Federal Register / Vol. 69, No. 190 / Friday, October 1, 2004 / Notices 58929

The agenda for the public meeting 

will be made available on October 8, 

2004, on the Internet at http://

www.fda.gov/cder/meeting/

ICH_10192004.htm.

Dated: September 23, 2004.

Jeffrey Shuren,

Assistant Commissioner for Policy.

[FR Doc. 04–22053 Filed 9–30–04; 8:45 am] 

BILLING CODE 4160–01–S

DEPARTMENT OF HEALTH AND 

HUMAN SERVICES 

Office of Inspector General 

Program Exclusions; Correction

AGENCY: Office of Inspector General, 

HHS.

ACTION: Notice of program exclusions; 

correction. 

SUMMARY: The HHS Office of Inspector 

GeneralPublished a document in the 

Federal Register of September 15, 2003, 

imposed exclusions. The document 

contained an incorrect exclusion type.

FOR FURTHER INFORMATION CONTACT:

Jacqueline Freeman, (410) 786–5197. 

Correction 

In the Federal Register of September 

15, 2004, in FR Doc. 20710, on page 

55641, correct the exclusion date to 

read:

LABONTE, MARY .................. 9/20/2004

SCOTTSDALE, AZ 

Dated: September 21, 2004. 

Katherine B. Petrowski, 

Director, Exclusions Staff, Office of Inspector 

General.

[FR Doc. 04–22046 Filed 9–30–04; 8:45 am] 

BILLING CODE 4150–04–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. 

Cytonectin, Cytonectin Gene and 

Cytonectin Inhibitors and Binding 

Ligands and Their Use in the Diagnosis 

and Treatment of Disease 

Soni J. Anderson et al. (NCI) 

U.S. Provisional Application No. 60/

553,977 Filed 18 Mar 2004 (DHHS 

Reference No. E–128–2004/0–US–01); 

U.S. Provisional Application No. 60/

578,068 Filed 09 Jun 2004 (DHHS 

Reference No. E–128–2004/1–US–01) 

Licensing Contact: Fatima Sayyid; 

(301) 435–4521; sayyidf@mail.nih.gov. 

Cytonectin is a 35K molecular weight 

protein that displays ion-independent 

adherence properties, is expressed in a 

variety of organs and tissues and is 

evolutionarily conserved from human to 

rodent and avian species. Within the 

body it is thought to serve the function 

of ‘‘super glue’’ contributing to cell-cell 

interactions and 3-dimensional tissue 

structure and a physiologic ‘‘do not 

attack’’ signal molecule that prevents 

tissue destruction by cells of monocyte 

lineage including odontoclasts in 

secondary teeth. It also plays an 

important role in the pathology 

associated with cancer, arthritis, 

Alzheimer’s and Parkinson’s disease. 

The present invention relates to 

cytonectin, to polynucleotides that 

encode cytonectin, to inhibitors and 

antibodies that bind to cytonectin and to 

the use of compositions in the diagnosis 

and treatment of cytonectin-related 

diseases and conditions. 

Genetic Fingerprint of Acute Stroke 

Alison E. Baird (NINDS) 

U.S. Provisional Application No. 60/

575,279 Filed 27 May 2004 (DHHS 

Reference No. E–306–2003/0–US–01) 

Licensing Contact: Fatima Sayyid; 

(301) 435–4521; sayyidf@mail.nih.gov. 

Stroke is the third leading cause of 

death and the leading cause of adult 

disability in developed countries. 

Despite the prevalence and burden of 

this disease, stroke precipitants and 

pathophysiological mechanisms in 

individual patients are often unknown. 

It is also difficult to accurately predict 

whether a stroke will lead to only minor 

neurological sequelae or more serious 

medical consequences. Although animal 

experiments in focally ischemic brain 

tissue have indicated that there are 

alterations in gene expression following 

a stroke, gene expression profiling has 

not yet been applied to clinical human 

stroke, primarily because brain tissue 

samples are inaccessible and rarely 

justified. 

The present provisional patent 

application discloses methods of 

determining whether a subject had an 

ischemic stroke, methods of 

determining the prognosis of a subject 

who had an ischemic stroke, as well as 

methods of determining an appropriate 

treatment regimen for a subject who had 

an ischemic stroke. 

Inhibition of Smad3 To Prevent Fibrosis 

and Improve Wound Healing 

Anita B. Roberts et al. (NCI) 

U.S. Patent Application No. 10/299,886 

Filed 18 Nov 2002 (DHHS Reference No. 

E–070–2000/0–US–06), claiming 

priority to PCT Application No. PCT/

US00/13725 Filed 19 May 2000 (DHHS 

Reference No. E–070–2000/0–PCT–01)

Licensing Contact: Marlene ShinnAstor; (301) 435–4426; 

shinnm@mail.nih.gov. 

Millions of dollars are spent each year 

to heal chronic non-healing wounds and 

in the treatment of severe burn patients. 

The NIH announces a new technology 

that may lead to improved approaches 

to treatment of burn patients and the 

reduction of scarring and more rapid 

closure of both acute (surgical) and 

chronic wounds (e.g., diabetic, 

decubitus, and venus statis ulcers). 

Smad2 and Smad3 are highly 

homologous cytoplasmic proteins which 

function to transduce signals from 

Transforming Growth Factor–beta 

(TGF–beta) and activin receptors to 

promoters of target genes found in the 

nucleus. This new technology indicates 

that interference with specific signaling 

pathways downstream of TGF–beta may 

be more selective and have a better 

outcome than approaches aimed at 

blocking all effects of this pleiotropic 

cytokine. 

Specifically, it is proposed that 

elimination or inhibition of Smad3 may 

interfere with fibrogenic mechanisms 

and reduce the accumulation of scar 

tissue associated with high dose 

radiation and wound healing, while 

increasing the rate of re-epithelialization 

of wounds.