NON-MOUSE MODELS OF DIABETES COMPLICATIONS IN CARDIOVASCULAR AND MICROVASCULAR
DISEASES
Release Date: November 20, 2000
RFA: HL-01-010
National Heart, Lung, and Blood Institute
http://www.nhlbi.nih.gov/
National Institute of Diabetes and Digestive
and Kidney Diseases
http://www.niddk.nih.gov
Letter of Intent Receipt Date: February 26, 2001
Application Receipt Date: March 21, 2001
PURPOSE
The purpose of this solicitation is to support efforts to develop non-mouse
animal models of diabetic complications. The animal models are expected to
mimic vascular diseases in patients with type 1 or type 2 diabetes mellitus
with an emphasis on, but not limited to, cardiovascular disorders of coronary
heart disease, stroke, peripheral arterial disease, cardiomyopathy, and
congestive heart failure. Improved animal models of microvascular
complications are also needed. The goal of this initiative is to obtain these
non-mouse animal models, through the use of selective breeding, dietary
manipulation, or molecular genetic approaches. Applicants to this initiative
are also expected to characterize and validate the models for use in various
aspects of basic, developmental, or translational research including testing
prevention, early detection, therapeutic, or diagnostic imaging strategies.
Applicants should also propose plans to make these models available to other
research investigators for studies to advance our understanding of the
etiology, pathobiology, clinical progression, management and prevention of
diabetic vascular diseases.
A companion RFA (DK-01-009, Mouse Models of Diabetic Complications:
Consortium) solicits applications to develop mouse models of diabetic
complications in order to take advantage of unique genetic technologies that
are applicable in the mouse.
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),
Non-Mouse Models Of Diabetes Complications In Cardiovascular And Microvascular
Diseases, is related to the priority areas, "Heart Disease and Stroke", and
"Chronic Disabling Conditions". Potential applicants may obtain a copy of
AHealthy People 2010" at http://www.health.gov/healthypeople/.
ELIGIBILITY REQUIREMENTS
Applications may be submitted by domestic and foreign, for-profit and non-
profit organizations, public and private, such as universities, colleges,
hospitals, laboratories, units of State or local governments, and eligible
agencies of the Federal government. Racial/ethnic minority individuals,
women, and persons with disabilities are encouraged to apply as Principal
Investigators.
All current policies and requirements that govern the research grant programs
of the NIH will apply to grants awarded under this RFA. Awards under this RFA
to foreign institutions will be made only for research of very unusual merit,
need, and promise, and in accordance with Public Health Service policy
governing such awards. Cell biology, molecular biology, nutrition,
biochemistry, physiology, pathology, genetics, and imaging modalities are
among the disciplines and expertise that may be appropriate for this research
program.
MECHANISM OF SUPPORT
This RFA will use the National Institutes of Health (NIH) research project
grant (R01) award mechanism. Responsibility for the planning, direction, and
execution of the proposed project will be solely that of the applicant. The
total project period for an application submitted in response to this RFA may
not exceed 5 years. This RFA is a one-time solicitation. Future unsolicited
competing continuation applications will compete with all investigator-
initiated applications and be reviewed according to the customary peer review
procedures. The anticipated award date is September 30, 2001.
FUNDS AVAILABLE
The NHLBI and NIDDK intend to commit approximately $1,500,000 in FY 2001 to
fund three to five new grants in response to this RFA. An applicant may
request a project period of up to five years and a budget for direct costs of
up to $350,000 per year. The Facilities and Administrative costs for
collaborating institutions are excluded from this ceiling and a maximum
increase of no more than three percent is allowed in each additional year
requested in the application. Because the nature and scope of the research
proposed may vary, it is anticipated that the size of each award will also
vary. Although the financial plans of both Institutes provide support for
this program, awards pursuant to this RFA are contingent upon the availability
of funds and the receipt of a sufficient number of meritorious applications.
At this time, it is not known if this RFA will be reissued.
Equipment is included in the budget limitation. However, requests for major
equipment that cause an application to exceed this limit may be permitted on a
case-by-case basis following staff consultation. Such equipment requires in-
depth justification. Final decisions will depend on the nature of the
justification and the Institute"s fiscal situation.
Because we expect that there will not be any applications requesting less that
$250,000 in first year direct costs, applications should be in the standard
(non-modular) format with a detailed budget.
Consortium Arrangements
When a grant application includes research activities that involve
institutions other than the grantee institution, it is considered a consortium
effort. Such activities may be included in a grant application, but it is
imperative that a consortium application be prepared so that the programmatic,
fiscal, and administrative considerations are explained fully. Facilities and
administrative costs paid as part of a consortium agreement are excluded from
the limit on the amount of direct costs that can be requested. The published
policy governing consortia is available in the business offices of
institutions that are eligible to receive Federal grants-in-aid. Consult the
latest published policy governing consortia before developing the application.
RESEARCH OBJECTIVES
Background
Prevention and treatment of long-term micro- and macro-vascular complications
remain a critical problem in the management of patients with type 1 or type 2
diabetes mellitus. In the United States, diabetes is the leading cause of new
blindness in adults, of new cases of end stage renal disease and of non-
traumatic lower leg amputations. In addition, cardiovascular complications are
now the leading cause of diabetes-related morbidity and mortality particularly
among women and the elderly. In adult patients with diabetes, the risk of
cardiovascular disease (CVD)is three to five fold greater than in
nondiabetics, up to three fourths of all deaths among diabetics can be
directly attributed to accelerated atherosclerosis and CVD. A number of known
risk factors for CVD, such as hypertension, central obesity, and dyslipidemia,
are more common in diabetics than in the general population. However, no more
than 25% of the excess coronary artery disease (CAD) risk in diabetics can be
accounted for by known risk factors such as high plasma cholesterol, low
plasma HDL, high plasma triglycerides, and hypertension, suggesting the
presence of other factors contributing to the development of CVD in patients
with diabetes.
The 1998 Diabetes Research Working Group report noted that a lack of good
animal models has been a major impediment to research on the long-term micro-
and macrovascular complications of diabetes. Improved animal models are
critical for understanding the pathogenesis of complications and for testing
potential new prevention and treatment modalities. Animal models can be used
to conduct studies at the molecular, cellular and tissue level not feasible in
humans. Thus, there is an urgent need to derive, thoroughly characterize, and
validate animal models for their relevance to human biology, and to use these
models for testing therapeutic, prevention, early detection or diagnostic
imaging strategies.
Clinical studies have repeatedly shown a strong correlation between
susceptibility to micro- and macrovascular complications, especially in
patients with diabetic nephropathy. Cardiovascular events are much more
frequent in patients with diabetic nephropathy. In addition, renal artery
atherosclerosis may contribute to renal disease, likewise, accelerated lower
extremity arterial disease interacts with neuropathy, resulting in the high
rate of lower extremity amputations in patients with diabetes. In addition, it
is becoming increasingly clear that the pathogenesis of microvascular
complications, as well as of macrovascular disease, includes disordered
function of endothelial cells.
There is a growing recognition that diabetes may be increasing the risk of CVD
partly due to its association with a variety of metabolic abnormalities.
Hyperglycemia, the defining metabolic change in diabetes, may accelerate the
development of atherosclerosis. However, the specific contribution of
hyperglycemia has been difficult to demonstrate in either population studies
or animal models. Moreover, hyperglycemia alone is unlikely to play a role in
the development of atherosclerosis that is seen in individuals with impaired
glucose tolerance (IGT) who usually
demonstrate only modest postprandial hyperglycemia. Therefore, it has been
suggested that, in addition to glucose levels, other factors associated with
IGT are likely to contribute to the development of atherosclerosis and CVD in
type 2 diabetes.
Thus, it is clear that the pathogenesis of diabetes-related CVD, and the
mechanisms by which known risk factors may enhance atherosclerosis and CAD are
poorly understood. In addition, factors contributing to type 1 and type 2
diabetes, such as autoimmune inflammatory and immunological responses, insulin
resistance and clustering of CVD risk factors need to be better understood.
Experimental verification of these potential mechanisms has been greatly
hindered by a lack of appropriate animal models. Existing animal models of
diabetes, CVD and atherosclerosis, although providing useful information, have
suffered from serious problems.
A separate RFA (DK-01-009) has been issued which focuses on the development of
mouse models of diabetic complications. This initiative solicits applications
to generate animal models in other species. There is a sizable body of work
that establishes a number of features in other species which are relevant to
diabetes-associated vascular disease.
Nonhuman primates fed atherogenic diets have been used to model human
atherosclerosis for many years. However, in some instances, as in the
squirrel monkey, the plasma cholesterol elevation that develops following
increased dietary cholesterol results from increases in -VLDL rather than in
LDL. Glucose intolerance and insulin resistance do develop spontaneously in
some nonhuman primates, although the development of diabetes is much more rare
than in humans. Therefore, diabetes is most often induced artificially which
has been problematic as the degree of beta cell damage and the need for
insulin vary greatly. Moreover, maintaining stable hyperglycemia and healthy
animals is costly and requires intensive monitoring and care.
Pigs have been frequently favored as an animal model because of their close
cardiovascular and metabolic similarities to humans. Natural mutations have
been identified for the development of hypercholesterolemia. These animals
developed advanced atherosclerotic lesions, morphologically similar to humans,
that resulted in their deaths. However, no attempts were made to selectively
breed these animals for diabetic states. Another pig model, the Yucatan
miniature swine, was developed by genetic selection for altered glucose
clearance during a glucose tolerance test. These animals display insulin
resistance and a diabetic-like state. On a high fat diet, these animals become
more glucose intolerant and diabetic. The cardiovascular and metabolic
abnormalities in this model have yet to be explored.
There are currently several animal models of insulin resistance induced by
high fructose diets. Although this approach has been used in dogs and
hamsters, fructose enriched diets are most frequently used to induce a
hyperinsulinemic, euglycemic insulin resistant condition in rats. These diets
also induce enhanced hepatic secretion of VLDL, frequently resulting in
moderate hypertriglyceridemia. Although all of these animal models have proven
useful for studies of insulin resistance, they do not develop extensive
atherosclerosis or CVD.
The New Zealand White rabbit has also been widely used as a model for
atherosclerosis. When fed high cholesterol diets, these rabbits develop
marked hypercholesterolemia and extensive atherosclerosis. However,
surprisingly, cholesterol fed rabbits made diabetic by alloxan treatment
developed less atherosclerosis compared to their nondiabetic controls. This
apparent paradox has not been explained. Rabbits lacking functional LDL
receptors (WHHL rabbits) also develop marked hypercholesterolemia and
extensive aortic lesions. However, the WHHL rabbit has not been used for
studies of diabetes and atherosclerosis. Given the absence of spontaneously
diabetic rabbits and the high mortality of alloxan treated rabbits, rabbits
have not proven as yet to be a useful model of diabetic atherosclerosis.
Another animal model commonly used for atherosclerosis studies is the hamster.
However, attempts to chemically induce diabetes have produced variable
results, with some animals showing marked hyperglycemia, weight loss and poor
survival, while others develop only moderate hyperglycemia and demonstrate
prolonged survival. Diabetic hamsters fed standard or cholesterol enriched
diets showed ultrastructural changes in the aorta consistent with
atherosclerosis development. However, the extent of atherosclerosis that
develops in the diabetic hamster model is modest, and more information is
needed on the changes in lipoprotein levels and composition that occur.
Several different strains of rats have been proposed as models of type 2
diabetes. These models were the result of naturally occurring mutations in
laboratory animals and the recognition that some rats are uniquely susceptible
to develop insulin resistance and diabetes on special diets. Rats homozygous
for the "fatty"(fa) or "corpulent"(cp) genes are typically obese,
hyperlipidemic, hyperinsulinemic and insulin resistant. The "fatty" (Zucker)
rat has been used primarily as a model of obesity. However, because of the
accompanying hyperglycemia and insulin resistance it is also useful as a model
of type 2 diabetes. As in most animal models of insulin resistance, there is
no evidence of advanced arterial lesion formation in the Zucker rat model.
The corpulent (JCR:LA-cp) rat has marked hyperinsulinemia that develops
shortly after birth and persists throughout life. This strain develops
spontaneous arterial lesions that resemble fatty streaks in humans. However,
these fatty streaks do not progress to fully developed atherosclerotic
lesions. This suggests that different etiologies for lesion formation may
exist in humans and the JCR:LA-cp rat.
Another rat model of type 2 diabetes and atherosclerosis is the sand rat. When
fed standard rat chow, the sand rat becomes obese, hyperglycemic,
hyperinsulinemic and insulin resistant. When made hypothyroid and fed a
cholesterol-enriched diet, they develop cardiovascular lesions. However, it
remains unknown whether factors other than lipid levels contribute to the
development of atherosclerosis in this strain.
Models of type I diabetes are usually generated by administration of chemicals
toxic to the pancreas, these animals require insulin to avoid developing
marked hyperglycemia, dehydration and ketosis. Using low doses of insulin to
avoid wasting and death while maintaining hyperglycemia to induce
complications is difficult and time consuming. Therefore, mortality rates are
frequently high and the possibility that poor health may influence metabolic
parameters and development of atherosclerosis always remains a concern. As
noted above, a common limitation of many of the existing animal models of
diabetes is that they develop only very modest atherosclerosis. Some species,
particularly the rat and the dog are naturally resistant to developing
atherosclerosis. In addition, lipoprotein patterns and metabolism in some
animal models are sufficiently different from those in humans to raise
concerns about the relevance of risk factors identified in studies using these
animal models.
To date, available animal models of microvascular complications have also
shared these limitations. Most of these models have not been fully validated,
or they reproduce only a small portion of the full human disease. For example,
there are several rodent models of diabetes associated with renal damage.
However, these animals generally lack a number of the key pathological
features seen in human disease. Thus, no animal model consistently exhibits
the vascular abnormalities, basement membrane thickening and nodule formation
characteristic of human diabetic nephropathy.
Objectives
The objective of this initiative is to accelerate the pace at which accurate
and reproducible non-mouse animal models of diabetic vascular complications
are developed. The animal models are expected to mimic disease in patients
with type 1 or type 2 diabetes mellitus. The major focus of this RFA is on
diabetes-associated cardiovascular disorders, including coronary heart
disease, stroke, peripheral arterial disease, cardiomyopathy, and congestive
heart failure. However, animals models of microvascular disease are also
acceptable. The goal of the program is to obtain these non-mouse animal
models, through selective breeding, dietary or molecular genetic approaches.
Once the models are developed, characterized and validated, it will be
important to disseminate the models and information related to them to the
research community, for studies to advance our understanding of the etiology,
pathobiology, clinical progression, management and prevention of diabetes
related cardiovascular and microvascular diseases. Specific areas of interest
would include identification of 1) genes which confer protection or induce
initiation and progression of diabetic vascular disease, 2) environmental
components that contribute to disease progression and 3) new therapeutic
strategies to block or retard progression of vascular disease.
It is hoped that rapid progress in creating animal models will be stimulated
by attracting investigators to integrate approaches involving animal breeding
and nutrition, vascular physiology, tissue-specific pathology, vascular cell
biology, molecular analysis of gene expression, clinical investigations, and
genetics. More careful characterization and creative utilization of tissue
and animal resources would expedite this effort. In addition, cross-breeding
experiments to explore the interactions of specific genes with various genetic
backgrounds could be useful.
Proposed Research
Appropriate investigations under this RFA would include, but not be limited
to, the generation and characterization of non-mouse animal model(s) of
insulin resistance or diabetes, which develop vascular disease which resembles
that seen in humans with type 1 or type 2 diabetes. Applicants must also
outline their proposed plans to make these animals available to the research
community.
It is envisaged that the most appropriate animal models of type I diabetes
would have low insulin levels, while models of type 2 diabetes would have
normal or slightly elevated plasma insulin. The models should also have
moderate to severe hyperglycemia and lipoprotein patterns typical of those
present in human diabetes. Atherosclerotic lesions in these models should have
many of the morphologic and cellular features characteristic of early and
advanced human lesions. Finally, the models should fulfill several practical
criteria for in vivo studies of atherosclerosis such as development of
atherosclerotic lesions and/or kidney dysfunction within a relatively short
time to allow the detection of differences between experimental and control
groups. Similarly, new models of diabetic microvascular disease must
demonstrate pathology analogous to human disease.
EXCLUSIONS
This RFA is intended to support R01 research programs to create, characterize,
evaluate, and disseminate non-mouse animal models to study diabetes
complications of accelerated atherosclerosis, and other cardiovascular
diseases, as well as microvascular disease cardiovascular and kidney diseases.
Applications that propose mouse models will be considered unresponsive to this
initiative. Investigators proposing mouse models may wish to consider RFA :
DK -01-009 entitled "Mouse Models of Diabetic Complications Consortium" or
consult with the NHLBI and NIDDK staff at the address listed under INQUIRIES.
SPECIAL REQUIREMENTS
Upon initiation of the program, the NHLBI and the NIDDK will sponsor periodic
meetings to encourage exchange of information among investigators who
participate in this program. Applicants should request travel funds for a 1
day meeting each year, most likely to be held in Bethesda, Maryland.
Applicants should include a statement in their applications indicating their
willingness to participate in these meetings.
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 February 26, 2001 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, and does not enter into the
review of a subsequent application, the information that it contains allows
staff to estimate the potential review workload and to plan the review.
The letter of intent is to be mailed, or faxed, to: Dr. Deborah Beebe at the
address listed under INQUIRIES.
APPLICATION PROCEDURES
The research grant application form PHS 398 (rev. 4/98) is to be used in
applying for these grants, with the modifications noted below. These forms
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.
Because we expect that there will not be any applications requesting less that
$250,000 in first year direct costs, applications should be in the standard
(non-modular) format with a detailed budget.
The RFA label found in the PHS 398 (rev. 4/98) application form must be
affixed to the bottom of the face page of the application. 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. In addition, the RFA title
(Non-Mouse Models of Diabetes Complications in Cardiovascular and Kidney
Diseases) and number (HL -01-010) must be typed on line 2 of the face page of
the application form and the YES box must be marked.
The sample RFA label available at: email:
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.
Submit a signed typewritten original of the application and three signed,
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/courier service)
At the time of submission, two additional copies of the application must be
sent to Dr. Deborah Beebe, Chief, Review Branch at the address listed under
INQUIRIES. It is important to send these two copies at the same time as the
original and three copies are sent to the Center for Scientific Review (CSR),
otherwise the NHLBI cannot guarantee that the application will be reviewed in
competition for this RFA.
Applications must be received by March 21, 2001. If an application is received
after that date, it will be returned to the applicant without review.
The Center for Scientific Review (CSR) will not accept any application in
response to this RFA that is essentially the same as one currently pending
initial review, unless the applicant withdraws the pending application. The
CSR will not accept any application that is essentially the same as one
already reviewed. This does not preclude the submission of substantial
revisions of applications already reviewed, but such applications must include
an introduction addressing the previous critique.
REVIEW CONSIDERATIONS
Upon receipt, applications will be reviewed for completeness by the CSR, and
responsiveness by NHLBI and NIDDK. 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 NHLBI 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 advisory councils of NHLBI and NIDDK.
Review Criteria
The goals of NIH-supported research are to advance our understanding of
biological systems, improve the control of disease, and enhance health. In
the written comments reviewers will be asked to discuss the following aspects
of the application in order to judge the likelihood that the proposed research
will have a substantial impact on the pursuit of these goals. Each of these
criteria will be addressed and considered in assigning the overall score,
weighting them as appropriate for each application. Note that the application
does not need to be strong in all categories to be judged likely to have major
scientific impact and thus deserve a high priority score. For example, an
investigator may propose to carry out important work that by its nature is not
innovative but is essential to move a field forward.
1) Significance
Does this study address an important problem? If the aims of the application
are achieved, how will scientific knowledge be advanced? What will be the
effect of these studies on the concepts or methods that drive this field?
2) Approach
Are the conceptual framework, design, methods, and analyses adequately
developed, well integrated, and appropriate to the aims of the project? Does
the applicant acknowledge potential problem areas and consider alternative
tactics? Once the models are developed, characterized and validated, does the
applicant propose plans for the efficient dissemination of the models and
information related to them to the research community?
3) Innovation
Does the project employ novel concepts, approaches or method? Are the aims
original and innovative? Does the project challenge existing paradigms or
develop new methodologies or technologies?
4) Investigator
Is the investigator appropriately trained and well suited to carry out this
work? Is the work proposed appropriate to the experience level of the
principal investigator and other researchers (if an)?
5) Environment
Does the scientific environment in which the work will be done contribute to
the probability of success? Do the proposed experiments take advantage of
unique features of the scientific environment or employ useful collaborative
arrangements? Is there evidence of institutional support?
In addition to the above criteria, in accordance with NIH policy, all
applications will also be reviewed with respect to the following:
o The reasonableness of the proposed budget and duration in relation to the
proposed research.
o The adequacy of the proposed protection for animals or the environment, to
the extent they may be adversely affected by the project proposed in the
application.
o The adequacy of the proposed plan to share and disseminate the animal
models.
SCHEDULE
Letter of Intent Receipt Date: February 26, 2001
Application Receipt Date: March 21, 2001
Review by NHLBI Advisory Council: September 6-7, 2001
Anticipated Award Date: September 30, 2001
AWARD CRITERIA
Applications will receive a secondary level of review by advisory councils of
NHLBI and NIDDK in September, 2001. The earliest anticipated date of award is
September 2001. Applicants should be aware that, in addition to scientific
merit, program priorities and program balance, the total costs of the proposed
project and the availability of funds will be considered by NHLBI staff as
well as NHLBAC in making funding recommendations. In addition, NHLBI
appreciates the value of complementary funding from other public and private
sources including foundations and industrial concerns. In circumstances in
which applications have similar scientific merit, but vary in cost
competitiveness, NHLBI is likely to select the more cost competitive
application for funding.
INQUIRIES
Inquiries concerning this RFA are encouraged. Potential applicants should
request a copy of the full RFA, which will include sample budget pages. The
opportunity to clarify any issues or questions from potential applicants is
welcome.
Direct inquiries regarding programmatic issues to:
Momtaz Wassef, Ph.D.
Leader, Atherosclerosis Research Group
Division of Heart and Vascular Diseases
National Heart, Lung, and Blood Institute
6701 Rockledge Drive, Suite 10186
Bethesda, MD 20892-7956
Telephone: (301) 435-0550
FAX: (301) 480-2848
E-mail: WASSEFM@NIH.GOV
Barbara Linder, M.D.
Division of Diabetes, Endocrinology
and Metabolic Diseases
National Institute of Diabetes and Digestive
and Kidney Diseases
6707 Democracy Blvd
Bethesda, MD 20892-5460
Telephone: (301) 594-0021
Fax: (301) 480-3503
E-mail: LINDERB@NIH.GOV
Direct inquiries regarding review issues, send letter of intent and two copies
of the application to:
Dr. Deborah Beebe
Division of Extramural Affairs
National Heart, Lung, and Blood Institute
6701 Rockledge Drive, Room 7178, MSC 7924
Bethesda, MD 20892-7924
Telephone: (301)435-0270
FAX: (301) 480-3541
E-mail: Beebeb@NIH.GOV
Direct inquiries regarding fiscal matters to:
Mr. Owen Bobbitt
Grants Operations Branch
National Heart, Lung, and Blood Institute
6701 Rockledge Drive, Suite 7156
Bethesda, MD 20892-7926
Telephone: (301)435-0177, FAX: (301)480-3310
E-mail: BobbittO@NIH.GOV
AUTHORITY AND REGULATIONS
This program is described in the Catalog of Federal Domestic Assistance No.
93.837, and 93.121. Awards are made under authorization of the Public Health
Service Act, Title IV, Part A (Public Law 78-410, as amended by Public Law
99-158, 42 USC 241 and 285) and administered under PHS grants" policies and
Federal Regulations 42 CFR 52 and 45 CFR Part 74. This program is not subject
to the intergovernmental review requirements of Executive Order 12372 or
Health Systems Agency review.
The PHS 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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