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PubMedDate not supplied

Hereditary vestigial pulmonary arterial trunk and related defects in rabbits.

In a population of IIIVO/J rabbits at the Jackson Laboratory a vestigial pulmonary arterial trunk is the commonest expression of a malformation involving the heart and great vessels. There appears to be a series of effects from a completely absent pulmonary trunk through a vestigial but patent pulmonary trunk and/or pulmonary valve stenosis on the one hand to a vestigial or absent ascending aorta on the other. In a few cases the pulmonary trunk is bulbous and the ductus arteriosus is vestigial or absent. In almost all cases of this syndrome, there is also a high ventricular septal defect. The animals appear perfectly normal in every other respect. In its extreme forms this mutation is lethal, but those few animals that are somewhat less severely affected may live for a short time. No effect was seen on birth weight or litter size. Inheritance of vestigial pulmonary arterial trunk appears to be due to two autosomal recessive factors both of which must be homozygous for the expression of the condition. We propose the symbols vpt-1 and vpt-2 for the genes responsible for vestigial pulmonary arterial trunk and its related abnormalities.

Animals↗
PubMed2001

Genetic analysis of intestinal cholesterol absorption in inbred mice.

A genetic mapping strategy was employed to identify chromosomal regions harboring genes that influence the absorption of intestinal cholesterol in the mouse. Analysis of seven inbred strains of male mice (129P3, AKR, BALB/c, C3H/He, C57BL/6, DBA/2, and SJL, all from Jackson Laboratories) revealed substantial differences in their abilities to absorb a bolus of cholesterol delivered by gavage. Crosses between high (AKR, 129) and low (DBA/2, SJL) absorbing strains revealed evidence for the presence of dominant genes that increase and decrease cholesterol absorption. Backcrosses between F1 offspring and parental strains (DBA/2xAKD2F1 and 129xSJL129F1) followed by linkage analyses revealed four quantitative trait loci that influenced cholesterol absorption. Analyses of recombinant inbred strains identified an additional three loci affecting this phenotype. These seven quantitative trait loci, which map to different chromosomes and are termed Cholesterol absorption 1-7 (Chab1-7) loci, together influence the absorption of intestinal cholesterol in mice and are likely to be involved in different steps of this complex pathway.

Animals↗
PubMed1975

[The development of microangiopathic hemolytic anemia in the model of a transplantable hemangioendothelioma of the J 129 mouse (author's transl)].

INTRODUCTION: In earlier reports we have described the morphological findings of microangiopathic hemolytic anemia (MHA) in autopsy cases. The aim of this publication is to show more exactly the close correlation between microangiopathy and intravascular hemolysis in a transplantable hemangioendothelioma of the mouse. This animal model is suitable for study of the MHA, which develops within short time, with various morphological and biochemical parameters. MATERIAL AND METHODS: 100 J 129 mice (Jackson Laboratory, Bar Harbor, Me) with transplanted hemangioendothelioma and 20 healthy controls were studied. For transplantation the tumors were removed in toto from donors and mined in 0.9% sterile saline; 0.7 ml of this tumor suspension was injected subcutaneously in the lateral flank of the recipients...

Anemia, Hemolytic↗
PubMed2002

Parkinson's disease mice and human umbilical cord blood.

In 1995, it was suggested that immature stem cells (Berashis Cells) existing in human cord blood might have an ameliorating effect on such neurological diseases as Alzheimer's, amyotrophic lateral sclerosis and Parkinson's disease. Since these predictions, we have been able to successfully extend the length of life of mice with amyotrophic lateral sclerosis [B6SJL-TgN(SOD1-G93A)IGUR], Huntington's Disease (B6CBA-TgN(H.Dexon1)62Gpb and Alzheimer's mice [Tg(HuAPP695.SWE)2576]. Recently we expanded the studies to include mice with Parkinson's Disease. 32 mice, 6-12 weeks old B6CBACa-AW-J/A-Kcnj6 were obtained from Jackson Laboratory, Bar Harbor, Maine. The mice were divided into 3 groups: (A) 10 untreated control mice, (B) 10 mice treated with 5.6 x 10(6) congenic bone marrow mononuclear cells and (C) 12 mice receiving 100-110 x 10(6) HUCB mononuclear cells intravenously. No immunosuppression was used. When 50% of the controls were dead only 1 of the 10 mice receiving congenic marrow and 2 out of 12 mice that received cord blood mononuclear cells were dead. This preliminary study was terminated when the animal's were 200 days old, at that time one out of 10 controls was alive. Out of 10 mice that received congenic bone marrow, 2 were alive. Out of 12 mice that received megadoses of cord blood mononuclear cells 4 were alive. Survival curve of mice that had congenic marrow had a p value of <.05; the survival curve of mice receiving cord blood mononuclear cells had a p value <.001 (Fig 1) compared to controls. Human umbilical cord blood mononuclear cells significantly delayed the onset of symptoms and death of Parkinson's disease mice. This effect was greater than that produced by congenic bone marrow cells.

Animals↗
PubMed2005

[Participation of transfused bone marrow cells in reparative osteohistogenesis].

The participation of skeletal tissue cell precursors in the repairing regeneration of bone tissue was studied. Bone marrow was taken from donor animals--mice of C57Bl/6-TgN(ACTbGFP) 1 Osb line (The Jackson Laboratory Bar Harbor ME USA line). Nucleated cell fraction was isolated by centrifugation on a density percoll gradient. Recipient mice C57Bl/6 line were irradiated by 7.0-7.5 Gr dose. Intravenous infusion of donor cells and osteoclasts of tibia was done after irradiation of recipient mice. Histological preparations of bone regenerate tissues were studied on 15, 30, and 60 days by confocal microscopy. Donor cells were found as skeletal tissue precursors into periost, endost, bone marrow, and as differentiated cells of newborn tissue of regenerate--osteoblasts, osteocytes, chondrocytes. The data obtained indicate that part of donor bone marrow cells are able to progressive differentiation under recipient bone fractures.

Animals↗
PubMed1990

[Characterization of gonadotropic cells in a new pituitary tumor cell line].

The pituitary tumor cell line RC-4B/C was established in The Jackson Laboratory from an aged rat pituitary adenoma. Immunocytochemical studies of this cell line showed that all pituitary cell types were present. Approximately 20% reacted with antisera (AS) to ovine (o) LH beta, 8.6% with AS to oFSH beta, 15% with AS to rat PRL, 12% with AS to equine GH, 9% with AS to porcine TSH beta and 8.6% with AS to ACTH1-24. Using NIDDK rat kits, RIA showed about 0.38, 0.08 and 607.50 ng per 10(6) cells of LH, FSH and PRL, respectively, vs 33.9, 75.6 and 573 ng in freshly dispersed rat pituitary cells. The GnRH receptor content of the cell line was about a half that of normal rat pituitary cells but the receptor affinity was the same. A chronic treatment of the cells for about 5 months with a "sub-physiological" concentration (3.7 pM) of a GnRH agonist had 3 major effects: 1) as compared to the controls, a 3-fold increase in the cell number in the log phase; 2) an increase of the percentage of FSH beta cells from 8.6 to 21.9% whereas LH beta cells and the cell content of LH and FSH remained stationary; 3) a decrease of the percentage of PRL cells from 15 to 6.5% and an almost 250-fold decrease of PRL cell content. Incorporation studies with [35S] Met demonstrated that the alpha subunit in the cell line was only partly glycosylated. Pretreatment of the cells with 5 nM estradiol restored, at least partly, glycosylation of alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1988

Schistosoma mansoni and S. japonicum worm numbers in 129/J mice of two types and dominance of susceptibility in F1 hybrids.

In a study on the genetics of resistance to schistosomiasis in WEHI 129/J mice, susceptibility to either Schistosoma mansoni or Schistosoma japonicum was shown to be unequivocally dominant in F1 hybrid crosses between genetically resistant WEHI 129/J and susceptible BALB/c mice. The operation of only 1 or 2 genes in the expression of resistance to S. mansoni was suggested by backcross analysis. Thus, approximately 25% of (BALB/c x WEHI 129/J) F1 x WEHI 129/J mice were resistant to S. mansoni infection, whereas resistance was manifest in approximately 50% of WEHI 129/J mice. The data are consistent with resistance being controlled by 1 recessive gene having 50% penetrance. We also report that 129/J mice obtained directly from the Jackson Laboratories (Bar Harbor, Maine) (designated JAX 129/J), differ from locally bred WEHI 129/J in being entirely susceptible to S. mansoni infection. However, both WEHI 129/J and JAX 129/J are relatively resistant to S. japonicum infection.

Animals↗
PubMed1988

Corticosteroid-induced cleft palate in short-ear mice.

Corticosteroid-induced facial clefting was examined in short-ear mice (inbred strain SEA/GnJ from Jackson Laboratory). They were found to be gentle, prolific breeders (average litter size 7.3 +/- 2.6), with no increased fetal loss due to treatment. Although they have the most "resistant" H-2 haplotype (H-2d), they were found to be highly susceptible to corticosteroid-induced clefting, demonstrating that loci other than H-2 are involved in susceptibility. The short-ear locus itself is a plausible candidate, given that this gene on chromosome 9 leads to defective mesenchymal condensation, which in turn may render these mice extremely sensitive to teratogen exposure. Another gene or genes on chromosome 9 are also possibilities.

Animals↗
PubMed1983

The William Allan Memorial Award. Presented to Elizabeth F. Neufeld, Ph. D., at the annual meeting of the American Society of Human Genetics Detroit, September 29-October 2, 1982.

The opportunity for this presentation provides me with three gratifications. The first and most important is that the scientist being honored is Elizabeth Neufeld. The second is the honor bestowed upon me by being selected to introduce Dr. Neufeld. Finally, the preparation of this introduction has provided me with the opportunity to reconstruct a scientific career from its beginnings to its present exciting momentum, an exercise in which I was helped with great enthusiasm by a number of people who have known Liz during the various phases of her scientific life. I am particularly pleased to note that our awardee is the product of that unique breeding ground of success stories, the special New York education system. After arriving in New York in 1940 at the age of 12 from Paris, a refugee from Nazi persecutions in Europe, Liz Neufeld, like so many other young refugees at the time, qualified for one of the specialized schools in New York--the Hunter College High School. From there she went to Queens College, one of the major high-quality free institutions of higher learning of the New York City college system, and graduated with a Bachelor of Science degree in 1948. Obviously turned on to a scientific career, she successfully applied for a research assistantship at the Jackson Laboratory in Bar Harbor, Maine, where she worked with the first of her mentors, Dr. Elizabeth Russell, to this day her good friend and enthusiastic admirer. Her first publications are derived from that experience and are concerned with hematologic genetics of mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Awards and Prizes↗
PubMed1981

Venereal spirochetosis of rabbits: eradication.

Venereal spirochetosis of rabbits, caused by Treponema cuniculi, have been observed since the 1940's in the rabbit colony maintained at The Jackson Laboratory. Treatment of individual rabbits with obvious clinical lesions using a product containing crystalline penicillin and dihydrostreptomycin caused lesions to heal but venereal spirochetosis persisted in the colony. Clinical and serological responses of rabbits receiving three subcutaneous injections of benzathine penicillin G-procaine penicillin G (either 42,000 or 84,000 IU/kg body weight/week) at 7 day intervals were monitored. Both doses were effective. Lesions healed within 2 weeks of the first treatment. Rapid plasma reagin titers declined markedly or disappeared by the sixth week after the first treatment. Based upon the above findings and results of previous epizootiological studies, a program to eradicate venereal spirochetosis from this enzootically infected colony was successfully undertaken.

Animals↗
PubMed1981

The production of anti-IgG2a autoantibody in the 129/Sv mouse: onset in the lymph nodes draining the intestinal tract and prevention by neonatal thymectomy.

The histological distribution of anti-IgG-secreting cells was studied by measuring the amount of anti-IgG autoantibodies produced in vitro by cells isolated from various lymphoid organs. Before 20 wk, the production of anti-IgG autoantibody in 129/Sv mice from our Institute predominated in the mesenteric and caudal lymph nodes, which both drain the intestinal tract. After 20 wk, the production extended to the spleen and bone marrow. At that time no production was detected in the mediastinal, lumbar, and inguinal lymph nodes. A similar distribution of anti-IgG-secreting cells was observed in 25-wk-old 129/J mice from the Jackson Laboratory. These data indicate that anti-IgG autoimmunity in the 129 primarily results from a local immune response, probably induced by a specific stimulus of intestinal origin. Neonatal thymectomy prevented the production of anti-IgG, demonstrating that the mesenteric anti-IgG production did not result from the direct stimulation of B lymphocytes by endotoxin-like polyclonal activators. It was found that the anti-IgG produced in vitro had the same narrow specificity against IgG2a as its serum counterpart, indicating that this specificity resulted from the selective stimulation of anti-IgG2a-secreting cells rather than from in vivo consumption of anti-IgG antibodies recognizing other IgG subclasses.

Aging↗
PubMed1982

Identification of genetically homozygous rapid and slow acetylators of drugs and environmental carcinogens among established inbred rabbit strains.

Liver and gut mucosa N-acetyltransferase (NAT) cytosol (105,000 x g) was prepared from selected lines of New Zealand White rapid and slow acetylator rabbits bred and housed at the University of Michigan, and from inbred and partially inbred rabbits obtained from The Jackson Laboratory. Liver NAT activity was determined with p-aminobenzoic acid, p-aminosalicyclic acid, procainamide, sulfamethazine, isoniazid and 2-aminofluorene as substrates. Gut mucosal NAT activity was determined with 2-aminofluorene. A gene dose-response relationship was observed for both liver NAT and gut mucosa NAT with all substrates tested. Highest levels were always observed in homozygous rapid acetylator inbred strains (B/J, III/J, IIIC/J, III/DwJ, IIIEP/J and IIIVO/J), lower levels in obligate heterozygous rapid acetylator rabbits and lowest levels in homozygous slow acetylator inbred (ACEP/J, III/cdJ, IIIVO/ahJ, and IIIVO/vptJ) and outbred rabbits. The differences in magnitude of liver NAT activity level between acetylator genotypes was dependent on the substrate employed, progressively increasing in the following order: p-aminobenzoic acid, p-aminosalicyclic acid, procainamide, sulfamethazine, isoniazid, 2-aminofluorene. The determination of kinetic constants for liver p-aminosalicyclic acid NAT activity indicated a 2-fold difference in apparent Vmax between rapid acetylator genotypes and a 30-fold difference between rapid and slow acetylator phenotypes. In addition, the apparent Km for p-aminosalicyclic acid was significantly lower in the slow acetylators than in the rapid acetylators.

Acetylation↗
PubMed1982

[Maintenance of inbred and genetic control--the significance in cancer research].

Implications of the maintenance of mouse inbred strains were discussed from the view point of experimental animals in the cancer research. Firstly, the genetically controlled inbred strains can provide us the experimental materials having homogeneous genetic characters. Secondly, they are able to serve as the reference by which we could equalize our experimental systems with the standard ones such as the stocks in the Jackson Laboratory. As to the markers for the genetic control of laboratory mice, the following four are introduced. (1) Morphological markers such as coat color genes: a, b, c and d. (2) Biochemical markers either in some serum proteins and in liver, kidney and erythrocytic allozymes. (3) Immunological markers, mainly H-2 private specificities. (4) Cytogenetical markers. Chromosome Q- and C-banding.

Animals↗
PubMed1993

Matching references with MEDLINE via TCP/IP.

Bibliographic references are an important part of databases and information resources used by clinicians and biomedical researchers. In addition to the obvious clerical advantages of standard references, bibliographic references can also be used as links to related items in different data sets. This paper describes an effort that involved matching references from a variety of disparate databases to canonical MEDLINE references. The references matched were those involved in a database unification project which is part of the Mouse Genome Informatics effort at The Jackson Laboratory. Software was developed to take advantage of a commercially available retrieval engine which accesses MEDLINE on CD-ROM disks. The software permits client programs on UNIX/C, and potentially other environments, to access unabridged MEDLINE via networks supporting the TCP/IP protocols. The matching process described can be used as a model for similar efforts with different research or clinical data sets, as well as different hardware or software environments.

Animals↗
PubMedDate not supplied

Determination of methylene chloride acceptability and its "purification" for ethylenethiourea methodology.

A liquid chromatographic-electrochemical method for the determination of ethylenethiourea (ETU) residues uses methylene chloride in the cleanup. Distilled-in-glass grade methylene chloride produced erratic ETU recoveries ranging from 0 to 106% for vacuum rotary evaporation of the solvent. ETU recoveries were found to be dependent on the bottle of methylene chloride used, not on supplier or lot. When GC2 grade methylene chloride from Burdick & Jackson Laboratories was used, ETU recoveries ranged from 92 to 110%. "Acceptable" ETU recoveries were defined as those values between 90 and 110%. Passing "unacceptable" methylene chloride through a column containing anhydrous sodium sulfate, sodium carbonate, and alumina was found to adequately purify methylene chloride. Treated methylene chloride provided acceptable ETU recoveries for up to 1 month after "purification."

Chromatography, Liquid↗
PubMed1997

Harlequin ichthyosis (ichq): a juvenile lethal mouse mutation with ichthyosiform dermatitis.

The harlequin ichthyosis (ichq) mouse mutation arose spontaneously in 1989 in a colony of BALB/cJ mice at The Jackson Laboratory. Affected mice developed thick skin due to formation of compact, orthokeratotic scales that fractured over articular surfaces, secondary to bending. Harlequin ichthyosis mice on the inbred BALB/cJ background died between 9 and 12 days of age. Onset of the clinical phenotype corresponded with emergence of hair fibers from follicles at 5 days of age. There was marked proliferation of the root sheaths of anagen hair follicles, limited to the region within the dermis. Sebaceous glands were present but small compared with those of littermate controls. Emerging hair fibers were surrounded by a thick, compact sheath of cornified cells. Mutant skin contained large mitochondria with lamellar-shaped, electron-dense structures at the ultrastructural level. Keratohyalin granules were smaller and less pleomorphic than those in control mice. Lamellar bodies were not evident in either mutant or littermate control mice. Using a panel of antibodies to evaluate changes in keratinocyte differentiation, mouse-specific keratin 6 was overexpressed in the suprabasilar, hyperplastic epidermis. Loricrin expression, within the cytoplasm of cells in the stratum granulosum, decreased rapidly postmortem, unlike that in normal mice where it was stable for over 24 hours postmortem. Filaggrin expression, within granules of cells in the stratum granulosum, was prominent, corresponding to hypergranulosis evident by light microscopy in mutant mouse skin. Skin grafts from harlequin ichthyosis mice grafted onto immunodeficient nude mice maintained the phenotype for the 10-week observation period. The mutant gene locus mapped to the proximal end of mouse chromosome 19 and is inherited as a fully penetrant autosomal recessive gene. The harlequin ichthyosis mouse mutation is very similar to human type 2 harlequin ichthyosis for which it may be a good model.

Animals↗
PubMed1997

Expression and chromosomal mapping of mouse Gpx2 gene encoding the gastrointestinal form of glutathione peroxidase, GPX-GI.

GPX-GI is a cytosolic tetrameric Se-dependent glutathione peroxidase, similar in properties to GPX-1. Unlike the almost ubiquitous GPX-1, GPX-GI is mainly expressed in the epithelium of gastrointestinal tract. GPX-GI contributes to at least fifty percent of GPX activity in rodent small intestinal epithelium. The total GPX activity consists of at least 70% of selenium-dependent GPX activity in this compartment. By analyzing a panel of mouse interspecies DNA from the Jackson Laboratory's backcross resource, we mapped Gpx2 gene to mouse chromosome 12 between D12Mit4 and D12Mit5, near the Ccs1 locus which contains a colon cancer susceptibility gene. A pseudogene, Gpx2-ps is mapped to mouse chromosome 7. Comparison of Gpx2 gene expression in three pairs of C57BL/6Ha and ICR/Ha mice which are respectively resistant and sensitive to dimethylhydrazine-induced colon cancer, we found a higher Gpx2 mRNA level in C57BL/6Ha colon than ICR/Ha colon. Interestingly, a lower level of GPX activity is found in the resistant strain of mice. Because GPX-1 has three times higher specific activity than GPX-GI, our data suggest that the decreased GPX activity may result from a higher level of Gpx2 gene expression in those cells co-express Gpx1 gene.

Amino Acid Sequence↗