This Program Announcement expires on July 1, 2004, unless reissued.


Release Date:  March 14, 2001

PA NUMBER:  PA-01-067

National Institute on Aging
National Institute of Arthritis and Musculoskeletal and Skin Diseases
National Institute of Child Health and Human Development
National Institute of Diabetes and Digestive and Kidney Diseases


This Program Announcement replaces Program Announcement,  PA-95-006 
(Biology of the Menopause: Change of Ovarian Function), which was 
published in the NIH Guide November 18, 1994.


The National Institute on Aging (NIA), in collaboration with the 
National Institute of Arthritis and Musculoskeletal and Skin Diseases 
(NIAMS), the National Institute of Child Health and Human Development 
(NICHD), and the National Institute of Diabetes, Digestive and Kidney 
Diseases (NIDDK), invite applications to support research that 
elucidates molecular and cellular mechanisms underlying the menopausal 
process, and the pathophysiologic connections of that process with 
various health problems and conditions of peri- and postmenopausal 
women.  This program announcement addresses a) the underlying biology 
of age- and menopause-related changes in the hypothalamic-
pituitary-ovarian (H-P-O) axis that result in the dramatic hormonal 
changes experienced across the menopausal transition, and b) how the 
biology of menopause impacts the menopause-related increase in health 
problems and conditions associated with the brain, cardiovascular, 
skeletal, genitourinary and other physiologic systems.  


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 Program 
Announcement (PA), Biology of the Menopause and Associated Health 
Conditions, is related to one or more of the priority areas. Potential 
applicants may obtain a copy of "Healthy People 2010" at


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 and 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.


The mechanism of support will be the National Institutes of Health 
(NIH) individual research project grant (R01). Responsibility for the 
planning, direction, and execution of the proposed project will be 
solely that of the applicant.

Specific application instructions have been modified to reflect 
"MODULAR GRANT" and "JUST-IN-TIME" streamlining efforts being examined 
by NIH. Complete and detailed instructions and information on Modular 
Grant applications can be found at: 


The ovary of the premenopausal non-pregnant human female, as well as 
the ovary of various animal species, serves as the body's primary 
source of estradiol-17 beta (E2), the steroid hormone associated with 
protection of the premenopausal woman from a variety of potential 
postmenopausal health problems, such as increased risk for decline in 
cardiovascular, skeletal, and genitourinary system function, and for 
increased incidence of hot flashes.  In addition to E2, the 
premenopausal ovary also secretes other steroid hormones, such as 
progestins and androgens, and the glycoprotein, inhibin.  Progestins, 
androgens and inhibin all have incompletely understood functions  
within the hypothalamic-pituitary-ovarian (H-P-O) axis and much less 
well-defined roles in the proper functioning of peripheral tissues.

The change in ovarian function across the menopause is accompanied by 
the loss of virtually all of the primordial and developing follicles 
residing within the ovary.  From a non-replenishable store of several 
million primordial follicles formed within the developing human ovary 
during gestation, approximately 25,000 follicles remain at the start of 
the final 12-15 years of menstrual cycling.  These remaining follicles 
appear to undergo an accelerated rate of loss of over twice that of the 
first two decades of reproductive life.  The molecular and cellular 
mechanisms responsible for this acceleration of follicular loss are 
virtually unknown.   Consequently only several hundred or less 
apparently gonadotropin-insensitive follicles remain in the ovary at 
the time of menopause, a number likely to be too small to sustain the 
H-P-O interactions required for regular menstrual cyclicity.  
Follicular atresia is the predominant fate of ovarian follicles.  Of 
the millions of follicles initially present in the ovary, well over 99 
percent are depleted over the woman's reproductive life span through 
atresia.  Except for the single ovulatory follicle per month in a 
normally cycling woman, all of the growing pool of antral follicles is 
resorbed within the ovary by atresia.  Even women not cycling due to 
oral contraceptive usage or pregnancy lose ovarian follicles at rates 
comparable to those in cycling women.  The underlying mechanism of 
atresia of antral follicles in diverse species, including humans, 
appears to involve apoptosis in various follicular cells.  The 
molecular and cellular mechanisms through which these apoptotic 
processes are regulated are just starting to be explored.
Menstrual cycles in regularly cycling middle-aged women gradually grow 
shorter due to a shorter follicular phase, while the length of the 
luteal phase generally remains constant.  As women enter the 
perimenopausal period, their cycles gradually lengthen, as the fraction 
of ovulatory cycles declines and cycles become irregular.  Early 
follicular phase FSH levels begin to rise about five years preceding 
the menopause, even in regularly cycling women.  Inhibin B, a potential 
biomarker of ovarian follicular function in the pre- and perimenopausal 
woman, is reported to decline in older ovulatory women with increased 
serum FSH levels.  Characteristics of pulsatile pituitary gonadotropin 
secretion driven by changes in hypothalamic GnRH secretion in women in 
their 40s with normal cycles and hormonal levels may explain the rise 
in FSH levels.  Thus, age-related changes in the H-P-O axis may to play 
an important role in the menopausal process.
LH levels become elevated roughly one year prior to menopause. Data on 
serum levels of E2 and progesterone suggest elevated levels of E2 and 
diminished levels of progesterone relative to young premenopausal women 
during at least part of the peri-menopause. Changes in the formation 
and function of the corpus luteum during the perimenopause are not well 

Thus, menopause marks a dramatic change in ovarian function.  Prior to 
menopause, the ovary participates as a key component of the dynamic 
hormonal orchestration of the H-P-O axis resulting in the periodic 
release of oocytes; subsequent to menopause, the ovary functions as a 
relatively quiescent androgen-secreting organ in a hypergonadotropic 
environment.  The molecular and cellular mechanisms involved in the 
increased magnitude of the rise in early follicular phase FSH, the 
development of menstrual cycle irregularity, the rise in LH late in the 
menopausal process, the regulation of E2, progesterone and inhibin 
levels during the menopausal process, and the apparent acceleration in 
the rate of follicular loss early in the menopausal process are largely 

By what molecular mechanisms do the menopause-related changes in the aging H-
P-O axis interact with non-reproductive tissues leading to the health 
problems and conditions associated with peri- and postmenopausal women?  
Clearly the loss of ovarian estrogen is a major factor involved in this 
process, as we learn that many non-reproductive tissues are responsive to 
protection by estrogen.  Increased estrogen levels during the perimenopause 
coupled with declining progesterone levels may explain abnormal uterine 
bleeding and perhaps the development of uterine fibroids.  Several non-
reproductive somatic tissues associated with postmenopausal health problems, 
such as bone and cardiovascular tissue, make their own supply of estrogen via 
endogenous estrogen synthetase (aromatase) and/or activate estrogen within 
the tissue via endogenous 17-beta hydroxysteroid dehydrogenase activity.

Other H-P-O axis factors may also be involved.  For example, the observations 
that a) gonadotropin levels are increased in estrogen-deficient 
postmenopausal women, b) glycosylated forms of serum LH and FSH are altered 
in the postmenopause, and c) gonadotropin receptors have been detected in 
non-reproductive tissue, increase the possibility that these altered 
postmenopausal levels and forms of gonadotropins may have physiologic or 
pathophysiologic roles outside of the reproductive system.  Also, loss of 
gonadal inhibin in peri- and postmenopausal women may affect 
osteoblastogenesis and osteoclastogenesis, thereby contributing to bone loss 
during and subsequent to the menopause.   The frequently greater complaint of 
menopausal symptoms in surgically menopausal women suggests either the 
severity is related to the abrupt loss of ovarian estrogen or the 
postmenopausal ovary may secrete protective factors to modulate symptoms.  
Still another largely unexplored possibility is age-related alteration in 
tissue sensitivity to estrogen and/or other bioregulatory factors secreted by 
the H-P-O axis.

A recent international conference (International Conference on Biology 
of Menopause, September 10-13, 1998, Newport Beach, CA), co-sponsored 
by Serono Symposia USA and the National Institute on Aging, was devoted 
to basic research issues related to the menopausal process and its 
interaction with the brain, cardiovascular, and skeletal systems.  The 
proceedings of this conference, containing further information 
regarding studies that resulted in the findings described above, is 
available in the Serono Symposia USA Series (Bellino, FL (ed) Biology 
of Menopause, Springer-Verlag, New York, 2000).

Goals of the Program Announcement
This program announcement invites research applications focused on the 
underlying biologic mechanisms of molecular regulatory factors (a) 
acting within and external to the H-P-O axis that are responsible for 
female reproductive aging processes, and (b) secreted from the H-P-O 
axis of women that serve to maintain extra-ovarian tissue (e.g., 
cardiovascular, bone, urinary, brain) function and diminish their 
protective effects during the peri- or postmenopausal periods.
The goal is to increase our understanding of the molecular basis of the 
normal menopausal process occurring in women generally between the ages 
of 45 and 55.  Premature ovarian failure, due either to iatrogenic or 
pathologic processes, is not within the scope of this program 
announcement.  However, this restriction is not intended to exclude 
research with animal or other models in which ovarian follicular 
exhaustion is manipulated experimentally or genetically to explore 
relationships of reproductive aging with follicular number. 
Although molecular and cellular mechanistic approaches to the issues 
described in this program announcement are strongly desired, the 
acquisition of more baseline data may be necessary in some areas to 
formulate a mechanistic hypothesis.  Research questions of interest 
include, but are not limited to, the following:
o  What regulates the process responsible for the enhanced rate of 
follicular loss in the last 12 to 15 years of menstrual cycling; what 
role do the hormonal interactions of the H-P-O axis play in this 
o  How do the declining numbers of ovarian follicles, and associated 
changes in the secretory products, in the aging ovary influence the 
process of the H-P-O axis intercommunication to result in acyclicity 
and eventual cessation of menstruation;
o  How do paracrine and autocrine processes within the aging ovary 
influence its function, and how are these processes regulated by 
extra-ovarian tissues;
o  What is the role of age-, central nervous system-, and 
ovarian-related changes in the pattern of pulsatile hypothalamic GnRH 
secretion on gonadotropin synthesis and release; how do these changes 
affect ovarian function;

 o  What changes occur during the peri- and postmenopause in 
posttranslational processing, including glycosylation, of the pituitary 
gonadotropins; do these changes affect function of various reproductive 
and non-reproductive tissues relative to the menopausal process and the 
development of associated health problems; by what mechanisms do these 
changes occur;
o  Are there age- or menopause-related changes in tissue sensitivity to 
estrogens and other bioregulatory factors secreted by the H-P-O axis; 
by what molecular and cellular mechanisms do these changes occur;
o  Does the reproductive history, as expressed by altered ovarian 
cellular components (due to, for example, different extents of 
regressed follicular or luteal tissue) affect the reproductive aging 
process or mechanisms underlying peri- or postmenopausal health 
o  What is the role of endogenous estrogen made in non-reproductive 
tissues associated with peri- and postmenopausal health problems, such 
as bone and cardiovascular tissue, relative to serum estrogen supplied 
by the ovary;  why are apparent estrogen-protective effects diminished 
in these tissues after menopause;
o  If age-related changes in vascular supply to the ovary play an 
important role in change of ovarian function across the menopause, what 
are the mechanisms for these changes and how do they influence ovarian 

o The NIDDK is interested in basic molecular mechanisms of how hormonal 
signals and other regulatory factors impact upon the function of the 
hypothalamic-pituitary-ovarian axis.

o The NICHD is particularly interested in the perimenopausal or age-
associated factors that may influence fertility in the last 12-15 years 
of menstrual cycling.

Research Resources
The ability to conduct definitive studies into the molecular and 
cellular mechanisms of the  menopausal transition and the associated 
change in non-reproductive tissue function is restricted in women by 
ethical concerns as well as by issues of practicality and experimental 
design. Consequently, it is necessary to utilize appropriate 
experimental models of the human menopausal process and development of 
pathophysiologic sequelae associated with the menopause.
Investigators are encouraged to develop and/or utilize appropriate 
animal models.  A non-primate animal model of menopause may be 
acceptable for particular studies provided that the selection of the 
animal model is based on current and expanding knowledge available 
regarding (a) the human menopausal process and associated changes in 
tissue or organ function, and (b) characteristics and appropriateness 
of particular animal species to answer the research questions posed 
using relevant experimental approaches (Bellino FL, Nonprimate Animal 
Models of menopause: Workshop Report, Menopause 7: 14-24, 2000)  .  For 
example, it may be possible to experimentally manipulate in a 
physiologic fashion ovarian follicle number or rate of follicular 
decline in order to explore their relationship to reproductive aging 
and associated tissue decline.  Although extensive research experience 
and background data on female reproductive aging has been accumulated 
in the rodent, some features of reproductive aging in the female rodent 
are substantially different from the human menopausal process.  Since 
for other species less extensive background data on female reproductive 
aging are available, more preliminary data from the investigator will 
be required if use of these animal species is proposed.
A potential choice for a model of the human menopause based both on the 
phylogenetic relationship of species and the known physiologic 
similarities is the non-human primate.  From the limited data 
available, the rhesus monkey and baboon may be suitable animal models 
of both the menopausal process and the subsequent decline in tissue 
function due to both menopause and aging.  Investigators may choose to 
utilize non-human primates, particularly in collaboration with 
established primate research centers, including the Regional Primate 
Research Centers (RPRC) supported by the National Center for Research 
Resources (NCRR), NIH.  However, there are drawbacks to the extensive 
and immediate use of these species, such as the high cost of husbandry 
(which is partially offset by maintenance of groups of aging animals at 
the RPRC by the NIA), relatively long life span, limited availability, 
and the limited published baseline data on female reproductive aging in 
non-human primates.   For further information on the use and 
availability of middle-aged and older non-human primates, please 
contact the Head of the Office of Biological Resources and Resource 
Development at the NIA, Dr. Nancy Nadon, at 301 496-6402 (phone), 301 
402-0010 (fax), or by email (

Other appropriate experimental models include (a) in vitro cell and 
tissue culture models using human tissues, or specimens derived from 
human tissues, (b) use of human post-mortem tissue where appropriate, 
and (c) implantation of relevant human tissues into pertinent animal 
species to approach questions regarding the behavior of that tissue 
under suitable experimental conditions. While clinical and 
epidemiological studies are not encouraged in response to this program 
announcement, the use of clinically derived data in characterizing the 
human tissues used for these studies would be appropriate.


It is the policy of the NIH that women and members of minority groups 
and their sub-populations 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 
indicating 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 

All investigators proposing research involving human subjects should 
read the UPDATED "NIH Guidelines for Inclusion of Women and Minorities 
as Subjects in Clinical Research," published in the NIH Guide for 
Grants and Contracts on August 2, 2000 
(; a 
complete copy of the updated Guidelines are available at  
The revisions relate to NIH defined Phase III clinical trials and 
require: a) all applications or proposals and/or protocols to provide a 
description of plans to conduct analyses, as appropriate, to address 
differences by sex/gender and/or racial/ethnic groups, including 
subgroups if applicable; and b) all investigators to report accrual, 
and to conduct and report analyses, as appropriate, by sex/gender 
and/or racial/ethnic group differences.


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.


Applications are to be submitted on grant application form PHS 398 
(rev. 4/98) and will be accepted at the standard application deadlines 
as indicated in the application kit. Application kits are available at 
most institutional offices of sponsored research and may be obtained 
from the Division of Extramural Outreach and Information Resources, 
National Institutes of Health, 6701 Rockledge Drive, MSC 7910, 
Bethesda, MD 20892-7910, Phone (301) 710-0267, Email:  
GRANTSINFO@NIH.GOV. Applications are also available on the internet at

Applicants planning to submit an investigator-initiated new (type 1), 
competing continuation (type 2), competing supplement, or any 
amended/revised version of the preceding grant application types 
requesting $500,000 or more in direct costs for any  year are advised 
that they must contact the Institute or Center (IC) program staff 
before submitting the application, i.e., as plans for the study are 
being developed. Furthermore, applicants must obtain agreement from the 
IC staff that the IC will accept the application for consideration for 
award. Finally, applicants must identify, in a cover letter sent with 
the application, the staff member and Institute or Center who agreed to 
accept assignment of the application.

This policy requires applicants to obtain agreement for acceptance of 
both any such application and any such subsequent amendment. Refer to 
the NIH Guide for Grants and Contracts, March 20, 1998 at:

Submit a signed, typewritten, original of the application, including 
the checklist and five signed photocopies in one package to:

BETHESDA, MD 20892-7710
BETHESDA, MD 20817 (for express/courier service)

The title and number of the program announcement must be typed on line 
2 of the face page of the application form and the YES box must be 


The modular grant concept establishes specific modules in which direct 
costs may be requested as well as a maximum level for requested 
budgets. Only limited budgetary information is required under this 
approach. The just-in-time concept allows applicants to submit certain 
information only when there is a possibility for an award. It is 
anticipated that these changes will reduce the administrative burden 
for the applicants, reviewers and Institute staff. The research grant 
application form PHS 398 (rev. 4/98) is to be used in applying for 
these grants, with the modifications noted below.


Modular Grant applications will request direct costs in $25,000 
modules, up to a total direct cost request of $250,000 per year. 
(Applications that request more than $250,000 direct costs in any year 
must follow the traditional PHS398 application instructions.) The total 
direct costs must be requested in accordance with the program 
guidelines and the modifications made to the standard PHS 398 
application instructions described below:

PHS 398

o  FACE PAGE:  Items 7a and 7b should be completed, indicating Direct 
Costs (in $25,000 increments up to a maximum of $250,000) and Total 
Costs [Modular Total Direct plus Facilities and Administrative (F&A) 
costs] for the initial budget period.  Items 8a and 8b should be 
completed indicating the Direct and Total Costs for the entire proposed 
period of support.

Page 4 of the PHS 398.  It is not required and will not be accepted 
with the application.

the categorical budget table on Form Page 5 of the PHS 398.  It is not 
required and will not be accepted with the application.

o  NARRATIVE BUDGET JUSTIFICATION - Prepare a Modular Grant Budget 
Narrative page. (See for sample 
pages.)  At the top of the page, enter the total direct costs requested 
for each year. This is not a Form page.

o  Under Personnel, list all project personnel, including their names, 
percent of effort, and roles on the project. No individual salary 
information should be provided. However, the applicant should use the 
NIH appropriation language salary cap and the NIH policy for graduate 
student compensation in developing the budget request.

For Consortium/Contractual costs, provide an estimate of total costs 
(direct plus facilities and administrative) for each year, each rounded 
to the nearest $1,000.  List the individuals/ organizations with whom 
consortium or contractual arrangements have been made, the percent 
effort of all personnel, and the role on the project. Indicate whether 
the collaborating institution is foreign or domestic. The total cost 
for a consortium/contractual arrangement is included in the overall 
requested modular direct cost amount. Include the Letter of Intent to 
establish a consortium.

Provide an additional narrative budget justification for any variation 
in the number of modules requested.

o  BIOGRAPHICAL SKETCH - The Biographical Sketch provides information 
used by reviewers in the assessment of each individual's qualifications 
for a specific role in the proposed project, as well as to evaluate the 
overall qualifications of the research team.  A biographical sketch is 
required for all key personnel, following the instructions below.  No 
more than three pages may be used for each person.  A sample 
biographical sketch may be viewed at:

- Complete the educational block at the top of the form page;
- List position(s) and any honors;
- Provide information, including overall goals and responsibilities, on 
research projects ongoing or completed during the last three years;
- List selected peer-reviewed publications, with full citations.

o  CHECKLIST - This page should be completed and submitted with the 
application.  If the F&A rate agreement has been established, indicate 
the type of agreement and the date. All appropriate exclusions must be 
applied in the calculation of the F&A costs for the initial budget 
period and all future budget years.

o  The applicant should provide the name and phone number of the 
individual to contact concerning fiscal and administrative issues if 
additional information is necessary following the initial review.


Applications will be assigned on the basis of established Public Health 
Service referral guidelines.  Applications will be reviewed for 
completeness by the Center for Scientific Review (CSR) and 
responsiveness by the Institutes (ICs).  Applications that are complete 
will be evaluated for scientific and technical merit by an appropriate 
peer review group convened in accordance with NIH peer review 
procedures. 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 applications under review, will be discussed, assigned a 
priority score, and receive a second level review by the appropriate 
national advisory council or board.

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?

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 

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 any)?

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 adequacy of plans to include minorities and their subgroups, as 
appropriate for the scientific goals of the research.  Plans for the 
recruitment and retention of subjects will also be evaluated.

o  The reasonableness of the proposed budget and duration in relation 
to the proposed research.

o  The adequacy of the proposed protection for humans, animals or the 
environment, to the extent they may be adversely affected by the 
project proposed in the application.


Applications will compete for available funds with all other 
recommended applications.  The following will be considered in making 
funding decisions:

o  Quality of the proposed project as determined by peer review
o  Availability of funds
o  Program priority.


Inquiries are encouraged. The opportunity to clarify any issues or 
questions from potential applicants is welcome.

Direct inquiries regarding programmatic issues to:

Frank Bellino, Ph.D.
Biology of Aging Program
National Institute on Aging
7201 Wisconsin Avenue, Suite 2C231 MSC 9205
Bethesda, MD  20892-9205
Telephone:  (301) 496-6402
FAX:  (301) 402-0010

William J. Sharrock, Ph.D.
Musculoskeletal Diseases Branch
National Institute of Arthritis and Musculoskeletal and Skin Diseases
45 Center Drive, Natcher Building, Room 5AS-37A, MSC 6500
Bethesda, MD  20892-6500
Telephone:  (301) 594-5055
FAX: (301) 480-4543
Estella Parrott, M.D., M.P.H.
Center for Population Research
National Institute of Child Health and Human Development
6100 Executive Boulevard, Room 8B01, MSC 7510
Bethesda, MD  20892-7510
Telephone:  (301) 496-6515
FAX:  (301) 496-0962

Sheryl M. Sato, Ph.D.
Director, Cellular Basis of Metabolic Diseases Program
National Institute of Diabetes and Digestive and Kidney Diseases
2 Democracy Plaza, Room 6105
6707 Democracy Boulevard, MSC 5460
Bethesda, MD  20892
(301) 594-8811
FAX (301) 480-3503

Direct inquiries regarding fiscal matters to:

Linda Whipp
Grants and Contracts Management Office
National Institute on Aging
7201 Wisconsin Avenue, Suite 2N212, MSC 9205
Bethesda, MD  20892-9205
Telephone:  (301) 496-1472
FAX:  (301) 402-3672

Melinda Nelson 
Grants Management Officer
Grants Management Branch
National Institute of Arthritis and Musculoskeletal and Skin Diseases
45 Center Drive, Room 5AS49 
Bethesda, Maryland  20892 
Telephone:   (301) 435-5278 
Fax:  (301) 480-5450 

Kathy Hancock
Lead Grants Management Specialist
National Institute of Child Health and Human Development
6100 Executive Boulevard, Room 8A17M, MSC 7510
Bethesda, MD 20892-7510
Phone:	301-496-5482
Fax:	301-402-0915

Mr. Kieran Kelley
Grant Management Specialist
National Institute of Diabetes and Digestive and Kidney Diseases
2 Democracy Plaza
6707 Democracy Boulevard, MSC 5456
Bethesda, MD  20892
(301) 594-0417
FAX (301) 480-3504


This program is described in the Catalog of Federal Domestic Assistance 
Nos. 93.866 (NIA), 93.864 (NICHD), 93.846 (NIAMS), 93.847 (NIDDK). 
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 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 

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