Federal Register / Vol. 62, No. 156 / Wednesday, August 13, 1997 / Notices 43333

orally or in writing, on issues pending

before the committee. Written

submissions may be made to the contact

person by August 22, 1997. Oral

presentations from the public will be

scheduled between approximately 8:30

a.m. to 9 a.m., and between

approximately 1 p.m. to 2 p.m. on

September 4, 1997. Time allotted for

each presentation may be limited. Those

desiring to make formal oral

presentations should notify the contact

person before August 22, 1997, and

submit a brief statement of the general

nature of the evidence or arguments

they wish to present, the names and

addresses of proposed participants, and

an indication of the approximate time

requested to make their presentation.

The agency encourages investigators,

academicians, members of the

pharmaceutical industry, consumer

groups, and others with information

relevant to the topic to respond to the

contact person.

Notice of this meeting is given under

the Federal Advisory Committee Act (5

U.S.C. app. 2).

Dated: August 7, 1997.

William B. Schultz,

Acting Lead Deputy Commissioner.

[FR Doc. 97–21434 Filed 8–12–97; 8:45 am]

BILLING CODE 4160–01–F

DEPARTMENT OF HEALTH AND

HUMAN SERVICES

Food and Drug Administration

Advisory Committee; Notice of Meeting

AGENCY: Food and Drug Administration,

HHS.

ACTION: Notice.

This notice announces a forthcoming

meeting of a public advisory committee

of the Food and Drug Administration

(FDA). At least one portion of the

meeting will be closed to the public.

Name of Committee: Hematology and

Pathology Devices Panel of the Medical

Devices Advisory Committee.

General Function of the Committee:

To provide advice and

recommendations to the agency on FDA

regulatory issues.

Date and Time: The meeting will be

held on September 5, 1997, 10 a.m. to

5 p.m.

Location: Corporate Bldg., conference

room 020B, 9200 Corporate Blvd.,

Rockville, MD.

Contact Person: Veronica J. Calvin,

Center for Devices and Radiological

Health (HFZ–440), Food and Drug

Administration, 2098 Gaither Rd.,

Rockville, MD 20850, 301–594–1243, or

FDA Advisory Committee Information

Line, 1–800–741–8138 (301–443–0572

in the Washington, DC area), code

12515. Please call the Information Line

for up-to-date information on this

meeting.

Agenda: The committee will discuss

quality control issues for home-use

prothrombin time devices.

Procedure: On September 5, 1997,

from 10:30 a.m. to 5 p.m., the meeting

is open to the public. Interested persons

may present data, information, or views,

orally or in writing, on issues pending

before the committee. Written

submissions may be made to the contact

person by August 22, 1997. Oral

presentations from the public will be

scheduled between approximately 11

a.m. and 12:15 p.m. Time allotted for

each presentation may be limited. Those

desiring to make formal oral

presentations should notify the contact

person before August 22, 1997, and

submit a brief statement of the general

nature of the evidence or arguments

they wish to present, the names and

addresses of proposed participants, and

an indication of the approximate time

requested to make their presentation.

Closed committee deliberations. On

September 5, 1997, from 10 a.m. to

10:30 a.m., the meeting will be closed to

permit discussion and review of trade

secret and/or confidential information.

(5 U.S.C. 552b(c)(4)). FDA staff will

present trade secret and/or confidential

commercial information regarding

present or future issues.

Notice of this meeting is given under

the Federal Advisory Committee Act (5

U.S.C. app. 2).

Dated: August 11, 1997.

Michael A. Friedman,

Deputy Commissioner for Operations.

[FR Doc. 97–21552 Filed 8–12–97; 8:45 am]

BILLING CODE 4160–01–F

DEPARTMENT OF HEALTH AND

HUMAN SERVICES

National Institutes of Health

Government-Owned Inventions;

Availability for Licensing

AGENCY: National Institutes of Health.

ACTION: Notice.

SUMMARY: The inventions listed below

are owned by agencies of the U.S.

Government and are available for

licensing in the U.S. in accordance with

35 U.S.C. 207 to achieve expeditious

commercialization of results of federally

funded research and development.

Foreign patent applications are filed on

selected inventions to extend market

coverage for U.S. companies and may

also be available for licensing.

ADDRESSES: Licensing information and

copies of the U.S. patent applications

listed below may be obtained by writing

to the indicated licensing contact at the

Office of Technology Transfer, National

Institutes of Health, 6011 Executive

Boulevard, Suite 325, Rockville,

Maryland 20852–3804; telephone: 301/

496–7057; fax: 301/402–0220. A signed

Confidential Disclosure Agreement will

be required to receive copies of the

patent applications.

Dvl1-Deficient Mice

AJ Wynshaw-Boris, N Lijam, D

Sussman, R Paylor, J Crawley (NHGRI)

OTT Reference No. E–100–97/0

Licensing Contact: David Sadowski;

phone: 301/496–7735 ext. 288; e-mail:

DS27A@NIH.GOV

Genetic factors are important

modifiers of a variety of simple and

complex behaviors in virtually all

organisms. Genetic effects have been

inferred from inbred strain analysis in

rodents and from linkage analysis in

rodents and humans. More recently,

genes influencing specific behaviors

have been identified by analyzing

behavioral abnormalities in mice with

targeted gene disruption.

In the present invention, mice

completely deficient for Dvl1, a mouse

homolog of the Drosophila segment

polarity gene Dishevelled, were created

by gene targeting. These mice

demonstrate that Dvl1 participates in

complex behaviors in mammals. Dvl1-

deficient mice exhibit reduced social

interaction, including differences in

whisker-trimming, deficits in nestbuilding, less huddling contact during

home cage sleeping, and subordinate

responses in a social dominance test. In

addition, Dvl1-deficient mice display

striking abnormalities in sensorimotor

gating, as indicated by attenuation of

prepulse startle inhibition in the mutant

mice. Prepulse inhibition is abnormal in

several human neuropsychiatric

disorders including schizophrenia,

schizotypal personality disorders,

obsessive-compulsive disorders,

Huntington’s disease, and Tourette

syndrome. In addition, many of these

disorders (as well as autism) are

characterized by abnormal social

interaction. Hence, Dvl1-deficient mice

provide a genetic animal model of

aspects of several human psychiatric

disorders and serve as a useful model

for screening drugs that modify
43334 Federal Register / Vol. 62, No. 156 / Wednesday, August 13, 1997 / Notices

abnormal social interaction and

sensorimotor gating.

Transgenic and Chimeric Viral Delivery

Systems

WJ Ramsey, RM Blaese (NHGRI)

OTT Reference No. E–011–97/0 filed 11

Apr 97

Licensing Contact: Larry Tiffany; phone:

301/496–7056 ext. 206; e-mail:

LT10X@NIH.GOV

The development of eukaryotic viral

vectors has generally focused on

delivery of one or more heterologous

genes to target cells, particularly for

gene therapy. Such development has

primarily involved vector systems

utilizing retrovirus, adenovirus, herpes

virus, vaccinia virus, and adenoassociated virus particles. However,

each of these viral vector systems has

presented one or more of several

obstacles including low viral titers,

induced host immune responses,

inefficient transduction, and transient

expression of the desired heterologous

gene. This invention addresses the need

for improved eukaryotic viral vectors for

diagnostic applications and for

delivering heterologous genes to cells in

vitro, ex vivo, and in vivo.

The present invention provides a

system for the production of viral

vectors (secondary viruses) whose

genome is encoded within another virus

with a different life cycle and biologic

characteristics (primary virus). For

example, chimeric primary viruses with

high transduction efficiencies

(adenoviruses) can be used to direct the

production of secondary viruses

(retroviruses) in a wide range of

producer cell types. Thus single (or

panels of) secondary viral vectors

containing identical secondary vector

genomes can easily and rapidly be

produced in retroviral vector packaging

cells containing different envelope

targeting components with the

additional advantage that there will be

little chance for vector rearrangement or

recombination. Secondary viruses also

can be readily produced in cells

obtained from the eventual gene therapy

target species so that enveloped viruses

will contain membrane constituents

from the same, rather than a xenogeneic

species, lessening the chance for

neutralizing immune responses to the

vectors. Similarly, serum complementmediated lysis of retroviral vectors may

be eliminated by the ability to easily use

vector producer cells from the same

species as the species to be treated by

gene therapy. Such secondary viruses

may comprise an expression cassette

constituting a nucleic acid encoding a

heterologous protein and/or an

antisense nuclei acid. Hence, this

invention overcomes obstacles

occurring with the in vitro, ex vivo, and

in vivo use of common viral vector

systems. In addition, these chimeric

primary viruses can be used to rescue

unknown viral genomes from host cells

for use in the development of diagnostic

tests or in the development of novel

viral vector systems.

MEN1, The Gene For Multiple

Endocrine Neoplasia Type 1

SC Chandrasekharappa (NHGRI), AM

Spiegel (NIDDK), LA Liotta (NCI) et al.

OTT Reference No. E–094–97/0 filed 05

Mar 97

Licensing Contact: Ken Hemby; phone:

301/496–7735 ext. 265; e-mail:

JH259B@NIH.GOV

Multiple endocrine neoplasia type 1

(MEN1) is an autosomal dominant

familial cancer syndrome characterized

by occurrence of tumors in

parathryroids, enteropancreatic

endocrine tissues, the anterior pituitary,

and occasionally other sites. The

present invention provides an isolated

DNA sequence encoding a gene which

when mutated in the germline is

associated with the development of

MEN1. This invention also comprises

polyclonal and monoclonal antibodies

which selectively bind to menin, the

protein encoded by MEN1. In addition,

the present invention provides methods

for immunological detection of menin in

biological samples as well as methods

for detecting the presence, alteration, or

absence of MEN1 DNA or RNA. This

research has been published in Science

276: 404–407 (1997).

Potential areas of application of this

invention include sporadic and familial

MEN1 diagnostics using immunoassays

and nucleic acid hybridizations, and

gene therapy.

Invaginated Liposome Delivery System

N Smyth-Templeton, GN Pavlakis (NCI)

Serial No. 60/024,386 Filed 19 Aug 96

Licensing Contact: Larry Tiffany; phone:

301/496–7056 ext. 206; e-mail:

LT10X@NIH.GOV

Liposome formulations for in vivo

delivery are valuable alternatives to

viral vectors and avoid the inherent

problems associated with modifying

viral genomes to create expression

vehicles. Previous liposome

formulations limited therapeutic

efficacy due to generally low expression

of the DNA being delivered. In contrast,

these novel liposomes are able to

transfect a broad host range and express

the encoded proteins at high titers.

The present technology involves

highly efficient cationic liposomes for

increased in vivo delivery of

biologically active agents. These

extruded DOTAP:cholesterol complexes

allow gene expression to be improved

up to 150-fold over previous liposomes.

This improvement is due to the novel

morphology of the DNA:liposome

complexes. The complexes are vaselike

structures which invaginate and

condense DNA between two protective

lipid bilayers. Because the outside of the

DNA:liposome complexes is

substantially free of DNA, targeting

ligands may be placed on the outside of

the complexes, without compromising

the effect of the targeting ligand or the

ability of DNA to be delivered and

expressed.

The present technology may be used

for: systematic or site-specific delivery

and expression of nucleic acid products;

production of kits capable of carrying

any biologically active agent; delivery of

reagents for human gene therapy in the

treatment of disease; and providing a

method for long term expression of a

gene product from a non-integrated

nucleic acid.

Licensees are currently being sought

for all therapeutic applications.

In Vitro Determination Of CD4+ T Cell

Depletion In HIV–1 Seropositive

Subjects as a Predictor of Future CD4+

T Cell Decline In Vivo

D Zella, A Riva, M Reitz (NCI)

OTT Reference No. E–061–96/0

Licensing Contact: George Keller; phone:

301/496–7735 ext. 246; e-mail:

GK40J@NIH.GOV

The current invention embodies a

prognostic method for determining

whether an asymptomatic HIV–1

seropositive individual is a progressor

or a non-progressor to AIDS. The

inventors have discovered that in HIV–

1 seropositive persons in the

asymptomatic stage of the disease,

peripheral blood mononuclear cells

(PBMCs) respond in one of two ways

when isolated and subsequently

activated in vitro by IL–2. Either (1) the

CD3+CD4+ cell number increases in

culture (non-progressor subjects) or (2)

the CD3+CD4+ number does not

increase or decreases in culture

(progressor subjects). This analysis was

performed by an automated flow

cytometer. This method, when

developed as a commercially-available

test, may represent an economical and

accurate assay to determine when

detrimental changes for the immune

system occur in asymptomatic HIV–1

seropositive subjects, and for this reason

to predict whether an individual is
Federal Register / Vol. 62, No. 156 / Wednesday, August 13, 1997 / Notices 43335

progressing to AIDS. This assay may

therefore be a valuable tool to use in

determining the appropriate course of

therapy to target not only HIV–1

replication but also to monitor the

effects of therapeutic drugs on the host

immune system response.

Avian Based Retrovirus Vectors

E Barsov, SH Hughes (NCI)

Serial No. 08/445,462 filed 22 May 95

Licensing Contact: Larry Tiffany; phone:

301/496–7056 ext. 206; e-mail:

LT10X@NIH.GOV

Recombinant retrovirus vectors based

on the Rous sarcoma virus (RSV) are

valuable alternatives to murine based or

replication-defective vectors because

they do not require a packaging or

helper cell line. Previous RSV vectors

limited efficacy due to their inability to

infect a broad range of mammalian

species. In contrast, these novel vectors

are able to infect a wider range of host

at high titers while remaining inherently

defective in mammalian cells.

The present technology involves

recombinant avian sarcoma leukosis

virus (ASLV) derived retroviral vectors

having an expanded host range.

Specifically, the ASLV envelope gene is

replaced by the env region derived from

a virus capable of infecting both

mammalian and avian cells. This

improvement allows the vectors to

produce high titer stock in avian cells

and the resulting virus can infect both

avian and mammalian species

efficiently.

The present technology may be used

for in vitro and in vivo delivery of

nucleic acid sequences to avian or

mammalian cells and for treatment or

prevention of diseases involving transfer

by recombinant retroviral vectors.

Licensees are currently being sought

for all therapeutic applications.

Nucleotide and Deduced Amino Acid

Sequences of a New Tumor Gene, Int6

R Callahan, A Marchetti, F Buttitta, G

Smith (NCI)

OTT Reference Nos. E–265–94/0 and E–

265–94/1

Licensing Contact: Ken Hemby; phone:

301/496–7735 ext. 265; e-mail:

JH259B@NIH.GOV

Murine retroviruses have been useful

in the identification of mammalian

genes involved in tumor development.

Five loci have been previously

identified as integration sites for one

specific retrovirus, mouse mammary

tumor virus (MMTV). This work

describes a sixth site of integration for

MMTV, the Int6 gene. The Int6 gene is

highly conserved among vertebrate

species, including humans. This

invention embodies a series of reagents

derived from the nucleic acid and

amino acid sequences of the Int6 gene

and the use of these reagents in

diagnostic methods, immunotherapy,

gene therapy, and as vaccines.

N-(1-thienylcycloalkyl)alkenyl-amines

For Treatment Of Neurotoxic Injury

KC Rice, AE Jacobson, A Thurkauf, MV

Mattson, TL O’Donohue, PC Contreras,

NM Gray (NIDDK)

Serial No. 08/344,433 Filed 23

November 94; U.S. Patent 5,604,255

issued 18 February 97

Licensing Contact: Leopold Luberecki,

Jr.; phone: 301/496–7735 ext. 223; email: LL87A@NIH.GOV

This invention describes compounds,

compositions, and methods for

neuroprotective purposes such as

controlling brain damage which occurs

during periods of anoxia, or ischemia

associated with stroke, cardiac arrest or

perinatal asphyxia. The treatment

includes administration of an N-(1-

thienylcycloalkyl) alkylamine

compound as an antagonist to inhibit

excitotoxic actions at major neuronal

excitatory amino acid receptor sites.

Compounds of most interest are

described in detail.

Brain tissue is particularly sensitive to

deprivation of oxygen or energy;

permanent damage to neurons can occur

during brief periods of hypoxia, anoxia

or ischemia. Neurotoxic injury is known

to be caused or accelerated by certain

excitatory amino acids (EAA) found

naturally in the central nervous system.

Neurons, which have EEA receptors on

their dendritic or somal surface,

undergo acute excitotoxic degeneration

when these receptors are excessively

activated by glutamate. Thus agents

which selectively block or antagonize

the action of glutamate at the EAA

synaptic receptors of central neurons

can prevent neurotoxic injury associated

with anoxia, hypoxia or ischemia

caused by stroke, cardiac arrest or

perinatal asphyxia.

The method embodied in the

invention may prove valuable for the

control of neuropathological processes

and the neurodengenerative

consequences thereof in mammals by

treating a mammal susceptible to

neurotoxic injury with an antiexcitotoxic effective amount of a

compound of a class described herein.

A Method for the Liposomal Delivery of

Nucleic Acids

AR Thierry (NCI)

Serial No. 08/286,730 Filed 05 August

94 and Serial No. 08/522,246 Filed 04

September 95 (CIP of 08/286,730)

Licensing Contact: Larry Tiffany; phone:

301/496–7056 ext. 206; e-mail:

LT10X@NIH.GOV

The present invention is directed to a

liposomal preparation of nucleic acids

or analogues and specific lipids which

form liposomes. Liposome vesicles are

prepared from a mixture of cationic

lipopolyamine and a neutral lipid.

Nucleic acids are associated with the

liposomes in two ways: (1) Complex

formation between the cationic lissome

vesicle and negatively charged nucleic

acid or (2) partial encapsulation and

partial complex formation in and with

the cationic liposome vesicle.

Liposome-encapsulated nucleic acids

have been shown to be more efficient in

transducing cells in cell cultures.

Sonication of liposome-complexed

nucleic acids allow for more

homogenized and smaller liposome

particles, and consequently for the

ability to circulate for longer periods in

blood following systemic injection.

Nucleic acids associated with the

liposomal carrier are completely

protected from enzymatic attack such as

nucleases, and stability in circulating

blood after administration can be

achieved. The present invention

provides for the highly efficient delivery

of nucleic acids to cells in vitro or in

vivo. Therefore, this invention provides

a method for gene therapy. This

liposome method does not have safety

concerns associated with gene therapy

based upon viral vectors. However,

liposomal delivery in accordance with

the present invention may be used for

increasing recombinant retrovirus

infection by enhancing the penetration

and/or expression of the viral agents.

The patent application includes

claims to liposome compositions and

method of use. These materials and

methods are useful in the delivery of

nucleic acids to cells and tissues.

Nitrogen-Containing Cyclohetero

Alkylamino Aryl Derivatives for CNS

Disorders

BR De Costa, WD Bowen, X-S He, L

Radesca, KC Rice (NIDDK)

Serial No. 08/261,796 Filed 20 June 94;

U.S. Patent 5,571,832 Issued 05 Nov 96

Licensing Contact: Leopold Luberecki,

Jr.; phone: 301/496–7735 ext. 223; email: LL87A@NIH.GOV

This invention describes a class of

therapeutically useful compounds
43336 Federal Register / Vol. 62, No. 156 / Wednesday, August 13, 1997 / Notices

comprising a pyrrolidinyl ring,

compositions and methods for treatment

of Central Nervous System (CNS)

dysfunctions, neurotoxic damage, or

neurodegenerative diseases. These

compounds are particularly useful for

treating neurotoxic injury which follows

periods of hypoxia, anoxia or ischemia

associated with stroke, cardiac arrest or

perinatal asphyxia. In addition these

compounds are also useful as

antipsychotics and anticonvulsives.

Unlike other tissues which can

survive extended periods of hypoxia,

brain tissue is particularly sensitive to

deprivation of oxygen or energy.

Permanent damage to neurons can occur

during brief periods of hypoxia, anoxia

or ischemia. Neurotoxic injury is known

to be caused or accelerated by certain

excitatory amino acids (EAA) found

naturally in the CNS. Compounds as

described herein block the action of

EEA synaptic receptors and thus can

prevent neurotoxic injury.

Treatment of CNS disorders and

diseases such as cerebral ischemia,

psychotic disorders, convulsions and

parkinsonism, as well as prevention of

neurotoxic damage and

neurodegenerative diseases, may be

accomplished by administration of a

therapeutically-effective amount of a

compound of a class described herein.

Severe Renal Glomerular Disease in

Mice Homozygous for Targeted

Disruption of Uteroglobin Gene: A

Model for Human Hereditary

Glomerulopathies

AB Mukherjee, Z Zhang (NICHD)

OTT Reference No. E–164–96/0

Licensing Contact: David Sadowski;

phone: 301/496–7735 ext. 288; e-mail:

DS27A@NIH.GOV

Uteroglobin (UG) is a protein fraction

of pregnant uterine fluid which can

induce and regulate blastocystic

development and also possesses

important anti-inflammatory properties.

This invention describes a novel

physiological function of UG, which is

its role in preventing severe fibronectin

(Fn) deposit-associated renal glomerular

disease. Uteroglobin binds to Fn thereby

inhibiting the formation of Fn-Fn

aggregates and Fn-collagen aggregates,

thus preventing the disease. Uteroglobin

knockout mice (UG-/-) were generated

by targeted disruption of the UG gene.

These mice developed glomerular

disease, became cachectic and died

within 4–5 weeks after birth.

This mouse could potentially be a

valuable model system for the study and

treatment of glomerular disease.

A description of this research may be

found in Science, vol. 276, pp. 1408–

1412, 1997.

A Method for Producing Retrovirus

RNA Packaging Cassettes Amplified in

the Cytoplasm by Autocatalytic

Togavirus Vectors

R Morgan, J Wahlfors, K Xanthopoulos

(NHGRI)

OTT Reference No. E–135–96/0 filed 25

Sep 96

Licensing Contact: Larry Tiffany; phone:

301/496–7056 ext. 206; e-mail:

LT10X@NIH.GOV

Retroviral vectors are currently the

most advanced system available for

mammalian gene therapy. The major

obstacle with the previous methods is

that the transfer of complex or large

genomic elements is virtually

impossible. This technology obviates

the need for the retrovirus DNA

provirus stage of the life cycle via

retroviral RNA vectors. Specifically, this

invention utilizes Togaviruses,

especially the Semliki Forest virus

(SFV), to produce recombinant

retroviral vector RNA in the cytoplasm

of a retrovirus packaging cell. Using the

SFV system, a retroviral cassette with a

heterologous gene is cloned into an SFV

expression vector. This in vitro

transcribed RNA vector is used to

transduce packaging cells. The retroviral

RNA vector is amplified in the

cytoplasm using the SFV system, and

packaged into infectious viral particles.

This system represents a means by

which large fragments of viral RNA, or

complex gene structures, can be

transferred via retroviral vectors. An

additional advantage is that by using the

SFV production system, it is able to

produce high titers of retrovirus

particles, due to its self-amplification

capabilities.

Potential areas of application include:

ex vivo and in vivo gene therapy for

infectious (e.g., HIV) and noninfectious

(e.g., cancer, birth defects) disease;

untranslated genomic regions of DNA

may be important for regulation of gene

expression.

Dated: August 5, 1997.

Barbara M. McGarey,

Deputy Director, Office of Technology

Transfer.

[FR Doc. 97–21401 Filed 8–12–97; 8:45 am]

BILLING CODE 4140–01–P

DEPARTMENT OF HEALTH AND

HUMAN SERVICES

National Institutes of Health

National Eye Institute

Notice of the meeting of the National

Advisory Eye Council Pursuant to Pub.

L. 92–463, notice is hereby given of the

meeting of the National Advisory Eye

Council (NAEC) on September 11–12,

1997, Executive Plaza North, Conference

Room G, 6130 Executive Boulevard,

Bethesda, Maryland.

The NAEC meeting will be open to

the public on September 11, from 8:30

a.m. until approximately 11:30 a.m.

Following opening remarks by the

Director, NEI, there will be

presentations by the staff of the Institute

and discussions concerning Institute

programs and policies. Attendance by

the public at the open session will be

limited to space available.

In accordance with provisions set

forth in sec. 552b(c)(4) and 552b(c)(6),

Title 5, U.S.C. and sec. 10(d) of Pub. L.

92–463, the meeting of the NAEC will

be closed to the public on September 11

from approximately 11:30 a.m. until

adjournment at approximately 5:00 p.m.

for the review, discussion, and

evaluation of individual grant

applications. These applications and the

discussions could reveal confidential

trade secrets or commercial property

such as patentable material, and

personal information concerning

individuals associated with the

applications, the disclosure of which

would constitute a clearly unwarranted

invasion of personal privacy.

Ms. Lois DeNinno, Council Assistant,

National Eye Institute, EPS, Suite 350,

6120 Executive Boulevard, MSC–7164,

Bethesda, Maryland 20892–7164, (301)

496–9110, will provide a summary of

the meeting, roster of committee

members, and substantive program

information upon request. Individuals

who plan to attend and need special

assistance, such as sign language

interpretation or other reasonable

accommodations, should contact Ms.

DeNinno in advance of the meeting.

(Catalog of Federal Domestic Assistant

Program No. 93.867, Vision Research:

National Institutes of Health)

Dated: August 7, 1997.

LaVerne Y. Stringfield,

Committee Management Officer, NIH.

[FR Doc. 97–21423 Filed 8–12–97; 8:45 am]

BILLING CODE 4140–01–M