Hereditary Differences in Serum Proteins of Normal Mice.

Thompson, Sarane; Foster, Joseph F.; Gowen, John W.; Tauber, Oscar E.

doi:10.3181/00379727-87-21367

Cited by 19 publications

(6 citation statements)

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“…The electrophoretic results, and the findings of Thompson et al (1954) (if applicable), are consistent with the conclusion that the transferrins of Trf A jTrf A and Trf B jTrf B mice differ in charge, rather than in size. The electrophoretic results, and the findings of Thompson et al (1954) (if applicable), are consistent with the conclusion that the transferrins of Trf A jTrf A and Trf B jTrf B mice differ in charge, rather than in size.…”

Section: Discussionsupporting

confidence: 85%

“…They described the presence in one strain (E) of a /^-globulin not present in the remaining six strains (BALB/Gw, LGW, K, RI, S, Z) and presented evidence that this /3 Xglobulin could be detected in the F x progeny of crosses between E and S strain mice. It is, therefore, a reasonable assumption that the /?-globulins which Thompson et al (1954) found to show hereditary variation were, in fact, transferrins. However, from the results of two-dimensional electrophoresis (Fig.…”

Section: Introductionmentioning

confidence: 99%

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Genetics of plasma transferrins in the mouse

Cohen

1960

Genet. Res.

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1. The plasma proteins of six inbred strains of mice have been studied, using starch-gel electrophoresis.2. The existence of two alternative plasma transferrin (β-globulin) phenotypes has been demonstrated. Five of the strains have one of these and one strain has the other. Each of the two transferrin patterns comprises three (or possibly only two) electrophoretic bands. The two patterns differ in all of these bands.3. The two transferrin types recognized are determined by a pair of allelic, autosomal genes (designated TrfA and TrfB). The TrfA phenotype (CBA strain) is determined by the genotype TrfA/TrfA, and the TrfB phenotype (A, C57BL, JU, KL, RIII strains) by the genotype TrfB/TrfB. The phenotype TrfAB, of the heterozygote (genotype TrfA/TrfB), is distinguishable and shows four (or possibly only three) bands. In this way it closely resembles a mixture of equal parts of TrfA and TrfB plasma.4. No linkage was detected between the Trf locus and sex, the agouti locus or the haemoglobin locus.5. The possible molecular basis of the action of the transferrin alleles in the mouse, and the widespread distribution in mammals of polymorphism involving the transferrins, are discussed.

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Genetics of plasma transferrins in the mouse

Cohen

1960

Genet. Res.

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“…At the walls the no-slip condition was imposed. Regarding the fluid parameters, the density was set to 1060 kg/m³ [7,8,26] and the blood was modeled as a Newtonian fluid with a constant dynamic viscosity of 0.0035 Pa s [7,8,27]. The pressure and velocity fields were solved using the SIMPLE algorithm with second-order upwind discretization for the momentum equations and standard pressure interpolation (i.e.…”

Section: Fluid Dynamics Modelmentioning

confidence: 99%

An Animal-Specific FSI Model of the Abdominal Aorta in Anesthetized Mice

et al. 2015

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Recent research has revealed that angiotensin II-induced abdominal aortic aneurysm in mice can be related to medial ruptures occurring in the vicinity of abdominal side branches.Nevertheless a thorough understanding of the biomechanics near abdominal side branches in mice is lacking. In the current work we present a mouse-specific fluid-structure interaction (FSI) model of the abdominal aorta in ApoE -/-mice that incorporates in vivo stresses. The aortic geometry was based on contrast-enhanced in vivo micro-CT images, while aortic flow boundary conditions and material model parameters were based on in vivo high-frequency ultrasound. Flow waveforms predicted by FSI simulations corresponded better to in vivo measurements than those from CFD simulations. Peak-systolic principal stresses at the inner and outer aortic wall were locally increased caudal to the celiac and left lateral to the celiac and mesenteric arteries. Interestingly, these were also the locations at which a tear in the tunica media had been observed in previous work on angiotensin II-infused mice. Our preliminary results therefore suggest that local biomechanics play an important role in the pathophysiology of branch-related ruptures in angiotensin-II infused mice. More elaborate follow-up research is needed to demonstrate the role of biomechanics and mechanobiology in a longitudinal setting.

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“…Hereditary group differences of serum are known, the ABO-Secretor -Lewis group differences being reflected also in serum. Hereditary differences between beta-globulins of strains of inbred mice have been found ( Thompson et al 1954). Hereditary human serum groups identifiable by zone electrophoresis have recently been described (Smithies 1955 a, b ) .…”

Section: Discussionmentioning

confidence: 99%

Hereditary Serological Human Serum Groups

Grubb¹

1956

Hum Hered

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Hereditary Differences in Serum Proteins of Normal Mice.

Cited by 19 publications

References 0 publications

Genetics of plasma transferrins in the mouse

Genetics of plasma transferrins in the mouse

An Animal-Specific FSI Model of the Abdominal Aorta in Anesthetized Mice

Hereditary Serological Human Serum Groups

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