21404 Federal Register / Vol. 66, No. 83 / Monday, April 30, 2001 / Notices

44231) to describe the Medicare

Coverage Advisory Committee (MCAC),

which provides advice and

recommendations to us about clinical

issues. This notice announces the

following public meeting of the

Diagnostic Imaging Panel (the Panel) of

MCAC.

Current Panel Members

Frank Papatheofanis, MD, PhD;

Barbara McNeil, MD, PhD; Carole

Flamm, MD, MPH; Jeffrey Lerner, PhD;

Michael Manyak, MD; Donna Novak,

BA; Manuel Cerqueira, MD; Kim

Burchiel, MD; Steven Guyton, MD; Sally

Hart, JD; Michael Klein, MBA

Meeting Topic

The Panel will hear and discuss

presentations from interested persons

regarding FDG Positron Emission

Tomography imaging for breast cancer

diagnosis and staging.

Procedure and Agenda

This meeting is open to the public.

The Panel will hear oral presentations

from the public for approximately 1.5

hours. The Panel may limit the number

and duration of oral presentations to the

time available. If you wish to make

formal presentations, you must notify

the respective Executive Secretary listed

in the FOR FURTHER INFORMATION

CONTACT section of this notice, and

submit the following by the Deadline for

Presentations and Comments date listed

in the DATES section of this notice: A

brief statement of the general nature of

the evidence or arguments you wish to

present, and the names and addresses of

proposed participants. A written copy of

your presentation must be provided to

each panel member prior to offering

your public comments. We will request

that you declare at the meeting whether

or not you have any financial

involvement with manufacturers of any

items or services being discussed (or

with their competitors).

After the public and HCFA

presentations, the Panel will deliberate

openly on the topic. Interested persons

may observe the deliberations, but the

Panel will not hear further comments

during this time except at the request of

the chairperson. The Panel will also

allow approximately a 30-minute open

public session for any attendee to

address issues specific to the topic. At

the conclusion of the day, the members

will vote and the Panel will make its

recommendation.

Authority: 5 U.S.C. App. 2, section 10(a)(1)

and (a)(2).

(Catalog of Federal Domestic Assistance

Program No. 93.774, Medicare—

Supplementary Medical Insurance Program)

Dated: April 6, 2001.

Jeffrey L. Kang,

Director, Office of Clinical Standards and

Quality, Health Care Financing

Administration.

[FR Doc. 01–10638 Filed 4–27–01; 8:45 am]

BILLING CODE 4120–01–P

DEPARTMENT OF HEALTH AND

HUMAN SERVICES

National Institutes of Health

Proposed Collection; Comment

Request; Extended Lung Cancer

Incidence Follow-Up for the Mayo Lung

Project Participants

SUMMARY: In compliance with the

requirement of section 3506(c)(2)(A) of

the Paperwork Reduction Act of 1995,

for opportunity for public comment on

proposed data collection projects, the

National Center Institute (NCI), the

National Institutes of Health (NIH) will

publish periodic summaries of proposed

projects to be submitted to the Office of

Management and Budget (OMB) for

review and approval.

Proposed Collection

Title: Extended Lung Cancer

Incidence Follow-Up for the Mayo Lung

Project Participants. Type of

Information Collection Request: NEW.

Need and Use of Information Collection:

The Mayo Lung Project (MLP) was an

NCI-funded randomized collection trial

(RCT) of lung cancer screening

conducted among 9,211 male smokers

from 1971 to 1983. No reduction in lung

cancer mortality was observed in the

MLP with an intense regimen of x-ray

and sputum cytology screening. Recent

analysis of updated mortality and case

survival data (through 1996) suggests

that lesions with little-to-no clinical

relevance (over-diagnosis) may have

been detected through screening in the

MLP intervention arm. Over-diagnosis

leads to unnecessary medical

interventions, including diagnostic and

treatment procedures that carry with

them varying degrees of risk.

Consequently, over-diagnosis can result

in considerable harm, including

premature death, which would not have

occurred in the absence of screening.

The persistence, after screening ends, of

an excess of lung cancer cases in the

intervention arm is the strongest

evidence in support of over-diagnosis,

but this information cannot be

adequately obtained with available MLP

data. Therefore, we propose to recontact the MLP participants and/or

their next-of-kin to determine the

participants who were diagnosed with

lung cancer after the formal end of the

Project. These data will allow the NCI

to either more-convincingly state or

perhaps refute the possibility of overdiagnosis in lung cancer screening, and

may be used to guide future research

agendas and lung cancer screening

policies. Frequency of response: Once.

Affected public: Individuals. Type of

respondents: MLP participants or their

next-of-kin. The annual reporting

burden is as follows: Maximum number

of respondents: 9200; Estimated number

of Responses per Respondent: 1.

Average Burden Hours Per Response:

0.25; Estimated Maximum Total Annual

Burden Hours Requested: 2300. The

annualized cost to respondents is

estimated at zero. There are no Capital

Costs to report. There are no Operating

or Maintenance Costs; to report.

Request for Comments

Written comments and/or suggestions

from the public and affected agencies

should address one or more of the

following points: (1) Evaluate whether

the proposed collection of information

is necessary for the proper performance

of the function of the agency, including

whether the information will have

practical utility; (2) Evaluate the

accuracy of the agency’s estimate of the

burden of the proposed collection of

information, including the validity of

the methodology and assumptions used;

(3) Enhance the quality, utility, and

clarity of the information to be

collected; and (4) Minimize the burden

of the collection of information on those

who are to respond, including the use

of appropriate automated, electronic,

mechanical, or other technological

collection techniques or other forms of

information technology.

FOR FURTHER INFORMATION CONTACT: To

request more information on the

proposed project or to obtain a copy of

the data collection plans and

instruments, contact: Dr. Pamela

Marcus, Epidemiologist, Biometry

Research Group, Division of Cancer

Prevention, National Cancer Institute,

Suite 344 EPN, 6130 Executive Blvd,

Bethesda, MD 20892–7354; or call nontool free 301–496–7468; or email

pm145q@nih.gov.

Comments due date: Comments

regarding this information collection are

best assured of having their full effect if

received on or before June 29, 2001.

Dated: April 20, 2001.

Reesa L. Nichols,

NCI Project Clearance Liaison.

[FR Doc. 01–10582 Filed 4–27–01; 8:45 am]

BILLING CODE 4140–01–M

Federal Register / Vol. 66, No. 83 / Monday, April 30, 2001 / Notices 21405

DEPARTMENT OF HEALTH AND

HUMAN SERVICES

National Institutes of Health

Government-Owned Inventions;

Availability for Licensing

AGENCY: National Institutes of Health,

Public Health Service, DHHS.

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 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.

Enhanced Homologous Recombination

Mediated by Lambda Recombination

Proteins

Drs. E. Lee, N. Copeland, N. Jenkins,

and D. Court (NCI)

DHHS Reference No. E–077–01/0 filed

Feb 26, 2001

Licensing Contact: John Rambosek; 301/

496–7056 ext. 270; e-mail:

rambosej@od.nih.gov

The present invention concerns a

method to enhance homologous

recombination in bacteria using the Red

recombination system derived from a

defective lambda prophage. This lambda

system, like the RecET system, uses

homologous recombination proteins to

protect and recombine the

electroporated linear DNA. However,

the lambda system is at least 50 to 100

times more efficient than the RecET

system. The high recombination

efficiency offered by this system makes

it possible to manipulate DNA without

drug selection. Point mutations,

deletions, or insertions can be

engineered into any gene on plasmids or

bacterial artificial chromosomes (BACs)

for gene functional analysis. This

recombination system also can be used

to subclone DNA fragments as large as

80 kb from BACs by gap repair.

Targeting vectors for embryonic stem

cells or transgenic constructs by BAC

engineering can now be subcloned with

ease, and virtually any region of the

engineered BAC may be included in the

final subclone. The ability to efficiently

and precisely modify genes or

regulatory sequences on BACs,

combined with the ability to include or

exclude them during the subcloning

process, should make it possible to

dissect the function of these sequences

in the whole animal at a high-throughput level not previously possible.

This lambda recombination system

has been used to introduce a Cre

recombinase gene into the coding region

of the mouse neural-specific enolase

gene carried on a 250 kb mouse BAC

after transfer of the mouse BAC into

DY380 E. coli cells which carry the

lambda recombination system.

Transgenic mice that were subsequently

generated which carry this modified

BAC specifically expressed Cre in all

mature neurons and Cre expression

mirrored that of the mouse neuralspecific enolase gene.

This abstract modifies an abstract for

this technology published in the

Federal Register on Thursday, April 5,

2001 (66 FR 18098).

Use of Endogenous Vertebrate Phytase

to Increase Capacity To Utilize Phytic

Acid in Livestock Feed

Stephen Shears (NIEHS), Paul Reynolds,

Jim Petitte

DHHS Reference No. E–139–00/0 filed

Aug 11, 2000

Licensing Contact: John Rambosek; 301/

496–7056 ext. 270; e-mail:

rambosej@od.nih.gov

This invention discloses the concept

of creating transgenic farm animals that

secrete a native phytase enzyme into

their digestive tracts. It has long been

recognized that monogastric animals

(e.g. pigs and chickens) do not utilize

dietary phosphorus as efficiently as

possible. This is because a high

percentage of total phosphorus (70% in

cereals, 50% in legume seeds) is present

as phytic acid and its salts—phytate.

Monogastric animals utilize phytate

inefficiently because they lack the

enzyme phytase in their digestive

systems. Phytase liberates the

phosphorus from phytate, thereby

making dietary phosphorus available to

the animals. This has the dual effect of

both promoting more efficient growth of

the animals, as well as imposing less of

an environmental burden in the form of

excess phosphorus in water streams.

Use of phytase as a growth feed

supplement is well known. However, in

the past the focus has always been on

adding exogenous phytase to animal

feed, or to increase the level of phytase

expression in the seeds making up the

feed. The inventors’ novel concept is to

redirect expression of a naturally

occurring phytase gene so that the

enzyme will be secreted into the

intestinal lumen. This will create farm

animals that can more efficiently utilize

unsupplemented feeds. Another

problem with existing phytases that the

present invention overcomes is that

phytase tends to be unstable during the

heat treatment used to process feed.

This invention overcomes this

limitation because the phytase does not

have to incorporated into feed at all.

Cloning of the Human Nuclear Receptor

Co-Repressor Gene

Dr. Johnson M. Liu (NHLBI)

DHHS Reference Number E–088–99/0

filed Aug 3, 1999

Licensing Contact: John Rambosek; 301/

496–7056 ext. 270; e-mail:

rambosej@od.nih.gov

Alteration in the expression of human

genes is critical to the development and

progression of many diseases. These

include, among others, cancer,

inflammation, cardiovascular disease,

hypercholesterolemia, blood pressure,

and diabetes. The Human Nuclear

Receptor Co-Repressor (HuN-Cor) gene

represents a technology that may be

used to alter the transcription of genes.

It provides a general mechanism by

which many genes may be modulated

throughout the entire range of being

turned on to being completely turned

off. The HuN-Cor gene encodes for a

ubiquitously expressed protein that

silences other genes. It does this by

specifically recruiting an enzyme

complex that causes local folding of

chromatin, not allowing other

transcription factors to access the DNA.

HuN-Cor represents a powerful research

tool that can be used to study gene

expression and characterization of many

different genes. It may ultimately have

great utility in controlling gene

expression via gene therapy technology,

and may also be useful as a target for the

isolation of pharmaceutical compounds

that enhance or inhibit expression of

genes. For example, it may be possible

to engineer mutations of the HuN-Cor

gene that dominantly inhibit its

function; these mutants could then be

expressed in appropriate target tissues

or cells in order to control gene

expression. Finally, the gene product

may have utility in the discovery of

therapeutic compounds that modulate

gene expression via HuN-Cor.

Antibodies That Selectively Detect the

Human Nestin Protein

Conrad Messam et al. (NINDS)