I'm also trekking to the gym, if only for the steam bath, a few times
a week.  Maybe 25-30 minutes in, concentrating on breathing in
through
the nose.  Again: effective?  Who knows....

good thought.

Another thing to try, a good mask. One that is comfortable enough to
sleep in. You can use a scarf or hankie
to just try it out. Anyway wearing a mask traps heat and humidity. you
might try taking some of your mucus and watching how it runs at
different temperatures.

I have found that mine is a lot less viscus at higher temps, and I
found that my fungal cultures do not like to grow over the frig,
which was my 87 degree F spot.  Dimorphic beasties tend to be round at
higher temps and filiments at lower temps.

Anyway I could breath at night if I wore a mask while I was trying to
figure out what else worked.

by the way. I agree with Susan that you might want to back down on the
steroids and see how you feel.

About the pepcid.  It is only antifungal topically and in a low PH
environment, but that should not have stopped them from
packageing it with an acidifier.  i kinda think that Bayer,  just did
not want to have to deal with the associations
that surround antifungal drugs. Even if it had a med/mld of 1/300,
they still would have been in more years of tests
to make oz OTC if they had mentioned it was antifungal because Ampho
is such a bugger.
.

Neil;
Oz is NOT an antiacid. it is a Pma1p inhibitor which only forms at a
ph of less than 4.
I don't think there are supposed to BE any such proton pumps active in
your nose. Yours are in your stomach.
I think the only active Pma1p pumps in acid secreting cells your nose
belong to the other guys.

I know you have the eye trouble so I have pulled out the revelant bit,
and then it is shown in context below, and then there is a link to the
whole artical.

[[[Significant conversion of the pro-drug to the reactive sulfenamide
species requires a pH<4.0 (pKa omeprazole ~ 4.0) (a ph of less than 4)
with more than 99.9% of the drug being rapidly converted at pH 1-2
(Brandstrom et al., 1989a).]]]

So Oz requires a ph of 4 or less to become active.

For reference, a Sprite has a PH of about 4, I would not go below
that.

"The proton pump inhibitors omeprazole (losec), lansoprazole
(prevacid), and pantoprazole belong to the chemical family of
substituted benzimidazoles (Fig. 3), and exist as pro-drugs that need
activation for interaction with the gastric H+,K+-ATPase (Lorentzon et
al., 1997). The compounds are chemically stable weak bases at neutral
pH, and can be orally administered. The stable pro-drugs reach the
parietal cells from the blood and are transported into the strongly
acidic environment of the secretory canaliculi. Protonation of these
compounds results in extensive molecular rearrangement followed by the
formation of a positively charged, sulfenamide species that has low
permeability coefficient across membranes and reacts covalently with
free sulfhydryl group(s) on the extracellular surface of the H+,K+-
ATPase (Sachs et al., 1995). Significant conversion of the pro-drug to
the reactive sulfenamide species requires a pH<4.0 (pKa omeprazole ~
4.0) with more than 99.9% of the drug being rapidly converted at pH
1-2 (Brandstrom et al., 1989a). Unreacted sulfenamide is rapidly
hydrolyzed in the aqueous compartment (Brandstrom et al., 1989a). The
sulfenamide forms a disulfide that covalently modifies the enzyme from
its extracellular domain and inhibits it with a stoichiometry of
approximately 2 molecules of drug per a -subunit of the H+,K+-ATPase.
Inhibition by omeprazole is believed to result from covalent
modification of Cys813 (or Cys822) and Cys892 located in the
extracellular loop regions joining TM5/TM6 and TM7/TM8 (Fig. 1)
(Lorentzon et al., 1997;Shin et al., 1997). These transmembrane
segments have been implicated in ion transport by P-type enzymes
suggesting that enzyme inhibition may result from a defect in ion
translocation. Such a defect would be expected to have a pronounced
affect on ATP hydrolysis by the enzyme as is observed, since ion
translocation and ATP hydrolysis are tightly coupled in these enzymes.
Enzyme inhibition can be reversed in vitro by the addition of reducing
agents such as b -mercaptoethanol, but it is essentially irreversible
under physiological conditions. New acid secretion will only result
from biosynthesis and assembly of new enzyme, since the turnover rate
of the enzyme is ~50h (Sachs et al., 1995). Thus, the antagonistic
affects of the drugs persist long after plasma clearance, which helps
account for their therapeutic efficacy."

http://www.ejbiotechnology.info/content/vol1/issue2/full/2/index.html

Part of a paper about drug development.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=538910

Pma1p was validated as an antifungal target by demonstrating that acid-
activated omeprazole is a fungicidal Pma1p inhibitor that acts from
outside the cell (25, 37). This paper describes a drug discovery
strategy that targets Pma1p. Screening of a compact 324-pool d-
octapeptide library, which comprises 1.8 million combinatorial
pentapeptides linked to a C-terminal amidated triarginine motif, has
identified a potent, broad-spectrum, surface-active fungicidal Pma1p
inhibitor that circumvents three clinically important (43) mechanisms
of energy-dependent azole resistance. Such inhibitors may provide a
novel and timely avenue for antifungal drug discovery.