[extropy-chat] BIO: Stem Cell Genes

[Damien Broderick]

From: "Brett Paatsch" <bpaatsch at bigpond.net.au>
Sent: Friday, December 26, 2003 8:02 AM
Subject: Re: [extropy-chat] BIO: Stem Cell Genes


[Rafal Smigrodzki wrote:]
> > ### Oh, the technology is patented already (as a preliminary
> > patent)

> "Preliminary patent" seems like slightly confused lay-speak to me.
> I think the process that would be used in the circumstance you've
> 'outlined' would have been a provisional application for patent.

My JD legal adviser informs me that `provisional patent' is indeed what
Rafal would be writing about.

Meanwhile, here's an interesting patent that was granted more than two and
half years ago. It'll fix hangnails, cancer, migrims, Alzheimers, and a
gallon or two should have your car running like new. :)

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1
&u=/netahtml/srchnum.htm&r=1&f=G&l=50&s1=6,268,398.WKU.&OS=PN/6,268,398&RS=P
N/6,268,398

Compounds and methods for treating mitochondria-associated diseases


Abstract
Compounds, compositions and methods are disclosed for treating
mitochondria-associated diseases, such as cancer, psoriasis, stroke,
Alzheimer's Disease and diabetes. The compounds of this invention have
structure (I) below, including stereoisomers, prodrugs and pharmaceutically
acceptable salts thereof, wherein Ar and L are as defined herein. The
methods of this invention are directed to treating a mitochondria-associated
disease by administering to a warm-blooded animal in need thereof an
effective amount of a compound of structure (I), typically in the form of a
pharmaceutical composition. ##STR1##


.......
a sample from the lengthy text:

< Oxidatively stressed mitochondria may release a pre-formed soluble factor
that can induce chromosomal condensation, an event preceding apoptosis
(Marchetti et al., Cancer Res. 56:2033-38, 1996). In addition, members of
the Bcl-2 family of anti-apoptosis gene products are located within the
outer mitochondrial membrane (Monaghan et al., J. Histochem. Cytochem.
40:1819-25, 1992) and these proteins appear to protect membranes from
oxidative stress (Korsmeyer et al, Biochim. Biophys. Act. 1271:63, 1995).
Localization of Bcl-2 to this membrane appears to be indispensable for
modulation of apoptosis (Nguyen et al., J. Biol. Chem. 269:16521-24, 1994).
Thus, changes in mitochondrial physiology may be important mediators of
apoptosis. To the extent that apoptotic cell death is a prominent feature of
neuronal loss in AD. mitochondrial dysfunction may be critical to the
progression of this disease and may also be a contributing factor in other
mitochondria associated diseases.

Focal defects in energy metabolism in the mitochondria, with accompanying
increases in oxidative stress, may be associated with AD.  > etc etc

Damien Broderick