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PubMedDate not supplied

Manipulation of intra- and extracellular pH in spontaneous canine tumours by use of hyperglycaemia.

We evaluated the use of hyperglycaemia to reduce tumour pH in dog with spontaneous tumours. Dogs were randomized to two groups: control and glucose. Intravenous administration of 20% glucose was used to induce and maintain hyperglycaemia. Extra- and intracellular tumour pH were measured using interstitial pH microelectrodes and 31P-MRS, respectively. During the administration of glucose, the mean (+/- SEM) blood glucose concentration was 419.8 (+/- 32.8) and 121.1 (+/- 8.0) mg/dl for the glucose and control groups, respectively. The mean extracellular tumour pH before and following 90 min of hyperglycaemia was 7.15 (+/- 0.08) and 7.15 (+/- 0.09). During consecutive measurements, intracellular tumour pH did not change significantly for the control group or the group subjected to hyperglycaemic manipulation. In contradistinction to previous rodent studies, our results demonstrate that hyperglycaemia alone is not sufficient to manipulate either intra- (pHi) or extracellular (pHe) hydrogen ion concentration in spontaneous canine soft tissue tumours.

Animals↗
PubMed1988

Malaria in beta-thalassemic mice and the effects of the transgenic human beta-globin gene and splenectomy.

To investigate the protective effects of beta-thalassemia against malaria, rodent malaria parasites were studied in C57BL/6J mice with beta-thalassemia, in mice in which the thalassemia had been transgenically corrected with the human beta A-globin gene, and in hematologically normal mice. In thalassemic mice, Plasmodium chabaudi adami infection was inhibited and peak parasitemia was variably delayed. In transgenically corrected mice, infection proceeded as in normal mice. Plasmodium berghei infection proceeded more rapidly in thalassemic mice, but survival was not different. Splenectomized normal mice displayed high-level parasitemia that peaked twice and persisted as a low-level parasitemia for more than 20 days after normal intact mice were free of all parasites. Splenectomized thalassemic mice showed a delay of 5 days in attaining peak parasitemia, but the parasitemia persisted as in normal splenectomized mice. Thus, for P. chabaudi, which displayed no preference for immature erythrocytes, beta-thalassemia offers enhanced resistance for the host. However, for P. berghei, which preferentially invades reticulocytes, thalassemia is not protective. The protective effects of the normal mouse spleen were observed, but the paradoxical facilitation of parasite growth by the thalassemic spleen is a new finding that will require further experimentation to explain. This new in vivo laboratory documentation of thalassemic protection against some rodent malaria parasites may serve as a useful model in further efforts to control this major infectious disease.

Animals↗
PubMed1985

Mechanisms for changing gene expression and their possible relationship to carcinogenesis.

Several genetic or epigenetic events can alter gene expression and we assess their importance in multistage carcinogenesis. Mutation and chromosome rearrangement can produce changes in DNA sequence which have been identified in some cancer cells. Recombination and non-disjunction can lead to the expression of recessive alleles. Overexpression of genes by amplification has also been observed in certain tumours. Heteroploidy, resulting from karyotypic instability, is a common feature of tumorigenicity. Although the pattern of DNA methylation is heritable, there is considerable evidence that genes can be activated by loss of methylation or inactivated by de novo methylation. Hypomethylation is frequently observed in tumour cells. Mutation and chromosome translocation can produce rare specific changes which may be important as initiating events. In contrast, the extent of karyotypic instability and hypomethylation shows some correlation with the stage of tumour progression, and these changes may be important in generating the phenotypic diversity which allows the selection of variants during neoplasia and metastasis. The striking differences between the frequencies of cellular transformation in rodents and man may be more easily explained by differences in the epigenetic controls of gene activity, than by abnormalities in DNA sequence.

Animals↗
PubMedDate not supplied

[In vivo experimental models of amebiasis].

In vivo experimental models for amebiasis have provided important information about the mechanisms of host-parasite interaction which determine the production of disease. In the laboratory, several species of rodents have been used to study the intestinal and hepatic amebiasis. For the former, the model of "washed-closed cecal loop" in guinea-pig and hamster has been useful to study the early invasive events. In gerbils we also produced early intestinal lesions by intracecal inoculation with monoxenically cultured amebas. Hamsters and gerbils have been used as susceptible animals for hepatic amebiasis, and rats and guinea-pigs as resistant animals. Morphological analysis of hepatic lesions of susceptible animals showed the role of host inflammatory cells in the process of liver damage. The resistance in the production of liver abscess in rats and guinea-pigs is due in part to the action of polymorphonuclear leukocytes in the rat and the macrophages in the guinea pigs. Complete characterization and standardization of the various models of amebiasis in rodents constitute the bases for other important biomedical studies aimed to the disease control.

Animals↗
PubMedDate not supplied

[The results of a 15-year study of the persistence of Yersinia pestis L-forms].

New diagnostic preparations for the detection of L-forms, immunoglobulin erythrocyte diagnosticum and luminescent antimembrane immunoglobulins, are described. Proofs indicating that Y.pestis L-forms are constantly isolated from wild rodents and their ectoparasites in the natural foci of plague are given. To control the effectiveness of the sanitation of such natural foci, the use of the radioimmunoassay and the enzyme immunoassay, known to be the most sensitive techniques, are recommended. The facts indicating that Y.pestis contaminating ticks and fleas are converted into L-forms, capable of persisting for several years, are presented. After their reversion to back the initial rod-shaped form the transmission of infection is possible. A suggestion is put forward that the persisting forms of Y.pestis play an important role in the preservation of this infective agent in the natural focus of infection.

Animals↗
PubMed2000

In vivo rodent erythrocyte micronucleus assay. II. Some aspects of protocol design including repeated treatments, integration with toxicity testing, and automated scoring.

An expert working group on the in vivo micronucleus assay, formed as part of the International Workshop on Genotoxicity Test Procedures (IWGTP), discussed protocols for the conduct of established and proposed micronucleus assays at a meeting held March 25-26, 1999 in Washington, DC, in conjunction with the annual meeting of the Environmental Mutagen Society. The working group reached consensus on a number issues, including: (1) protocols using repeated dosing in mice and rats; (2) integration of the (rodent erythrocyte) micronucleus assay into general toxicology studies; (3) the possible omission of concurrently-treated positive control animals from the assay; (4) automation of micronucleus scoring by flow cytometry or image analysis; (5) criteria for regulatory acceptance; (6) detection of aneuploidy induction in the micronucleus assay; and (7) micronucleus assays in tissues (germ cells, other organs, neonatal tissue) other than bone marrow. This report summarizes the discussions and recommendations of this working group. In the classic rodent erythrocyte assay, treatment schedules using repeated dosing of mice or rats, and integration of assays using such schedules into short-term toxicology studies, were considered acceptable as long as certain study criteria were met. When the micronucleus assay is integrated into ongoing toxicology studies, relatively short-term repeated-dose studies should be used preferentially because there is not yet sufficient data to demonstrate that conservative dose selection in longer term studies (longer than 1 month) does not reduce the sensitivity of the assay. Additional validation data are needed to resolve this point. In studies with mice, either bone marrow or blood was considered acceptable as the tissue for assessing micronucleus induction, provided that the absence of spleen function has been verified in the animal strains used. In studies with rats, the principal endpoint should be the frequency of micronucleated immature erythrocytes in bone marrow, although scoring of peripheral blood samples gives important supplementary data about the time course of micronucleus induction. When dose concentration and stability are verified appropriately, concurrent treatment with a positive control agent is not necessary. Control of staining and scoring procedures can be obtained by including appropriate reference samples that have been obtained from a separate experiment. For studies in rats or mice, treatment/sampling regimens should include treatment at intervals of no more than 24 hr (unless the test article has a half-life of more than 24 hr) with sampling of bone marrow or blood, respectively, within 24 or 40 hr after the last treatment. The use of a DNA specific stain is recommended for the identification of micronuclei, especially for studies in the rat. In the case of a negative assay result with a non-toxic test article, it is desirable that systemic exposure to the test article is demonstrated. The group concluded that successful application of automated scoring by both flow cytometry and image analysis had been achieved, and defined criteria that should be met if automated scoring is employed. It was not felt appropriate to attempt to define specific recommended protocols for automated scoring at the present time. Other issues reviewed and discussed by the working group included micronucleus assays that have been developed in a number of tissues other than bone marrow. The group felt that these assays were useful research tools that could also be used to elucidate mechanisms in certain regulatory situations, but that these assays had not yet been standardized and validated for routine regulatory application.

Animals↗
PubMed1990

Cell replication and unscheduled DNA synthesis (UDS) activity of low molecular weight chlorinated paraffins in the rat liver in vivo.

The rodent carcinogen C12-chlorinated paraffin (C12-CP) has been evaluated for unscheduled DNA synthesis (UDS) activity in the rat liver in vivo. Evidence of cell proliferation was also assessed by measuring cells undergoing semi-conservative DNA activity (S phase). No evidence of UDS was observed at doses up to 2 g/kg at either 2 or 12 h after dosing. Concomitant positive UDS responses were observed for the liver genotoxins N-nitrosodimethylamine, 4-aminobiphenyl, methyl methanesulphonate, 2-acetylaminofluorene, benzidine and 6-dimethylaminophenylazobenzthiazole. A strong positive response was observed in the cell proliferation assay for the test agent and the positive control agents quinoline and 4-acetylaminofluorene. These observations are discussed within the context of the rodent carcinogenicity reported for the same sample of C12-CPs as studied by the US National Toxicology Program.

Animals↗
PubMed1991

The epidermal pentapeptide pyroGlu-Glu-Asp-Ser-GlyOH inhibits murine hair growth in vivo and in vitro.

Tissue growth may be controlled by negative feedback mechanisms. Recently, a pentapeptide, pyroGlu-Glu-Asp-Ser-GlyOH ('epidermal pentapeptide', EPP), which slows the growth of mouse epidermis in vivo and of mouse keratinocytes in vitro, was isolated from mouse epidermis. Since inhibitory molecules like EPP might be part of the feedback systems underlying hair growth control, we assessed the effect of synthesized EPP on the growth of hair follicles, using rodent in vivo and in vitro assays. We report for the first time that intraperitoneally injected EPP (30 nmol/animal/day over 6 days) significantly slows the growth of hair follicles in plucking-induced anagen skin of C57 B1-6 mice (as assessed by microscopic morphometry). Using an in vitro organ culture assay, EPP inhibits the incorporation of 3H-thymidine into mouse pelage anagen follicles. That this epidermal-derived peptide affects hair growth raises the possibility that hair growth may be regulated by an inhibition/disinhibition mechanism under participation of EPP-like molecules and that the epidermis may play a role in the control of hair growth.

Alopecia↗
PubMed2000

Aerosol delivery of muramyl dipeptide to rodent lungs.

Tuberculosis is the single most serious infectious disease worldwide. The respiratory tract is the primary site of infection by Mycobacterium tuberculosis(MTB). A number of immunogenic components of the cell wall of MTB, if delivered to the lungs as aerosols, can be used to study the local immune response. The site of deposition of these aerosols can be employed to control their residence time in the lungs. Muramyl dipeptide (MDP) aerosols were delivered to alveolar macrophages in the lungs of rodents. Guinea pig macrophages harvested by bronchoalveolar lavage were examined by differential interference contrast microscopy for morphological changes indicative of activation. Bronchoalveolar lavage fluid was analyzed for the presence of alkaline phosphatase, lactate dehydrogenase, N-acetyl-glucosaminidase (NAG), and total protein content. Rat alveolar macrophages were studied for the production of nitric oxide, by induction of nitric oxide synthase. Twenty-four hours following exposure to an aerosol of MDP, alveolar macrophages exhibited morphological characteristics (spreading and pseudopodia), enzyme activity (NAG 50% above control), and production of the reactive intermediate nitric oxide. Rat macrophages subjected to aerosol exposure to MDP when challenged with a second dose of MDP or lipopolysaccharide exhibited a linear dose response as measured by nitric oxide production. These studies indicate that the topical delivery of an MTB bacterial cell wall component, muramyl dipeptide, results in activation of alveolar macrophages. This approach may be useful in elucidating elements of the immune response to MTB.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1983

Control of glycosaminoglycan synthesis and connective tissue differentiation in culture by solubilized bone matrix fractions.

Implantation of decalcified bone matrix in rodents induces the formation of new cartilage and bone by responding cells. Extraction of the bone matrix with high ionic strength solutions, followed by solubilization of part of the extract in isotonic salt solution, yielded material which stimulated glycosaminoglycan (GAG) synthesis by monolayers of fibroblastic cells. Bone is greatly enriched in this stimulatory activity compared to other connective tissues. However, fibroblastic cells from different sources respond to the stimulatory effect of low concentrations of the solubilized material. Kinetic studies of the GAG synthesized and secreted by the cultured cells revealed that a major stimulation of GAG secretion occurred at the cell surface as an early event following stimulation with the bone matrix extract. GAG accumulation in the culture medium occurs at a greater rate in cultures that have been stimulated with the bone matrix extract than in controls.

Animals↗
PubMed1998

Controlled release of TGF-beta1 impedes rat colon carcinogenesis in vivo.

Transforming growth factor beta1 (TGF-beta1) is a cytokine known to play a key role in the control of cell growth. TGF-beta1 potently inhibits the proliferation of human and rodent-derived epithelial cells. Colonic precancerous and moderately differentiated cancer cells are responsive to TGF-beta1, whereas malignant colon cancer cells are resistant to the inhibitory action of the cytokine. These observations have been derived exclusively from in vitro studies. Therefore, the main aim of our study was to determine whether TGF-beta1 exerts a growth-restraining action on colon carcinogenesis in vivo. TGF-beta1 was sequestered into ethylene acetate copolymer matrices and "loaded" preparations were implanted intraperitoneally (i.p.) in rats. One week later, the animals were treated with dimethylhydrazine (DMH), a colon procarcinogen. Empty matrices devoid of TGF-beta1 but containing bovine serum albumin (BSA) carrier served as the appropriate control preparations. The number of aberrant crypt foci (ACF), considered to be preneoplastic lesions of the colon, was scored. Tumor formation and size were assessed at the appropriate times. TGF-beta1 released in a sustained manner from copolymer matrices: (i) markedly inhibited colonic ACF formation and the number of aberrant crypts and (ii) significantly reduced colonic tumor formation and size.

1,2-Dimethylhydrazine↗
PubMed1991

A consideration of the factors which influence and control the viability and developmental potential of the preimplantation embryo.

The advent of the new reproductive technologies (including in vitro fertilization) has led to a revolution in the treatment of infertility. It has not yet led to a marked improvement in our understanding of the control of development and of viability of the early embryo. It is the poor viability of embryos, with consequent implantation failure, which is the major limiting factor to successful outcomes. While much of the research in this area has concentrated on strategies of ovulation induction, experimental models have shown that the major cause of reduced embryo viability is due to the actual process of fertilization in vitro and subsequent culture of the preembryo in synthetic culture medium. It is likely that this is due to the absence of critical nutrients or trophic factors of maternal origin and work with co-culture of embryos with somatic cells suggests improved viability can be achieved. Such co-culture is not an option for routine clinical use, however. It is essential therefore to understand by detailed study of the physiology of embryonic development their requirements for optimal development. The empirical approach of comparing different formulations of culture media is unlikely to be successful because of the vast range of parameters to be tested and the large number of pregnancies required to demonstrate a significant improvement in outcome. The strategy that is most likely to be successful in the future, therefore, is the use of appropriate experimental models, such as the developing rodent embryo, to understand the essential physiological changes in the embryo during its development, the control processes in place, and the effect of the embryo's environment on the processes. This will allow the rational design of culture media which can then be rigorously tested for improved outcome. An example of successful application of this approach is the discovery of embryo-derived platelet activating factor (PAF). The production of embryo-derived PAF was first described and validated in the rodent. In the same species it was shown to have an essential role in pregnancy and to act as an autocrine mediator of embryo viability. This fundamental observation in rodents was then confirmed in humans, and recent work has shown that supplementation of culture human embryo media with PAF results in a dramatic increase in their developmental and pregnancy potential. This example should be the first of many such improvements based on a more fundamental understanding of the embryo's developmental requirements.

Animals↗
PubMed2001

Alternative splicing and tissue-specific transcription of human and rodent ubiquitous 5-aminolevulinate synthase (ALAS1) genes.

The rate of haem synthesis in non-erythroid mammalian tissues is controlled by the ubiquitous isoform of 5-aminolevulinate synthase (ALAS1). In order to explore the regulation of mammalian ALAS1 genes, we have investigated the transcription of the human and rat genes. The 17 kb human gene differs from the rat gene in containing an additional untranslated exon that is alternatively spliced to produce a longer, minor mRNA transcript. Relative amounts of the two transcripts were similar in all tissues examined. Analysis of mRNA transcripts in human and rat tissues revealed tissue-specific differences in the use of transcription start sites by closely similar core promoters. In brain, initiation was from sites within and upstream from the TATA box, including an initiator-like element. In liver, initiation was TATA-driven from a single downstream site that appeared to be used exclusively for induction by drugs. Intermediate patterns were observed in other tissues and cell lines. Mutation of the TATA box did not impair transcription in transfected HeLa cells but activated upstream start sites, recapitulating the brain pattern. Our findings indicate that the conformation of the core ALAS1 promoter that directs assembly of the transcription pre-initiation complex may vary between tissues and have implications for understanding the tissue-specific regulated expression of this gene.

5-Aminolevulinate Synthetase↗
PubMed2002

Inhibition of the MAPK and PI3K pathways enhances UDCA-induced apoptosis in primary rodent hepatocytes.

The mechanisms by which bile acids induce apoptosis in hepatocytes and the signaling pathways involved in the control of cell death are not understood fully. Here, we examined the impact of mitogen-activated protein kinase (MAPK) and phosphatidyl inositol 3-kinase (PI3K) signaling on the survival of primary hepatocytes exposed to bile acids. Treatment of hepatocytes with deoxycholic acid (DCA), chenodeoxycholic acid (CDCA) or ursodeoxycholic acid (UDCA) caused sustained MAPK activation that was dependent on activation of the epidermal growth factor receptor (EGFR). Activation of MAPK was partially blocked by inhibitors of PI3K. Inhibition of DCA-, CDCA-, and UDCA-stimulated MAPK activation resulted in approximately 20%, approximately 35%, and approximately 55% apoptosis, respectively. The potentiation of DCA- and CDCA-induced apoptosis by MEK1/2 inhibitors correlated with cleavage of procaspase 3, which was blocked by inhibitors of caspase 8 (ile-Glu-Thr-Asp-p-nitroanilide [IETD]) and caspase 3 (DEVD). In contrast, the potentiation of UDCA-induced apoptosis weakly correlated with procaspase 3 cleavage, yet this effect was also blocked by IETD and DEVD. Incubation of hepatocytes with the serine protease inhibitor AEBSF reduced the death response of cells treated with UDCA and MEK1/2 inhibitor to that observed for DCA and MEK1/2 inhibitor. The apoptotic response was FAS receptor- and neutral sphingomyelinase-dependent and independent of FAS ligand expression, and neither chelation of intracellular and extracellular Ca(2+) nor down-regulation of PKC expression altered the apoptotic effects of bile acids. In conclusion, bile acid apoptosis is dependent on the production of ceramide and is counteracted by activation of the MAPK and PI3K pathways.

Animals↗
PubMed1989

Nuclear factor EF-1A binds to the adenovirus E1A core enhancer element and to other transcriptional control regions.

We have identified a cellular enhancer-binding protein, present in nuclear extracts prepared from human and rodent cells, that binds to the adenovirus E1A enhancer element I sequence. The factor has been termed EF-1A, for enhancer-binding factor to the E1A core motif. EF-1A was found to bind to two adjacent, related sequence motifs in the E1A enhancer region (termed sites A and B). The binding of EF-1A to these adjacent sites, or to synthetic dimerized sites of either motif, was cooperative. The cooperative binding of EF-1A to these sites was not subject to strict spacing constraints. EF-1A also bound to related sequences upstream of the E1A enhancer region and in the polyomavirus and adenovirus E4 enhancer regions. The EF-1A-binding region in the E1A enhancer stimulated expression of a linked gene in human 293 cells when multimerized. Based on the contact sites for EF-1A binding determined by chemical interference assays, this protein appears to be distinct from any previously characterized nuclear binding protein.

Adenoviridae↗
PubMed2005

The effect of ethanol on uncontrolled hemorrhage in a rodent model.

OBJECTIVES: Ethanol intoxication has hemodynamic and metabolic effects after hemorrhage according to studies using fixed-volume controlled blood loss models. The authors tested the null hypothesis that after uncontrolled hemorrhage there would be no difference in the hemodynamic responses between ethanol-intoxicated (EtOH+) and nonintoxicated (EtOH-) rats. METHODS: Forty Sprague-Dawley rats were anesthetized with althesin intraperitoneally. Twenty EtOH+ rats received a 3-g/kg dose of 20% ethanol intraperitoneally 60 minutes before hemorrhage. The EtOH- rats received an equivalent volume of normal saline intraperitoneally. The femoral artery was cannulated by cutdown to monitor the mean arterial blood pressure (MAP) and to obtain blood samples for lactate (LAC). Twenty rats (ten EtOH+ and ten EtOH-) underwent uncontrolled hemorrhage by 75% tail amputation. Twenty rats (ten EtOH+ and ten EtOH-) served as nonhemorrhage controls. The MAP, LAC, and cumulative hemorrhage volume were measured prehemorrhage and then every 15 minutes posthemorrhage for 120 minutes. Data were reported as mean +/- SEM. Group comparisons were analyzed by analysis of variance with repeated values and post hoc testing by Bonferroni (two tailed; alpha = 0.05). RESULTS: Initially, EtOH+ and EtOH- rats were evenly matched for LAC and MAP. The mean (+/-SD) baseline ethanol level was 170 (+/-68) mg/dL in EtOH+ rats. Cumulative hemorrhage volume was similar (p = 0.23) for the EtOH- (2.36 +/- 0.24 mL/100 g) and EtOH+ (1.87 +/- 0.32 mL/100 g) rats. No significant difference was noted in posthemorrhage MAP between EtOH- (68.6 +/- 6.8 mm Hg) and EtOH+ (69.3 +/- 7.2 mm Hg) rats (p = 1.00). The EtOH- group had a significantly higher LAC (4.94 +/- 1.07 mmol/L) than the EtOH+ group (2.27 +/- 0.59 mmol/L) (p < 0.03). CONCLUSIONS: Ethanol intoxication does not deleteriously affect the hemodynamic response to uncontrolled hemorrhage.

Alcoholic Intoxication↗