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Thread: Next year dr. young

  1. #11
    Hi Judy, I don't know what conferences Dr. Lima intends to attend. The information about Dr. Lima refining his procedure was based on a comment by Kahma who had been in touch with him.

  2. #12
    Senior Member Schmeky's Avatar
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    judykerperien,

    Lima visited the Australian (Brisbane) group and may be contemplating cultured OEG's instead of minced mucosa.

  3. #13
    Senior Member alan's Avatar
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    How about something simple - a med to relieve central pain while the SCI cure research continues on its way to success?

    Alan

    "Was it over when the Germans bombed Pearl Harbor?"

  4. #14
    Wise?

    You've concerned me when you said that taking 4-AP could limit your participation in other trials. Which trials? Why? Just because 4-AP doesn't help a person, that doesn't mean other experimental drugs won't. I'm confused.

    Jan

  5. #15
    Fellowhawkeye,

    I didn't mean for it to sound the way it did. Actually, 4-AP is less likely than other treatments to limit participation in other trials because it is a drug whose effects are perceived to go away when it is stopped. However, having taken 4-AP from compounding pharmacies has indeed limited the participation of many people in the 4-AP clinical trials. There are likely to be other clinical trials in the coming years, relating to better forms of 4-AP or other drugs such as one that Aventis is testing now in India.

    Wise.

  6. #16
    Wise, thanks for clearing that up. I didn't know there were better forms of 4-ap around the world or will be. Wouldn't they be enough different than compound 4-AP to be considered more effective? Otherwise why are they even making them? Seems silly.

    Jan

  7. #17
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    Wise,

    I guess you're referring to HP184 which seems to be both neuroprotective, improve myelination, and improve recovery of function.
    Do you've more info about the trial in India? I assume it's for acutes.But I am also curious when did they start the trial and how many people are involved.

  8. #18
    pecla, you are right. I first heard about the clinical trials in India at the Neuroscience meeting. When a company like Aventis talks about clinical trials, they are serious. So, I think that it is real. Wise.

  9. #19
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    At Aventis website they say that HP-184 has demonstrated improved nerve conduction and ambulation in animals.
    They also expect it reduces neuropathic pain and improves bladder function in humans.
    It was already in human trials in June 2002 or earlier and probably for chronic injuries because the head of the article is "HP-184; improving function in chronic spinal cord injury"

  10. #20
    Here are two references on HP-184

    • Smith CP, Woods-Kettelberger AT, Corbett R, Chesson SM, Bores GM, Petko WW, Roehr JE and Kongsamut S (1996). Serotonergic activity of HP 184: does spontaneous release have a role? Neurochem Res. 21: 575-83. Neuroscience Therapeutic Domain, Hoechst Marion Roussel, Somerville, NJ 08876, USA. Examination of HP 184, [N-n-propyl)-N-(3-fluoro-4-pyridinyl) -1H-3-methylindodel-1-amine hydrochloride], in a variety of tests for serotonergic activity revealed some unique properties of this compound. We report here that 100 microM HP 184 enhanced spontaneous release of [3H]serotonin (5-HT) from rat hippocampal slices. This release was independent of the uptake carrier. In vivo assays confirmed that HP 184 (20 mg/kg, i.p.) lacked significant interactions at the norepinephrine (NE) or 5-HT uptake carrier itself. Notably, HP 184 (15 mg/kg, i.p.) reduced drinking behavior in schedule-induced polydipsic (SIP) rats. We previously reported that some selective 5-HT reuptake inhibitors decrease SIP 30-40% after a 14-21 day treatment. In the current study, HP 184 decreased SIP beginning with the first treatment, and this reduction (30%) was maintained for 28 days. We further investigated HP 184 and serotonin metabolite levels. One hour after i.p. administration of 30 mg/kg HP 184, the ratio of whole brain 5-hydroxyindolacetic acid (5-HIAA) to 5-HT was increased, suggesting serotonergic activation. Under these conditions, the brainlasma ratio of HP 184 was approximately 2:1, with brain concentrations of 1.6 micrograms/gram. We speculate that the spontaneous release effects of HP 184 may be responsible for the behavioral effects observed.

    • Tang L and Kongsamut S (1996). Frequency-dependent inhibition of neurotransmitter release by besipirdine and HP 184. Eur J Pharmacol. 300: 71-4. Neuroscience Therapeutic Domain, Hoechst Marion Roussel, Sommerville, NJ 08876, USA. We have described the interaction of besipirdine (HP 749, N-(n-propyl)-N-(4-pyridinyl)-1H-indol-1-amine hydrochloride) with voltage-dependent Na+ channels (Tang et al., 1995, Br. J. Pharmacol. 116,2468). Here we describe studies with besipirdine and a related compound, HP 184 (N-(n-propyl)-3-fluoro-4-pyridinyl)-1H-3-methylindol-1-amine hydrochloride), showing that this interaction is voltage-dependent and leads to frequency-dependent inhibition of electrically stimulated neurotransmitter release. Thus, the inhibition of veratridine-induced increases in intracellular Ca2+ was enhanced by depolarization with KCl (IC50 shifted from 23.8 +/- 1.4 microM in 5 mM KCl to 7.3 +/- 1.2 microM in 15 mM KCl for besipirdine and from 58.2 +/- 1.3 microM for HP 184). Moreover, the enhancement of electrically stimulated [3H]norepinephrine release by besipirdine was diminished at higher frequencies of stimulation. As has been previously suggested for such compounds, we predict that besipirdine would act as a filter in the brain allowing signalling at low frequencies but blocking transmission at high frequencies.

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