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PubMed1991

Skeletal muscle metabolism in the offspring of trained rats.

To determine the effects of maternal exercise training during pregnancy on skeletal muscle metabolism of the progeny, eleven female Sprague-Dawley rats were divided into an exercise and a control group. The maternal training group (6) ran on a rodent treadmill for 4 weeks prior to pregnancy and daily throughout gestation (21 days) at 26.8 m/min, 1 hour/day, 5 days per week. The measurements were taken 28 days postpartum. No differences were noted between the sedentary and trained maternal animals for succinic dehydrogenase (SDH), phosphofructokinase (PFK), and myosin ATPase activities of the soleus, plantaris and gastrocnemius muscles. Maternal gastrocnemius SDH and soleus PFK levels were significantly (p less than 0.05) lower than levels found in the offspring. The liver glycogen of trained maternal animals was significantly higher than that found in all other groups. As well it was shown that maternal exercise had no effect on any of the aforementioned physiological parameters measured in the pups. The results indicate that exercise training during pregnancy does not modify the skeletal muscle metabolism of the offspring as observed 28 days after birth.

Adaptation, Physiological↗

PubMed1995

[Natural epidemiology of Lyme borreliosis with reference to clustered incidence of illnesses in the suburbs of a North Baden community].

Human infection with Borrelia burgdorferi, the causative agent of Lyme disease, is unusually common in the "Scheelkopf" area of the town Bruchsal in north Baden (Germany), a situation which has led to considerable publicity and public concern. This study was carried out in order to clarify this situation by determining the prevalence of B. burgdorferi in both the free-living tick populations (Ixodes ricinus) and the rodent population from the "Scheelkopf" as well as from surrounding control areas. The polymerase chain reaction (PCR) was used to determine the presence of infection in whole tick preparations and in mouse bladders. The prevalence of B. burgdorferi in freeland ticks ranged from 19% to 44% and in mice from 6% to 29% depending on the area studied. The "Scheelkopf", with prevalences for ticks and mice of 33% and 10% respectively, was not significantly different from the control areas. Our results indicate that there is a high risk of human infection throughout the study area. This is probably related to the intensive use of the area for gardens and the related recreational behaviour of the human population in conjunction with the high rate of infection prevailing in I. ricinus.

Animals↗

PubMed1997

Genetic determinants of teratogen-induced abnormal development in mouse and rat embryos in vitro.

The response of an embryo to a teratogenic treatment is often critically dependent on its genetic makeup. However, in conventional in vivo studies of gene-teratogen interactions it may be difficult to distinguish between the effects of genes that are carried by the embryo and those that are carried by the mother. It is likewise not easy to determine whether an observed interaction is between a particular gene and the parent compound administered, or whether it is with a metabolite that has been generated by the maternal system. The use of whole rodent embryo culture offers certain advantages in the study of gene-teratogen interactions. Not only can the effects of metabolism and the maternal genotype be more carefully controlled, but the stage of development at which embryos of different genotypes are exposed can be matched. Rodent whole embryo culture has been used to a limited extent to study interactions between single gene mutations and teratogenic treatments, variations in responses of different strains to teratogens, as well as species differences in response to teratogens. These studies point to the need to precisely control the stage of development at the time of treatment in order to be able to make valid comparisons. But, even more important, they highlight the versatility of the whole embryo culture technique, and underscore the need for its wider use in evaluating the relative contribution of genes and environment to abnormal embryonic development.

Animals↗

PubMedDate not supplied

Using remotely sensed data to identify areas at risk for hantavirus pulmonary syndrome.

The 1993 U.S. hantavirus pulmonary syndrome (HPS) outbreak was attributed to environmental conditions and increased rodent populations caused by unusual weather in 1991- 92. In a case-control study to test this hypothesis, we estimated precipitation at 28 HPS and 170 control sites during the springs of 1992 and 1993 and compared it with precipitation during the previous 6 years by using rainfall patterns at 196 weather stations. We also used elevation data and Landsat Thematic Mapper satellite imagery collected the year before the outbreak to estimate HPS risk by logistic regression analysis. Rainfall at case sites was not higher during 1992-93 than in previous years. However, elevation, as well as satellite data, showed association between environmental conditions and HPS risk the following year. Repeated analysis using satellite imagery from 1995 showed substantial decrease in medium- to high-risk areas. Only one case of HPS was identified in 1996.

Animals↗

PubMed1994

Induction of senescence and control of tumorigenicity in BK virus transformed mouse cells by human chromosome 6.

Viral transformation models may be useful to detect and map human tumor suppressor genes. BK virus (BKV), a human papovavirus, readily transforms rodent cells but is unable to transform human cells, suggesting that oncosuppressive functions expressed in human cells control BKV oncogenic activity. We have transferred human chromosome 6 to BKV-transformed mouse pRPcT1ss1 cells. The great majority of the colonies growing in selective medium degenerated by senescence. Only five hybrid pRPcT1ss1/H6 clones maintained the immortalized phenotype of the recipient cell line. All the immortalized clones had two common regions of deletion involving bands 6q21-22 and the SOD2 gene in 6q25. Senescent colonies carried an intact chromosome 6. A specific human sequence in 6q21-22 was amplified by PCR in senescent cells, suggesting that this region harbors a gene inducing senescence. The SOD2 deletion confirms recent data on the role of the Mn-dependent superoxide dismutase in inhibition of proliferation. The monochromosomic hybrids bearing a deleted chromosome 6 showed a reverted phenotype in vitro and a significantly longer latency period before they were tumorigenic in nude mice, indicating the presence of a tumor suppressor gene in the residual regions of chromosome 6. Molecular mapping suggests that this gene is located in 6q27. The BKV transformation model detects genes inducing senescence and tumor suppressor genes on human chromosome 6 and may represent a useful system to isolate and clone such genes.

Animals↗

PubMed1998

A telomere-independent senescence mechanism is the sole barrier to Syrian hamster cell immortalization.

Reactivation of telomerase and stabilization of telomeres occur simultaneously during human cell immortalization in vitro and the vast majority of human cancers possess high levels of telomerase activity. Telomerase repression in human somatic cells may therefore have evolved as a powerful resistance mechanism against immortalization, clonal evolution and malignant progression. The comparative ease with which rodent cells immortalize in vitro suggests that they have less stringent controls over replicative senescence than human cells. Here, we report that Syrian hamster dermal fibroblasts possess substantial levels of telomerase activity throughout their culture life-span, even after growth arrest in senescence. In our studies, telomerase was also detected in uncultured newborn hamster skin, in several adult tissues, and in cultured fibroblasts induced to enter the post-mitotic state irreversibly by serum withdrawal. Transfection of near-senescent dermal fibroblasts with a selectable plasmid vector expressing the SV40 T-antigen gene resulted in high-frequency single-step immortalization without the crisis typically observed during the immortalization of human cells. Collectively, these data provide an explanation for the increased susceptibility of rodent cells to immortalization (and malignant transformation) compared with their human equivalents, and provide evidence for a novel, growth factor-sensitive, mammalian senescence mechanism unrelated to telomere maintenance.

Animals↗

PubMed2002

Several subpopulations of neuropeptide Y-containing neurons exist in the infundibular nucleus of sheep: an immunohistochemical study of animals on different diets.

Conversely to rodents, the involvement of hypothalamic neuropeptide Y (NPY) neurons in the control of nutrition is poorly understood in ruminants such as sheep. Therefore, the aim of this work was to describe the NPY neurons of the diencephalon in ewes submitted to different diets. In colchicine-treated animals, large populations of NPY-immunoreactive (-ir) neurons were observed in a ventral and a lateral subpopulation of the infundibular nucleus (IN), in the median eminence, the pituitary stalk, and the dorsomedian and dorsocaudal nuclei. No labeled perikaryon was observed in the magnocellular neurons of the hypothalamus, although numerous labeled fibers were noted in the neural part of the pituitary. The pattern of distribution of NPY-ir neurons in the sheep hypothalamus is similar in many ways to those of rodents, but it presents also many specific characteristics that have not been previously described. In ewes that were fasted for 24 hours, or fed ad libitum, the number of NPY-ir neurons was the same whatever the hypothalamic structures. In underfed ewes (40% of maintenance for 24 weeks), the lateral subpopulation of the IN presented a higher number of NPY-ir neurons than observed in the 100% fed ewes. Conversely, in the ventral subpopulation, the animals refed ad libitum (at least 150% of maintenance for 4 days) presented a lower number of NPY-ir neurons than the other groups. The other NPY neuronal populations of the hypothalamus were not significantly modified by the dietary treatments. For the first time, we demonstrated the presence of two functionally distinct subpopulations of NPY neurons in the sheep IN. The variations of labeled neurons were correlated with plasma nonesterified fatty acid levels but not with leptinemia.

Animal Nutritional Physiological Phenomena↗

PubMed1992

Ultrastructural features of primate granule cell bodies show important differences from those of rats: axosomatic synapses, somatic spines and infolded nuclei.

Granule cells of the primate dentate gyrus were examined in the electron microscope where they displayed significantly less axosomatic synapses than granule cells in rodents. In addition, primate granule cells frequently had infolded cell nuclei and somal spines which are features that are both rare in rodents. Since the granule cell body is an important site for gamma-aminobutyric acid (GABA)ergic inhibitory control, the reduced number of axosomatic synapses in monkeys suggests that local inhibitory connections of primate granule cells are less than that of rodents. Together, these differences may indicate that the primate granule cells are physiologically more active than rat granule cells.

Animals↗

PubMed1998

Immunity to asexual blood stages of Plasmodium: is resistance to acute malaria adaptive or innate?

Current models of immunity to blood stages of Plasmodium invoke a primary role for T-cell dependent processes and much recent evidence implicates Th1-type responses as crucial to the control of acute malaria. But do these data stand up to close scrutiny? Here, Andy Fell and Nick Smith review recent data from rodent and human studies and suggest that Th1-type responses may not after all be important in controlling malaria infection in the blood.

Journal Article↗

PubMed2000

Correlations among tumor types in mouse cancer bioassays: liver adenomas, liver carcinomas, leukemias and lymphomas.

In an examination of rodent bioassays Young and Gries [Young S.S., and Gries C.L. Exploration of the negative correlation between proliferative hepatocellular lesions and lymphoma in rats and mice--establishment and implications. Fundam. Appl. Toxicol. 1984: 4: 632-6401 and Haseman et al. [Haseman J.K., et al. Body weight-tumor incidence correlations in long-term rodent carcinogenicity studies. Toxicol. Pathol. 1997: 25: 256-263] noticed that there is a negative correlation (anticorrelation) between development of liver tumors and leukemia or lymphomas. If an animal has a lymphoma or leukemia it is less likely to develop liver tumors. These studies noted that this applies to several strains of animals. The anticorrelation appeared in control animals. In this paper we study this anticorrelation in the quarter of a million rodents exposed in the Carcinogenesis Bioassay Database System (CBDS) database of the National Toxicology program in both control and dosed animals. We failed to completely replicate Young and Gries or Haseman et al. However, when benign liver tumors (adenomas or nodules) and malignant liver tumors (carcinomas) are considered separately AND different leukemia and lymphoma types are considered, a strong anticorrelation appears. We identify survival and the time period (in years) during which the bioassay was completed as an important factor in interpreting correlations and anticorrelations. Differences between liver adenomas and carcinomas and lymphoma types contribute to a more general question of grouping of the individual tumor types. In our classification scheme (originally developed about 1986 by Dr. Bailar) an effort is made to distinguish benign and malignant neoplasms, while other investigators group all tumors at a specific site. For many analyses liver adenomas and carcinomas have been lumped together. This is because it is suspected that the diagnoses by pathologists may not distinguish, or ignore the (benign) adenoma when a (malignant) carcinoma is present. Possible biological differences in tumor mechanisms may require separate evaluation of these tumors with all the dangers of "pathologist bias" that this introduces.

Adenoma↗

PubMed1993

Induction of an anti-vaccine response by T cell vaccination in non-human primates and humans.

Experimental and spontaneous autoimmune disease in animals can effectively be prevented and treated by application of pathogenic autoreactive T cells in an attenuated form. This approach has become known as T cell vaccination. T cell vaccination exploits specifically the ability of the immune system to regulate its autoreactive T cells by mechanisms of network control. The success of T cell vaccination in a variety of rodent animal models has raised hopes for its use as an effective and specific therapy in human autoimmune disease. The aim of this study was to induce an anti-T cell response by T cell vaccination in humans and primates as a pre-clinical study into the feasibility and toxicity of T cell vaccination. Using bulk cultures of T cells from the peripheral blood or an inflamed joint, it was possible to induce a T cell response specific for the injected vaccine and its activation state both in rhesus monkeys and in two patients with active rheumatoid arthritis. In one of the patients there was already a spontaneous T cell response against a mitogen driven T cell line from the peripheral blood, but not against a control T cell line specific for tetanus toxoid, suggesting that regulatory T cell networks are operative in patients with autoimmune disease. Significant clinical effects or side-effects were not observed. The results suggest that T cell vaccination in humans is feasible and non-toxic. It is likely to influence an already ongoing regulatory process. Conditions for making T cell vaccination an effective therapy need still to be worked out by further studies both in primates and in less complex human immune processes.

Animals↗

PubMed2001

Rationale for the existence of additional adipostatic hormones.

Parabiosis studies with obese rodents demonstrated that circulating factors are involved in the long-term control of food intake and energy balance. More than 40 years ago it was hypothesized that rats made obese by hypothalamic or dietary means, as well as genetically obese fa/fa rats and db/db mice, produce a circulating factor that either inhibits food intake or acts metabolically to reduce the fat content of non-obese ad libitum-fed partners. However, none of these obese rodents showed a significant change in weight when parabiosed to a normal animal. It was therefore postulated that these obese rodents produced a circulating lipostatic factor but were unable to respond to it. In contrast, genetically obese ob/ob mice were thought to be deficient in the circulating signal, as they lost weight when parabiosed to lean or obese db/db mice. The discovery of leptin suggested that the circulating lipostatic signal had been identified. However, a closer look at the outcome of the parabiotic studies reveals that leptin alone does not explain all of the findings of the parabiotic experiments. Another (or more than one) as yet unidentified factor(s) may be involved in energy balance regulation. The evidence for the existence of further leptin-like hormones comes from observations in which the direct effect of leptin has been eliminated or can be excluded.

Adipose Tissue↗

PubMedDate not supplied

A human putative lymphocyte G0/G1 switch gene homologous to a rodent gene encoding a zinc-binding potential transcription factor.

G0S24 is a member of a set of genes (putative G0/G1 switch regulatory genes) that are expressed transiently within 1-2 hr of the addition of lectin or cycloheximide to human blood mononuclear cells. Comparison of a full-length cDNA sequence with the corresponding genomic sequence reveals an open reading frame of 326 amino acids, distributed across two exons. Potential phosphorylation sites include the sequence PSPTSPT, which resembles an RNA polymerase II repeat reported to be a target of the cell cycle control kinase cdc2. Comparison of the derived protein sequence with those of rodent homologs allows classification into three groups. Group 1 contains G0S24 and the rat and mouse TIS11 genes (also known as TTP, Nup475, and Zfp36). Members of this group have three tetraproline repeats. Groups 1 and 2 have a serine-rich region and an "arginine element" (RRLPIF) at the carboxyl terminus. All groups contain cysteine- and histidine-rich putative zinc finger domains and a serine-phenylalanine "SFS" domain similar to part of the large subunit of eukaryotic RNA polymerase II. Comparison of group 1 human and mouse genomic sequences shows high conservation in the 5' flank and exons. A CpG island suggests expression in the germ line. G0S24 has potential sites for transcription factors in the 5' flank and intron; these include a serum response element. Protein and genomic sequences show similarities with those of a variety of proteins involved in transcription, suggesting that the G0S24 product has a similar role.

Amino Acid Sequence↗

PubMed1971

The effect of flea control on Yersinia (Pasteurella) pestis antibody rates in the California vole, Microtus californicus, and its epizootiological implications.

The effects of flea control on the prevalence of (Pasteurella) pestis antibody rates in the California vole, Microtus californicus, were studied in San Mateo County, California, USA. In this area, which had shown antibody prevalence rates of 50% or more during epizootics in previous years, continuous flea control measures reduced the antibody rate to virtually zero and held it at that level for 12 months, although a nearby area showed an incidence of 40-80% seropositive voles for 5 months during the same period. The striking correlation between the reduction of the flea population and the decline of Y. pestis antibody rates suggests that in the area studied there is no evidence that soil, or any factor other than the flea vector, was the agent of transmission of the infective agent in wild rodents.

Animals↗

PubMed2004

Prefrontal executive and cognitive functions in rodents: neural and neurochemical substrates.

The prefrontal cortex has been implicated in a variety of cognitive and executive processes, including working memory, decision-making, inhibitory response control, attentional set-shifting and the temporal integration of voluntary behaviour. This article reviews current progress in our understanding of the rodent prefrontal cortex, especially evidence for functional divergence of the anatomically distinct sub-regions of the rat prefrontal cortex. Recent findings suggest clear distinctions between the dorsal (precentral and anterior cingulate) and ventral (prelimbic, infralimbic and medial orbital) sub-divisions of the medial prefrontal cortex, and between the orbitofrontal cortex (ventral orbital, ventrolateral orbital, dorsal and ventral agranular cortices) and the adjacent medial wall of the prefrontal cortex. The dorso-medial prefrontal cortex is implicated in memory for motor responses, including response selection, and the temporal processing of information. Ventral regions of the medial prefrontal cortex are implicated in interrelated 'supervisory' attentional functions, including attention to stimulus features and task contingencies (or action-outcome rules), attentional set-shifting, and behavioural flexibility. The orbitofrontal cortex is implicated in lower-order discriminations, including reversal of stimulus-reward associations (reversal learning), and choice involving delayed reinforcement. It is anticipated that a greater understanding of the prefrontal cortex will come from using tasks that load specific cognitive and executive processes, in parallel with discovering new ways of manipulating the different sub-regions and neuromodulatory systems of the prefrontal cortex.

Acetylcholine↗

PubMed1984

Control of cage lighting by locomotor activity through feedback circuits.

This paper describes an electronic device through which environmental lighting conditions are linked to locomotor activity thus allowing only the photosensitive portions of a nocturnal rodents phase-response-curve to be exposed to light. In the past, this type of lighting schedule has been difficult, if not impossible, to present with an exogenously controlled lighting system due to the phase shifting ability of the rodent's circadian system. The feedback lighting system is made from components which can be purchased at most electronics outlets for less than $100.

Animals↗

PubMed2006

Thyroid function and reproductive success in rodents exposed to perchlorate via food and water.

The purpose of the present study was to determine if exposure to perchlorate via food items would have effects on mammals similar to those caused by exposure through drinking water at approximately equivalent doses. Prairie voles (Microtus ochrogaster) and deer mice (Peromyscus maniculatus) were used to assess the potential toxicity of perchlorate-contaminated food items. Voles and mice were divided randomly into three treatment groups--perchlorate-contaminated food (PCF), perchlorate-contaminated water (PCW), and control groups--such that each treatment group contained equal numbers of males and females. Rodents in PCF treatment groups were fed chow formulated with soybean plant matter that had been grown with perchlorate-contaminated irrigation water. Individuals in the control and PCF groups were provided distilled/deionized drinking water, whereas the PCW group received drinking water containing sodium perchlorate. Only slight differences among treatment groups were observed in a variety of endpoints, including reproductive success, tissue perchlorate concentrations, thyroid hormone concentrations, and thyroid histology. However, trends observed in the present study suggest that perchlorate exposure via water may result in slightly greater effects than exposure to perchlorate via food. These data and recent reports of perchlorate in a wide variety of food items indicate that exposure via food intake is an important consideration when examining cumulative risk among humans, livestock, and wildlife.

Animal Feed↗

PubMedDate not supplied

Plasma resistin levels in patients with type 1 and type 2 diabetes mellitus and in healthy controls.

Resistin is a recently discovered hormone that is exclusively expressed in adipose tissue. Its expression in rodents was reported to be elevated or suppressed in genetic and diet-induced obesity, respectively. Resistin treatment impaired glucose tolerance and insulin action. Immunoneutralization of resistin improved insulin sensitivity, while thiazolidinedione treatment reduced resistin expression. Therefore, resistin could play a critical role in the development of obesity and type 2 diabetes. In this study were determined resistin plasma levels in humans suffering from type 1 and type 2 diabetes and in healthy controls. Plasma levels of resistin in healthy controls were 38.78 ng/ml. They were not statistically different in individuals with a broad BMI range. Resistin plasma levels in type 2 diabetes were 38.7 ng/ml, and 39.4 ng/ml in type 1 diabetes. Thiazolidinedione treatment did not influence resistin plasma levels. We conclude from our data: 1. resistin can be detected in human plasma, 2. plasma resistin levels are not different in type 1 and type 2 diabetes.

Adult↗