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Biomedical subjects

D J Gilbert

Publications and source records attributed to D J Gilbert.

322 records · Page 18Linked to original sources
PubMed1991

Glucose transporter gene expression in early mouse embryos.

The glucose transporter (GLUT) isoforms responsible for glucose uptake in early mouse embryos have been identified. GLUT 1, the isoform present in nearly every tissue examined including adult brain and erythrocytes, is expressed throughout preimplantation development. GLUT 2, which is normally present in adult liver, kidney, intestine and pancreatic beta cells is expressed from the 8-cell stage onward. GLUT 4, an insulin-recruitable isoform, which is expressed in adult fat and muscle, is not expressed at any stage of preimplantation development or in early postimplantation stage embryos. Genetic mapping studies of glucose transporters in the mouse show that Glut-1 is located on chromosome 4, Glut-2 on chromosome 3, Glut-3 on chromosome 6, and Glut-4 on chromosome 11.

Amino Acid Sequence↗
PubMed1991

Structure, chromosome mapping, and expression of the mouse Lyl-1 gene.

The mouse Lyl-1 gene was cloned and shown to consist of four exons with extensive nucleotide and structural homology to the human LYL1 gene. The Lyl-1 gene was localized to the central region of mouse chromosome 8 which defines a new region of synteny with human chromosome 19p. The predicted mouse Lyl-1 protein is 78% identical to human LYL1. The region of highest similarity occurs in the basic DNA binding and helix-loop-helix dimerization motifs which are nearly identical in mouse and man differing by only one conservative amino acid substitution. Expression of the Lyl-1 gene was found to be low in murine spleen and undetectable in other tissues by Northern blot analysis. In lymphoid cell lines, Lyl-1 was expressed in most B lineage cells but downregulated during terminal differentiation and was not expressed in most T lineage cells. In a human T ALL cell line carrying a translocation that juxtaposed LYL1 with the beta TCR gene, the translocated LYL1 gene was transcriptionally active whereas the nontranslocated gene was transcriptionally silent. We conclude that LYL1 has the properties of a lineage- and differentiation-specific HLH protein that contributes to T-cell neoplasia through its deregulated expression following chromosomal translocation.

Amino Acid Sequence↗
PubMed1990

Mast cell growth factor maps near the steel locus on mouse chromosome 10 and is deleted in a number of steel alleles.

Many spontaneous, chemical-induced, and radiation-induced dominant white spotting (W) and steel (Sl) mutations have been identified in the mouse. W and Sl mutations have similar phenotypic effects including deficiencies in pigment cells, germ cells, and blood cells, Numerous studies have suggested that W acts within the affected cell while Sl instead exerts its effects in the extracellular environment. Recent findings demonstrating that W encodes the c-kit proto-oncogene, a tyrosine kinase membrane receptor, have suggested that Sl encodes a ligand for c-kit. In the accompanying article we report the identification and purification of mast cell growth factor (MGF), a c-kit ligand. Here we describe the cloning of sequences encoding MGF. Furthermore, we show that Mgf maps near Sl in the distal region of mouse chromosome 10 and is deleted in a number of Sl alleles. These findings strongly support the notion that Sl encodes the mast cell growth factor.

Alleles↗
PubMed1990

A genetic linkage map of mouse chromosome 10: localization of eighteen molecular markers using a single interspecific backcross.

Interspecific mouse backcross analysis was used to generate a molecular genetic linkage map of mouse chromosome 10. The map locations of the Act-2, Ahi-1, Bcr, Braf, Cdc-2a, Col6a-1, Col6a-2, Cos-1, Esr, Fyn, Gli, Ifg, Igf-1, Myb, Pah, pgcha, Ros-1 and S100b loci were determined. These loci extend over 80% of the genetic length of the chromosome, providing molecular access to many regions of chromosome 10 for the first time. The locations of the genes mapped in this study extend the known regions of synteny between mouse chromosome 10 and human chromosomes 6, 10, 12 and 21, and reveal a novel homology segment between mouse chromosome 10 and human chromosome 22. Several loci may lie close to, or correspond to, known mutations. Preferential transmission of Mus spretus-derived alleles was observed for loci mapping to the central region of mouse chromosome 10.

Animals↗
PubMed1989

Spontaneous germ line virus infection and retroviral insertional mutagenesis in eighteen transgenic Srev lines of mice.

SWR/J-RF/J hybrid mice spontaneously acquire new germ line ecotropic proviruses at high frequency. In the studies described here, we used these hybrids to produce 18 transgenic mouse lines, each carrying a single newly acquired Srev locus (SWR/J-RF/J ecotropic proviral locus). All of the newly acquired proviruses identified in mosaic founder SWR/J-RF/J mice that could be transmitted through the germ line were also present in somatic tissues, demonstrating that viral integration occurred before the germ line was set aside from the somatic lineages. Quantitative analysis of proviral DNA copy numbers in somatic and germinal tissues of mosaic founder parents combined with structural analysis of Srev loci indicated that these proviruses are acquired after multiple rounds of somatic viral reinfection and that most of these viral integration events occurred after DNA replication in the zygote and before DNA replication in the four-cell embryo. The frequency of provirus acquisition in Srev lines that expressed the infectious ecotropic virus was similar to that in SWR.RF mice carrying Emv-16 and Emv-17, suggesting that the chromosomal integration site of the parental locus is not an important determinant for high-frequency provirus acquisition. The frequency of recessive lethal mutations induced by spontaneous viral integration was 5%, which was similar to that induced by preimplantation embryo infection. This approach represents a simple and viable strategy for inducing and studying mutations that affect mammalian development.

Animals↗
PubMed1988

Studies of the mechanism of spontaneous germline ecotropic provirus acquisition in mice.

SWR/J--RF/J hybrid mice spontaneously acquire new germline ecotropic proviruses at high frequency. We have performed ovarian transplantation and in situ hybridization studies to delineate the mechanism and developmental stage of germline provirus acquisition. In addition, we have developed a novel, efficient and simple method to introduce single copy proviruses into the mouse germline. The results reported here have direct implications for understanding how proviruses are acquired in the germline, for using murine leukemia viruses as insertional mutagens, and for using retroviral vectors to introduce foreign genes into the mouse germline.

Animals↗
PubMed1987

Common sites of viral integration in lymphomas arising in AKXD recombinant inbred mouse strains.

Lymphomas from 21 AKXD recombinant inbred mouse strains were analyzed for retrovirally induced rearrangements in seven known or putative proto-oncogene loci. Among the rearrangements detected in the 258 lymphomas screened, most rearrangements appeared to be caused by viral integration. Rearrangements were detected in the Myc, Pvt-1, Pim-1, Mlvi-1, Mlvi-2, and Fis-1 loci, but not in the Myb locus. Seven lymphomas contained rearrangements in two loci. Nearly 90% of the rearrangements were observed in T cell lymphomas; few were detected in B cell or myeloid tumors. Rearrangements in Pvt-1, Fis-1, Mlvi-1, and Mlvi-2 were identified only in T cell lymphomas. Alterations in the Myc and Pim-1 loci, although occurring predominantly in T cell lymphomas, were occasionally detected in other types of lymphoma. These data suggest that the repertoire of cellular proto-oncogenes activated by integration of virus into lymphomas may be different for each hematopoietic cell lineage. The AKXD lymphomas represent a useful resource for identifying these sites.

Animals↗
PubMed1985

Efficacy in anterior uveitis of two known steroids and topical tolmetin.

We have compared the anti-inflammatory efficacy of 5% tolmetin sodium dihydrate, 0.5% prednisolone disodium phosphate, and 0.1% betamethasone disodium phosphate in 71 consecutive patients presenting with acute endogenous non-granulomatous uveitis randomly assigned to one of these treatment groups. Inflammatory symptoms and signs were scored during the course of the 21-day trial period. There was no statistically significant difference in the effect on the signs or symptoms of the three drugs tested. 90% of the Betnesol (betamethasone sodium phosphate, benzalkonium chloride) treated group were clinically judged cured compared with 68% of the Predsol (prednisolone sodium phosphate, benzalkonium chloride) treated group, and 57% of the tolmetin treated group.

Administration, Topical↗
PubMed1985

A non-invasive instrument for clinical assessment of the pre-corneal tear film stability.

A simple, non-invasive technique has been developed for assessment of the stability of the pre-corneal tear film. Changes are observed in the reflection of a grid pattern from the tear film surface. Breaks in the tear film appear as random discontinuities in the grid image. Using this non-invasive technique the stability of the pre-corneal tear film was assessed in nine normal subjects and twelve established dry-eye patients. The non-invasive tear film break-up time (NIBUT) of the dry-eye patients was on average only 25% to 32% of normal values. The non-invasive technique provides an alternative approach to diagnosing non-wetting disorders as well as a means of evaluating the efficacy of artificial tear solutions.

Adolescent↗
PubMed1985

Effect of fluorescein instillation on the pre-corneal tear film stability.

Non-invasive tear film break-up time (NIBUT) was measured in nine normal subjects to investigate the effect of fluorescein instillation of tear film stability. It was found that fluorescein instillation reduced the tear film stability in the treated group, compared with the control group (P less than 0.05). It is, therefore likely that the tear film stability may be greater than had hitherto been suggested by the fluorescein method.

Adult↗
PubMed1984

The effect of topical 0.5% triamterene suspension on the intraocular pressure of open angle glaucoma patients. A single dose study.

The effect of a topical 0.5% triamterene suspension on the intra-ocular pressure of 15 open angle glaucoma patients was investigated. On the first day measurements were made at 09.00, 12.00 and 16.30 hours without treatment. On the second day measurements were made at 09.00 hours and 1, 2, 4 and 6 hours following instillation of the suspension into the eye. Without treatment there were no significant changes in intra-ocular pressure. After topical triamterene the maximum group mean pressure reduction was -4.7 mm Hg at 6 hours and mean intra-ocular pressures were less than 22 mm Hg at both 4 and 6 hours. There was also a notable decrease in intra-ocular pressure in two thirds of the contralateral untreated eyes which was not attributable to diurnal variation. No local or systemic side effects were observed.

Administration, Topical↗
PubMed1980

Generalized morphea with peripheral eosinophilia, fasciitis and myositis.

The distinctions between eosinophilic fascitis (Shulman's syndrome) and scleroderma may sometimes be unclear. We describe a patient with generalized morphea who also had peripheral blood eosinophilia, fibrosis and inflammation of fascia, and hyper-globulinemia, features usually attributed to Shulman's syndrome. The latter diagnosis should be restricted to those patients whose history, clinical and laboratory findings, and response to therapy closely resemble Shulman's original description. Scleroderma and eosinophilic fasciitis may represent slightly differing aspects of the same disease spectrum, with a similar immunologic pathogenesis.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Sequence, genomic organization, and chromosome localization of the mouse TRADD gene.

Signals triggered by tumor necrosis factor (TNF) are mediated by its two receptors: the 55 kDa TNF receptor one (TNF-R1) and the 75 kDa TNF receptor two (TNF-R2). Activation of TNF-R1 induces cell death, NF-kappa B activation, inflammatory response and anti-viral activity, while TNF-R2 mainly stimulates cell proliferation and NF-kappa B activation. The TNF-R2-associated factor TRAF2 has been shown to mediate activation of NF-kappa B by TNF-R2 and CD40. The human TNF-R1-associated death domain protein (TRADD) induces cell death and NF-kappa B activation when overexpressed. Here we describe the cloning and gene structure of the mouse homolog of TRADD. Mouse TRADD shares 75% overall amino acid sequence identity with human TRADD, suggesting high conservation of function. Mouse TRADD specifically interacts with wild type TNF-R1 but not with a truncated mutant TNF-R1 lacking its C-terminal 20 amino acids. Like human TRADD, mouse TRADD also induces activation of NF-kappa B and cell death. The expression of TRADD in mouse embryo appears developmentally regulated. The mTRADD gene contains four exons, with the fourth exon encoding all of the death domain. The mouse TRADD gene was localized to the distal region of chromosome 8.

Amino Acid Sequence↗