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HHS Recovery Act Recipient Reporting Readiness Tool

Step 4. Review and Copy the Grant Awards Data

TAGGS provides some – but not all – of the data needed for the Recipient Report. Recipients are responsible for directly collecting and reporting all required data to FederalReporting.gov. Data that HHS does not currently collect are highlighted in yellow. Do not copy this highlighted information. Please enter the appropriate data for your organization in these required fields. For assistance with entering these data please contact FederalReporting.gov.

You may capture the data HHS does provide by copying data from this screen and pasting it into the reporting format of your choice, such as the Excel spreadsheet template, the XML template, or by logging into the online form. For assistance with copying and pasting these data please email our help desk at Readiness Help


Prime Recipient Report

Award Detail for: HEME OXYGENASE-1/CARBON MONOXIDE IN LUNG VASCULAR INJURY
Recipient Name:BRIGHAM & WOMEN`S HOSPITAL
DUNS Number: 030811269
10 VINING STREET
BOSTON, MA 02115-6114

Reporting Information

Award Type*: Grant

Award Number*: 5R01HL060234-11

Final Report*: Recipient responsible for this data

Award Recipient Information

Recipient DUNS Number*: 030811269

Recipient Account Number: Recipient responsible for this data

Recipient Congressional District*: 8

Award Information

Funding Agency Code*: 7529

Awarding Agency Code*:7529

Award Date*: 08-26-2010

Amount of Award*: $ 549,013

Program Source (TAS)*: 750871

CFDA Number*: 93.701

Sub Account Number for Program Source (TAS)*: Recipient responsible for this data

Total Number of Sub Awards to Individuals*: Recipient responsible for this data

Total Amount of Sub Awards to Individuals*: Recipient responsible for this data

Total Number of Payments to Vendors less than $25,000/award*: Recipient responsible for this data

Total Amount of Payments to Vendors less than $25,000/award*: Recipient responsible for this data

Total Number of Sub Awards less than $25,000/award*: Recipient responsible for this data

Total Amount of Sub Awards less than $25,000/award*: Recipient responsible for this data

Award Description* DESCRIPTION (provided by applicant): Autophagy is manifested by degradation of cytoplasmic organelles via a lysosomal pathway, involving rearrangement of intracellular membranes to sequester damaged proteins or organelles within formed membrane vesicles, or autophagosomes. Autophagosomes then fuse with lysosomes where the content is degraded and recycled to become an endogenous source of energy and nutrients. Autophagy has been described in the yeast system for decades; however, we have witnessed the explosion of this field in the mammalian system in recent years. Little is known on the role of autophagy in lung disease, and the role of autophagy in pulmonary hypertension (PH) has not been rigorously explored. We have obtained intriguing preliminary data that human PH and experimental models of PH exhibit marked induction of autophagy. Our laboratory and others have started to unravel the mechanisms and signaling pathways by which carbon monoxide (CO) imparts protective effects in various models of cellular and tissue injury. Importantly, our recent study illustrates that CO can protect against hypoxia or MCT-induced PH in mice and rats, respectively, even after the development of PH suggesting that CO may affect vascular remodeling processes including vascular cell proliferation and apoptosis. Interestingly, we have obtained preliminary data that CO regulates the autophagic process both in cultured vascular cells and in the lung. We hypothesize that autophagy represents an adaptive stress response to protect against PH, and that CO prevents PH via regulating autophagy. Furthermore, we hypothesize that autophagy regulated inflammasomes can potentially serve as diagnostic biomarker in predicting severity of PH. We will test the hypothesis by addressing the following aims: Specific Aim #1: To determine the mechanism by which CO-induced autophagy functions to provide cytoprotection in experimental PH Specific Aim 2: To determine the mechanism by which CO dampens the inflammasome pathway in experimental PH Specific Aim #3: To determine whether CO inhibits inflammasome and its regulated cytokines in human PH PUBLIC HEALTH RELEVANCE: Pulmonary arterial hypertension (PAH) is a dreadful disease with no effective therapies. An improved understanding of the pathogenesis of PAH will potentially provide new therapeutic targets. We hope to identify new molecules involved in the autophagy pathway which potentially could represent novel targets for therapy in PAH in the future.

Project Information

Project Name or Project/Program Title*: HEME OXYGENASE-1/CARBON MONOXIDE IN LUNG VASCULAR INJURY

Project Status*: Recipient responsible for this data

Total Federal Amount of ARRA Funds Received/Invoiced*: Recipient responsible for this data

Number of Jobs*: Recipient responsible for this data

Description of Jobs Created*: Recipient responsible for this data

Quarterly Activities/Project Description*: Recipient responsible for this data

Activity Code (NAICS or NTEE-NPC)*: Recipient responsible for this data

Total Federal Amount of ARRA Expenditure* (Enter the cumulative total amount of Recovery Funds received that were expended to projects or activities. Refer to the Data Model for details on how to calculate this amount.): Recipient responsible for this data

Total Federal ARRA Infrastructure Expenditure Recipient responsible for this data

Infrastructure Contact Name: Recipient responsible for this data

Infrastructure Contact Email: Recipient responsible for this data

Infrastructure Contact Phone: Recipient responsible for this data

Infrastructure Contact Phone Ext: Recipient responsible for this data

Infrastructure Contact Street Address 1: 10 VINING STREET

Infrastructure Contact Street Address 2: Not Available

Infrastructure Contact Street Address 3: Recipient responsible for this data

Infrastructure City: BOSTON

Infrastructure State: MA

Infrastructure ZIP Code+4: 02115-6114

Infrastructure Purpose and Rationale (If applicable, enter an explanation about how the infrastructure investment will contribute to one or more purposes of the Recovery Act. Refer to the Data Model for details on what to report. 4000 characters or less.): Recipient responsible for this data

Primary Place of Performance

Street Address 1: 20 SHATTUCK ST.

Street Address 2: BOSTON

City*: BOSTON

State*: MA

ZIP Code+4*: 021156110

Congressional District*: 8

Country*: US

Recipient Highly Compensated Officers

Prime Recipient Indication of Reporting Applicability*: Recipient responsible for this data

  1. Officer Name and Compensation: Recipient responsible for this data
  2. Officer Name and Compensation: Recipient responsible for this data
  3. Officer Name and Compensation: Recipient responsible for this data
  4. Officer Name and Compensation: Recipient responsible for this data
  5. Officer Name and Compensation: Recipient responsible for this data

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Use in the Recipient Report

The information provided by this tool is baseline data that the Recipient should include in the Recipient Report that must be submitted to FederalReporting.gov beginning October 1, 2009. The data from this tool can be cut and pasted directly into the Recipient Report.