IMMUNOPATHOGENESIS OF CHRONIC GRAFT REJECTION
Release Date: May 30, 2000
RFA: AI-00-013
National Institute of Allergy and Infectious Diseases
(http://www.niaid.nih.gov)
National Heart, Lung, and Blood Institute
(http://www.nhlbi.nih.gov)
Letter of Intent Receipt Date: September 1, 2000
Application Receipt Date: October 23, 2000
APPLICATIONS IN RESPONSE TO THIS REQUEST FOR APPLCATIONS (RFA) MUST BE
PREPARED USING A MULTI-PROJECT GRANT APPLICATION FORMAT; SPECIFIC
INSTRUCTIONS FOR COMPLETING THE APPLICATIONS ARE IN AN NIAID BROCHURE
ENTITLED INSTRUCTIONS FOR APPLICATIONS FOR MULTI-PROJECT AWARDS.
PURPOSE
The Division of Allergy, Immunology and Transplantation (DAIT) of the
National Institute of Allergy and Infectious Diseases (NIAID), and the
Divisions of Heart and Vascular Diseases (DHVD) and Lung Diseases (DLD)
of the National Heart, Lung, and Blood Institute (NHBLI) invite
applications for program projects in the immunopathogenesis of chronic
graft rejection. Programs should be designed to: elucidate the cellular
and molecular mechanisms involved in chronic allograft rejection;
implement new, or improve upon existing therapeutic approaches to
enhance graft survival; or, develop new prognostic tools which will aid
in diagnosing the outcome of allograft transplant.
HEALTHY PEOPLE 2010
The Public Health Service (PHS) is committed to achieving the health
promotion and disease prevention objectives of "Healthy People 2010," a
PHS-led national activity for setting priority areas. This Request for
Applications (RFA), Immunopathogenesis of Chronic Graft Rejection , is
related to: Heart Disease and Stroke, Respiratory Diseases, Diabetes and
Chronic Disabling Diseases. Potential applicants may obtain a copy of
"Healthy People 2010" at http://www.health.gov/healthypeople/
ELIGIBILITY REQUIREMENTS
Applications may be submitted by domestic, for-profit and non-profit
organizations, public and private, such as universities, colleges,
hospitals, laboratories, units of State and local governments, and
eligible agencies of the Federal government. Multi-institutional
applications are acceptable and encouraged. Foreign institutions are
not eligible to apply. Racial/ethnic minority individuals, women, and
persons with disabilities are encouraged to apply as Principal
Investigators.
MECHANISM OF SUPPORT
The mechanism of support will be the program project (P01) grant. This
type of award supports broadly based multidisciplinary research programs
that have a well-defined central research focus or objective. An
important feature of the program project is that the interrelationships
of the individual scientifically meritorious projects will result in a
greater contribution to the overall program goals than if each project
were pursued individually. Standard NIH policy requires P01 applications
to consist of a minimum of three interrelated individual research
projects that contribute to the program objective. This type of award
also can provide support for certain common resources termed cores. Such
resources should be utilized by two or more projects within the award.
Responsibility for the planning, direction, and execution of the
proposed project will be solely that of the applicant. The total
project period may not exceed 5 years. The anticipated award date is
July 1, 2001.
FUNDS AVAILABLE
The estimated total funds [direct & facilities + administration (F&A)]
available for the first year of support for this RFA will be $5 million.
In fiscal year 2001, the NIAID and the NHLBI plan to make approximately
4 awards related to this RFA. This level of support is dependent on the
receipt of a sufficient number of applications of high scientific merit.
Applications in excess of $1,250,000 in total (direct and F&A) costs in
the first year will be returned as non-responsive. Because the nature
and scope of the research proposed may vary, it is anticipated that the
size of each award will also vary.
The usual NIH policies governing grants administration and management
will apply. Although this program is provided for in the financial
plans of the NIAID and the NHBLI, awards pursuant to this RFA are
contingent upon the availability of funds for this purpose. Funding
beyond the first and subsequent years of the grant will be contingent
upon satisfactory progress during the preceding years and availability
of funds. At this time, the NIAID and NHLBI have not determined whether
or how this solicitation will be continued beyond the present RFA.
RESEARCH OBJECTIVES
Background
With the advent of modern immunosuppressive therapies, one-year post-
engraftment survival approaches 90% for some organs. However, long-term
graft survival still remains poor, with 25% to 65% of all grafts failing
within five years post-transplantation. While many of the pathological
mechanisms which cause acute rejection have been defined and are
effectively treated or prevented with standard immunosuppressive
therapies and modern HLA typing techniques, these therapies have not
significantly improved long-term clinical outcomes for many transplant
patients.
The complex, multistage processes that result in chronic rejection of
vascularized allografts are poorly understood. While the determination
of organ failure often relies on measurable physiological parameters,
the early stages of chronic rejection are difficult to diagnose.
Detection requires invasive procedures to obtain graft biopsies for
histological evaluation. Organs undergoing chronic rejection manifest
some common pathologic criteria such as: progressive vascular
obliteration; infiltration of immunocytes; interstitial and tubular
atrophy; graft arteriosclerosis; and a marked fibrotic response. The
cellular and molecular mechanisms underlying these histopathological
hallmarks remain obscure.
Research Objectives and Scope
Organ transplantation is the definitive therapy for most forms of end-
stage organ disease; however, chronic graft rejection, the deleterious
effects of global, life-long immunosuppressive therapy, and the shortage
of donor organs continue to limit its success. Chronic graft rejection
is the primary obstacle to long-term successful organ transplantation.
While the armamentarium of immunosuppressive agents is impressive and
the future prospect of tolerance induction to alleviate allograft
rejection holds considerable promise, little is known about the
pathologic mechanisms that effect chronic rejection. To better
integrate basic science and clinical medicine, this RFA seeks to focus
these disciplines on the pathogenesis of chronic graft rejection, the
processes which foreshadow rejection of allografts long-term, and the
development of diagnostic procedures which will aid in predicting the
prognosis of allograft transplants. To this end, this RFA will fund
research to: 1) elucidate the cellular and molecular events during the
induction and effector phases of chronic solid organ graft rejection; 2)
develop improved therapeutic approaches to enhance long-term graft
survival; and 3) develop better prognostic tests to define and predict
outcomes of allograft transplants.
Many cell-cell, cell-matrix, and intracellular pathways have been
implicated in the complex pathogenesis of chronic rejection. Recent
studies have focused on chemokine/growth factor-receptor intracellular
signaling pathways and on genes induced during the early onset of
rejection. These pathways and genes lend themselves as targets for
pharmacological and therapeutic intervention for both early diagnosis
and possible prevention of graft rejection. In addition, cell-cell
interaction between T cells, macrophages, and endothelial cells and
interactions of cells with the extracellular matrix have been implicated
in the onset and progression of chronic rejection. Thus, studies
focused on these and other relevant cellular and molecular pathways that
can serve as potential targets for intervention are of major interest.
Applications that capitalize on the strengths of collaboration between
physicians and scientists to maximize the potential for discovering
novel approaches relevant to transplantation for human diseases are
strongly encouraged. To foster the teamwork between basic scientists
and transplant clinicians, NIH is especially interested in program
projects that define the pathogenesis of chronic graft rejection in
humans. Areas of particular interest are: identification of the targets
recognized by the immune response in chronic rejection; definition of
the relative contributions of immunocytes to the process of chronic
rejection; studies of the response of targets cells (e.g. endothelial
cells, smooth muscle cells) to lymphocytes, cytokines and growth
factors; delineation of the molecular process(es) of chronic rejection,
including studies of cytokines, infiltrating cell types, and methods to
attenuate the actions of these cells and their products; development of
new therapeutic approaches and improvement of existing therapeutic
approaches for the treatment and/or prevention of chronic rejection.
Examples of relevant studies include, but are not limited to, the
following:
o Recent scientific findings have highlighted the involvement of T
cells, macrophages and their respective gene-products as causal for
chronic rejection. The interaction of these cells and their factors
with endothelial cells of the allograft may, in part, determine the
success of the match. Studies which further analyze the infiltrating
cellular components and their soluble mediators in in vivo human models
are encouraged.
o Cytokines are expressed in heart, kidney, lung, liver and skin
allografts following engraftment and during acute and chronic rejection.
While the majority of information concerning cytokine biology in
transplantation has come from animal models, little is known about the
role of cyokines in human allograft rejection. Cytokines and growth
factors may play important mechanistic roles in transplant rejection.
For example, IL-2, IL-6, IL-10, IL-1beta and TNF-alpha have been
implicated in the pathogenesis of arteriosclerosis, and IL-4, TGF-beta
may be involved in chronic allograft nephropathy. Alternatively, the
mediators might serve as diagnostic indicators for the analysis of
allograft rejection or graft dysfunction. A better understanding of the
role these factors play in chronic rejection may provide justification
for their use as interventional targets.
o Certain solid organ allografts display alterations in adhesion
molecules and extracellular matrix (ECM) components upon rejection.
However, it has yet to be determined whether these alterations are a
consequence or a cause of the pathogenesis of allograft rejection. If
causal in nature, could these molecules be used as targets or markers to
prevent chronic rejection? For example, in several organs, upregulation
of endothelial adhesion molecules in the vascularized allograft is
hypothesized to function in T cell recruitment to the graft site.
Analysis of T cell:endothelial cell interactions in vivo and new
information concerning the potential inhibition of such associations by
anti-ICAM-1, -VCAM, or E-selectin may lead to strategies to decrease
the risk of graft failure.
o Although the long-term rejection of allografts is sometimes
accompanied by the presence of infectious agents, the role of infections
in chronic rejection is poorly understood. Recent studies have
demonstrated a correlation between the presence of certain pathogens
(e.g., cytomegalovirus, Mycobacterium tuberculosis, and Microsporidia)
and a poor prognosis for long-term graft survival. Do these pathogens
ignite an immune response which is detrimental to the allograft? Is
the pathogenesis by which infectious agents induce chronic rejection
similar/identical to naturally occurring chronic rejection in the
absence of infection? Studies which aim to analyze the basic science
behind the pathogenesis, with the goal of clinical intervention, are
encouraged.
o With the aim of developing new approaches, or improving existing
approaches for the early detection of chronic organ rejection,
applicants are encouraged to create and test novel, non-invasive
diagnostic techniques for the early detection of chronic rejection.
Technical applications are sought which partner basic science principles
with clinical approaches. These techniques are particularly needed in
the post-transplantation period during which the early stages of chronic
rejection should be defined, characterized and potentially eliminated.
SPECIAL AREAS OF INTEREST
Heart
A number of cardiac diseases result in heart failure, for which cardiac
transplantation is the only successful treatment. The primary
indications for heart transplantation are coronary artery disease and
cardiomyopathy in adults, and congenital heart disease and
cardiomyopathy in children. Nearly 5 million people in the United
States have some form of heart failure and 20,000 to 40,000 of these
could benefit from a heart transplant. In patients who survive the first
year after transplant, chronic rejection is the major cause of death,
arising in 50-60 percent of patients surviving five years post-
transplant. Chronic rejection is manifested in the coronary arteries of
the transplanted heart as a concentric and diffuse intimal hyperplasia
such that distal portions of the coronary vessels occlude. There are
multiple theories as to the etiology of this disease, but few confirmed
risk factors have been defined. There are no proven therapies to prevent
or treat chronic rejection, and the only cure is re-transplantation.
Current methods of diagnosis include intravascular ultrasound and/or
coronary angioscopy.
Chronic rejection in heart transplantation is recognized by a variety of
names: cardiac allograft vasculopathy (CAV), cardiac transplant
atherosclerosis, and accelerated graft arteriosclerosis. The disease is
believed to be caused by the immune response of the recipient to the
donor organ and such responses have been shown to involve humoral and
cellular immune components, as well as, complement, cytokines and growth
factors. More studies are needed to: 1) define the risk factor(s) that
contribute to CAV and their mechanism(s) of action; 2) develop new or
improved methods to predict and diagnose early onset of CAV; and 3)
identify viable targets for prevention and/or treatment of chronic
rejection in the heart; and 4) determine the role, if any, of non-
antigen specific responses, such as ischemia/reperfusion injury or brain
death, in the development of chronic rejection.
Kidney
Kidney disease is a severe and costly public health problem that is
increasing in the U.S. An estimated 10.9 million Americans suffer from
kidney disease, including more than 360,000 who depend on dialysis or a
kidney transplant to survive. Kidney transplantation accounts for 57
percent of all transplant procedures. This statistic reflects the fact
that many common diseases, including diabetes and glomerulonephritis (a
heterogeneous group of immunological diseases), result in end-stage
renal disease (ESRD), for which transplantation is the preferred
treatment.
Unfortunately, chronic allograft dysfunction is the most common cause of
ESRD beyond the post-transplantation periods, accounting for 25-30
percent of patients awaiting re-transplantation. While the exact
mechanism(s) responsible for chronic renal allograft failure remain
obscure, it is generally agreed that both alloantigen-dependent and
alloantigen-independent factors influence chronic allograft nephropathy.
These immune-mediated attacks often result in chronic allograft
nephropathy (CAN) and are characterized by obliterative vasculopathy,
glomerulosclerosis, and interstitial fibrosis. One of the major
hypotheses for the etiology of CAN argues that destruction of the donor
tissue arises due to a response from the recipient's allo-immune
response to nonself antigens. Numerous immune cell types,
immunoregulatory molecules, and cytokines have been implicated in the
pathologic processes associated with CAN. Advanced studies are needed
to define the: relative contributions of the humoral and cellular based
immune systems in CAN; mechanisms responsible of the pathogenesis of
chronic dysfunction in solid renal grafts; and, approaches to better
diagnosis, management and treatment of CAN.
Lung
Lung transplantation is a viable therapeutic option and its use has
increased since the first successful operations in the early 1980s.
Most lung transplantations are performed for four major disease
processes: chronic obstructive lung disease (COPD), cystic fibrosis
(CF), idiopathic pulmonary fibrosis (IPF) and pulmonary hypertension
(PH). As a result of improvements in surgical techniques,
immunosuppression and postoperative management, the one-year survival
rate is approximately 80 percent. In 50 percent of long-term lung
transplant recipients, chronic lung allograft rejection manifests as
bonchiolitis obliterans (OB), a complication involving scar formation
and fibrosis in small airways accompanied by intimal thickening and
sclerosis of vessels (chronic vascular rejection). Studies are
necessary to identify and characterize the events that initiate and
maintain repetitive injury to endothelium or epithelium that is followed
by repair and proliferation of smooth muscle cells or fibroblasts,
leading to development of fibrotic obstructive lesions. Further,
studies focused on antigen-dependent processes, influenced by early
immunologic events such as acute rejection and continuing host allo-
responsiveness, or alloantigen-independent processes, such as prolonged
ischemia, reperfusion injury or recurrent infection, are necessary to
understand the progressive changes that occur in chronic rejection and
the pathogenesis of OB.
SPECIAL REQUIREMENTS
Applications should emphasize: collaborative research between basic
scientists and clinical investigators; the use of new and innovative
approaches to enhance understanding of the immunopathogenesis of chronic
graft rejection and the clinical application and relevance of such
approaches; and the use of the most up-to-date concepts and techniques.
Applications from multi-institutional consortia are encouraged in order
to unsure the appropriate mix of scientific and clinical interests of
transplantation in humans within the RFA.
For applications in heart transplantation, clinical research must be
included in one of two ways: 1) a clinical project involving human
patients or material from human patients; or 2) one or more clinical
aims in each project. The clinical project may be a clinical study or a
mechanistic study attached to an ongoing trial. Projects that are
descriptive only will not be acceptable. Projects may include animal
models but only when the animal model can be definitely shown to be
relevant to the human disease; and not in lieu of the requirement for
either or both 1) or 2) above.
For studies of lung transplantation, animal models are acceptable.
However, evidence must be provided that it is a valid model of chronic
rejection/bronchiolitis obliterans following lung transplantation. In
addition, the proposed applications must have at least one clinical
project involving human patients or utilizing human cells and/or tissue.
A single application may contain projects related to chronic rejection
in the heart, lung and/or kidney.
Basic research and preclinical studies using laboratory animals is not
encompassed under this solicitation for other transplantation systems.
It is imperative that all applications focus on the immunopathogenesis
of chronic rejection in humans. Clinical trials evaluating the safety
and efficacy of therapeutic regimens in humans will not be supported
under this RFA; however, the analysis of data obtained from ongoing or
completed clinical trials related to chronic rejection that are
supported by public or private organization is highly encouraged.
Please note, in order to assure a strong level of commitment on the part
of the principal investigator of each project, a minimum of 15% effort
on the application is required. Projects not meeting this requirement
will be returned as non-responsive.
STUDY POPULATIONS
INCLUSION OF WOMEN AND MINORITIES IN RESEARCH INVOLVING HUMAN SUBJECTS
It is the policy of the NIH that women and members of minority groups
and their subpopulations must be included in all NIH supported
biomedical and behavioral research projects involving human subjects,
unless a clear and compelling rationale and justification are provided
that inclusion is inappropriate with respect to the health of the
subjects or the purpose of the research. This policy results from the
NIH Revitalization Act of 1993 (Section 492B of Public Law 103-43).
All investigators proposing research involving human subjects should
read the "NIH Guidelines for Inclusion of Women and Minorities as
Subjects in Clinical Research," published in the Federal Register of
March 28, 1994 (FR 59 14508-14513) and in the NIH Guide for Grants and
Contracts, Vol. 23, No. 11, March 18, 1994, and is available on the web
at: http://grants.nih.gov/grants/guide/notice-files/not94-100.html
INCLUSION OF CHILDREN AS PARTICIPANTS IN RESEARCH INVOLVING HUMAN
SUBJECTS
It is the policy of NIH that children (i.e., individuals under the age
of 21) must be included in all human subjects research, conducted or
supported by the NIH, unless there are scientific and ethical reasons
not to include them. This policy applies to all initial (Type 1)
applications submitted for receipt dates after October 1, 1998.
All investigators proposing research involving human subjects should
read the "NIH Policy and Guidelines" on the Inclusion of Children as
Participants in Research Involving Human Subjects that was published in
the NIH Guide for Grants and Contracts, March 6, 1998, and is available
at the following URL address:
http://grants.nih.gov/grants/guide/notice-files/not98-024.html
Investigators also may obtain copies of these policies from Lawrence
Kerr, Ph.D. listed under INQUIRIES. Program staff may also provide
additional relevant information concerning the policy.
URLS IN NIH GRANT APPLICATIONS OR APPENDICES
All applications and proposals for NIH funding must be self-contained
within specified page limitations. Unless otherwise specified in an NIH
solicitation, Internet addresses (URLs) should not be used to provide
information necessary to the review because reviewers are under no
obligation to view the Internet sites. Reviewers are cautioned that
their anonymity may be compromised when they directly access an Internet
site.
LETTER OF INTENT
Prospective applicants are asked to submit by September 1, 2000 a letter
of intent that includes a descriptive title of the proposed research,
the name, address, and telephone number of the Principal Investigator,
the identities of other key personnel and participating institutions,
and the number and title of the RFA in response to which the application
may be submitted. Although a letter of intent is not required, is not
binding, does not commit the sender to submit an application, and does
not enter into the review of a subsequent application, the information
that it contains allows NIAID staff to estimate the potential review
workload and plan the review.
The letter of intent is to be sent to Dr. Meherotra listed under
INQUIRIES.
APPLICATION PROCEDURES
Applicants for P01 grants must follow special application guidelines in
the NIAID Brochure entitled INSTRUCTIONS FOR APPLICATIONS FOR MULTI-
PROJECT AWARDS (April 1999); this brochure is available via the WWW at:
http://www.niaid.nih.gov/ncn/grants/multibron.htm
The research grant application form PHS 398 (rev. 4/98) is to be used in
applying for these grants. Application kits are available at most
institutional offices of sponsored research and from the Division of
Extramural Outreach and Information Resources, National Institutes of
Health, 6701 Rockledge Drive, MSC 7910, Bethesda, MD 20892-7910,
telephone (301) 710-0267, email: GrantsInfo@nih.gov. Applications are
also available on the World Wide Web at
http://grants.nih.gov/grants/forms.htm.
For purposes of identification and processing, item 2a on the face page
of the application must be marked "YES" and the RFA number AI-00-013
and the words "IMMUNOPATHOGENESIS OF CHRONIC REJECTION" must be typed
in.
The RFA label and line 2 of the application should both indicate the RFA
number. The RFA label must be affixed to the bottom of the face page.
Failure to use this label could result in delayed processing of the
application such that it may not reach the review committee in time for
review.
The sample RFA label available at:
http://grants.nih.gov/grants/funding/phs398/label-bk.pdf
has been modified to allow for this change. Please note this is in pdf
format.
Applications must be received by October 23, 2000. Applications that
are not received as a single package on the receipt date or that do not
conform to the instructions contained in PHS 398 (rev. 4/98) Application
Kit (as modified in, and superseded by, the NIAID BROCHURE ENTITLED
"INSTRUCTIONS FOR APPLICATIONS FOR MULTI-PROJECT AWARDS"), will be
judged non-responsive and will be returned to the applicant.
It is highly recommended that the appropriate NIAID or NHBLI program
contact be consulted before submitting the letter of intent and during
the early stages of preparation of the application. (See program
contact under INQUIRIES).
Submit a signed, typewritten original of the application, including the
Checklist, and three signed, exact, single-sided photocopies, in one
package to:
CENTER FOR SCIENTIFIC REVIEW
NATIONAL INSTITUTES OF HEALTH
6701 ROCKLEDGE DRIVE, ROOM 1040 - MSC 7710
BETHESDA, MD 20892-7710
BETHESDA, MD 20817 (for express mail or courier service)
At the time of submission, two additional exact copies of the grant
application and all five sets of any appendix material must be sent to
Dr. Meherotra listed under INQUIRIES.
Concurrent submission of an R01 and a Component Project of a Multi-
project Application: Current NIH policy permits a component research
project of a multi-project grant application to be concurrently
submitted as a traditional individual research project (R01)
application. If, following review, both the multi-project application
and the R01 application are found to be in the fundable range, the
investigator must relinquish the R01 and will not have the option to
withdraw from the multi-project grant. This is an NIH policy intended
to preserve the scientific integrity of a multi-project grant, which may
be seriously compromised if a strong component project(s) is removed
from the program. Investigators wishing to participate in a multi-
project grant must be aware of this policy before making a commitment to
the Principal Investigator and awarding institution.
Applicants from institutions that have a General Clinical Research
Center (GCRC) funded by the NIH National Center for Research Resources
may wish to identify the GCRC as a resource for conducting the proposed
research. If so, a letter of agreement from either the GCRC program
director or principal investigator could be included with the
application.
SPECIAL INSTRUCTIONS FOR COMPLETION OF APPLICATIONS IN RESPONSE TO THIS
RFA
Applicants for P01 grants must follow special application guidelines in
the NIAID Brochure entitled INSTRUCTIONS FOR APPLICATIONS FOR MULTI-
PROJECT AWARDS (April 1999); this brochure is available via the WWW at:
http://www.niaid.nih.gov/ncn/grants/multibron.htm
The brochure presents specific instructions for sections of the PHS 398
(rev. 4/98) application form that should be completed differently than
usual. For all other items in the application, follow the usual
instructions in the PHS 398.
REVIEW CONSIDERATIONS
Review Procedures
Upon receipt, applications will be reviewed for completeness by the NIH
Center for Scientific Review and for responsiveness by NIAID staff.
Incomplete and/or non-responsive applications will be returned to the
applicant without further consideration.
Applications that are complete and responsive to the RFA will be
evaluated for scientific and technical merit by an appropriate peer
review group convened by the Division of Extramural Activities, NIAID in
accordance with the review criteria stated below. As part of the initial
merit review, all applications will receive a written critique and
undergo a process in which only those applications deemed to have the
highest scientific merit, generally the top half of the applications
under review, will be discussed, assigned a priority score, and receive
a second level review by the National Advisory Allergy and Infectious
Diseases Council.
Review Criteria
The general criteria for P01 grant applications are presented in the
NIAID brochure entitled INSTRUCTIONS FOR APPLICATIONS FOR MULTI-PROJECT
AWARDS (April 1999). Additional review criteria specific to this RFA
are:
Schedule
Letter of Intent Receipt Date: September 1, 2000
Application Receipt Date: October 23, 2000
Scientific Review Date: February, 2001
Advisory Council Date: June, 2001
Earliest Date of Award: July, 2001
AWARD CRITERIA
Funding decisions will be made on the basis of scientific and technical
merit as determined by peer review, program balance, and the
availability of funds.
INQUIRIES
Written and telephone inquiries concerning this RFA are encouraged. The
opportunity to clarify any issues or questions from potential applicants
is welcome.
Requests for the NIAID brochure "INSTRUCTIONS FOR APPLICATIONS FOR
MULTI-PROJECT AWARDS" as well as inquiries regarding programmatic
(eligibility and research scope) issues, may be directed to:
Lawrence D. Kerr, Ph.D.
Division of Allergy, Immunology and Transplantation (DAIT)
National Institute of Allergy & Infectious Diseases (NIAID)
National Institutes of Health
6700-B Rockledge Rd., Rm. 5129
Bethesda, Maryland 20892-7640
Telephone: (301) 496-5598
Fax: (301) 402-2571
Email: LKerr@niaid.nih.gov
National Heart, Lung, and Blood Institute (NHBLI)
For chronic rejection in the heart:
Judith Massicot-Fisher, Ph. D.
National Heart, Lung and Blood Institute
Division of Heart and Vascular Diseases
6701 Rockledge Drive MSC 7940
Bethesda, MD 20892-7940
Telephone: (301) 435-0528
Fax: (301) 480-1454
E-mail : massicoj@nhlbi.nih.gov
For chronic rejection in the lung(s):
Susan Garfinkel, Ph.D.
NHLBI, Division of Lung Diseases
2 Rockledge Center
6701 Rockledge Drive
Bethesda, MD 20892-7952
Telephone: (301)435-0222
FAX: (301)480-3557
E-mail: GarfinkS@NHLBI.NIH.GOV
Direct inquiries regarding preparation of the application and review
issues, and address the letter of intent to, and mail two copies of the
application and all five sets of appendices to:
Dr. Priti Meherotra
Division of Extramural Activities
National Institute of Allergy and Infectious Diseases
Room (insert), MSC-7616
6700-B Rockledge Drive
Bethesda, MD 20892-7616
Telephone: (301)(435-9369)
FAX: (301)(402-2638)
Email: PM158@nih.gov
Direct inquiries regarding fiscal matters to:
Ms. Pamela Fleming
Division of Extramural Activities
National Institute of Allergy and Infectious Diseases
Room 2119, MSC-7614
6700-B Rockledge Drive
Bethesda, MD 20892-7614
Telephone: (301) 402-6580
FAX: (301) 480-3780
E-mail: PFlemming@niaid.nih.gov
AUTHORITY AND REGULATIONS
This program is described in the Catalogue of Federal Domestic
Assistance No. 93.855, (DAIT) and 93.837 (DHVD) and 93.838 (DLD). Awards
are made under authorization of Sections 301 and 405 of the Public
Health Service Act, as amended (42 USC 241 and 284) and administered
under NIH grants policies and Federal Regulations 42 CFR 52 and 45 CFR
Parts 74 and 92. This program is not subject to the intergovernmental
review requirements of Executive Order 12372 or Health Systems Agency
review.
The Public Health Service strongly encourages all grant and contract
recipients to provide a smoke-free workplace and promote the non-use of
all tobacco products. In addition, Public Law 103-227, the Pro-Children
Act of 1994, prohibits smoking in certain facilities (or, in some cases,
any portion of a facility) in which regular or routine education,
library, day care, health care or early childhood development services
are provided to children. This is consistent with the PHS mission to
protect and advance the physical and mental health of the American
people.
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