| 1. |
- Schon, M P, et al.
(författare)
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Mucosal T lymphocyte numbers are selectively reduced in integrin alpha E (CD103)-deficient mice
- 1999
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Ingår i: Journal of Immunology. - 1550-6606. ; 162:11, s. 6641-6649
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Tidskriftsartikel (refereegranskat)abstract
- The mucosal lymphocyte integrin alpha E(CD103)beta 7 is thought to be important for intraepithelial lymphocyte (IEL) localization or function. We cloned the murine integrin gene encoding alpha E, localized it to chromosome 11, and generated integrin alpha E-deficient mice. In alpha E-/- mice, intestinal and vaginal IEL numbers were reduced, consistent with the known binding of alpha E beta 7 to E-cadherin expressed on epithelial cells. However, it was surprising that lamina propria T lymphocyte numbers were diminished, as E-cadherin is not expressed in the lamina propria. In contrast, peribronchial, intrapulmonary, Peyer's patch, and splenic T lymphocyte numbers were not reduced in alpha E-deficient mice. Thus, alpha E beta 7 was important for generating or maintaining the gut and vaginal T lymphocytes located diffusely within the epithelium or lamina propria but not for generating the gut-associated organized lymphoid tissues. Finally, the impact of alpha E deficiency upon intestinal IEL numbers was greater at 3-4 wk of life than in younger animals, and affected the TCR alpha beta+ CD8+ T cells more than the gamma delta T cells or the TCR alpha beta+ CD4+CD8- population. These findings suggest that alpha E beta 7 is involved in the expansion/recruitment of TCR alpha beta+ CD8+ IEL following microbial colonization. Integrin alpha E-deficient mice will provide an important tool for studying the role of alpha E beta 7 and of alpha E beta 7-expressing mucosal T lymphocytes in vivo.
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| 2. |
- Weston, M. D., et al.
(författare)
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Myosin VIIA mutation screening in 189 Usher syndrome type 1 patients
- 1996
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Ingår i: American Journal of Human Genetics. - 0002-9297 .- 1537-6605. ; 59:5, s. 1074-1083
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Tidskriftsartikel (refereegranskat)abstract
- Usher syndrome type 1b (USH1B) is an autosomal recessive disorder characterized by congenital profound hearing loss, vestibular abnormalities, and retinitis pigmentosa. The disorder has recently been shown to be caused by mutations in the myosin VIIa gene (MYO7A) located on 11q14. In the current study, a panel of 189 genetically independent Usher I cases were screened for the presence of mutations in the N-terminal coding portion of the motor domain of MYO7A by heteroduplex analysis of 14 exons. Twenty-three mutations were found segregating with the disease in 20 families. Of the 23 mutations, 13 were unique, and 2 of the 13 unique mutations (Arg212His and Arg212Cys) accounted for the greatest percentage of observed mutant alleles (8/23, 31%). Six of the 13 mutations caused premature stop codons, 6 caused changes in the amino acid sequence of the myosin VIIa protein, and 1 resulted in a splicing defect. Three patients were homozygotes or compound heterozygotes for mutant alleles; these three cases were Tyr333Stop/Tyr333Stop, Arg212His-Arg302His/Arg212His-Arg302His, and IVS13nt-8c-->g/Glu450Gln. All the other USH1B mutations observed were simple heterozygotes, and it is presumed that the mutation on the other allele is present in the unscreened regions of the gene. None of the mutations reported here were observed in 96 unrelated control samples, although several polymorphisms were detected. These results add three patients to single case reported previously where mutations have been found in both alleles and raises the total number of unique mutations in MYO7A to 16.
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| 3. |
- Zabel, B A, et al.
(författare)
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Human G protein-coupled receptor GPR-9-6/CC chemokine receptor 9 is selectively expressed on intestinal homing T lymphocytes, mucosal lymphocytes, and thymocytes and is required for thymus-expressed chemokine-mediated chemotaxis
- 1999
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Ingår i: Journal of Experimental Medicine. - 1540-9538. ; 190:9, s. 1241-1256
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Tidskriftsartikel (refereegranskat)abstract
- TECK (thymus-expressed chemokine), a recently described CC chemokine expressed in thymus and small intestine, was found to mediate chemotaxis of human G protein-coupled receptor GPR-9-6/L1.2 transfectants. This activity was blocked by anti-GPR-9-6 monoclonal antibody (mAb) 3C3. GPR-9-6 is expressed on a subset of memory alpha4beta7(high) intestinal trafficking CD4 and CD8 lymphocytes. In addition, all intestinal lamina propria and intraepithelial lymphocytes express GPR-9-6. In contrast, GPR-9-6 is not displayed on cutaneous lymphocyte antigen-positive (CLA(+)) memory CD4 and CD8 lymphocytes, which traffic to skin inflammatory sites, or on other systemic alpha4beta7(-)CLA(-) memory CD4/CD8 lymphocytes. The majority of thymocytes also express GPR-9-6, but natural killer cells, monocytes, eosinophils, basophils, and neutrophils are GPR-9-6 negative. Transcripts of GPR-9-6 and TECK are present in both small intestine and thymus. Importantly, the expression profile of GPR-9-6 correlates with migration to TECK of blood T lymphocytes and thymocytes. As migration of these cells is blocked by anti-GPR-9-6 mAb 3C3, we conclude that GPR-9-6 is the principal chemokine receptor for TECK. In agreement with the nomenclature rules for chemokine receptors, we propose the designation CCR-9 for GPR-9-6. The selective expression of TECK and GPR-9-6 in thymus and small intestine implies a dual role for GPR-9-6/CCR-9, both in T cell development and the mucosal immune response.
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| 4. |
- Boström, Ragnhild, et al.
(författare)
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Mörbylånga kyrkor
- 1997
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Bok (övrigt vetenskapligt/konstnärligt)
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| 5. |
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| 6. |
- Crispin, Xavier, et al.
(författare)
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Chemisorption of acrylonitrile on the Cu(100) surface: A local density functional study
- 1999
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Ingår i: Journal of Chemical Physics. - : American Institute of Physics (AIP). - 0021-9606 .- 1089-7690. ; 111:7, s. 3237-3251
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Tidskriftsartikel (refereegranskat)abstract
- The possibility of chemically grafting polyacrylonitrile onto transition metal electrodes via electropolymerization leads to promising applications in the fields of corrosion protection or metal surface functionalization. The initial step of the electrografting mechanism is the adsorption of the acrylonitrile monomer on the metal surface from solution. Here, we investigate theoretically this adsorption process on the copper (100) surface; Density Functional Theory is used in the Local Spin Density approximation to describe the electronic and structural properties of acrylonitrile adsorbed on copper clusters. The chemisorption of acrylonitrile on the copper surface is confirmed experimentally via X-Ray Photoelectron Spectroscopy. The thermodynamic characteristics of the adsorption process are also studied via statistical mechanics. Finally, determining the influence of the copper cluster size on the adsorption of acrylonitrile allows to extrapolate the properties of the acrylonitrile/Cu(100) surface from those of acrylonitrile/copper clusters. (C) 1999 American Institute of Physics. [S0021-9606(99)70231-X].
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| 7. |
- Eudy, James D., et al.
(författare)
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Mutation of a gene encoding a protein with extracellular matrix motifs in Usher syndrome type IIa
- 1998
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 280:5370, s. 1753-1757
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Tidskriftsartikel (refereegranskat)abstract
- Usher syndrome type IIa (OMIM 276901), an autosomal recessive disorder characterized by moderate to severe sensorineural hearing loss and progressive retinitis pigmentosa, maps to the long arm of human chromosome 1q41 between markers AFM268ZD1 and AFM144XF2. Three biologically important mutations in Usher syndrome type IIa patients were identified in a gene (USH2A) isolated from this critical region. The USH2A gene encodes a protein with a predicted size of 171.5 kilodaltons that has laminin epidermal growth factor and fibronectin type III motifs; these motifs are most commonly observed in proteins comprising components of the basal lamina and extracellular matrixes and in cell adhesion molecules.
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| 8. |
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| 9. |
- Luepker, Russell V., et al.
(författare)
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Community education for cardiovascular disease prevention. Morbidity and mortality results from the Minnesota Heart Health Program
- 1996
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Ingår i: American Journal of Epidemiology. - 0002-9262. ; 144:4, s. 351-362
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Tidskriftsartikel (refereegranskat)abstract
- The Minnesota Heart Health Program was a community trial of cardiovascular disease prevention methods that was conducted from 1980 to 1990 in three Upper Midwestern communities with three matched comparison communities. A 5- to 6-year intervention program used community-wide and individual health education in an attempt to decrease population risk. A major hypothesis was that the incidence of validated fatal and nonfatal coronary heart disease and stroke in 30- to 74-year-old men and women would decline differentially in the education communities after the health promotion program was introduced. This hypothesis was investigated using mixed-model regression. The intervention effect was modeled as a series of annual departures from a linear secular trend after a 2-year lag from the start of the intervention program. In the education communities, 2,394 cases of coronary heart disease and 818 cases of stroke occurred, with 2,526 and 739 cases, respectively, being seen in the comparison communities. The overall decline in coronary heart disease incidence was 1.8 percent per year in men (p = 0.03) and 3.6 percent per year in women (p = 0.007). For stroke, there were no significant secular trends. The authors recently published findings showing minimal effects of sustained intervention on risk factor levels. In the current report, there was no evidence of a significant intervention effect on morbidity or mortality, either for coronary heart disease or for stroke.
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| 10. |
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