Evidence for the Activation of 3-Methylcholanthrene as a Carcinogen in vivo and as a Mutagen in vitro by P1-450 from Inbred Strains of Mice

1975 ◽  
pp. 127-149 ◽  
Author(s):  
Daniel W. Nebert ◽  
James S. Felton
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice

scholarly journals Enhancement of coxsackievirus B3 infection by antibody to a different coxsackievirus strain

2002 ◽  
Vol 83 (2) ◽  
pp. 351-358 ◽  
Author(s):  
Jaskamal Girn ◽  
Mojgan Kavoosi ◽  
Janet Chantler
Keyword(s):  
Viral Myocarditis ◽  
Neutralizing Antibody ◽  
Inbred Strains ◽  
Inbred Strains Of Mice ◽  
Infected Cells ◽  
Group B ◽  
Multiple Strains ◽  
Old Mice

Group B coxsackieviruses (CVBs) are a major cause of viral myocarditis and pancreatitis in humans and produce a similar pattern of disease in inbred strains of mice. As there are six strains of CVBs, individuals can be infected with multiple serotypes. This raises the possibility of antibody enhancement of infectivity (AEI) by cross-reactive but non-neutralizing antibody to a different strain from a prior infection. To determine whether AEI plays a role in coxsackievirus pathogenesis, an in vitro system using the murine macrophage cell line J774.1 was tested for enhanced infection when incubated with CVB3 plus anti-CVB2 antibody. Yields of virus were found to increase by 10–50-fold and the percentage of infected cells increased proportionately. The effect was Fc-mediated as F(ab′)2 fragments of the antibody could not mediate the effect. To determine whether AEI could also be demonstrated in vivo CVB3 was injected into 5-week-old mice together with mouse polyclonal anti-CVB2. Controls included mice injected with PBS or CVB3 alone. Results showed that the titres of virus in tissues of animals injected with virus plus antibody were 1–2 logs higher than when virus was injected alone. This was accompanied by greater histopathological damage, particularly in the heart. These results have implications for human disease as infection with multiple strains likely occurs during the lifetime of an individual.

In vivo and in vitro glycogenic effects of methionine sulfoximine are different in two inbred strains of mice

2002 ◽  
Vol 929 (2) ◽  
pp. 147-155 ◽  
Author(s):  
Katy Bernard-Hélary ◽  
Marie-Yvonne Ardourel ◽  
Tobias Hévor ◽  
Jean-François Cloix
Keyword(s):  
Inbred Strains ◽  
Methionine Sulfoximine ◽  
Inbred Strains Of Mice

Strain difference in the timing of meiosis resumption in mouse oocytes: involvement of a cytoplasmic factor(s) acting presumably upstream of the dephosphorylation of p34cdc2 kinase

Zygote ◽  
1997 ◽  
Vol 5 (2) ◽  
pp. 105-109 ◽  
Author(s):  
Zbigniew Polanński
Keyword(s):  
Extreme Values ◽  
Strain Difference ◽  
Germinal Vesicle ◽  
Inbred Strains ◽  
Germinal Vesicle Breakdown ◽  
Cytoplasmic Factor ◽  
Inbred Strains Of Mice ◽  
The Difference

SummaryOocytes from eight inbred strains of mice were screened for the timing of germinal vesicle breakdown (GVB) in vitro. This characteristic varied between strains, reaching most extreme values in oocytes from AKR and BALB/c mice (3.1 and 1.6h after release from dibutyryl cAMP block, respectively; p<0.0001). The difference between AKR and BALB/c mice was confirmed in experiments in which GVB was induced in vivo by stimulation with exogenous gonadotrophins. Analysis of the rate of GVB in hybrids obtained after fusion of nuclear and cytoplamic fragments of oocytes from both strains suggests that the factor responsible for the difference between AKR and BALB/c mice is located in the cytoplasm of the proghase oocytes. Finally, in oocytes from both strains stimulated to resume meiotic maturation with okadaic acid, an inhibitor of protein phosphatases types 1 and 2A the rate of GVB was the same (2.2h and 2.3h for AKR and BALB/c, respectively; p= 0.48). This suggests that the difference between strains is not related to the amount or quality of the pre-MPF (Maturation Promoting Factor) stored in the prophase oocyte, but to the factor(s) acting upstream of the dephosphorylation of p34cdc2. kinase in the pathway leading to pre-MPF activation.

In vitro tracheal responses from mice chosen for in vivo lung cholinergic sensitivity

1990 ◽  
Vol 69 (1) ◽  
pp. 274-280 ◽  
Author(s):  
G. G. Weinmann ◽  
C. M. Black ◽  
R. C. Levitt ◽  
C. A. Hirshman
Keyword(s):  
Linear Regression Analysis ◽  
Inbred Strains ◽  
Multiple Linear Regression Analysis ◽  
Maximal Response ◽  
Inbred Strains Of Mice ◽  
Cholinergic Agents ◽  
Cholinergic Sensitivity

We selected two inbred strains of mice based on their different in vivo lung responses to intravenous acetylcholine for studies on the in vitro tracheal responses to contractile and relaxing agents. In addition, we studied the role of cyclooxygenase products on the in vitro responses. Tracheal rings were contracted with increasing concentrations of carbachol and KCl and relaxed with increasing concentrations of isoproterenol after contraction with carbachol at the concentration that produced 30, 50, and 70% of the maximal contraction (EC30, EC50, and EC70, respectively) and KCl at the EC50. Half the tracheae simultaneously underwent the same protocols after pretreatment with indomethacin (3 X 10(-6) M). Despite a severalfold difference in the maximal response to cholinergic agents in vivo, there were no significant differences between the strains in the tracheal responses to carbachol (P = 0.78) or KCl (P = 0.13) in vitro. Both strains showed inhibition of the isoproterenol relaxation by carbachol (P less than 0.0001). Multiple linear regression analysis showed that the strain that was more sensitive to carbachol in vivo was also more sensitive to isoproterenol in vitro after carbachol contraction (P = 0.014). The greater isoproterenol sensitivity of the tracheae from this strain was not present after contraction with KCl, nor were these tracheae more sensitive to relaxation with sodium nitroprusside. Indomethacin pretreatment of the tissues in vitro augmented the maximal response and the sensitivity to carbachol (P less than 0.001) and KCl (P = 0.0006), and this effect was similar in both strains. Evaluation of isoproterenol relaxation after indomethacin pretreatment was confounded by the lower concentrations of carbachol needed for contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Exclusive involvement of H-2D(b) or H-2K(d) product in the interaction between T-killer lymphocytes and syngeneic H-2(b) or H-2(d) viral lymphomas

1977 ◽  
Vol 146 (4) ◽  
pp. 909-922 ◽  
Author(s):  
E Gomard ◽  
V Duprez ◽  
T Reme ◽  
MJ Colombani ◽  
JP Levy
Keyword(s):  
Inbred Strains ◽  
Antigenic Specificity ◽  
Target Cells ◽  
Chromium Release ◽  
Viral Budding ◽  
Inbred Strains Of Mice ◽  
Murine Sarcoma Virus ◽  
Specific Association

It was demonstrated previously that the cytolysis of murine viral lymphoma cells by anti-murine sarcoma virus (MSV) syngeneic T-killer lymphocytes was restricted by some products of the H-2 complex. The respective role of the products of different regions of the H-2 complex were studied with six H-2(b) and three H-2(d) lymphomas induced by five different type C viruses. They were tested in a classical chromium release test against anti-MSV T-killer cells obtained from different inbred strains of mice, including several H-2 recombinants. Tumors o£ the H-2(b) haplotype were lysed only when effectors and target cells have in common the D(b) region. On the contrary an identity limited to the K end of the H-2 complex is necessary and sufficient in the H-2(d) haplotype. An in vitro restimulation of the spleen cells with concanavalin A strongly increased the activity of in vivo-primed T lymphocytes but did not provide any response for in vivo-primed but nonresponder cells. Preincubation of the tumor cells with anti-H-2 sera abolished the lysis by syngeneic anti-MSV effector lymphocytes. The same results were obtained by preincubating the H-2(b) targets with anti-H-2D(b), or the H-2(d) target with anti-H-2K(d). Preincubation with anti-H-2K(b) or anti- H-2D(d) were ineffective. These results show that the T-killer/target cells interaction in the MSV system involved some products of the H-2 complex which might be different with the various H-2 haplotypes and could possibly vary according to the antigenic specificity. A specific association of a viral product with a normal cellular structure, directed by the H-2 region during the viral budding could explain the observed results.

Effect of murine strain on metabolic pathways of glucose production after brief or prolonged fasting

2005 ◽  
Vol 289 (1) ◽  
pp. E53-E61 ◽  
Author(s):  
Shawn C. Burgess ◽  
F. Mark H. Jeffrey ◽  
Charles Storey ◽  
Angela Milde ◽  
Natasha Hausler ◽  
...  
Keyword(s):  
Genetic Manipulation ◽  
Glucose Production ◽  
Tca Cycle ◽  
Inbred Strains ◽  
Mouse Strains ◽  
Background Strain ◽  
Metabolic Fluxes ◽  
Inbred Strains Of Mice ◽  
Total Glucose

Background strain is known to influence the way a genetic manipulation affects mouse phenotypes. Despite data that demonstrate variations in the primary phenotype of basic inbred strains of mice, there is limited data available about specific metabolic fluxes in vivo that may be responsible for the differences in strain phenotypes. In this study, a simple stable isotope tracer/NMR spectroscopic protocol has been used to compare metabolic fluxes in ICR, FVB/N (FVB), C57BL/6J (B6), and 129S1/SvImJ (129) mouse strains. After a short-term fast in these mice, there were no detectable differences in the pathway fluxes that contribute to glucose synthesis. However, after a 24-h fast, B6 mice retain some residual glycogenolysis compared with other strains. FVB mice also had a 30% higher in vivo phospho enolpyruvate carboxykinase flux and total glucose production from the level of the TCA cycle compared with B6 and 129 strains, while total body glucose production in the 129 strain was ∼30% lower than in either FVB or B6 mice. These data indicate that there are inherent differences in several pathways involving glucose metabolism of inbred strains of mice that may contribute to a phenotype after genetic manipulation in these animals. The techniques used here are amenable to use as a secondary or tertiary tool for studying mouse models with disruptions of intermediary metabolism.

Examining basal chloride transport using the nasal potential difference response in a murine model

2001 ◽  
Vol 281 (5) ◽  
pp. L1173-L1179 ◽  
Author(s):  
Kristine G. Brady ◽  
Thomas J. Kelley ◽  
Mitchell L. Drumm
Keyword(s):  
Cystic Fibrosis ◽  
Chloride Transport ◽  
Inbred Mice ◽  
Inbred Strains ◽  
Potential Difference ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Inbred Strains Of Mice ◽  
Cystic Fibrosis Transmembrane

Epithelia of humans and mice with cystic fibrosis are unable to secrete chloride in response to a chloride gradient or to cAMP-elevating agents. Bioelectrical properties measured using the nasal transepithelial potential difference (TEPD) assay are believed to reflect these cystic fibrosis transmembrane conductance regulator (CFTR)-dependent chloride transport defects. Although the response to forskolin is CFTR mediated, the mechanisms responsible for the response to a chloride gradient are unknown. TEPD measurements performed on inbred mice were used to compare the responses to low chloride and forskolin in vivo. Both responses show little correlation between or within inbred strains of mice, suggesting they are mediated through partially distinct mechanisms. In addition, these responses were assayed in the presence of several chloride channel inhibitors, including DIDS, diphenylamine-2-carboxylate, glibenclamide, and 5-nitro-2-(3-phenylpropylamino)-benzoic acid, and a protein kinase A inhibitor, the Rp diastereomer of adenosine 3′,5′-cyclic monophosphothioate ( Rp-cAMPS). The responses to low chloride and forskolin demonstrate significantly different pharmacological profiles to both DIDS and Rp-cAMPS, indicating that channels in addition to CFTR contribute to the low chloride response.

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