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Institution

National Jewish Health

HealthcareDenver, Colorado, United States
About: National Jewish Health is a healthcare organization based out in Denver, Colorado, United States. It is known for research contribution in the topics: T cell & Asthma. The organization has 883 authors who have published 833 publications receiving 79201 citations. The organization is also known as: National Jewish Medical and Research Center.
Topics: T cell, Asthma, Population, Lung, Antigen


Papers
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Journal ArticleDOI
01 Jan 2013
TL;DR: This review focuses specifically on the differentiation of innate effector cells, particularly the role of cytokine signaling in the differentiated cells of Bone marrow progenitors.
Abstract: Innate effector cells, including innate effector cells of myeloid and lymphoid lineages, are crucial components of various types of immune responses. Bone marrow progenitors differentiate into many subsets of innate effector cells after receiving instructional signals often provided by cytokines. Signal transducer and activator of transcription (STATs) have been shown to be essential in the differentiation of various types of innate effector cells. In this review, we focus specifically on the differentiation of innate effector cells, particularly the role of cytokine signaling in the differentiation of innate effector cells.

14 citations

Journal Article
TL;DR: These secreted immunoregulatory molecules have the Ag/MHC specificity of the T cells producing them and are structurally and serologically related to the TCR-alpha/beta, and suggest that for some hapten-specific/class I MHC-restricted TCR, the alpha-chain may have avidity for the haptens and the beta- chain may dictate the MHC restriction element recognized by the receptor.
Abstract: To examine in greater detail the relationship between DNP-specific/class I MHC-restricted suppressor molecules (SSF) that inhibit contact sensitivity to 2,4-dinitrofluorobenzene and the receptors on the T cells that produce them, we have generated two T cell hybridomas that can be induced to produce and secrete these molecules. In order to become activated to produce SSF, the Ts 15.15 and 15.31 cells required recognition of complexes of DNP/Dd on presenting cells. The suppressor molecules produced by each of the Ts hybrids had the same specificity, recognizing DNP/Dd on cells in the immune lymph node cell target population. The activation of the Ts hybrids was blocked when the cells were treated with the anti-V beta 8 antibody F23.1 before coculture with the DNP-presenting cells. Reduction of the 15.15 and 15.31 SSF followed by affinity chromatography on DNP-bovine-gamma-globulin-Sepharose beads indicated that these molecules are dimers and that one of the chains (Ag-binding(AgB] binds to cellfree DNP and one (non-Ag-binding (NAgB) chain) does not. The AgB chain was found to express an epitope bound by a mAb specific for a TCR alpha-chain-constant region determinant. Alternatively, the NAgB chain expressed an epitope bound by the anti-V beta 8 mAb F23.1. Active hybrid suppressor molecules were generated by combining the NAgB chain from a DNP-specific/H-2Kd-restricted SSF (produced by Ts hybridoma 3-10) with the AgB chain from Ts 15.31 and by combining the NAgB chain from Ts cell 15.15 with the 3-10 AgB chain. In each case, the class I MHC element (i.e., Kd or Dd) restricting the activity of these hybrid SSF correlated with the source of the V beta 8+, NAgB chain. Thus, these secreted immunoregulatory molecules have the Ag/MHC specificity of the T cells producing them and are structurally and serologically related to the TCR-alpha/beta. The results further suggest that for some hapten-specific/class I MHC-restricted TCR, the alpha-chain may have avidity for the hapten and the beta-chain may dictate the MHC restriction element (K or D) recognized by the receptor.

14 citations

Patent
14 Feb 2008
TL;DR: In this article, the authors proposed methods of inhibiting biofilm formation or reducing biofilms in a subject or on a device or surface by administering a charged compound such as a polyamino acid to a subject, device, or surface.
Abstract: The invention relates to methods of inhibiting biofilm formation or reducing biofilms in a subject or on a device or surface by administering a charged compound such as a polyamino acid to a subject, device or surface. The invention also relates to compositions for inhibiting biofilm formation or reducing biofilms.

14 citations

Patent
09 Mar 2011
TL;DR: In this paper, an airway stent with an integral suture anchor is used to prevent migration of the stent within the airway and the anchor is incorporated by percutaneous placement of a suture through the neck.
Abstract: An airway stent with an integral suture anchor is used to prevent migration of the stent within the airway. The suture anchor is incorporated by percutaneous placement of a suture through the neck and into the stent. The distal end of the suture includes an anchor element to secure the suture to the stent. The opposite end of the suture is tensioned and held in place by a suture clamp and a pledget routed over the stent and placed against the neck. Airway stents such as tracheal stents are effective at maintaining airway patency however; a common complication is stent migration. The integral suture anchor provides a reliable, economical, and non-intrusive solution to stent migration.

14 citations

Posted ContentDOI
28 Jun 2017-bioRxiv
TL;DR: The findings indicate that both population specific and shared genetic variation contributes to differences in BDR in minority children with asthma, and that the genetic underpinnings of BDR may differ between racial/ethnic groups.
Abstract: Background: Short-acting B2-adrenergic receptor agonists (SABAs) are the most commonly prescribed asthma medications worldwide. Response to SABAs is measured as bronchodilator drug response (BDR), which varies among racial/ethnic groups in the U.S. However, the genetic variation that contributes to BDR is largely undefined in African Americans with asthma. Objective: To identify genetic variants that may contribute to differences in BDR in African Americans with asthma. Methods: We performed a genome-wide association study of BDR in 949 African American children with asthma, genotyped with the Axiom World Array 4 (Affymetrix, Santa Clara, CA) followed by imputation using 1000 Genomes phase 3 genotypes. We used linear regression models adjusting for age, sex, body mass index and genetic ancestry to test for an association between BDR and genotype at single nucleotide polymorphisms (SNPs). To increase power and distinguish between shared vs. population-specific associations with BDR in children with asthma, we performed a meta-analysis across 949 African Americans and 1,830 Latinos (Total=2,779). Lastly, we performed genome-wide admixture mapping to identify regions whereby local African or European ancestry is associated with BDR in African Americans. Two additional populations of 416 Latinos and 1,325 African Americans were used to replicate significant associations. Results: We identified a population-specific association with an intergenic SNP on chromosome 9q21 that was significantly associated with BDR (rs73650726, p=7.69x10-9). A trans-ethnic meta-analysis across African Americans and Latinos identified three additional SNPs within the intron of PRKG1 that were significantly associated with BDR (rs7903366, rs7070958, and rs7081864, p≤5x10-8). Conclusions: Our findings indicate that both population specific and shared genetic variation contributes to differences in BDR in minority children with asthma, and that the genetic underpinnings of BDR may differ between racial/ethnic groups.

14 citations


Authors

Showing all 901 results

NameH-indexPapersCitations
Thomas V. Colby12650160130
John W. Kappler12246457541
Donald Y.M. Leung12161450873
Philippa Marrack12041654345
Jeffrey M. Drazen11769352493
Peter M. Henson11236954246
David A. Schwartz11095853533
David A. Lynch10871459678
Norman R. Pace10129750252
Kevin K. Brown10038747219
Stanley J. Szefler9955437481
Erwin W. Gelfand9967536059
James D. Crapo9847337510
Yang Xin Fu9739033526
Stephen D. Miller9443330499
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20233
202214
202113
202017
201917
201841