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At least 19 recordsLinked to original sources
PubMed1989

DNA excision-repair ability of embryonic fibroblasts measured by UDS and thymine dimer excorporation in four inbred mice strains.

Differences in the excision-repair capability of embryonic fibroblasts of four inbred strains of mice following various degrees of UV irradiation were assessed. Two methods of determination were used: (1) the incorporation of 3H-thymidine during unscheduled DNA synthesis (UDS) as measured by an autoradiographic technique; (2) the rate of excision of thymine dimers (TT) in the acid-insoluble fraction of the cellular DNA as determined by a dimerspecific radioimmuno-assay. Based on UDS, the repair rates of the four strains could be ranked in decreasing order as follows: DBA/2 (DB); C57BL/6J (B6); AKR/N (AK); CBA/J (CB). The calculated rate for DBA/2 (DB) is approximately twice that of CBA/J (CB). The determination of the TT excision rate indicates that 72 h after irradiation a maximum of 50% of the original UV-induced dimers in the DB strain could be repaired. In the three remaining strains the relatively reduced repair rates of 15% - 40% did not differ significantly.

Animals↗
PubMed1992

Toxic effect of lead on fertility of inbred strain mice.

Males of inbred strains were orally given lead acetate water solution during 150 days. Changes were found in the structure of the seminiferous tubules and in spermatozoa. The pathological changes in Leydig cells brought about a decline in levels of androgens.

Androgens↗
PubMed1975

Role of complement components in the susceptibility to Plasmodium berghei infection among inbred strains of mice.

Inbred strains of mice, sensitive and resistant to Plasmodium berghei infections, including a complement deficient strain were infected with P. berghei. Daily levels of parasitaemia were determined and serum levels of complement components (C3 and C5) measured by standard haemolytic assay. Serum levels of C3 and C5 were depressed in all strains of mice infected with P. berghei. There was no difference in the infectivity and course of P. berghei infection in the co-isogenic C5 deficient and non-deficient strains. The significance of these observations is discussed.

Agglutination Tests↗
PubMed1978

[Renewal of noradrenaline in different zones of the central nervous system of inbred mice strains and their recombinants].

A good correlation exists between the learning capacity and norepinephrine metabolism in the neocortex of C57 and Balb inbred Mice strains, as well as their F1 hybrids and seven recombinant inbred strains derived from their cross. The animals with a better learning performance are characterised by low levels of norepinephrine, as well as a slow metabolic rate of this neurotransmitter in the cortex. Such a correlation has not been found to exist in the other cerebral regions studied.

Animals↗
PubMed1988

Genetic complementation of defects in vaccine-induced immunity against Schistosoma mansoni in P- and A-strain inbred mice.

Inbred P- and A-strain mice are deficient in their capacity to develop resistance to challenge infection in response to vaccination with irradiated cercariae of Schistosoma mansoni and are also defective in their cell-mediated response as assessed by the activity of antigen-elicited macrophages in killing schistosome larvae in vitro. In contrast, vaccinated (P x A)F1 mice displayed high levels of both immunity to challenge and macrophage larvicidal activity, indicating that the P- and A-strain defects in the vaccine-induced response are controlled by distinct genetic loci.

Animals↗
PubMed1992

Induction of tumor necrosis factor alpha by Leishmania infantum in murine macrophages from different inbred mice strains.

The present study was undertaken to determine whether the viscerotropic species, Leishmania infantum, endemic in Italy, could induce tumor necrosis factor alpha (TNF alpha) in murine macrophages. Genetically susceptible (Lshs) and resistant (Lshr) mice were used in the attempt to correlate TNF alpha production with the ability to control parasite growth and replication. Resident peritoneal macrophages of C3H/HeN, DBA/2, CBA (Lshr), C57BL/10 and BALB/c (Lshs) mice were infected in vitro with promastigotes at a parasite to cell ratio of 8:1. No significant differences in the percentages of infected peritoneal cells of Lshs versus Lshr mice were observed until 72 h of in vitro culture. On the contrary, Kupffer cells from Lshr mice inhibited Leishmania replication. Peritoneal macrophages of resistant mice produced significantly higher amounts of TNF alpha as compared to susceptible mice. TNF alpha production of both resistant and susceptible mice peaked at about 5 h after the challenge with the parasite. No TNF alpha was found in supernatants of infected Kupffer cells from all the strains tested. The ability of macrophages from susceptible or resistant mice strains to produce TNF alpha after challenge with Leishmania infantum does not seem related to their capacity to control parasite replication in vitro.

Animals↗
PubMed1991

Quantitative morphological analysis of hippocampal structures in DBA1 and DBA2 inbred mice strains with genetically determined different shuttle box behavior: the mossy fiber system with reference data to the C3H strain.

The present work deals with morphological aspects which are likely related to a genetically determined learning behavior in the shuttle box paradigm. Subregions of the hippocampal mossy fiber system in two closely related inbred mice strains, DBA1 as a bad active avoider and DBA2 as a good one, are compared. Additionally, data derived from C3H (bad active avoider) studies are analyzed. Beside of certain structural similarities in DBA1 and DBA2 such as the elongation of infrapyramidal mossy fibers along the CA3 neurons this study pays attention to the topography of hilus and basal CA3 mossy fiber innervation.

Animals↗
PubMed1985

Variation in susceptibility to atherosclerosis among inbred strains of mice.

Ten inbred strains of mice were fed an atherogenic diet containing 1.25% cholesterol, 0.5% cholic acid and 15% fat. The strains were examined for plasma cholesterol and triglyceride levels and for formation of lipid-containing lesions in the aortic wall. The strains differed considerably in the frequency of lesion formation after 14 weeks on the atherogenic diet with a range of 0-1.8 lesions/mouse. The order of susceptibility to lesion formation from the least susceptible to the most susceptible was BALB/cJ, C3H/J, A/J, SWR/J, NZB/J, less than 129/J, AKR/J, DBA/2J, less than C57L/J less than C57BL/6J. Total plasma cholesterol after 5 weeks on the diet varied from 131 mg/dl to 328 mg/dl among strains; however, there was little correlation between total cholesterol levels and susceptibility to lesion formation (r = 0.29). Plasma triglycerides after 5 weeks on the diet varied less than cholesterol with a range of 137-220 mg/dl. An analysis of the genetic differences among inbred strains of mice might provide useful insights into lipid metabolism and the development of atherosclerosis.

Animals↗
PubMed1987

Muscarinic receptors in brain from four strains of inbred mice.

The density of brain muscarinic receptors from four strains of inbred mice was determined. C57BL/6J mice had a significantly higher density of muscarinic receptors in the forebrain than Balb/cJ or C57BL/10J mice. In the midbrain, C57BL/6J mice also had the highest density of receptors and in the hindbrain, C57BL/6J and AKR/J mice had a two fold higher receptor density compared to the other two strains. These findings demonstrate that inbred strains of mice which exhibit a range of genetically-determined behaviors, have varying densities of muscarinic receptors.

Animals↗
PubMed1987

An immunogenetic analysis of resistance to herpes simplex virus retinitis in inbred strains of mice.

Specific inbred strains of mice have been shown to vary considerably in their resistance and susceptibility to herpes simplex virus (HSV) infection. We injected 2 X 10(5) plaque forming units (PFU) of the KOS strain of HSV-1 intracamerally into one eye of BALB/c, C57Bl/6, and F1 (BALB/c X C57Bl/6) mice. HSV-1 antigens were localized in frozen sections of enucleated eyes at 10 to 14 days post-inoculation. Injected eyes of BALB/c mice showed an anterior uveitis with HSV-1 antigens in the anterior segment and an intact retina free of HSV antigens. The retina of the contralateral uninjected eye was necrotic and contained HSV-1 antigens. In both C57Bl/6 and F1 mice, HSV antigens were limited to anterior segment structures in the injected eye, whereas, in contrast to BALB/c mice, the contralateral retina appeared histologically normal and contained no viral antigens. The C57Bl/6 and F1 strains remained relatively resistant to retinal infection even if pretreated with up to 800 Rads of irradiation. The retinas of normal or sublethally irradiated C57Bl/6 and F1, but not BALB/c strains, were also resistant to intravitreal injection of HSV. These results suggest that resistance to HSV retinitis is a dominantly inherited trait, which depends only partly upon immunologic factors and may be heavily influenced by the inherent ability of host cells from different murine strains to support a productive viral infection.

Animals↗
PubMed1987

The virulence of Trypanosoma congolense can be determined by the antibody response of inbred strains of mice.

Three inbred strains of mice, BALB/c, C57Bl/6 and CBA/J were infected with three clones of Trypanosoma congolense, DIND/3.1, SAM/28.1 and KAR/57.1, which were obtained from three different stocks. DIND/3.1 was of high virulence for BALB/c and CBA/J but of negligible virulence for C57Bl/6. SAM/28.1 was of high virulence and KAR/57.1 of negligible virulence for the three strains of mice. In each case, high virulence was correlated with a late, transient and low titre protective antibody response measured by complement mediated lysis of live organisms. Negligible virulence was correlated with an early, high titre protective antibody response. Suppression of the antibody response by sub-lethal irradiation or cyclophosphamide treatment of the host turned a trypanosome infection of negligible virulence into one of high virulence. In mice with mixed infections it was shown that highly virulent trypanosomes did not influence the course of infection and antibody response to trypanosomes of negligible virulence and vice-versa. The relationship of total antigen mass to the kinetics of the antibody response suggests that 1000- to 10,000-fold less antigen is required in good responder than in bad responder mice to trigger the immune response. Thus the virulence of T. congolense can be determined by the antibody response of inbred strains of mice. The specificity and dose dependency of this antibody response seem to implicate the involvement of Ir genes.

Animals↗
PubMed1975

Emotionality, exploratory behavior, and locomotion in aging inbred strains of mice.

Two inbred strains of mice, C57BL/6J and DBA/2J, ranging in age from 2 to 38 months, were tested in an open field using the free exploration method. Scores were obtained for locomotor activity, exploratory behavior and emotionality. Strain differences were observed for all three variables. Beginning at late maturity (12 months), locomotor activity decreased with increasing age. Exploratory behavior was at a low level for DBA/2J mice at all ages. For C57BL/6J mice, exploratory behavior decreased significantly between 2 and 6 months and remained stable thereafter. Emotionality remained unchanged with advancing age for both strains of mice.

Aging↗
PubMed1991

Colony-stimulating factors increase resistance to atypical mycobacteria in resistant mice, whereas they decrease resistance in susceptible strains of mice.

Inbred strains of mice, notably the susceptible C57BL/6 and the resistant A/J strains of mice, were infected with a strain of Mycobacterium evium. The infection in the visceral organs of mice was then studied, and the effect of colony-stimulating factors, i.e., interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), and macrophage colony-stimulating factor (CSF-1) on the infectious process was evaluated. Infusion of GM-CSF, CSF-1, and IL-3 led to a significant, albeit rather modest, increase in the mycobacterial resistance of A/J mice, as seen by a decrease in the number of colony-forming units (CFU) in the organs. Conversely, these CSFs dramatically increased the susceptibility of C57BL/6 mice, as seen by increased bacterial numbers in the spleens and livers. In vitro studies demonstrated that resident peritoneal macrophages from susceptible mice were more permissive than cells from resistant mice for mycobacterial growth. Application of CSFs on peritoneal macrophage monolayers led to an increased growth in both A/J and C57BL/6 monolayers for IL-3 and CSF-1 and a small microbiostatic effect for GM-CSF. Cytokine treatment did not, however, change the resistance/susceptibility phenotype of isolated macrophages. Our results indicate that CSFs may exert beneficial or detrimental effects on resistance to mycobacteria depending on the host genetic make up.

Animals↗
PubMed1977

Genetic variation in brain L-glutamate decarboxylase activity from two inbred strains of mice.

Two inbred strains of mice, C57BL/6Bg and DBA/1Bg, were compared for genetic varaition in brain L-glutamate decarboxylase (GAD) activity. Although no large difference was found between the strains in whole brain GAD activity at adult age (27--45 days postnatally), regional examination revealed a difference in GAD activity in the cerebral cortex (15% higher in DBA); subcellular examination revealed a difference in synaptosomal fraction (21% higher in DBA). When GAD activity was measured in synaptosomal fractions prepared from dissected cerebral cortex, DBA was 34% higher than C57BL. In addition, differences in GAD activity between the two strains could be observed even in the whole brain (10--15% higher in DBA) during earlier development (15--23 days postnatally). These data indicate that at adult age, genetic difference in GAD activity between the two strains exists mainly in nerve terminals of the cerebral cortex. It is postulated that the difference may be due to a genetically mediated mechanism regulating GAD in the presynaptic terminals of GABA neurons of the cerebral cortex.

Age Factors↗