[bionet.sci-resources] NIH Guide 6/2/89

CZJ@nihcu.bitnet (06/06/89)

Attached is the Table of Contents
and items of interest
from the NIH Guide to Grants and Contracts - 6/2/89

Jim Cassatt

-------






Vol. 18, No. 19, June 2, 1989


                     DATED ANNOUNCEMENTS (RFPs AND RFAs)


SEER/SURVEILLANCE QUALITY CONTROL UNIT (RFP) ..............(84/124).......... 1
National Cancer Institute
Index:  CANCER


LARGE-SCALE AUTOMATED DNA SEQUENCING OF NEUROTRANSMITTER
RECEPTOR GENES (RFP) ......................................(127/184)......... 1
National Institute of Neurological Disorders and Stroke
Index:  NEUROLOGICAL DISORDERS, STROKE


DIABETES CENTERS (RFA) ....................................(187/292)......... 2
National Institute of Diabetes and Digestive and Kidney Diseases
Index:  DIABETES, DIGESTIVE AND KIDNEY DISEASES


MINORITY-BASED COMMUNITY CLINICAL ONCOLOGY PROGRAM (RFA) ..(295/409)......... 3
National Cancer Institute                                  (1124/2381)
Index:  CANCER


NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUPS FOR THE
ACQUIRED IMMUNODEFICIENCY SYNDROME (RFA) .............(412/488, 2384/3254)... 5
National Institute of Allergy and Infectious Diseases
Index:  ALLERGY, INFECTIOUS DISEASES


MURINE IMMUNODEFICIENCY LENTIVIRUS MODEL FOR AIDS (RFA) ...(491/532)......... 6
National Institute of Allergy and Infectious Diseases      (3257/3556)
Index:  ALLERGY, INFECTIOUS DISEASES


                        ONGOING PROGRAM ANNOUNCEMENTS


MOLECULAR MECHANISMS OF CELL DEATH DURING AGING ...........(538/818)......... 6
National Institute on Aging
Index:  AGING


THE AGING OF RETARDED ADULTS ..............................(821/1099)........10
National Institute on Aging
Index:  AGING




LARGE-SCALE AUTOMATED DNA SEQUENCING OF NEUROTRANSMITTER RECEPTOR GENES

RFP AVAILABLE:  NIH-NINDS-89-10

P.T. 34;  K.W. 0760050, 0760075, 0755045

National Institute of Neurological Disorders and Stroke

The National Institute of Neurological Disorders and Stroke has a new
requirement which involves research to improve and provide large-scale DNA
template production applicable to large-scale automated DNA sequence analysis.

The Contractor shall be required to work from established protocols to 1)
provide single-stranded DNA templates to the Government and 2) improve upon
the methods used to produce these templates.  In most cases this shall include
restriction endonuclease digest analysis of DNA fragments from lambda or
cosmid clones and the use of the resulting information to subclone fragments
of the cloned insert DNA into phagemid or plasmid vectors.  The next step
shall be the production of ordered, unidirectional deletions of DNA fragments
from phagemids containing cloned DNA using exonuclease III and the analysis of
these deleted subclones.  The final step shall be the production of
single-stranded DNA templates from phagemids or plasmids for use in automated
DNA sequencing.  The Contractor may be required to carry out alternate
procedures which shall be either subsets of the above procedures or closely
related procedures.

The Contractor shall be required to develop new procedures to accomplish the
goals achieved by carrying out the procedures above or develop variations of
the above procedures that allow more rapid sample preparation, greater number
of samples to be processed simultaneously, and less variation in experimental
results.  An example of an improvement that the Contractor may perfect is the
use of polymerase chain reaction to prepare single-stranded template DNA.  To

                    Vol. 18, No. 19, June 2, 1989 - Page 1
accomplish these goals, offerors shall have expertise and experience in the
areas of microbiology, molecular biology and nucleic acids biochemistry.

It is anticipated that one contract award will be made under this RFP, for a
three-year period.

RFP No. NIH-NINDS-89-10 will be issued on or about June l, l989, with a
tentative date for receipt of proposals set at August l, l989.

To receive a copy of the RFP, please submit a written request and two
self-addressed mailing labels to the following address.

All responsible sources may submit a proposal which shall be considered by the
Government.

Contracting Officer
Contracts Management Branch, DEA
National Institute of Neurological
Disorders and Stroke, NIH
Federal Building, Room 90l
7550 Wisconsin Avenue
Bethesda, Maryland  20892

Attn: RFP-NINDS-89-10


DIABETES CENTERS

RFA AVAILABLE:  89-DK-09

P.T. 04;  K.W. 0715075, 0785050, 0710030

National Institute of Diabetes and Digestive and Kidney Diseases

Application Receipt Date:  November 20, 1989

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
invites applications for a Center grant to be awarded in Fiscal Year 1991.
NIDDK anticipates the competitive award of one Diabetes Endocrinology Research
Center (DERC) in Fiscal Year 1991.

BACKGROUND

The NIDDK-supported DERCs are part of an integrated program of
diabetes-related research support provided by NIDDK.  These centers have
provided a focus for increasing collaboration and cost effectiveness among
groups of successful investigators at institutions with established
comprehensive diabetes research bases.

OBJECTIVES AND SCOPE

The objectives of the DERCs are to bring together investigators from relevant
disciplines in a manner which will enhance and extend the effectiveness of
research related to diabetes and its complications.  A diabetes center must be
an identifiable unit within a single university medical center or a consortium
of cooperating institutions, including an affiliated university.  The overall
goal of the DERC is to bring together on a cooperative basis, clinical and
basic science investigators in a manner which will enrich the effectiveness of
diabetes research.  An existing program of excellence in biomedical research
in the area of diabetes and related metabolic and endocrine disorders is
required.  This research should be in the form of NIH-funded research
projects, program projects, or other peer-reviewed research that is in
existence at the time of submission of a center application.  Close
cooperation, communication, and collaboration among all involved personnel of
all professional disciplines are ultimate objectives.  Applicants should
consult with NIDDK staff concerning plans for the development of the center.

The DERCs are based on the core concept.  Cores are defined as shared
resources that enhance productivity or in other ways benefit a group of
investigators working in diabetes or diabetes-related areas to accomplish the
stated goals of the center.  Two other types of activities may also be
supported with center funding - a pilot and feasibility program and an
enrichment program.  The pilot and feasibility program provides modest support
for new initiatives or feasibility research studies.  This program is directed
at new or established investigators in other research disciplines where their
expertise may be applied to diabetes research.  The center grant may also
include limited funds for program enrichment such as seminars, visiting
scientists, consultants, workshops, etc.

                    Vol. 18, No. 19, June 2, 1989 - Page 2
MECHANISM OF SUPPORT

NIDDK expects to award one DERC Grant in Fiscal Year 1991 on a competitive
basis.  The receipt of one competitive continuation application is
anticipated, which will compete for the award along with other applications
received in response to this announcement.  Foreign institutions are not
eligible to apply.  The anticipated award will be for five years and is
contingent upon the availability of appropriated funds.  The RFA (general
description and Guidelines for the DERC) and consultation may be obtained
from:

Dr. Sanford A. Garfield
Diabetes Centers Program Director
Division of Diabetes, Endocrinology, and Metabolic Diseases
Westwood Building, Room 626
National Institute of Diabetes and Digestive and Kidney Diseases
Bethesda, Maryland  20892
Telephone:  (301) 496-7418

REVIEW PROCEDURES

Applications for a DERC grant will be evaluated in national competition by the
NIH grant peer review process.  Applications will be reviewed initially by a
special review committee convened by the NIDDK and subsequently by the
National Diabetes and Digestive and Kidney Diseases Advisory Council.

METHOD OF APPLYING

Potential applicants are urged to submit a letter of intent regarding their
application.  The letter of intent is nonbinding and is not a precondition for
an award.  The letter of intent should include the name(s) of the principal
investigator and principal collaborators, descriptive titles of the core
facilities and pilot/feasibility projects, and the organization(s) involved.

Applications must be submitted using PHS Form 398 (Rev. 10/88).  The RFA
label contained in the application kit must be affixed to the bottom of the
face page of the original copy of the application.  Failure to use this label
could result in delayed processing and review of your application.

Mail the completed application (original and four copies) to:

Application Receipt Office
Division of Research Grants
Westwood Building, Room 240
National Institutes of Health
Bethesda, Maryland  20892**

Simultaneously submit two copies to Dr. Sanford A. Garfield at the address
noted above.

The special single receipt date for submissions in response to this
announcement is November 20, 1989, with earliest funding December 1, 1991.
NATIONAL COOPERATIVE VACCINE DEVELOPMENT GROUPS FOR THE ACQUIRED
IMMUNODEFICIENCY SYNDROME

RFA AVAILABLE:  89-AI-16

P.T. 34;  K.W. 0715008, 0740075, 1002045, 0760080, 1002008, 0710030

National Institute of Allergy and Infectious Diseases

Letter of Intent Receipt Date:  June 19, 1989
Application Receipt Date:  August 10, 1989

The National Institute of Allergy and Infectious Diseases (NIAID) announces
the availability of an RFA for the funding of National Cooperative Vaccine
Development Groups for the Acquired Immunodeficiency Syndrome (NCVDG).  The
RFA (available on request) invites applications aimed at the development of
effective vaccines for the prevention of AIDS.  Scientific approaches to the
development of effective AIDS vaccines appropriate to the RFA may range from
research on whole virus vaccines, through the production of preparations with
recombinant DNA techniques and synthetic approaches, to the use of viral
vectors to deliver antigenic materials.  Applications directed towards vaccine
development for AIDS-associated opportunistic infections are not invited.
Otherwise, scientific approaches to the development of effective vaccines
appropriate to the RFA are broad and limited only by the creativity and
ability of the applying group to exploit leads from basic studies in virology,
molecular biology, and immunology.

Each NCVDG will be assembled by the Principal Investigator to form a
multidisciplinary consortium representing the various skills needed to
successfully design and evaluate vaccine entities and strategies for the
prevention of AIDS.  Inasmuch as it is unlikely that all of the outstanding
talents required to exploit fundamental leads from various scientific
disciplines will be found in a single institution, each Group is envisioned as
being multi-institutional as well.  Thus each NCVDG will be assembled by the
Principal Investigator and may consist of a number of Laboratory Projects
representing the scientific disciplines required to attain the Group's goal
and objectives.  The various Laboratory Projects, including that of the
Principal Investigator, may be mobilized from academic or research
institutions, and industry.  It is expected that the rationale for design of
potential vaccines, the synthesis or production of specific candidates, and
the models for evaluation will originate within the Group and be based on
leads from their own and others' fundamental research.

Awards will be made as Cooperative Agreements.  Assistance via a Cooperative
Agreement differs from the research grant in that the Government component (in
this instance, the NIAID) awarding the Cooperative Agreement anticipates
substantial involvement during performance.  The nature of NIAID staff
participation is described in the RFA.  However, the applying Group must
define its objectives in accord with its own interests and perceptions of
approaches to vaccines for AIDS prevention.

It is anticipated that 5 to 7 awards will be made, each averaging $500,000 to
$750,000 in direct costs.

The proposed applicant institution will be responsible for the Group's
application.  Awards will be made to the applicant institution on behalf of
the group as a whole and not to individual Laboratory Projects within the
Group.  The applicant institution will provide a Central Operations Office for
the Group.  The applicant institution will be responsible for the performance
of the entire Group and will be accountable for the funds awarded.  The
participation of the Government through the NIAID extramural staff is aimed at
facilitating a concerted effort by the Group.  The interaction of academic and
non-profit research institutions with commercial organizations and Government
is expected to favor efficient development of AIDS vaccines and will
facilitate their subsequent refinement and evaluation in clinical trials.



                    Vol. 18, No. 19, June 2, 1989 - Page 5
The RFA is available from:

Dr. Dale R. Spriggs
NIAID, AIDS Program
Vaccine Research and Development Branch
6003 Executive Blvd., Room 234P
Rockville, Maryland  20892
Telephone:  (301) 496-8200


MURINE IMMUNODEFICIENCY LENTIVIRUS MODEL FOR AIDS

RFA AVAILABLE:  89-AI-17

P.T. 34;  K.W. 0715008, 0755020, 1002045, 0765033

National Institute of Allergy and Infectious Diseases

Letter of Intent Receipt Date:  July 14, 1989
Application Receipt Date:  August 25, 1989

The National Institute of Allergy and Infectious Diseases (NIAID) announces
the availability of an RFA for the development of a murine immunodeficiency
lentivirus model for the acquired immunodeficiency syndrome (AIDS).  The RFA
(available on request) invites applications to develop a murine
immunodeficiency lentivirus model for AIDS which would expedite studies of
pathogenesis, and evaluation of potential therapies and vaccines.  Applicants
are encouraged to propose novel strategies for obtaining such a model with a
rational approach for the identification, isolation, and molecular and
biological characterization of naturally occurring murine lentiviruses.  It
will be important to address multiple alternatives since there will be no way
to guarantee success of a single search strategy.  Scientific and technical
merit of the zoology/ecology collaborators or contractors will be critical in
the evaluation of the applications.

Mouse strains and viruses developed in this research must be made available to
the AIDS Research and Reference Reagent Program for world-wide distribution to
qualified researchers.

Awards will be made as individual research (RO1) grants.

Investigators from any institution, foreign or domestic, are eligible to apply
for this funding.

This RFA is available from:

Dr. Linda M. Muul
Pathogenesis Branch
NIAID, AIDS Program
6003 Executive Blvd., Room 214N
Rockville, Maryland  20892
Telephone:  (301) 496-8378


                        ONGOING PROGRAM ANNOUNCEMENTS


MOLECULAR MECHANISMS OF CELL DEATH DURING AGING

P.T. 34;  K.W. 0710010, 1002004, 0765010, 0765033, 0790005, 0705055

National Institute on Aging

INTRODUCTION

Cell death in multicellular organisms takes place in a variety of
circumstances.  For example, the death of certain cells may occur as part of a
developmental program; in connection with organ involution or regression as in
the adult thymus; during cell renewal processes where specialized,
differentiated, non-dividing effete cells such as granulocytes and
erythrocytes are replaced by newly-formed cells; as a consequence of toxic or
harmful environmental conditions; when potentially harmful cells such as
neoplastic or virus-infected cells are targeted for destruction by
surveillance systems; or because of senescence of the cells themselves or the
host organism.  In an entity as complex as the cell there are processes such
as nucleic acid and protein synthesis, transport of ions, nutrients and other
metabolites across membranes, and structures such as membranes and
cytoskeleton whose function and integrity must be faithfully maintained

                    Vol. 18, No. 19, June 2, 1989 - Page 6
because they are essential for cell viability.  Defense mechanisms such as DNA
repair and heat shock proteins have evolved which allow the cell to repair, or
prevent injury to vital molecules when faced with stressful or potentially
harmful environmental conditions.

In some cases, the molecular events that lead to cell death are reasonably
well known.  For example, in complement-mediated lysis the membrane attack
complex causes the formation of channels in the target cell's membrane, which
therefore becomes leaky and no longer functions as a permeability barrier.  In
other cases, however, the critical event(s) in cell death is not known; nor is
it known which molecular lesions are irreversible and which can be repaired or
prevented by the cell's protective mechanisms.  Questions such as why and how
senescent cells die are relevant to understanding the aging process in complex
organisms.  Furthermore, the role of cell death in age-related diseases and
degenerative conditions is unknown.  This question is particularly important
in neural tissue, where cell regeneration is either non-existent or at best
quite limited.

SPECIFIC OBJECTIVES

The National Institute on Aging (NIA) wishes to encourage applications for
research projects investigating the molecular events that may lead to, or
accompany, cell death during aging.  While the study of cell death in any
circumstance may be appropriate under this program, its relevance to the aging
process must be explicit.  The following questions illustrate the type of
research that this program announcement intends to foster.

BASIC MECHANISMS OF CELL DEATH

  o  What intracellular conditions predispose the cells to irreversible
     damage, e.g., elevation of calcium ion concentration, oxidizing
     agents, etc.?  By what mechanisms?

  o  What are the critical sites or molecules which, when damaged,
     result in cell death if not repaired?

  o  Which potentially lethal lesions can be repaired by the cell, and
     which lesions are irreversible?

  o  What are the cellular mechanisms that prevent or reverse
     potentially lethal lesions, and how do they work?  Are these
     defense mechanisms impaired in senescence?

  o  Do senescent cells die because they are programmed to die, do they
     die because of damage resulting from the accumulation of damage
     inflicted by a hostile environment, or both?

  o  What tissues are most sensitive to loss of function due to cell
     death?

  o  Although cells may die for a variety of reasons, are there common
     steps in the pathways leading to cell death?

  o  What naturally-occurring molecules are toxic to cells leading to
     cell death, and how do they function?

CELL DEATH IN AGE-ASSOCIATED DISEASES AND DEGENERATIVE CONDITIONS

The role of cell death in the pathogenesis of several age-related diseases and
degenerative conditions is an intriguing and largely unexplored possibility.
Explorations of this possibility are limited by technical difficulties in
determining the extent of cell death in many tissues.  Important avenues for
research thus include the following:

  o  Testing new techniques to determine the rate and extent of in vivo
     cell loss and/or cell death in tissues susceptible to age-related
     diseases (e.g. articular cartilage, bone, cardiac muscle, vascular
     endothelium; cell loss in the CNS is discussed in the next
     section).

  o  Studies to determine the possible role of cell loss and/or cell
     death in specific age-associated diseases and conditions.  Examples
     include the possible role of chondrocyte loss in osteoarthritis,
     loss of osteoblasts or osteoblast progenitor cells in osteoporosis,
     loss of striated muscle fibers in age-associated degenerative
     muscular conditions, loss of parietal cells in atrophic gastritis,
     cell loss associated with disorders of gait and balance, and cell
     loss in the sinoatrial node in age-associated arrhythmias.

                    Vol. 18, No. 19, June 2, 1989 - Page 7
  o  Studies to determine the role of cell in age-associated changes in
     renal, pulmonary, muscular, and other physiologic functions.

CELL DEATH IN THE AGING NERVOUS SYSTEM

One of the most critical issues in the neurobiology of aging concerns the
specific mechanisms of selective cell loss in the brain.  Neuronal death is
especially critical due to the non-replicative nature of most cells in the
central nervous system; CNS structural change and/or loss of neurons is the
hallmark of many of the age-associated disorders of the brain such as
Alzheimer's disease.  The inability of the CNS to replace lost neurons and the
complex structure of the brain raise a number of unique research questions.

  o  Is there significant cell loss associated with normal healthy aging
     of the brain as there is during early development or is it only as
     a result of incipient disease?

  o  Do the mechanisms of cell loss associated with normal brain aging
     differ from those associated with diseases of the CNS?

  o  What accounts for the selective vulnerability of specific neurons
     in various diseases?

  o  What is the role of trophic factors in the survival and death of
     neurons in the aging CNS?

  o  Is there increased vulnerability to endogenous and environmental
     toxins in the aging CNS and if so what is the nature of this
     vulnerability?

  o  Under what conditions do excitatory amino acid neurotransmitters
     become excitotoxic?

  o  What are the molecular mechanisms by which toxins trigger cell
     death in the aging CNS?

  o  What role does neuronal connectivity and activity play in the
     survival or death of neurons in the adult and aging CNS?

  o  What is the role of altered gene expression in neuronal cell death?

  o  How does the aging CNS compensate for cell loss?

  o  What roles do vascular and glial elements play in neuronal survival
     and death; are changes in the transport mechanisms for glucose,
     oxygen and other essential elements involved?

  o  Are the quantitative methods used for estimating cell loss in the
     aging nervous system accurate or are new methods needed?

  o  What role do changes in neuroendocrine and immune factors play in
     neuronal cell death in the aging nervous system?

  o  What is the role of stress and glucocorticoids in neuronal cell
     death?

  o  Are intracellular metabolic changes such as modifications in
     mitochondrial oxidative metabolism primary or secondary causes of
     neuronal cell death?

  o  How do membrane changes affect inter- and intracellular signal
     transduction during normal aging and diseases of aging?

  o  How do changes in homeostatic mechanisms that regulate cytosol
     calcium concentration lead to cell death?

Qualified scientists who plan to investigate these issues, or other issues of
similar nature, are invited to apply for research grants under this program.

APPLICATION AND REVIEW PROCEDURES

The primary mechanisms for support of this program are:

o  Research grant (R01)

o  Program Project Award (P01)



                    Vol. 18, No. 19, June 2, 1989 - Page 8
o  First Independent Research Support and Transition (FIRST)
   Award (R29)

o  Career grants, which include:
     Research career development award (K04)
     Clinical investigator award (K08)

o  Training grants (T32)

o  Fellowships (F32, F33)

Research project grant (R01 and R29) applications, fellowships (F32, F33) and
research career development awards (K04) will be reviewed for scientific and
technical merit by an appropriate study section in the Division of Research
Grants.  All other applications will be reviewed by an appropriate peer review
group.  Secondary review will be by an appropriate National Advisory Council.

There are no set-aside funds for these applications.  Applications compete on
the basis of scientific merit with all other applications.  The review
criteria are the traditional ones underlying scientific merit.

Researchers who are considering making an application in response to this
announcement are welcome to discuss their project, and the range of grant
mechanisms available, with NIA staff in advance of formal submission.  This
can be done either through a telephone conversation or a brief letter giving
the descriptive title of the proposed project and identifying the principal
investigator and, when known, other key participants.  Applications related to
the health of women and minorities are particularly encouraged.

Applicants should use the regular research project and program project grant
application form 398 (Rev. 9/86) for R01, R29, P01, T32, K04 and K08
applications, and form 416-1 (revised 7/88) for F32 and F33 applications.
These are available at the applicant's institution or from:

Office of Grants Inquiries
Division of Research Grants
Westwood Building, Room 449
National Institutes of Health
Bethesda, Maryland  20892
Telephone:  (301) 496-7441

To expedite the application's routing within NIH, please check "Yes" on item 2
of the face sheet of the application indicating that your proposal is in
response to this announcement and print "Mechanisms of Cell Death."  In
assigning applications to NIA or other Institutes, accepted referral
guidelines will be followed.

Mail the completed application (with 6 copies) to:

Division of Research Grants
National Institutes of Health
Westwood Building, Room 240
Bethesda, Maryland  20892**

Receipt dates for Research Grant, Program Project Grant, Research Career
Development Award and First Award applications are February 1, June 1, and
October 1; those for Institutional Training Grant and Fellowship applications
are January 10, May 10, and September 10.

Depending on your particular research interests, correspondence and inquiries
should be directed to:

Basic mechanisms of cell death

Huber Warner, Ph.D.
Molecular Biology Program Administrator
Biomedical Research and Clinical Medicine
Building 31, Room 5C21
National Institute on Aging
Bethesda, Maryland 20892
Telephone:  (301) 496-6402








                    Vol. 18, No. 19, June 2, 1989 - Page 9
Role of cell death in age-associated diseases

Evan Hadley, M.D.
Chief, Geriatrics Branch
Biomedical Research and Clinical Medicine
Building 31, Room 5C27
Bethesda, Maryland  20892
Telephone:  (301) 496-6761

Cell death in the aging nervous system

Creighton Phelps, Ph.D.
Neuroplasticity Program Administrator
Neuroscience and Neuropsychology of Aging
Building 31, Room 5C32
National Institute on Aging
Bethesda, Maryland  20892