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EXTRAMURAL RESEARCH FACILITIES IMPROVEMENT

校外研究设施的改善

基本信息

批准号：
6829193
负责人：
Richard Banfield Marchase
金额：
$ 360万
依托单位：
UNIVERSITY OF ALABAMA AT BIRMINGHAM
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-09-30 至 2009-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/6829193
关键词：
EXTRAMURAL RESEARCH FACILITIES IMPROVEMENT

项目摘要

DESCRIPTION (provided by applicant): This proposal requests $4 million of NCRR funding to assist in the completion of 45,996 gsf of research and research support space. When matched with $5.746 million from the University of Alabama at Birmingham, this award will fit out two of twelve levels (Levels 6 and 11) in the Richard C. and Annette N. Shelby Interdisciplinary Biomedical Research Building as Phase 2 of construction. The first aim is to finish and equip 22,998 gsf of space for the Mucosal Immunology Program on Level 6. This space will house an interdisciplinary research group with the relocation of six current investigators from three departments and two future recruits. The long-term objective of this group is to advance the understanding of mucosal immunology in human diseases, with a particular emphasis on inflammatory bowel disease. The second aim is to finish and equip 22,998 gsf of space for the Interdisciplinary Neurosciences Program. The goal of this unit is to advance the understanding of learning and memory, behavior, cognition, and brain cancers. Six investigators from four departments will occupy Level 11, and space will be provided for two recruits. This project will also provide space for a shared imaging facility. Space liberated by the relocation of these investigators will provide local relief for space-limited departments and an opportunity to modernize older space to create additional, efficient worksites for research. This project will thus provide state-of-the-art facilities to support federally funded research in areas emerging as high priorities for the University and the nation.

描述（由申请人提供）：

项目成果

期刊论文数量（20）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

SOCS3 Deficiency in Myeloid Cells Promotes Tumor Development: Involvement of STAT3 Activation and Myeloid-Derived Suppressor Cells.

DOI：
10.1158/2326-6066.cir-15-0004
发表时间：
2015-07
期刊：
Cancer immunology research
影响因子：
10.1
作者：
Yu H;Liu Y;McFarland BC;Deshane JS;Hurst DR;Ponnazhagan S;Benveniste EN;Qin H
通讯作者：
Qin H

Adaptive immunity in the host-microbiota dialog.

DOI：
10.1038/mi.2010.60
发表时间：
2011-01
期刊：
Mucosal immunology
影响因子：
8
作者：
Feng T;Elson CO
通讯作者：
Elson CO

Autoimmune-mediated reduction of high-density lipoprotein-cholesterol and paraoxonase 1 activity in systemic lupus erythematosus-prone gld mice.

DOI：
10.1002/art.27764
发表时间：
2011-01
期刊：
ARTHRITIS AND RHEUMATISM
影响因子：
0
作者：
Srivastava, Roshni;Yu, Shaohua;Parks, Brian W.;Black, Leland L.;Kabarowski, Janusz H.
通讯作者：
Kabarowski, Janusz H.

Th17 cells induce colitis and promote Th1 cell responses through IL-17 induction of innate IL-12 and IL-23 production.