Federal Register / Vol. 70, No. 186 / Tuesday, September 27, 2005 / Notices 56473 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

National Institutes of Health/National 

Institute of Environmental Health 

Sciences; Submission for OMB 

Review; Comment Request; Active 

Living by Design Program Evaluation 

SUMMARY: Under the provisions of 

Section 3507(a)(1)(D) of the Paperwork 

Reduction Act of 1995, the National 

Institute of Environmental Health 

Sciences (NIEHS), the National Institute 

of Health (NIH) has submitted to the 

Office of Management and Budget 

(OMB) a request to review and approve 

the information collection listed below. 

This proposed information collection 

was previously published in the Federal 

Register on February 14, 2005 (Volume 

70, Number 29, Pages 7508–7509, and 

allowed 60–days for public comment. 

No public comments were received. The 

purpose of this notice is to allow an 

additional 30 days for public comment. 

The National Institutes of Health may 

not conduct or sponsor, and the 

respondent is not required to respond to 

the collection of information unless it 

displays a currently valid OMB control 

number. 

Proposed Collection: Title: Active 

Living by Design Program Evaluation. 

Type of Information Collection Request: 

NEW. Need and Use of Information 

Collection: The purpose of this study is 

to provide NIEHS with an overall 

evaluation of the Active Living by 

Design (ALbD) program to determine the 

extent to which program strategies to 

increase physical activity influence 

change, as measured by increased 

physical activity and reduction of Body 

Mass Index (BMI), in residents of 

participating communities. The 

objective of this study is to determine 

the degree to which the changes in the 

built environment, communication 

strategies and policy as a result of 

ALbD’s program has impacted physical 

activity and BMI in residents within the 

twenty-five (25) participating 

communities relative to a set of ten (10) 

control communities. 

Two types of data collection will 

occur throughout the study. A telephone 

survey, which relies on self-reports, and 

a clinical survey, which will collect 

physical activity data using measures of 

physical activity such as, 

accelerometers; measures of BMI and an 

interview on respondents’ perceptions 

of their neighborhood. The findings of 

this study will provide valuable 

information concerning (1) The Impact 

ALbD strategies have on increasing 

physical activity and bringing about 

positive changes in health associated 

with exercise, such as weight loss; and 

(2) possible reduction of health risks 

and diseases related to physical 

inactivity through implementation of 

ALbd strategies. Frequency of Response: 

Three times over a period of five (5) 

years, during three rounds of data 

collection. Affected Public: Individuals 

or households. Type of Respondents: 

Respondents includes adults and 

children ages 13 through 17 years and 

their parents. The clinical procedures 

require respondents under 18 years of 

age to be accompanied by their parent/ 

guardian, therefore the burden has been 

doubled for these respondents. The 

annual reporting burden is respected in 

the following table: 

Type of respondents Number of 

respondents 

Frequency of 

response 

Average time 

per response 

Annual hour 

burden 

Respondents to Telephone Survey ................................................................. 2,450 1 .334 818.3 

Respondents to Clinical Study—Adults ........................................................... 1,855 1 .9185 1,703.8 

Respondents to Clinical Study—Children/Parent ............................................ 595 1 1.837 1,093.0 

Total .......................................................................................................... ........................ ........................ ........................ 3,615.1 

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 appropriated automated, electronic, 

mechanical, or other technological 

collection techniques or other forms of 

information technology. 

Direct Comments To OMB: Written 

comments and/or suggestions regarding 

the item(s) contained in this notice, 

especially regarding the estimated 

public burden and associated response 

time, should be directed to the: Office 

of Management and Budget, Office of 

Regulatory Affairs, New Executive 

Office Building, Room 10235, 

Washington, DC 20503, Attention: Desk 

Officer for NIH. To request more 

information on the proposed project or 

to obtain a copy of the data collection 

plans and instruments, contact: Shobha 

Srinivasan, Ph.D., Division of 

Extramural Research and Training, 

National Institute of Environmental 

Health Sciences, P.O. Box 12233, MD 

EC–21, 111 T.W. Alexander Drive, RTP, 

NC 27709. Phone: (919) 541–2506. Fax: 

(919) 316–4606. E-mail: 

ss688k@nih.gov. 

Comments Due Date: Comments 

regarding this information collection are 

best assured of having their full effect if 

received within 30-days of the date of 

this publication. 

Dated: September 15, 2005. 

Richard A. Freed, 

NIEHS, Associate Director for Management. 

[FR Doc. 05–19175 Filed 9–26–05; 8:45 am] 

BILLING CODE 4140–01–M 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Government-Owned Inventions; 

Availability for Licensing 

AGENCY: National Institutes of Health, 

Public Health Service, HHS. 

ACTION: Notice. 

SUMMARY: The inventions listed below 

are owned by an agency 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 

56474 Federal Register / Vol. 70, No. 186 / Tuesday, September 27, 2005 / Notices 

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. 

Methods for Introducing Homologous 

Recombination in a Wide Variety of 

Bacteria Using Plasmids and Prophage 

Donald L. Court (NCI). 

U.S. Provisional Application No. 60/ 

573,504 filed 21 May 2004 (HHS 

Reference No. E–207–2004/0–US–01; 

U.S. Provisional Application No. 60/ 

653,259 filed 14 Feb 2005 (HHS 

Reference No. E–207–2004/1–US–01); 

U.S. Provisional Application No. 60/ 

655,729 filed 22 Feb 2005 (HHS 

Reference No. E–207–2004/2–US–01); 

U.S. Patent Application filed 20 May 

2005 (HHS Reference No. E–207–

2004/3–US–01). 

Licensing Contact: Norbert Pontzer; 301/ 

435–5502; pontzern@mail.nih.gov. 

Homologous recombination is the 

process of exchanging DNA between 

two DNA molecules through regions of 

identical sequence. Homologous 

recombination provides an alternative to 

using restriction endonucleases and 

ligases for producing recombinant DNA. 

Although the background level of 

homologous recombination in native E. 

coli is very low even with long 

homology arms, it is possible to modify 

or clone nucleic acids using 

homologous recombination in specific 

genetically modified strains of E. coli. 

Whereas, a defective prophage used in 

these recombineering strains is 

optimally suited for expression of the 

lambda RED functions for homologous 

recombination it is hard for 

experimenters not familiar with E. coli 

genetics to move the defective prophage 

from strain to strain. Thus, methods of 

introducing the defective prophage and 

its recombineering functions into other 

strains of E. coli and other bacteria, 

including other gram negative bacteria, 

are also needed. 

This invention provides plasmids and 

methods of use that confer the 

recombineering function to a variety of 

cells, including strains like DH10B of E. 

coli, as well as other species like 

Salmonella, Pseudomonas, 

Cyanobacteria, and Yeresinia, among 

others. These plasmids can be isolated 

in vitro and can be used to transform 

bacterial cells, such as gram negative 

bacteria. 

This research is described, in part, in: 

Thomason, L.C., Costantino, N., 

Sawitzke, JA., Datta, S., Bubunenko, M., 

Court, DL., Myers, R.S., Oppenheim, 

AB. 2005. Recombineering in 

Prokaryotes. In Phages: Their Role in 

Bacterial Pathogenesis and 

Biotechnology. pp. 383–399. (MK. 

Waldor, DI. Friedman, and SL. Adhya) 

ASM Press, Herndon, VA. 

Also provided are Lambda phages and 

methods of use for their introduction as 

prophages to provide recombineering 

functions into E. coli cells (Virology 

319: 185–189, 2004). These phages 

include appropriate amber mutations in 

genes to prevent cell death and allow 

high expression of lambda RED 

recombination functions. The phage 

also carry a selectable drug marker used 

to make lysogens. The phages can be 

used to infect an E. coli cell that 

includes a suppressor of the amber 

mutations which allows the phage to 

reproduce, lyse the infected cell, and 

produce high titers of the phage. 

However, the phage will not be able to 

destroy cells that do not carry the 

suppressor mutations and in these cells 

the phage can lysogenise and be used as 

a defective prophage to generate 

recombination activity in those cells. 

Such cells lacking the suppressor are 

DH10B cells in which genomic libraries 

of BACs are cloned. Such random 

libraries can be lysogenized in mass (or 

individually) with these phages by 

selecting for the drug marker they carry. 

These lysogens can then be manipulated 

for homologous recombination in the 

same way as BAC containing derivatives 

off DY380 described elsewhere. 

In addition to licensing, the 

technology is available for further 

development through collaborative 

research opportunities with the 

inventors. 

Regulation of INS (3456) P4 Signalling 

by a Reversible Kinase/Phosphatase 

and Methods and Compositions Related 

Thereto 

Stephen Shears (NIEHS) et al. 

U.S. Patent Application No. 10/508,363 

filed 16 Sep 2004 (HHS Reference No. 

E–105–2002/0–US–03), claiming 

priority to 18 Mar 2002. 

Licensing Contact: Marlene Shinn-Astor; 

301/435–4426; shinnm@mail.nih.gov. 

Receptor-dependent changes in Ins 

(3,4,5,6) P4 levels is a topic of general 

biological significance, since this 

regulates the activities of chloride 

channels that in turn regulate salt and 

fluid and mucus secretion from 

epithelial cells, cell volume 

homeostasis, and electrical excitability 

in neurons and smooth muscle. 

The NIH announces new treatment 

methods for asthma, bronchitis and 

cystic fibrosis. The treatments consist of 

either increasing or decreasing the 

activity of inositol 1,3,4,5,6 

pentakisphosphate 1-phosphatase in a 

patient, thereby controlling Ins (3,4,5,6) 

P4-signaling which in turn affects the 

chloride channels, ultimately regulating 

salt, fluid and mucus secretion. This 

modulation of inositol 1,3,4,5,6 

pentakisphosphate 1-phosphatase is 

accomplished by either pharmacological 

or genetic intervention. 

In addition to licensing, the 

technology is available for further 

development through collaborative 

research opportunities with the 

inventors. 

Cancer Therapy Using Vasoactive 

Intestinal Peptide Antagonists 

T. Moody (NCI), D. Brenneman 

(NICHD), et al. 

U.S. Patent No. 5,217,953 issued 08 Jun 

1993 (HHS Reference No. E–009–

1991/0–US–01); U.S. Patent No. 

5,565,424 issued 15 Oct 1996 (HHS 

Reference No. E–009–1991/1–US–01); 

U.S. Patent No. 6,630,124 issued 07 

Oct 2003 (HHS Reference No. E–301–

1998/2–US–06); Worldwide IP 

coverage. 

Licensing Contact: Susan Carson; 301/ 

435–5020; carsonsu@mail.nih.gov. 

The second leading cause of death in 

the United States is cancer and more 

than one million Americans are 

diagnosed with cancer each year, with 

this number likely to increase as the 

population ages. There remains a need 

for effective therapeutics with improved 

safety profiles, and promising results 

can be obtained through targeting 

receptors which are highly expressed on 

specific cancers. Vasoactive Intestinal 

Peptide (VIP) is a 28 amino-acid peptide 

hormone and one of several small 

neuropeptides that can function as 

autocrine growth factors. VIP mediates a 

variety of physiological responses and 

has been shown to exert stimulating and 

trophic effects on neoplastic cells 

inducing its own receptors by feedback 

mechanisms. Studies have shown that 

VIP receptors are present in many 

epithelial cancers including breast, 

colon, non-small cell lung carcinoma, 

and pancreatic and prostate cancers. 

Work by NIH scientists and their 

collaborators has shown that VIP 

receptor antagonists such as the 

lipophilic VIP antagonist SNH inhibit 

the growth of cancer cell lines in vitro 

and in vivo and potentiate the 

cytotoxicity of chemotherapeutic drugs. 

For example, results have shown that 

Federal Register / Vol. 70, No. 186 / Tuesday, September 27, 2005 / Notices 56475 

SNH and taxol are synergistic at 

inhibiting breast cell cancer growth and 

can potentiate the cytotoxicity of taxol 

in an in vivo human xenograft breast 

cancer mouse model. 

Combination therapy using these 

agents may therefore greatly enhance 

the response rate of different cancers to 

these drugs and may significantly 

reduce side effects by permitting a lower 

therapeutic dose to be administered. 

Available for licensing are compositions 

of matter and methods of use of VIP 

receptor antagonists. 

Dated: September 15, 2005. 

Steven M. Ferguson, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

[FR Doc. 05–19172 Filed 9–26–05; 8:45 am] 

BILLING CODE 4140–01–P 

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

National Institutes of Health 

Government-Owned Inventions; 

Availability for Licensing 

AGENCY: National Institutes of Health, 

Public Health Service, HHS. 

ACTION: Notice. 

SUMMARY: The inventions listed below 

are owned by an agency 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. 

HIV-Encoded siRNA, microRNA and 

Suppressor of RNA Silencing 

Yamina Bennasser et al. (NIAID) 

U.S. Provisional Application No. 60/ 

677,839 filed 05 May 2005 (HHS 

Reference No. E–203–2005/0–US–01). 

Licensing Contact: Susan Ano; 301/435–

5515; anos@mail.nih.gov. 

The present invention relates to virusencoded siRNA and miRNA species and 

the use of such RNAs in the diagnosis, 

prevention and/or treatment of 

retroviral infection, especially HIV or 

SIV infection. This invention conveys 

the first evidence that HIV–1 encodes 

viral siRNA precursors in its genome 

and that natural HIV–1 infection 

provokes nucleic acid-based immunity 

in human cells. To overcome this 

cellular defense, the HIV–1 Tat protein 

has evolved to include a suppressor of 

RNA silencing (SRS) function. 

Additionally, this invention identifies 

five microRNA (miRNA) precursor 

candidates that regulate cellular gene 

expression at a post-transcriptional 

level. The five miRNA precursors (21–

25 nucleotides in length) are encoded in 

highly conserved regions of HIV such as 

TAR sequence, gag, pol and nef genes. 

These findings indicate that viruses 

utilize RNA interference as a 

mechanism to regulate cellular gene 

expression. 

This technology is further described 

in: Bennasser et al., ‘‘HIV–1 encoded 

candidate micro-RNAs and their cellular 

targets,’’ Retrovirology 2004 Dec 15, 

1(1):43, doi:10.1186/1742–4690–1–43; 

and Bennasser et al., ‘‘Evidence that 

HIV–1 encodes an siRNA and a 

suppressor of RNA silencing,’’

Immunity 2005 May, 22(5):607–619, 

doi:10.1016/j.immuni.2005.03.010. 

In addition to licensing, the 

technology is available for further 

development through collaborative 

research opportunities with the 

inventors. 

Miniature Laser-Induced Fluorescence 

Detector 

Paul Smith, Nicole Morgan, Edward 

Wellner, Terry Phillips (ORS) 

U.S. Provisional Application No. 60/ 

682,847 filed 20 May 2005 (HHS 

Reference No. E–129–2005/0–US–01). 

Licensing Contact: Michael Shmilovich; 

301/435–5019; 

shmilovm@mail.nih.gov. 

Available for licensing and 

commercial development is a miniature 

laser-induced fluorescence detector 

having an in-line microfluidic detection 

cell. The detection cell finds application 

in High Performance Liquid 

Chromatography (HPLC), Capillary 

Electrophoresis (CE) and Mass 

Spectroscopy (MS) applications, among 

others. The cell for fluorescence 

measurements can have a measurement 

volume of 1 nL or less and a sample can 

be excited using two excitation 

wavelengths. The detection cell can 

include a 5 mm to 5 cm long capillary 

tube and an excitation fiber proximate 

to the capillary tube. A detection fiber 

is also proximate to the capillary tube, 

and the detection fiber has a diameter 

the same size or larger than the external 

diameter of the capillary tube. A 

plurality of both excitation and 

detection fibers can be used. 

In addition to licensing, the 

technology may be available for further 

development through collaborative 

research opportunities with the 

inventors. 

Cellular Receptor for Varicella-Zoster 

Virus and Cell-to-Cell Spread of Virus 

Jeffery Cohen et al. (NIAID) 

U.S. Provisional Application No. 60/ 

684,526 filed 26 May 2005 (HHS 

Reference No. E–289–2004/0–US–01). 

Licensing Contact: Chekesha S. 

Clingman; 301/435–5018; 

clingmac@mail.nih.gov. 

This technology relates to 

identification of insulin degrading 

enzyme (IDE) as a cellular receptor for 

Varicella-Zoster-Virus (VZV), the 

etiologic agent of varicella (chickenpox) 

and zoster (shingles). Acute infection of 

VZV is followed by cell-associated 

viremia and the development of 

varicella rash. The virus establishes lifelong latency in the nervous system and 

can reactivate to cause zoster. The 

mechanism of VZV entry into target 

cells and spread from cell-to-cell is not 

well understood. The inventors have 

shown that antibodies to IDE and 

recombinant IDE partially inhibit 

infection with the virus in cell culture. 

Reducing the level of IDE in the cell 

(with siRNA), or blocking the ability of 

IDE to bind with a VZV glycoprotein, 

markedly diminishes cell-to-cell spread 

of the virus in cell culture and partially 

inhibits infection of cells with cell-free 

virus. This invention further describes 

molecules that may have a role in the 

treatment or prevention of VZV 

infections, including antibodies to IDE, 

peptides that block IDE–VZV 

interactions, and other molecules that 

block binding activity of IDE. 

In addition to licensing, the 

technology is available for further 

development through collaborative 

research opportunities with the 

inventors. 

A Novel Amplification Method Permits 

Pathogens To Be Detected With 

Microarrays 

Michael J. Brownstein, Charles Xiang, 

and Zhi-Qing Qi (NIMH) 

U.S. Provisional Application No. 60/ 

635,239 filed 09 Dec 2004 (DHHS 

Reference No. E–184–2004/0–US–01). 

Licensing Contact: Cristina 

Thalhammer-Reyero; 301/435–4507; 

thalhamc@mail.nih.gov.