Just a thought to start with... Are you really interested in
researching something, or just making arguements about stuff you
obviously don't know about?!?? I'd like to think you're serious about
researching something, but I've my doubts...
In article <Pine.ULT.3.91.960314194146.13504K-100000 at essex.UCHSC.edu>,
Teresa Binstock <binstoct at essex.UCHSC.edu> wrote:
>After reading and rereading Patel et al, I'm not convinced that they
>chose their STE2 and STE3 so carelessly. They were examining more than
>100 surface molecules and just coincidently picked alpha-numeric symbols
>that have been traditional and specific for many years; but perhaps that is
>what they did.
It's quite obvious to me what they're talking about, and why they
named their antibodies the way they did. You'll agree that they named
the antibodies as such, correct? What happens if they've got more than
one antibody against an antigen? Give it the same name? I don't think
so... Ever done a fusion? If they'd made specific antibody, they'd
have give the antibody a name, and not give it the antigens name. They
would've said, "anti-ste" for example. It's just how things are done,
and it makes sense.
Additionally, you've ignored my other points about the
databases. There are no other instances of anything remotely like
"Human STE" as a yeast homologue. Not in nucleotide or protein
databases, nor in the literature. See below.
>My hypothesis is not dependent upon STE2 and STE3, but is primarily based
>upon immunological cells within the nasal mucosa -- which, to my
>knowledge, has not yet been researched.
There are various data on leukocytes in the nasal mucosa. In fact,
there are conjectures about olfactory stimuli and neutrophil
accumulation in response to temporary ischemia there. Problem is,
there's nothing that suggests what you suppose. But you're right. No
one has specifically looked for antigen specific autoimmune T-cells
against vomeronasal antigens. But then, why would they?!?!
Your hypothesis is full of holes, and poorly stated. What do you want,
anyway?!? What is this "Collected writings copyright" for? If you're
trying for a patent position, I'm afraid you've a ways to go...
So, to take your meaning, you think that some sort of immune imbalance
leads to an improper signaling event in/from the nasal mucosa? You've
got no reason to think so, and no mechanism. You started out by
postulating that there's other pathways for odour sensing/processing
than known ones, without any good (or bad) reason at all.
You've concocted an entire position out of thin air. See below.
>If it turns out that Patel et al's STE2 and STE3 have zero homology with
>yeast molecules of similar alpha-numeric nomenclature, I will conclude
>that the Internet has in fact performed a useful function -- ie, that of
>pointing out a flaw prior to hundreds of thousands of dollars poured down
>yet another lab's drains.
Are you suggesting that you are in control of hundreds of thousands of
dollars for research?!?!!
The Internet already provides many useful functions, anyway. The real
conclusion is that you must form a prima facia case based on facts,
and not conjecture. The reasoning must be logical, the model must
explain the data and predict other untested outcomes, and hopefully be
testable. You've provided none of this. See below.
>In trying to pin down the STE2,3 ambiguity, I have written to the Patel
>et al corresponding author.
Good. Why don't you call them?
Department of Medicine, Duke University Medical Center, Durham,
North Carolina 27710, USA.
Name: Dhavalkumar Patel
Type: Faculty/Staff
Title/Class: Assistant Professor
Department/College: Div Of Rheumatology Immunology
Campus_Address: 222 Clin Res Labs
Mail_Address: Box 3258 Med Ctr Durham, NC 27710
Local/Office_Phone: (919) 684-5093
Fax: (919) 684-5230
Email: patel003 at mc.duke.edu
Name: Barton F Haynes
Type: Faculty/Staff
Title/Class: Frederic M Hanes Prof Of Med
Department/College: Department Of Medicine Chair Of Medicine Dir,
Duke Univ Arthritis Center
Campus_Address: 1102 Hosp North
Mail_Address: Box 3703 Med Ctr Durham, NC 27710
Local/Office_Phone: (919) 684-5384
Fax: (919) 681-8992
Email: hayne002 at mc.duke.edu
>I can't help but wonder, given the long-standing tradition of using ste2
>and ste3 in reference to S. Cerevisiae receptors, why would researchers
>and reviewers allow such a similar term to be used for molecules found in
>the human thymic epithelium?
Did you know that in the French, ste is an abbriviation for a female
saint? I bet you didn't. Have you done a medline search for the
keyword ste? I know you haven't. I know because you'll find:
1. Armengol X; Estelrich J.
Physical stability of different liposome compositions obtained by
extrusion method.
Journal of Microencapsulation, 1995 Sep-Oct, 12(5):525-35.
(UI: 96093127)
which contains:
"DPPC:CHOL:stearylamine (STE)"
2. Iskhakova FKh; Esipova OV; Zvonkova EN.
[Synthesis of stearoyl derivatives of proline-containing hydrophobic
peptides].
Bioorganicheskaia Khimiia, 1995 Aug, 21(8):596-603.
Language: Russian.
(UI: 96096913
which contains:
"compounds containing a Ste-Pro fragment"
3. Her C; Aksoy IA; Kimura S; Brandriff BF; Wasmuth JJ; Weinshilboum RM.
Human estrogen sulfotransferase gene (STE): cloning, structure, and
chromosomal localization.
Genomics, 1995 Sep 1, 29(1):16-23.
(UI: 96079087)
Reference number 4 referred to a cell line called "STE".
And so on. There are, dare I say, many more "researchers and
reviewers" who are carelessly throwing STE around than there might at
first seem. There were 102 refs that came up in my search from
above. The great bulk of them had little to do with yeast. In fact,
crossing the above result with keyword yeast, yielded 8 cites. I think
you're flogging a dead horse here.
>Regarding anecdotal evidence, you seem to have taken that notion out of
>its context wherein Wedekind et al MHC data and other immune-related data
>were cited. Often in human research, anecdotal data and hypotheses
>derived therefrom help to guide what become actual collectings of data,
>testing of hypotheses.
I simply pointed out that you base your assumptions on what your
friends do/say. If you want me to point out flaws in your other cites,
I'll do so. For example, you might start with how many genes are found
in the MHC region. Finding something there has become, dare I say,
almost routine? The fact that a gene lies close to another means
little by itself. All genes lie next to other genes. Besides which,
you've no link from any gene there, to your hypothesis.
>For the record, the seemingly higher than
^^^^^^^^^
>average presence of autoimmune dysregulations among HM was in fact first
>pointed out to me by several HM themselves. Certainly, their impression
^^^^^^^^^^
>may be a "false positive", but at least one that is consistent with
>MHC-related processes of human interactions as documented by Wedekind et al,
>Blanchard et al, and others cited previously in this thread.
Blanchard's data is that homosexuals with siblings often have male
older brothers. Wedekind had women smell T shirts (worn by males) and
rate them as pleasant or no, then compared with MHC. I'm afraid you've
got a long way to go before any reasonable person would take this as
significant support for your theory.
The other point in your original post was from WJ Turner, who proposes
that homosexuality in males might be X-linked. Neither does this
directly (or indirectly) support your theory.
>But thanks for making effort to address my hypothesis, including its
>portion based upon ste2 and ste3 and Patel et al.
No problem. You've got some rethinking to do, as I see it. Perhaps
you'll post an updated model? And perhaps an explaination of what it
is you're after? (eg, personal interest, research proposal, class
assignment, etc.)
Later,
Aaron
--
"Nothing more is needed to destroy a man, than the conviction that his
life's work is useless." -Antonin Artaud
erawtech at leland.stanford.edu (R. Aaron Warnock)
