Appeal No. 2001-1499 Page 8
Application No. 08/957,654
directs our attention to the last paragraph, on page 577 of Rao. According to
Rao (page 577, last paragraph):
Intact FN [fibronectin] may be required for the healing of
chronic wounds. The observations reported herein suggest that
the degradation of AT precedes the degradation of FN in chronic
wounds. We show here that AT [α1-antitrypsin] precedes the
degradation of FN in chronic wounds. We show here that AT
effectively prevented the degradation of FN by chronic wound fluid
serine proteinases. Therefore, topical AT may inhibit FN degrading
enzymes and increase the concentration of intact and functional FN
in chronic wounds [emphasis added].
According to appellants (Brief, page 15), “[a]t best, Rao postulates that
AAT may protect fibronectic in a chronic wound.” We agree. Our dissenting
colleague, however, cannot join with us because he believes that Rao’s results
illustrated in Figure 6, and explained in the paragraph bridging columns 1 and 2
of page 575 are sufficient to overcome the deficiencies of Gillis. Infra, page 14.
The portion of Rao, relied upon by the dissent, however, does nothing more than
document the results of an in vitro study to investigate if serine proteinases are
responsible for fibronectin degradation in chronic skin wounds, the stated “aim”
of Rao’s report. Rao, page 572, column 2. While Rao states (id.) that a further
aim of his study is to “examine the status of α1-antitrypsin…” Rao makes no
attempt to correlate his in vitro study, to an in vivo application. Instead, Rao
simply suggests (page 577, column 1, last sentence) that AAT regulates
fibronectin degradation in chronic wounds. In our opinion, Rao is at best an
invitation to explore a promising new field of experimentation. However, as set
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