needle, page-2

I will not get to meet Roland.....look anybody that can research hard and is prepared to back their abilities with hard earned - simply had to buy this stock.

Sure, smaller investors could have waited for results and then entered. I was of the view however, the number of shares I wanted (based on my belief of the upside potential) could not easily be purchased post the gap. Accordingly I went long prior to news.

Certainly I have no specific hard feelings towards the company.....just rather you develop a mechanical approach to changes in company fundamentals (eg that news from yesterday).......and trade and invest based on the obvious goal to make as much money (as quickly as possible).

I have sold completely. My stategy (based on this intense research is to seek out stocks with 300% or 400% upside). MBP does not fit that bill......however unless you are into six hours research a day and specifically seeking out multi-baggers..........why on earth would you sell shares in a company at less than their cash backing.

If it gets back to 10 cents (or a cap of $30 million).....thats a very handy 90% gain on todays shareprice.

Good luck to you jevalent.
____________________________________________

I had always known of this information....but had never presented it.

I won't be back on the MBP thread......in view of the current situation - why do you think this information is now of significance.

April 4, 2005, 16:5 > A conus peptide blocks nicotinic... < Previous | Next >
ARTICLE LINKS:
Fulltext | PDF (231 K)
A conus peptide blocks nicotinic receptors of unmyelinated axons in human nerves.

SOMATOSENSORY SYSTEMS, PAIN

Neuroreport. 16(5):479-483, April 4, 2005.
Lang, Philip M. 1; Burgstahler, Ralf 2; Haberberger, Rainer V. 3; Sippel, Wolfgang 2; Grafe, Peter 2 CA
Abstract:
The novel [alpha]-conotoxin Vc1.1 is a potential analgesic for the treatment of painful neuropathic conditions. In the present study, the effects of Vc1.1 were tested on the nicotine-induced increase in excitability of unmyelinated C-fiber axons in isolated segments of peripheral human nerves. Vc1.1 in concentrations above 0.1 [mu]M antagonized the increase in axonal excitability produced by nicotine; the maximal inhibition was observed with 10 [mu]M. We also demonstrate immunoreactivity for [alpha]3 and [alpha]5 subunits of neuronal nicotinic receptors on unmyelinated peripheral human axons. Blockade of nicotinic receptors on unmyelinated peripheral nerve fibers may be helpful in painful neuropathies affecting unmyelinated sympathetic and/or sensory axons.

(C) 2005 Lippincott Williams & Wilkins, Inc.



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