beplay苹果手机能用吗

发现奖计划

Program Goals

The main objective of the Discovery Award Program is to bring talented and accomplished basic and physician scientists together in an interdisciplinary manner promoting the generation of research that identifies viable targets for the treatment of various forms of lung disease. Teams of basic and physician scientists will propose research based on existing preliminary results that show promise. The competitive selection of projects will be conducted by an advisory board consisting of qualified outside and institutional scientists. Projects will be selected based upon the expertise of the team and the quality of preliminary data presented. The most feasible and highest quality proposals will be funded with the major goal of pushing forward translational research on pulmonary diseases. These proposals should be viewed as Pre-RO1 awards provided to help the investigative team generate findings that will lead to eventual high level extramural grant submissions. Success of this program will be measured by the quality of data generated and the securing of additional public or private funding to continue the research.

Measures of Success

质量数据生成
Publication in top journals
Successful grant applications
Patent filings

监督和评估

外部顾问委员会
中心领导
年度科学务虚会评估进度和展示结果

发现奖得主：研究摘要beplay苹果手机能用吗

  • Development of Patient-Specific Therapeutic Approaches for Cystic Fibrosis

    PI：布莱恩·戴维斯（Brian R. Davis），博士，布朗基金会分子医学研究所
    Co-Pi：WA Xian，博士，棕色基金会分子医学研究所
    Co-I：Ricardo Mosquera，医学博士，Uthealth儿科部 - McGovern医学院

    囊性纤维化(CF)基因遗传疾病引起的DNA mutations in a specific gene named CFTR, results in recurrent infections and inflammation in the lung. This project is focused on performing a detailed characterization of a specific population of cells in the lungs of CF patients, namely the stem cells. What we wish to determine is whether the stem cells, which are responsible for the ongoing maintenance and regeneration of the lung airway, are adversely affected — either as a direct consequence of the CFTR mutation or as an indirect consequence of continuous exposure to inflammation and injury. In addition, we wish to assess whether precise genetic correction of the CFTR mutation in these cells restores the ability of CF stem cells to give rise to functional lung tissue. If this latter possibility is demonstrated, then this will potentially lead to new therapeutic approaches in which CF patient-specific lung stem cells are corrected—either directly in the CF patient or first corrected in a clinical laboratory and then transplanted back into the lungs of the same patient. The hope is that that the presence of genetically corrected lung stem cells would result in restoration of healthy lung tissue.

  • MicroRNA and mRNA Epigenetics as Post-transcriptional Regulators of Allergic Airway Inflammation

    PI：Ann-bin Shyu，uthealth生物化学与分子生物学系博士 - 麦戈文医学院
    CO-I：杰弗里·T·张（Jeffrey T.
    Co-I: Chyi-Ying A. Chen, PhD, Department of Biochemistry and Molecular Biology, UTHealth – McGovern Medical School
    共同:琥珀陈德良,医学博士,Otorhinolaryngology, UTHealth – McGovern Medical School

    呼吸上皮细胞，在呼吸道内衬里，可以感觉到吸入过敏原，污染物，蛋白酶和微生物，并通过细胞表面受体反应，从而导致胁迫和炎症反应的激活。介导这些响应的一种关键信号通路称为NF-κB信号传导。我们最近通过微核酸揭示了一种新型的细胞调节，称为microRNA 26（miR-26）。这种小的RNA通过直接下调NF-κB信号传导来抑制人支气管上皮细胞的炎症反应。我们的第一个研究计划beplay苹果手机能用吗是研究miR-26对气道上皮细胞中炎症反应和组织重塑过程中NF-κB信号通路的影响。我们的研究计划的第二个方面是研究气道炎症与信使RNbeplay苹果手机能用吗A（mRNA）的概念新颖且在很大程度上未开发的关系。人mRNA包含许多甲基化腺苷（M6A）残基，这代表了先前未知的基因表达调节层。我们将测试M6A修饰动力学改变的患者是否会表现出与气道炎症和组织重塑有关的异常基因表达。总体而言，我们的研究具有巨大的潜力，可以洞悉新型治疗方法，以减轻与慢性气道疾病有关的气道炎症，例如慢性鼻窦炎，肺纤维化和哮喘。

  • CFIm25 Links Alternative Polyadenylation with Pulmonary Hypertension and Right Ventricle Hypertrophy

    pi：Harry Karmouty-Quintana博士，UTHEADY生物化学和分子生物学系助理教授 - 麦戈文医学院
    Co-I：Bindu Akkanti，医学博士
    Co-I：Leng Han博士，UTHEADY生物化学和分子生物学系助理教授 - 麦戈文医学院
    Co-I: Keith Adam Youker, Ph.D., Assistant Research Professor, Houston Methodist Hospital Research Institute

    The appearance of high blood pressure in the lungs, termed pulmonary hypertension (PH), is the one of the deadliest complication that affects many patients already suffering from chronic lung diseases such as chronic obstructive pulmonary disease (COPD) or idiopathic pulmonary fibrosis (IPF). Sadly, the mechanisms that lead to this deadly complication are not entirely understood and as a result there are no treatment options other than lung transplantation for patients with PH. PH is fatal because the wall of the arteries that carry blood in the lung thicken and eventually block the flow of blood, resulting in increased blood pressure in the lungs. This higher blood pressure means that the heart has to work harder to pump blood to the lungs causing the walls of the heart to also thicken and eventually fail; causing many patients die from right-heart failure. A new discovery of my lab is that a protein called CFIm25 appears to control the level of many molecules that regulate wall thickness. We believe that when CFIm25 levels are reduced more molecules that make the wall thicker are produced. As a result our research efforts focus on preventing CFIm25 to go down in disease, as a new way to treat both PH and prevent heart attacks.

  • Induced Pluripotent Stem (iPS) Cell-Derived Lung Progenitor Cells as Therapy for Lung Injury and Surfactant Protein Disorders

    pi：Rick A. Wetsel, PhD, Brown Foundation Institute of Molecular Medicine
    Co-I: Matthew T. Harting, MD, Pediatric Surgery, UTHealth – McGovern Medical School
    Co-I: Brian R. Davis, PhD, Brown Foundation Institute of Molecular Medicine
    Co-I: Dachun Wang, MD, Brown Foundation Institute of Molecular Medicine

    Respiratory diseases are a leading cause of mortality and morbidity worldwide, and are a major cause of death in babies less than 1 year of age. In the United States alone, 35 million Americans suffer with lung disease, accounting for approximately 400,000 deaths per year. Current treatments for lung disease at best provide symptomatic relief but offer no prospect of cure or disease reversal. Lung transplantation is the often the only viable option. Our research team is focused on developing novel cell based therapeutics to treat patients suffering from lung injury and from infants affected by genetically inherited diseases affecting normal lung function. Our overall approach will test the use of patient specific induced pluripotent stem cells (iPSCs). These iPSCs are derived from a small skin biopsy and can be differentiated into pure populations of lung cells that can be transplanted into the lungs of patients for repair of damaged pulmonary tissue caused by acute or chronic lung diseases, such as COPD. After genetic correction, they also can be used for gene therapy for patients with genetic disorders affecting normal lung function. Since these transplanted cells are derived from the patient undergoing therapy, there will be no graft rejection issues—thereby avoiding a major complication of lung transplantation.

  • 代谢组分析揭示了肺动脉高压的新见解，敏感的生物标志物和创新方法

    PI：Yang Xia，医学博士，博士，UTHealth生物化学和分子生物学系教授 - McGovern医学院
    CO-I：Harinder S. Juneja，医学博士，UTHealth内科学系教授兼主任 - McGovern医学院
    Co-I: Aravind Yadav, MD, Assistant Professor, Pulmonary Medicine, Department of Pediatrics, UTHealth – McGovern Medical School
    CO-I：Harry Karmouty-Quintana博士，UTHEADY生物化学与分子生物学系助理教授 - McGovern医学院

    Pulmonary hypertension (PH)由于缺乏早期症状检查和有效的疗法，是一种危险状况，具有高发病率和死亡率。氧气不足（缺氧）是促进pH值的主要初始触发因素之一。镰状细胞疾病（SCD）是一种毁灭性的遗传溶血疾病，不断面临缺氧，并且与pH有关。拟议的研究基于我们公正的高beplay苹果手机能用吗通量代谢组筛查的结果，表明adenosine (Ado),sphingosine 1 phosphate (S1P)和2,3-双磷酸甘油（2,3-bpg）are metabolites elevated in the blood of humans and mice with SCD and in healthy individuals adapting to high altitude hypoxia. Further studies showed that these metabolites collaboratively work together facilitating O2release from hemoglobin to prevent hypoxemia and progression to PH. However, this process is detrimental for SCD patients by promoting O2release, sickling and development of PH. Taken together, our innovative metabolomic screening revealed multiple common hypoxic responsive metabolites and opens up novel promising therapeutic approaches for the treatment of PH. Thus, the major goal of our proposed research is to determine whether our newly identified hypoxia-responsive circulating and erythrocyte metabolites are sensitive biomarkers for early prediction of PH in SCD patients and important therapeutic targets in pathogenesis of PH in non-SCD settings.