PCR) and indirect immunohistochemistry. For the rodent mammary gland, the study included different physiological stages of development during nonpregnancy, pregnancy, lactation, and postweaning. RT-PCR amplification revealed a constitutive expression of RNA for alpha 1 connexin in all three species. In contrast, both beta 1 and beta 2 transcripts were expressed only during lactation in the rodent mammary gland. Specifically, immunohistochemistry showed that the expression of all three connexins was restricted to specific cell types, and it varied according to the physiological activity of the organ. In particular, alpha 1 antigen was detected only between myoepithelial cells, the contractile cells surrounding alveoli and ductal systems in the mammary gland, while beta 1 and beta 2 antigens were localized solely at the basolateral border of alveolar secretory cells. The level of beta 1 and beta 2 connexins was increased in the rodent mammary gland during lactation. No staining for either beta connexin was detected in human mammary gland or in that of nonpregnant, pregnant, or postweaning rodents. The inducible coexpression of beta 1 and beta 2 antigens in luminal cells of the lactating rodent suggests a possible role for these connexins in the coordination of the secretory epithelium.

Adult↗
PubMed1994

The relationship between use of the maximum tolerated dose and study sensitivity for detecting rodent carcinogenicity.

The relationship between maximum tolerated dose (MTD) and study sensitivity for detecting rodent carcinogenicity was evaluated for 216 chemicals found to be carcinogens in laboratory animal studies conducted by the National Cancer Institute (NCI) and the National Toxicology Program (NTP). Approximately two-thirds of these rodent carcinogens would have been detected even without the top dose (estimated MTD), but in many of these studies, some site-specific carcinogenic effects would have been missed. Among the remaining one-third of the rodent carcinogens that required the top dose for statistical significance, approximately 80% had numerically elevated rates of the same site-specific tumors at lower doses as well. Only 13 of the NCI/NTP rodent carcinogens had increased tumor rates limited to the top dose for all sites of carcinogenicity. Alternatively, of the 838 site-specific carcinogenic effects observed in the NCI/NTP studies, 447 (53%) would have been detected even without the top dose. Of the remaining effects, 75% (294/391) showed numerically elevated site-specific tumor rates at lower doses. Our evaluation indicates that most carcinogenic effects observed at the top dose in rodent studies are also present (with reduced incidence that might or might not be statistically significant) at the lower doses typically employed (1/2MTD, 1/4MTD).

Animals↗
PubMed2000

A comparison of primate, carnivoran and rodent limb bone cross-sectional properties: are primates really unique?

The cross-sectional properties of mammalian limb bones provide an important source of information about their loading history and locomotor adaptations. It has been suggested, for instance, that the cross-sectional strength of primate limb bones differs from that of other mammals as a consequence of living in a complex arboreal environment (Kimura, 1991, 1995). In order to test this hypothesis more rigorously, we have investigated cross-sectional properties in samples of humeri and femora of 71 primate species, 30 carnivorans and 59 rodents. Primates differ from carnivorans and rodents in having limb bones with greater cross-sectional strength than mammals of similar mass. This might imply that primates have stronger bones than carnivorans and rodents. However, primates also have longer proximal limb bones than other mammals. When cross-sectional dimensions are regressed against bone length, primates appear to have more gracile bones than other mammals. These two seemingly contradictory findings can be reconciled by recognizing that most limb bones experience bending as a predominant loading regime. After regressing cross-sectional strength against the product of body mass and bone length, a product which should be proportional to the bending moments applied to the limb, primates are found to overlap considerably with carnivorans and rodents. Consequently, primate humeri and femora are similar to those of nonprimates in their resistance to bending. Comparisons between arboreal and terrestrial species within the orders show that the bones of arboreal carnivorans have greater cross-sectional properties than those of terrestrial carnivorans, thus supporting Kimura's general notion. However, no differences were found between arboreal and terrestrial rodents. Among primates, the only significant difference was in humeral bending rigidity, which is higher in the terrestrial species. In summary, arboreal and terrestrial species do not show consistent differences in long bone reinforcement, and Kimura's conclusions must be modified to take into account the interaction of bone length and cross-sectional geometry.

Animals↗
PubMed1996

A mechanistic interpretation of the oncogenicity of chlorothalonil in rodents and an assessment of human relevance.

Chronic dietary treatment of rodents with the fungicide chlorothalonil causes an increased incidence of papillomas and carcinomas of the forestomach squamous epithelium (rats and mice, both sexes) and adenomas and carcinomas of the renal proximal tubule epithelium (rats, both sexes; mice, males only); the product elicits no tumorigenic response in dogs. As a result, chlorothalonil is classified by EPA as a Group B2 "probable human carcinogen." However, chlorothalonil is not genotoxic and there is strong evidence that both the forestomach and renal tumors observed in rodents result from cytotoxicity followed by compensatory cell proliferation and hyperplasia. In the case of the forestomach, cytotoxicity results from sustained irritation of the squamous epithelium by chlorothalonil leading to inflammation, ulceration, and restorative hyperplasia. Cytotoxicity in the renal tubular epithelium is associated with formation of di- and trithiols that arise through the action of renal beta-lyase on cysteine S-conjugates derived from the corresponding glutathione conjugates of chlorothalonil. Renal cytotoxicity and cell necrosis in rodents result from the ability of the di- and trithiols to inhibit kidney mitochondrial respiration and disrupt cellular integrity. There is strong evidence that this mechanism is not operative in other species such as dogs and monkeys. The progression from cytotoxicity to hyperplasia to neoplasia is becoming increasingly well-recognized as a threshold-based mechanism of carcinogenesis. Unless exposure is excessively prolonged or intense, the cytotoxic effects will be fully reversible. Furthermore, the effects observed in rodents are not appropriate for evaluating the potential human cancer risk from chlorothalonil. Humans do not possess an organ equivalent to the rodent forestomach and the rat is a poor model for evaluating potential human risk for the renal tumorigenicity of chlorothalonil. Humans are likely to be very much less sensitive than rats to the nephrotoxic effects of chlorothalonil. In view of the fact that the tumorigenic effects of chlorothalonil are mediated through a well-understood, nongenotoxic, threshold-based mechanism of little or no relevance to humans, chlorothalonil should be a prime candidate for re-review under EPA's new risk assessment guidelines. Expert committees in both Europe and Canada have concluded that human risks to chlorothalonil should be evaluated by means of the NOEL/safety factor approach usually employed for noncarcinogenic materials.

Animals↗
PubMed1981

Assignment of adenosine deaminase complexing protein (ADCP) gene(s) to human chromosome 2 in rodent-human somatic cell hybrids.

The experiments reported in this paper indicate that the expression of human adenosine deaminase complexing protein (ADCP) in the human-rodent somatic cell hybrids is influenced by the state of confluency of the cells and the background rodent genome. Thus, the complement of the L-cell derived A9 or B82 mouse parent apparently prevents the expression of human ADCP in the interspecific somatic cell hybrids. In the a3, E36, or RAG hybrids the human ADCP expression was not prevented by the rodent genome and was found to be proportional to the degree of confluency of the cell in the culture as in the case of primary human fibroblasts. An analysis of human chromosomes, chromosome specific enzyme markers, and ADCP in a panel of rodent-human somatic cell hybrids optimally maintained and harvested at full confluency has shown that the expression of human ADCP in the mouse (RAG)-human as well as in the hamster (E36 or a3)-human hybrids is determined by a gene(s) in human chromosome 2 and that neither chromosome 6 nor any other of the chromosomes of man carry any gene(s) involved in the formation of human ADCP at least in the Chinese hamster-human hybrids. A series of rodent-human hybrid clones exhibiting a mitotic separation of IDH1 and MDH1 indicated that ADCP is most probably situated between corresponding loci in human chromosome 2.

Adenosine Deaminase↗
PubMed1988

Synonymous nucleotide substitution rates of beta-tubulin and histone genes conform to high overall genomic rates in rodents but not in sea urchins.

Sea urchin and rodent genomes have been posited to evolve rapidly as indicated by divergences in single copy nuclear DNA sequences. We have examined whether the synonymous substitution rates of three highly conserved genes, beta-tubulin, histone H4, and histone H3, adhere to these high genomic substitution rates by comparing sequences between two sea urchins, Strongylocentrotus purpuratus and Lytechinus pictus, and between rodents and humans. Whereas the rate of change between the 3' untranslated regions of the beta-tubulin cDNA of S. purpuratus (Sp-beta 1), sequenced in this study, and of L. pictus (Lp-beta 3) was consistent with the overall rate of change estimated from previous DNA hybridization results between these species, the synonymous substitution rates for the carboxyl domains of these beta-tubulins, as well as for the late histones H4 and H3, were significantly depressed. In contrast, synonymous nucleotide substitution rates between rodents and between rodent and human for the carboxyl domain proper of identical beta-tubulin isotypes and for histone H4 and H3.1 did not differ from the overall rate of change for the rodent genomes. Moreover, an analysis of paralogous human and mouse beta-tubulin sequences supported the conclusion that the synonymous substitution rates in the mouse were higher than those in the human. Differences in constraint on evolutionary change were not evident strictly from the conserved amino acid sequences and base compositions of these genes. Other constraining influences seemed more relevant to the departure of the synonymous substitution rates of the sea urchin beta-tubulin and histone coding regions from the average genomic rate.

Amino Acid Sequence↗
PubMed1999

Peroxisome proliferators: mechanisms of adverse effects in rodents and molecular basis for species differences.

Peroxisome proliferators (PPs), such as diethylhexylphthalate (DEHP), constitute a diverse class of chemicals with many therapeutic, industrial and environmental applications. In rodents, PPs are nongenotoxic hepatocarcinogens, raising concerns regarding the potential of PPs to harm human health. However, humans differ from rodents in their response to PPs and the weight of evidence supports the supposition that PPs do not pose a carcinogenic risk to humans. The effects of PPs in the rodent are mediated by peroxisome proliferator activated receptor alpha (PPARalpha). PPARalpha predominates in the liver whereas another isoform PPARgamma predominates in adipose tissue and in the immune system. This tissue-specific pattern of PPARalpha expression is consistent with a role for PPARalpha but not PPARgamma or PPARbeta in PP-induced rodent hepatocarcinogenesis. Humans, marmosets and guinea-pigs appear refractory or less responsive to the adverse liver effects of PPs. However, humans give a therapeutic response to the fibrate PPs via an alteration in lipid metabolism mediated by PPARalpha. Such marked species differences may be explained by quantity of PPARalpha and/or the quality of the PPARalpha-mediated response. The lower expression of full-length functional PPARalpha in humans could be attributed to the presence of a truncated, inactive form of PPARalpha, which appears to be present in most individuals examined to date. In addition, there are species differences in sequence and responsiveness of the acyl CoA oxidase (ACO) gene promoter, suggesting that even in the presence of sufficient PPARalpha, the human equivalent of rodent genes associated with peroxisome proliferation may remain inactive.

Animals↗
PubMed2003

Local molecular clocks in three nuclear genes: divergence times for rodents and other mammals and incompatibility among fossil calibrations.

Reconstructing the chronology of mammalian evolution is a debated issue between molecule- and fossil-based inferences. A methodological limitation of molecules is the evolutionary rate variation among lineages, precluding the application of the global molecular clock. We considered 2422 first and second codon positions of the combined ADRA2B, IRBP, and vWF nuclear genes for a well-documented set of placentals including an extensive sampling of rodents. Using seven independent calibration points and a maximum-likelihood framework, we evaluated whether molecular and paleontological estimates of mammalian divergence dates may be reconciled by the local molecular clocks approach, allowing local constancy of substitution rates with variations at larger phylogenetic scales. To handle the difficulty of choosing among all possible rate assignments for various lineages, local molecular clocks were based on the results of branch-length and two-cluster tests. Extensive lineage-specific variation of evolutionary rates was detected, even among rodents. Cross-calibrations indicated some incompatibilities between divergence dates based on different paleontological references. To decrease the impact of a single calibration point, estimates derived from independent calibrations displaying only slight reciprocal incompatibility were averaged. The divergence dates inferred for the split between mice and rats (approximately 13-19 Myr) was younger than previously published molecular estimates. The most recent common ancestors of rodents, primates and rodents, boreoeutherians, and placentals were estimated to be, respectively, approximately 60, 70, 75, and 78 Myr old. Global clocks, local clocks, and quartet dating analyses suggested a Late Cretaceous origin of the crown placental clades followed by a Tertiary radiation of some placental orders like rodents.

Animals↗
PubMed2001

The rates of molecular evolution in rodent and primate mitochondrial DNA.

A higher rate of molecular evolution in rodents than in primates at synonymous sites and, to a lesser extent, at amino acid replacement sites has been reported previously for most nuclear genes examined. Thus in these genes the average ratio of amino acid replacement to synonymous substitution rates in rodents is lower than in primates, an observation at odds with the neutral model of molecular evolution. Under Ohta's mildly deleterious model of molecular evolution, these observations are seen as the consequence of the combined effects of a shorter generation time (driving a higher mutation rate) and a larger effective population size (resulting in more effective selection against mildly deleterious mutations) in rodents. The present study reports the results of a maximum-likelihood analysis of the ratio of amino acid replacements to synonymous substitutions for genes encoded in mitochondrial DNA (mtDNA) in these two lineages. A similar pattern is observed: in rodents this ratio is significantly lower than in primates, again consistent only with the mildly deleterious model. Interestingly the lineage-specific difference is much more pronounced in mtDNA-encoded than in nuclear-encoded proteins, an observation which is shown to run counter to expectation under Ohta's model. Finally, accepting certain fossil divergence dates, the lineage-specific difference in amino acid replacement-to-synonymous substitution ratio in mtDNA can be partitioned and is found to be entirely the consequence of a higher mutation rate in rodents. This conclusion is consistent with a replication-dependent model of mutation in mtDNA.

Animals↗
PubMed1999

Microfungal Community Changes in Rodent Food Stores over Space and Time.

> Abstract This paper reports the changes over time in the microfungal communities that inhabit three rodent species' food stores at two climatically different locations. Results reveal that microfungal diversity values calculated from above-ground food stores are highest in the more commonly disturbed portions of the rodent dens. Interactions among food-inhabiting microbes and between the rodents and food-inhabiting microbes also appear to influence the microfungal communities within the rodent dens. For example, our data suggest that transport by animal vectors, and not by air currents, is more effective at dispersing microbial propagules. Furthermore, although fungal communities inhabiting food stores within dens varied in composition and diversity over time, standardized substrates (sorghum seeds) simultaneously placed within the food stores converged in microfungal composition the longer they were left within the dens. We hypothesize that animal vectors, including rodents, make neighboring fungal communities more alike by introducing similar communities of microbes, which in turn initiate a cascade of biological interactions that, over time, result in similar microfungal communities inhabiting newly stored food items.http://link.springer-ny.com/link/service/journals/00248/bibs/38n1p79.html

Journal Article↗