Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
1.acetylcholine C7H16NO2 2.melatonin C13H16N2O2 3.Warfarin (blood thinner also known to knock off Bb) C19H16O4 4.usnic acid C18H16O7 (we talked about usnic acid on this board years ago) 5.Rocephin C18H16N8Na2O7S3 * 3.5 H2O 6.Camphor C10H16 7.A terpene from the bark of a tree: C10H16 8.l-methone C10H16O 9.Malarone (atovaquone and proguanil hydrochloride) ...the chemical formula for proguanil hydrochloride is C11H16CIN5 * HCL 10.Biotin: Its molecular formula is C10H16N2O3S There is some evidence that it may have antioxidant activity. 11.Taurolidine to treat bacterial infections, particularly Helicobacter pylori infections. Taurolidine occurs as a white to off-white powder having the molecular formula - C7 H16 N4 O4 S2. 12.EDTA (or ethylenediamine tetra acetic acid, also known as edetic acid or tetra acetic acid) is a synthetic amino acid having a molecular weight of 292.25 and a molecule formula of C10H16N2O8 2-Dimethylaminoethyl 4 chlorophynoxyacetate hydrochloride. trade names Cerutil, Helfergin and Lucidri Molecular Formula: C(12)H(16)CINO(3), HCL Synonyms:Centrophenoxine Hydrochloride; Clofenoxine Hydrochloride; Clophenoxate Hydrochloride; Deanol 4 Chlorophenoxyacetate Hydrochloride; Meclofenoxane Hydrochloride. Go here: http://www.worldhealth.net/p/aadr-centrophenoxine.html (anti-aging) 13.IPRIFLAVONE, 7-isopropoxyisoflavone. Used in Europe as Osteofix for increasing bone density, this isoflavone may be the answer for osteoporosis at 300mg twice a day. Appearance: A almost white powder. Formula: C18-H16-O3 14.3-INDOXYL PHOSPHATE Molecular Weight: 257CAS Registry Number: 3318-43-2Molecular Formula: C8H16NNa2O4P 15.ATP: Formula: C10 H16 N5 O13 P3 http://xplor.csb.yale.edu/xplor/hetero/ATP.html 16.MAP Formula: C10 H16 N6 O12 MG1 P3 Name(s): magnesium-5p-adenylyl-imido-diphosphate 17.The results show that H16 of hEGF, although not essential for mitogenic activity, optimizes receptor recognition by hydrogen-bond donor/acceptor interactions and may share this feature with H18 of hTGFalpha.
Human epidermal growth factor (hEGF)
PMID: 10025663
18. Vitamin B1: C12H16 N4OS Thiamine...Valletta's patent...Mg pyrophosphate is phosphorous and thiamine and Mg.
19.Citrus D-Limonene - geeze...(I KNEW I should have brought some home from Capri!) Molecular Formula:C10H16 = 136.24
23. According to a detailed research on American peppermint oil by F. B. Power and C. Kleber (Pharm. Rundschau, 1894, p. 157), this oil contains the following substances: (1) Acetaldehyde; (2) isovaleric aldehyde; (3) amyl alcohol; (4) free acetic, and (5) isovalerianic acids; (6) pinene; (7) phellandrene; (8) l-limonene; (9) cadinene; (10) cineol; (11) a lactone (C10H16O2); (12) menthone; (13) menthol; (14) menthyl-acetate; (15) menthyl-isovalerianate; (16) menthylester of an acid, C8H12O2; (17) dimethyl sulphide (S[CH3]2). Substances 3 and 17 were additionally found in the laboratory of Schimmel & Co., in 1894 and 1896.
24. Chrysanthemic acid, C10H16O2
25. Ascaridole, C10H16O2
26. Oleum Chenopodii. Oil of Chenopodium. -- This volatile oil, obtained by distilling with water or superheated steam, is a colorless, pale yellowish liquid, peculiar, disagreeable odor, bitte burning taste, soluble in 70 p.c. alcohol (8), sp. gr. 0.967, levorotatory; contains a terpene-- pinene, C10H16, and a liquid oxygenated portion (C10H16O2), ascaridol. Chenopodium is a herb. It is called Mexican Tea. It has been used to treat roundworms. This is curious: We isolated ascaridol from a commercial preparation of Chenopodium oil and analyzed its activity against different tumor cell lines in vitro (CCRF-CEM, HL60, MDA-MB-231). Multidrug-resistant (MDR) counterparts of these cell lines express differentially the MDR-conferring ATP-binding cassette transporter genes MDR1, MRP1 and BCRP, respectively. We found that ascaridol exerts antineoplastic activity. The findings of the present investigation are the first hint that ascaridol may be an interesting novel candidate drug for cancer treatment.
27. Hypericinin , C30H16O8 St. John's Wort
28.Valporic acid C8H1602 anticonvulsant
29. Cimetidine (Tagamet) C10H16N6S
30. AZT Formula: C10 H16 N5 O13 P3
31. � Nabumetone - C15H16O2Nabumetone - C15H16O2
Nabumetone is used to relieve the pain, tenderness, inflammation (swelling), and stiffness caused by osteoarthritis and rheumatoid arthritis. Nabumetone is in a class of medications called nonsteroidal anti-inflammatory medications (NSAIDs). It works by stopping the body's production of a substance that causes pain, fever, and inflammation.
32. Fioricet Fioricet� (Butalbital, Acetaminophen, and Caffeine Tablets, USP) is supplied in tablet form for oral administration.
Each tablet contains:
butalbital*, USP ........................................................ 50 mg *warning: May be habit-forming. acetaminophen, USP .................................................325 mg caffeine, USP ............................................................ 40 mg Active Ingredients: butalbital, USP, acetaminophen, USP, and caffeine, USP
Inactive Ingredients: crospovidone, FD&C Blue #1, magnesium stearate, microcrystalline cellulose, povidone, pregelatinized starch, and stearic acid.
***Butalbital: (5-allyl-5-isobutylbarbituric acid), is a short to intermediate-acting barbiturate. It has the following molecular formula: C11H16N2O3 with molecular weight 224.26.
Acetaminophen: (4-hydroxyacetanilide), is a non- opiate, non-salicylate analgesic and antipyretic. It has the following molecular formula: C8H9NO2 with molecular weight 151.16.
Caffeine: (1 ,3,7- trimethylxanthine), is a central nervous system stimulant. It has the following molecular formula: C8H10N4O2 with molecular weight 194.19.
33.Clopidogrel bisulfate is : PLAVIX is proven to help keep platelets in the blood from sticking together and forming clots--which helps keep blood flowing. Taking PLAVIX daily can help reduce your risk of a future heart attack or stroke.
empirical formula of clopidogrel bisulfate is C 16 H 16 ClNO 2 S�H 2 SO 4
Too much of a co-incidence here!!! Hydrogen is a powerful "antioxidant"...it combines with oxygen to form a tight bond. Why only H16?
[ 27. October 2005, 12:41 PM: Message edited by: Marnie ]
Posts: 9426 | From Sunshine State | Registered: Mar 2001
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-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
"The effectiveness of dizocilpine and NBQX in preventing lethality in Soman poisoning was studied in our laboratory. The antilethal effects of dizocilpine were significantly weaker than those of diazepam; treatment with NBQX was more lethal than treatment without an anticonvulsant , using only atropine and the oxime HI-6 (1-(((4-amino-carbonyl)pyridino)methoxy)methyl)-2-(hydroxyimino)methyl)-pyridinium dichloride monohydrate), C14-H16-N4-O3.2Cl)" http://jmedchemdef.org/Issue_0101/Rump_0104.html
Still looking.....
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1991.02.21 910056 H16 - SEVERAL QUESTIONS 1. Documentation authorizing release and use of H16 (including any New Drug Submission made), and rights of military personnel to consent/refuse using it. 2. Costs of (i) helping develop and (ii) purchasing H16 supplies and injection kits, including contracts undertaken, royalties paid. 3. Costs of distributing H16 kits and information and how many kits were distributed and to which personnel. 4. Sale and amounts made of H16 supplies/kits to other combatants in the Gulf area, or to NATO allies. 5. DND's Surgeon General or other authorities review of that distribution/information program. 6. Review of actual use to date of H16 by military personnel. 7. Possession of any other chemical antidotes or other remedies in Gulf war area, their costs and distribution and use. 8. Canadian military personnel possession of any defensive/offensive chemical/biological materials/weaponry in the Gulf war zone. 9. Materials that the Surgeon General has declared as defence critical items to the Gulf crisis for saving military personnel. 10. Surgeon General or other senior personnel review of human tests done re H16, atropine, phenobarbital by DRES or contracts like with Laboratoire Bio-Reseaeche Ltee (Quebec). 11. Briefing notes 1990, 1991 on the above subjects that include DND dealing with H16, chemical warfare products, procedures to follow in release of chemical/biological war products.
Dept Date Request No Text Page: 24 Min Rec'v/Recue No. Demande Texte ____ ___________ ___________ _____________________________________________________________________________
Continued from previous page ... DND 1991.02.21 910056 12. Reaction to 1990, 1991 media stories on H16 testing, chemical defensive testing/product use.
1991.03.04 910067 DEFENCE PRODUCTION PERSIAN GULF I am applying under the Access Act for the following records: 9110054 points 1,2,4,8,11. Any changes given the Gulf war in defence production agreements or new ones with the United States, and the implications of such changes. Any declarations of certain Canadian industrial goods and service as critical defence items, or as mandatory to produce for Canadian and allies use in the Gulf war. Any new directives on critical defence items as they apply to the Gulf war. Re my access application 90-10112, any updates on tying North American Defence industries capabilities closer together.
More http://www.stormingmedia.us/11/1146/A114652.html A Comparison of the Efficacy of H16 and 2-PAM against Soman, Tabun, Sarin, an d VX in the RabbitAuthors: Irwin Koplovitz; James R. Stewart; ARMY MEDICAL RESEARCH INST OF CHEMICAL DEFENSE ABERDEEN PROVING GROUND MD
Abstract: The efficacy of HI6 and 2-PAM against nerve agent (soman (GD), tabun (GA), sarin (GB), and VX)induced lethality was investigated in atropinesterase- free rabbits pretreated with vehicle (controls) or pyridostigmine (PYR). Treatment was administered at signs or 2 min after agent challenge and consisted of oxime (100 umol/kg) + atropine (ATR) (13 mg/kg) (alone or together with- diazepam). Twenty-four-hour LD50s were calculated for GD and GAintoxicated animals whereas 24 hr survival was noted in animals given 10 LD50s of GB or VX. In PYR and control rabbits intoxicated with GD and treated with oxime + ATR (alone or together with diazepam), HI6 was 3-5 times more effective than 2-PAM. In contrast, HI6 was less effective than 2-PAM against GA poisoning. In PYR pretreated animals exposed to CA, efficacy was increased more than 3 fold when compared to GA-challenged animals treated with ATR + H16 alone. Both oximes were highly effective against GB and VX. These findings suggest that HI6 could replace 2-PAM as therapy for nerve agent poisoning, because it is superior to 2- PAM against GD, and when used in PYR pretreated animals, it affords excellent Soman, Sarin, Tabun, VX, Atropine, HI6, 2-PAM, Rabbits, Pyridostigmine, Diazepam. Description: Technical rept. Jun-Oct 90, Pages: 27 Report Date: JUN 92 Report number: A114652 Report Unavailable This title is unavailable from Storming Media. We do not know when it might be available, if at all. We list the report on our site for bibliographic completeness, to help our users know what other work has been performed in this field. Please note that as with all titles on this site, we do not have contact information for any of the authors. Nor can we give any suggestions on how one might obtain this report.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
"Three oximes currently being evaluated for adoption as replacement nerve agent therapies by various countries were compared for therapeutic efficacy against soman and tabun. These compounds, together with PAM-CI and toxogonin, were also compared against GF poisoning. The order of effectiveness against soman was HI-6 greater then HLo-7 greater than pyrimidoxime. HLo-7 was very effective against tabun poisoning while HI-6 and pyrimidoxime were of moderate value. Against GF, HI-6 and HLo-7 were highly effective, toxogonin was moderately effective, and PAM-CI and pyrimidoxime were the least effective."
posted
"Studies on the structural of acetyicholinesterase (AChE) as a target of organophosphate toxicity continue and have yielded several leads of significance and practical outcomes. First, studies on oxime reactivation reveal the importance of achieving a suitable angle of attack for the oxime within the confines of the active center gorge. Through the use of mutant AChE-oxime combinations, oxime assisted catalytic turnover of organophosphates can be achieved such that mutant AChE can be employed with oximes as a catalytic scavenger. Second, through cysteine substitution mutagenesis and acrylodan labeling we have developed a fluorescent enzyme whose emission spectrmn changes upon conjugation with organophosphate. These enzymes are now being immobilized and developed as a remote sensor for acetylcholinesterase. Third, we have developed mass spectrometry methods to detect directly the organophosphate conjugates with AChE. Lastly, we have developed several transgenic animal strains that enable us to study the roles cholinesterase inhibition centrally and in the periphery play in organophosphate toxicity and whether the antidotal actions of oximes arise solely through reactivation."
....and now. Back to our regularly scheduled program. Posts: 294 | From nevada | Registered: Sep 2005
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Evaluation of the toxicity, pathology, and treatment of cyclohexylmethylphosphonofluoridate (CMPF) poisoning in rhesus monkeys.
Koplovitz I, Gresham VC, Dochterman LW, Kaminskis A, Stewart JR.
US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010-5425.
Cyclohexylmethylphosphonofluoridate (CMPF) is an organophosphate cholinesterase inhibitor with military significance.
The purpose of these studies was 1) to determine the acute toxicity of CMPF in the male rhesus monkey, 2) to evaluate the efficacy of pyridostigmine (PYR) pretreatment plus atropine and oxime (2-PAM or H16) treatment, and 3) to evaluate the pathological consequences of acute poisoning.
An i.m. LD50 of CMPF was estimated using an up-and-down dose selection procedure and 12 animals. The 48-h and 7-day LD50 was 46.6 micrograms/kg, i.m. In the protection experiments, pyridostigmine (0.3-0.7 mg/kg/24 h) was administered by surgically implanted osmotic minipumps for 3-12 days resulting in 21-65% inhibition of erythrocyte acetylcholinesterase activity.
Animals were challenged with 5 x L50 CMPF (233 micrograms/kg) and treated with atropine (0.4 mg/kg) and either 2-PAM (25.7 mg/kg) or HI6 (37.8 mg/kg) at the onset of signs or 1 min after challenge.
Osmotic pumps were removed within 30 min after agent challenge.
Pyridostigmine, atropine, and either 2-PAM or H16 were completely effective against CMPF, saving ten of ten animals in each group.
In comparison, three of five animals challenged with 5 x LD50 of soman and treated with atropine and 2-PAM survived 7 days. The primary histologic lesions in the acute toxicity group were neuronal degeneration/necrosis and spinal cord hemorrhage.
The CMPF treated groups (total of 20 animals) had minimal nervous system changes with no significant lesion difference resulting from the different oxime therapies. The primary non-neural lesions were degenerative cardiomyopathy and skeletal muscle degeneration which occasionally progressed to necrosis and mineralization.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 1482284
J Neurochem. 2004 Jun;89(5):1119-25.
Regulation of protein kinase C by the anti-Parkinson drug, MAO-B inhibitor, rasagiline and its derivatives, in vivo.
Bar-Am O, Yogev-Falach M, Amit T, Sagi Y, Youdim MB.
Technion-Faculty of Medicine, Eve Topf and NPF Centers for Neurodegenerative Diseases, Department of Pharmacology, Haifa, Israel.
We have recently shown that the anti-Parkinson-propargyl-containing monoamine oxidase B (MAO-B) inhibitor drug, rasagiline [N-propargyl-(1R)-aminoindan],
and its cholinesterase inhibitor derivatives
TV3326 and TV3279, regulate amyloid precursor protein (APP) processing by a protein kinase C (PKC)-dependent mechanism
in SH-SY5Y neuroblastoma and PC12 cells. In the present study, we investigated the effect of rasagiline and its derivatives on the regulation of the PKC-dependent mechanism and APP processing under in vivo conditions.
Administration of rasagiline (0.1 mg/kg) to male C57/BL mice for 14 days significantly decreased membrane-bound holoprotein APP levels in the hippocampus. Additionally, we observed that rasagiline up-regulated p-PKC levels and the expression of alpha and epsilon PKC isozymes in the hippocampus, indicating that the mechanism by which rasagiline affects APP processing may be related to PKC-associated signalling.
The results also demonstrate that rasagiline treatment significantly elevated the levels of phosphorylated myristoylated alanine-rich C kinase substrate (p-MARCKS), a major substrate for PKC, as well as the levels of receptors for activated C kinase 1 (RACK1).
Similar effects on APP and PKC levels were also demonstrated for the two cholinesterase inhibitor derivatives of rasagiline, TV3326 and TV3279. These results indicate that rasagiline and its derivatives regulate PKC-dependent mechanisms and APP processing. The activation and induction of PKC and MARCKS by these drugs may have a crucial role not only in their neuroprotective activity, but also in their ability to affect neuronal plasticity and spatial learning processes.
PMID: 15147504
Bb contains a PKC inhibitor...
Trying to keep level of acetylcholine up. Bb needs acetyl CoA...
Trying to restore PKC...
Were the ticks exposed to pesticides? Did it alter the pathogens attached to them?
What is H16?
Posts: 9426 | From Sunshine State | Registered: Mar 2001
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It's HI-6. 1-(2-hydroxyiminomethyl pyridinium)-3-(4-carbamoylpyridinium)-2-oxapropane dichloride). An H-series (Hagedorn) bis-pyridinium oxime or methoxime. An effective reactivator of soman-inhibited acetylcholinesterase. Somewhat related to HL�-7. ---------------------------- "32. Fioricet Fioricet�" also known as Fiorinal. Great for headaches!!
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Cut and paste:
"atropine and oxime (2-PAM or H16) treatment."
that is definitely a #1.
"HI6 (37.8 mg/kg)"
That is definitely an I.
"and either 2-PAM or H16"
***********
Biochem Pharmacol. 1985 Oct 1;34(19):3606-8. Related Articles, Links
Reactivation of ethyl methylphosphonylated eel acetylcholinesterase in vitro by 2PAM, H16, and a series of nonquaternary alpha-ketothiohydroximates.
Kenley RA, Bedford CD, Howd RA, Jackson SE.
PMID: 4052103
That is a #1
That is definitely a #1.
"A Comparison of the Efficacy of H16 and 2-PAM against Soman, Tabun, Sarin, an d VX in the Rabbit"
That is definitely a #1
"Abstract: The efficacy of HI6 and 2-PAM against nerve agent (soman (GD), tabun (GA), sarin (GB), and VX)induced lethality was investigated in atropinesterase- free rabbits pretreated with vehicle (controls) or pyridostigmine (PYR)."
Another I.
"HI6 was 3-5 times more effective than 2-PAM. In contrast, HI6 was less effective than 2-PAM against GA poisoning."
2 more for the I's.
"animals treated with ATR + H16 alone."
1 for the #1's group.
"suggest that HI6 could replace 2-PAM as therapy for nerve agent poisoning"
1 for the I group.
How can a typist mistake 1 for I?
Still...there is SOMETHING about 16 hydrogens that looks to be critical.
This is curious:
(hEGF = human epidermal growth factor, H16 histadine 16)
The results show that H16 of hEGF, although not essential for mitogenic activity, optimizes receptor recognition by ***hydrogen-bond donor/acceptor interactions and may share this feature with H18 of hTGFalpha.
PMID: 10025663 (Receptor recognition by histidine 16 of human epidermal growth factor via hydrogen-bond donor/acceptor interactions.)
Epidermal growth factor (EGF) is a small protein hormone that plays a critical role in regulating cell growth and proliferation. Because it promotes healing, EGF is used clinically to treat severe burns, ulcers, and postsurgical wounds. (It can trigger epithelial growth factor in cancer.)
The results indicate that histidine-16 contributes to receptor binding and activation through ***hydrogen-bonding reactions. Replacement of histidine-16 with better hydrogen-bonders like glutamine and asparagine led to significantly (two- to four-fold) enhanced receptor binding and activation.
These results suggest the possibility of generating analogues of EGF with superior wound-healing properties by protein engineering.
Evidence is accumulating that histidine is an essential amino acid for adults. It was found that when uremic patients receiving mixtures of the Rose eight essential amino acids were given a histidine supplement, hemoglobin increased (8) and nitrogen retention improved (9).
ARMY MEDICAL RESEARCH INST OF CHEMICAL DEFENSE ABERDEEN PROVING GROUND MD
(U) A COMPARISON OF THE EFFICACY OF HI6 again with a I??[/b} AND 2- PAM AGAINST SOMAN, TABUN, SARIN, AND VX IN THE RABBIT
1994
12P MEDIA COST: $ 6.00 PRICE CODE: AA
PERSONAL AUTHORS: KOPLOVITZ, IRWIN; STEWART, JAMES R.
UNCLASSIFIED
ABSTRACT: (U)This Study Compared The Efficacy Of H16 And 2-Pam Against Nerve Agent (Soman Tabun Sarin And Vx) -Induced Lethality In The Atropinesterase-Free Rabbits Pretreated With Vehicle (Controls) Or Pyridostigmine. Treatment Was Administered At Signs Or 2 Min After Agent Challenge And Consisted Ofoxime (L00umol/Lkg) + Atropine (13 Mg(Kg) (Alone Or Together With Diazepam). Twenty-Four- H Ld50 Values Were Calculated For Soman- And Tabun-Intoxicated Animals, Whereas 24-H Survival Was Noted In Animals Given 10 Ld50s Of Sarin Or Vx. In Pyridostigmine And Control Rabbits Intoxicated With Soman And Treated With Oxime + Atropine (Alone Or Together With Diazepam), Hi6 another i?? Was 35 Times More Effective Than 2-Pam. In Contrast 1116 Was Less Effective Than 2-Pam Against Tabun Poisoning. In Pyridostigmine-Pretreated Animals Exposed To Tabun, Efficacy Was Increased More Than 3-Fold When Compare To Tabun-Challenged Animals Treated With Atropine + H16 Alone.Here its a Number one again?? Both Oximes Were Highly Effective Against Satin And Vx. These Findings Suggest That Hifi Could Replace 2-Pam As Therapy For Nerve Agent Poisoning Because It Is Superior To 2-Pam Against Soman, And When Used In Pyridostigmine- Pretreated Animals It Affords Excellent Protection Against All Four Nerve Agents When Used In Combination With Atropine (Alone Or Together With Diazepam) Therapy.
A. MBR INFO (AS PER PARA 3) AND DATE PRODUCT WAS RETURNED, AS APPLICABLE. (E.G. WHEN MBR RTN H16/ATROPINE AND DIAZEPAM AUTOINJECTORS)
B. PRODUCT, DOSE, LOT N0, MANUFACTURER
C. QTY IE NUMBER OF DOSES
9. THE FOL UNLICENSED DRUGS/BIOLOGICS ARE IN USE BY CF. THIS LIST MAY CHANGE TO REFLECT REQUIREMENTS
A. ANTHRAX VACCINE B. BOTULINUM PENTAVALENT VACCINE C. PLAGUE VACCINE D. SMALLPOX VACCINE E. TICK BORNE ENCEPHALITIS VACCINE F. ATROPINE 2 MG/ML MULTIDOSE VIAL G. ATROPINE/HI6 AUTOINJECTOR
DND 1991.01.03 1991.01.03 910002 ANTICIPATED ORAL QUESTIONS 30 JUN-31 DEC 90 A list, log or record of anticipated oral questions prepared for the period from June 30, 1990 to December 31, 1990. Please include the date and title of the anticipated oral questions.
1991.01.16 910009 RECORDS - EXAMINATION UNIT I would like to obtain copies of a number of previously-released records held by your institution concerning the Examination Unit, a code-breaking operation of the Canadian government which operated during the Second World War. I refer you to the letter written to me by your predecessor, Mr. C.J. Gauthier, dated 15 September 1988, in which Mr. Gauthier informed me that the records in question consist of 1345 pages, for which the reproduction fee would be $269. He also informed me that the normal access fee of $5 would be required for this request.
910010 THE TILLIAN I have become aware that your office holds a number of issues of the Tillian, a newsletter for members of the Commmunications Branch/ Communications Security Establishment, that have already been released in severed form. Some of these have also been released to me. I now request pages 153-270 inclusive of these records.
1991.02.21 910056 H16 - SEVERAL QUESTIONS 1. Documentation authorizing release and use of H16 (including any New Drug Submission made), and rights of military personnel to consent/refuse using it. 2. Costs of (i) helping develop and (ii) purchasing H16 supplies and injection kits, including contracts undertaken, royalties paid. 3. Costs of distributing H16 kits and information and how many kits were distributed and to which personnel. 4. Sale and amounts made of H16 supplies/kits to other combatants in the Gulf area, or to NATO allies. 5. DND's Surgeon General or other authorities review of that distribution/information program. 6. Review of actual use to date of [b]H16 by military personnel. 7. Possession of any other chemical antidotes or other remedies in Gulf war area, their costs and distribution and use. 8. Canadian military personnel possession of any defensive/offensive chemical/biological materials/weaponry in the Gulf war zone. 9. Materials that the Surgeon General has declared as defence critical items to the Gulf crisis for saving military personnel. 10. Surgeon General or other senior personnel review of human tests done re H16, atropine, phenobarbital by DRES or contracts like with Laboratoire Bio-Reseaeche Ltee (Quebec). 11. Briefing notes 1990, 1991 on the above subjects that include DND dealing with H16, chemical warfare products, procedures to follow in release of chemical/biological war products.
Dept Date Request No Text Page: 24 Min Rec'v/Recue No. Demande Texte ____ ___________ ___________ _____________________________________________________________________________
Continued from previous page ... DND 1991.02.21 910056 12. Reaction to 1990, 1991 media stories on H16 testing, chemical defensive testing/product use. From H16
::::::::::::::::: :::::::::::::: :::::::::::::::
This stuff must be something huh???
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
posted
Nerve gases and most pesticides block acetylcholine breakdown -- that is how they kill people and insects -- the nerves keep firing and wear themselves out -- end result is most likely a heart attack or stroke if I remember correctly.
Hubby was tested for pesticide toxicity because of his out of control tremors -- one blood test found small levels of a couple of pesticides -- can't remember which ones now, but fat biopsy came back normal so we did not pursue this further.
Acetylcholine (the gas) and dopamine (the brakes) are the neurotransmitters that control movement. Parkinson's patients do not have enough dopamine. Something like 80% of the dopamine producing cells have been destroyed before they become symptomatic.
Lyme does deplete acetylcholine but as far as I can determine it does not actually destroy dopamine producing cells -- the 2 neurotransmitters are just out of balance.
Also, the neurotoxins produced by Lyme may possibly interfere with acetylcholine production or breakdown -- can't say as I have never read where anyone has actually identified what these neurotoxins are.
Bea Seibert
[ 29. October 2005, 11:44 PM: Message edited by: seibertneurolyme ]
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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posted
Anticholinergic drugs include Benadryl, Artane and Ditropan -- anticholinergics stop spasms and slow movement.
Cholinergic drugs include Reglan -- cholinergics speed up movement including heartrate and peristalsis.
There are several more in each group that don't come to mind right off -- hubby has had all these and more for lifelong G.I. problems and tremors due to Lyme.
Atropine and scopolamine block cholinergic effects and are sometimes used as antidotes for cholinesterase inhibition I think. Atropine is actually the poisonous alkaloid found in deadly nightshade (Belladonna)-- in common use as the agent which is used to dilate eyes for eye exams.
Pamine is another newer G.I. drug but I forget which class it goes in.
It's been a while since I studied up on all this so I might not be 100 % accurate.
Bea Seibert
[ 29. October 2005, 11:49 PM: Message edited by: seibertneurolyme ]
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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Also, the neurotoxins produced by Lyme may possibly interfere with acetylcholine production or breakdown -- can't say as I have never read where anyone has actually identified what these neurotoxins are.
Bea Seibert
I was wondering that myself just the other day.
Anybody know what the chemical composition of the toxins are? Anybody? Marnie?
Posts: 294 | From nevada | Registered: Sep 2005
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Recently the new Hagedorn (H) oximes have been synthesised and these include the compounds H16 and HS6 as shown in Figure B-III.
c. The oximes are thought to act by combining with the modified nerve agent molecule and removing it from the acetylcholinesterase enzyme. They also have other pharmacological effects which may contribute to their efficacy.
posted
This may be a case of Optical Character Recognition (OCR) software incorrectly transcribing a "1" for an "I". I trust the Adobe pdf file transcripts which are basically direct pictures of the original abstracts. Sorry, but I'm pretty sure it's HI-6.
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