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Post by lilsissy on Dec 27, 2010 2:00:52 GMT -5
Sustances that are being banned peppermint in the U.K. www.rumormillnews.com/cgi-bin/forum.cgi?read=191086Menthol cigaretts here, Menthol is an organic compound made synthetically or obtained from peppermint or other mint oils. It is a waxy, crystalline substance, clear or white in color, which is solid at room temperature and melts slightly above. The main form of menthol occurring in nature is (-)-menthol, which is assigned the (1R,2S,5R) configuration. Menthol has local anesthetic and counterirritant qualities, and it is widely used to relieve minor throat irritation. www.cigarettesflavours.com/tag/menthol-cigarettesen.wikipedia.org/wiki/MentholDoes this relate to Morgellons and to the transfer of genes ? I noticed that Morgellons fibers are driven out when exposed to mentholated baby wash. hmmmm, what just turned up in our work with budding yeast and human cells? www.niehs.nih.gov/news/newsletter/2010/october/science-council.cfmAt the meeting of the National Advisory Environmental Health Sciences Council Sept. 1-2 (see related story (http://www.niehs.nih.gov/news/newsletter/2010/october/spotlight-council.cfm)), NIEHS once more honored the tradition of showcasing its science and giving members a welcome respite from the program reports. For its fall meeting, members enjoyed presentations by grantee Sven-Eric Jordt, Ph.D., and by NIEHS Principal Investigator Mike Resnick, Ph.D. In 2006, Jordt(http://info.med.yale.edu/pharm/faculty/index.php?bioID=39) was selected as one of the first NIEHS Outstanding New Environment Scientist (ONES) awardees and is the principal investigator of a grant under the NIH CounterACT program administered by NIEHS. The next year, Jordt became the first NIEHS grantee to be honored with a Presidential Early Career Award for Scientists and Engineers (PECASE). Resnick (http://www.niehs.nih.gov/research/atniehs/labs/lmg/cs/index.cfm) is head of the NIEHS Chromosome Stability Group and a veteran investigator with a long list of honors and outstanding publications (see this month's summary (http://www.niehs.nih.gov/news/newsletter/2010/october/science-intramural.cfm) of his most recent Paper of the Month). Resnick was honored as NIEHS Scientist of the Year in 2008, and since the inception of the "Best Paper of the Year" at NIEHS in 2003, his group has received this award for 2003, 2004, and 2007. Jordt and Resnick are examples of NIEHS-funded investigators involved in basic research, with promising translational potential for treating and preventing human injury and disease. TRP channels in chemical sensing and environmental disease Jordt's work has its roots in his postdoctoral research on the mechanisms of transient receptor potential (TRP) channel receptors, which are part of an early warning system of sensory neurons activated during injury and chronic painful conditions. These receptors trigger tears, sneezing, neurogenic inflammation, pain, and respiratory constriction in the upper airway. A series of important papers by Jordt's group over the past four years has uncovered the role of TRP channel activation, specifically TRPA1, in mammalian responses to noxious chemical and physical stimuli, such as cigarette smoke, tear gas agents, and chlorine. Recent work by the group has expanded investigations into the role of sensory neuronal ion channel activation in producing airway inflammation and hyperactivity in allergic asthma (see related story (http://www.niehs.nih.gov/news/newsletter/2009/july/science-jordt.cfm)). In his work with wildtype and TRPA1 knockout mice challenged with ovalbumin, Jordt and his colleagues have experimented with a TRPA1 antagonist, HC-030031, that was found to be protective in exposure to noxious gases. The antagonist, they found, also gave wildtype mice the same protection as that enjoyed by the genetically modified mice against the asthmatic response, inhibiting eosinophil infiltration and preventing the development of airway hyperreactivity. Jordt's recent work also addresses the TRPM8 cold-sensitive channel activated by menthol and may support efforts by public health advocates to end use of this anti-inflammatory agent in cigarettes. The expanding universe of p53 targets As the latest step in his basic research on genome stability, Resnick entered into an innovative Intramural Research Award collaboration last year (see related story (http://www.niehs.nih.gov/news/newsletter/2010/february/science-pritchard.cfm)) with two NIEHS clinical investigators, Michael Fessler, M.D., and Stavros Garantziotis, M.D. In his Council presentation, Resnick reviewed his group's findings from research on budding yeast and human cells and the work that informs the new paper that Resnick, Fessler, and Garantziotis, along with Chromosome Stability Group members Daniel Menendez, Ph.D., and Maria Shatz, Ph.D., have recently submitted for publication — "The human Toll-like receptor (TLR) family is integrated into the DNA damage and p53 response network." Resnick reviewed the tumor suppressor p53 as the "guardian of the genome" in its role as a sequence-specific transcription factor and master regulator of more than 200 genes and non-coding sequences in the human genome, and he described recent findings that greatly expand the p53 network of target genes. With his cross-disciplinary collaborations, Resnick is investigating the evolution of p53 networks, including ones that seem to be primate specific, and addressing what he calls "the dramatic synergy" of the estrogen receptor and p53 networks. Studies of human primary lymphocytes from healthy volunteers have revealed p53 control of most human TLR genes and shed light on the mechanisms of p53 control and its involvement in variations in innate immunity. These findings will likely have potential implications in terms of better understanding individual susceptibility to environmentally linked diseases and for the advancement of personalized medicine.
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Post by lilsissy on Dec 27, 2010 3:46:56 GMT -5
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Post by lilsissy on Dec 27, 2010 4:10:03 GMT -5
I have noticed that both menthol and caspaisin drive morgellons fibers crazy bu they have a antiinflammatory effect on the body as described in this article. This is a great blog on this with Dr. Ayers following the article Japanese Gain Ability to Digest Algal Polysaccharides from Marine Bacteria Gut flora adapt to the food nutrients that are prevalent in different parts of the world. Bacteria able to digest unusual nutrients, such as the sulfated porphyrans found in seaweed eaten in Japanese cuisine, are also consumed along with algae. Formation of bacterial biofilms triggers the exchange of genes among gut bacteria and the acquisition of new polysaccharide-degrading enzyme activities. reference: Hehemann JH, Correc G, Barbeyron T, Helbert W, Czjzek M, Michel G. Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota. Nature. 2010 Apr 8;464(7290):908-12. coolinginflammation.blogspot.com/2010/04/lateral-gene-transfer-in-gut-flora.htmlIn the blog area, a refernce to menthol and caspase www.blogger.com/profile/01727664149735013259Dr. Art Ayers said... Claire (1), My understanding of relapsing polychondritis, is that it is an autoimmune disease attacking cartilage. As you indicate, it is important that you reduce chronic, systemic inflammation as much as possible. Most people say that they are on an anti-inflammatory diet, but what they mean is the anti-inflammatory diets that are found in typical magazines, which are just inflammatory diets plus some veggies. The fact that you mention lingering symptoms of inflammation, indicates that your diet is still probably contributing to your problem. I will look up the info available on the typical cartilage protein that is the target in most polychondritis. That will just point back to other autoimmune diseases and ultimately to celiac or a viral infection. The disease can't start without chronic inflammation that is used based on diet. First aid: You can probably reduce the attack on cartilage in particular areas by applying a general tissue anti-inflammatory, such as castor oil, caspsaicin or menthol. These don't penetrate, but that isn't important, since they work on your nervous system: trigger hot/cold nerve sensors to produce anti-inflammatory response in the surrounding deep tissue. It also works well on sore joints/tendons. Vagal stimulation should also work throughout your body. Diet: Check your serum vitamin D level. I would expect that it is below 30. You will probably need more than 5,000 IU/day of vit.D3 supplement to get you into the 90 range. Check again after a month of supplements. Daily sunshine (never burn) over a large surface area will help a lot. Celiac to Hashimoto's thyroiditis to vasculitis to RPC is one path. That means that you are likely to have an intolerance to gluten that got you started. That means that you should stop eating grains. Most diets are much healthier without grains anyway, because they also provide excess starch that just spikes your insulin and contributed to your problems. Most nutritionists do not understand cell biology and only preach what their books say. They continue to preach moderate starch/sugar, when the biomedical literature says that depending on carbs for calories is unhealthy. Go to a low carb diet.
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Post by lilsissy on Dec 27, 2010 15:26:34 GMT -5
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Post by lilsissy on Dec 27, 2010 15:47:54 GMT -5
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Post by lilsissy on Dec 27, 2010 22:05:59 GMT -5
Looking for alternative energy cells , I think this will relate to the Cytoophdia by CPTS ,
CHECK OUT ELECTROSTATIC ACTION Whether polyphosphates are endogenous factors that interact with TRPA1 remains to be determined. Polyphosphates are major components of yeast and Escherichia coli, serve as a source of stored energy that can be used in times of stress, and participate in cell motility, biofilm formation, and virulence (Kornberg et al., 1999; Bolesch and Keasling, 2000; Zhang et al., 2005). Enzymes that synthesize (polyphosphate kinase) and degrade polyphosphates (exopolyphosphatase and endopolyphosphatase) are expressed in these organisms (Schroder et al., 2000; Saito et al., 2005; Zhang et al., 2005). Polyphosphates are also found in all eukaryotic cells, but their function is not well understood (Kumble and Kornberg, 1995, 1996; Kornberg et al., 1999). The enzymes that synthesize polyphosphates are also expressed in eukaryotic cells. A recent study showed that inorganic polyphosphates stimulate mammalian target of rapamycin, a kinase involved in the proliferation of mammary cancer cells (Wang et al., 2003). In our study, the activation of TRPA1 by pungent chemicals in inside-out patches was observed even when the concentration of polyphosphates was as low as 20–50 µM. The concentration of long-chain free polyphosphates in eukaryotic cells has been reported to range from 100 to 400 µM (Kornberg et al., 1999; Schroder et al., 2000). According to our concentration–response curves, these concentrations of polyphosphates are not high enough to restore full activation of TRPA1 by AITC. Therefore, polyphosphates may be only one of the factors responsible for keeping TRPA1 in the fully functional state. It is possible that cellular polyphosphates are present at high enough levels near the plasma membrane to keep TRPA1 in the functional conformation or that different combination of polyphosphates works more effectively. Whether a polyphosphate that has hundreds of phosphate groups also work on TRPA1 remain to be determined. IP3 and IP6 can make TRPA1 agonist sensitive but are unlikely to contribute significantly to the modulation of TRPA1 because their concentrations in the cell are below the submicromolar levels (Bezprozvanny and Ehrlich, 1993; Ehrlich et al., 1994). Free [PPi] in the cell is also in the low micromolar range (Guynn et al., 1974; Gitomer and Veech, 1986), indicating that endogenous PPi (K1/2 of 9 mM) is not a regulator of TRPA1. Additional studies on the biochemical properties of inorganic polyphosphates in eukaryotic cells are needed to understand their potential role in the regulation of TRPA1.
How do polyphosphates interact with TRPA1 and sensitize it to pungent chemicals? PPi and PPPi can block ATP hydrolysis in ATPases and ion channels (such as cystic fibrosis transmembrane regulator) by binding to the PPi-binding pocket (Baukrowitz et al., 1994; Gunderson and Kopito, 1994, 1995). However, TRPA1 has no known ATPase or phosphatase activities and has no ATP binding motif, and ATP does not activate TRPA1. Therefore, the effect of polyphosphates on TRPA1 function is unlikely to be related to inhibition of ATP hydrolysis. One obvious property of polyphosphates is its high number of phosphate groups and associated negative charges. Because of a large number of positively charged residues in TRPA1, it was not practical to mutate all of them to test their roles. Therefore, the possibility of an electrostatic interaction, although seemingly likely, is not yet proven. The lack of effect of Pi and polyglutamate, even at high concentrations, would suggest that, in addition to the negative charges, the structure of the polyphosphate is also important. This is supported by the failure of high concentrations of ATP or GTP to confer agonist sensitivity to TRPA1. The relatively bulky adenosine moiety of ATP probably hinders access to the interaction site of TRPA1. The much smaller inositol structure of IP3 and IP6 probably allows access to the interaction site, because they both can keep TRPA1 to the agonist-sensitive state. Positively charged molecules such as polylysine antagonized the effect of polyphosphates. Therefore, there is some basis for speculating that both the negative charges and the structure of polyphosphates are important for the TRPA1 function. The 16–18 ankyrin repeat domains present at the N terminus of TRPA1 may provide sites for protein–protein interaction (Mosavi et al., 2004; Jin et al., 2006), as well as interaction with other nonprotein molecules, such as polyphosphates. Unfortunately, no TRPA1 activity could be recorded when three and six ankyrin repeat domains from the N terminus or all of the N terminus was deleted. The possible interaction between polyphosphates and ankyrin repeat domains of TRPA1 needs additional investigation.
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Post by skyship on Dec 27, 2010 22:37:09 GMT -5
Works for me: in the cartilage, tendon area back of neck along hairline.
castor oil, caspsaicin or menthol.
castor oil, caspsaicin and vicks!
Also what pulls out the deep fibers wrapped around the nerves, vicks and fungal cream.============ repeating and disecting:Whether polyphosphates are endogenous factors that interact with TRPA1 remains to be determined. Polyphosphates are major components of yeast and Escherichia coli, serve as a source of stored energy that can be used in times of stress, and participate in cell motility, biofilm formation, and virulence (Kornberg et al., 1999; Bolesch and Keasling, 2000; Zhang et al., 2005). Enzymes that synthesize (polyphosphate kinase) and degrade polyphosphates (exopolyphosphatase and endopolyphosphatase) are expressed in these organisms TRPA1 = The nervous system senses peripheral damage through nociceptive neurons that transmit a pain signal.[b] TRPA1 is a member of the Transient Receptor Potential (TRP) family of ion channels and is expressed in nociceptive neurons[/b]. TRPA1 is activated by a variety of noxious stimuli, including cold temperatures, pungent natural compounds, and environmental irritants....... ......Structurally unrelated cysteine-modifying agents such as i odoacetamide (IA) and (2-aminoethyl)methanethiosulphonate (MTSEA) also bind and activate TRPA1. We identified by mass spectrometry fourteen cytosolic TRPA1 cysteines labelled by IA, three of which are required for normal channel function. ..... .....Collectively, our data indicate that covalent modification of reactive cysteines within TRPA1 can cause channel activation, rapidly signalling potential tissue damage through the pain pathway.,,,,,,, www.nature.com/nature/journal/v445/n7127/abs/nature05544.html=================== I would say the environmental irritants from chemtrails are IT! polyphosphate kinase Here is one, and guess where it is from the P. aeruginosa..... PPK1........ ================ A polyphosphate kinase 1 (ppk1) mutant of Pseudomonas aeruginosa exhibits multiple ultrastructural and functional defects WT- wild type mutant...... in the p aeruginosa..... www.pnas.org/content/104/9/3526/F2.expansion.html======================= So, some morgellons folks, died because of this mutant in the area where they lived. New Zeeland! Australia area? too.
So, in different areas different mutants were released!=====
then a new kinase is found from another organism and so on till it is perfect meanwhile the monitoring from other probes, indicate another type of kinase in that specific area or environment, say a dry environment, mountainous environment, water environment, swampy environment, using alterations in wild to affect the human by environmental stimulus, both from released mutant species and air borne released spores and microspheres, buckyballs and nanotubes from chemtrails. And finally the use of mere nanoparticles to alter anything. All you need is the right signal, sound, vibrations, resonance, radio freq. and light wave patterns.
Eyes to see, meaning light patterns Ears to hear, meaning vibrations, signals resonance,
================================== We will get this physics part, and it may involve the neutrinos. they go right through us............mmmmmm skysip, RED RED WINE!
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Post by skyship on Dec 27, 2010 23:13:22 GMT -5
....."failure of high concentrations of ATP or GTP to confer agonist sensitivity to TRPA1" So, ATP or GTP is not high enough to show or release sensitivity to TRPA1, no reaction, so goes past immune system? So TRPA1 then could lower the ATP or GTP? It appears the issues are in GDP and CTP? =============== thebiogrid.org/32060/summary/saccharomyces-cerevisiae/trp1.htmland yeast artificial chromosome was not used? They say they used it for study, but, did they use it to incorporate us into the biogrid? So, in a way we are confined to the earth's organic biogrid, which will become an artificial biogrid? We are connected by signal, by sound, by light wave, by protein-protein interaction, by chemical bonds, and by transitional metals and minerals to the earth itself. We are the earth, the earth is us. skyship
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Post by skyship on Dec 27, 2010 23:22:24 GMT -5
lil sis, this one is used for detection and screening, does not change genes, the only thing that can is viral mutations, chemical mutation, telomere issues, chromosome initiation which can be done using the methylation, but, it is specific to the epigenetic control of the genes, however going through the back door, through the histones. www.freepatentsonline.com/7375203.htmlskyship
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Post by skyship on Dec 28, 2010 0:06:50 GMT -5
It seems that TRPA1 works to stop:
formalin-induced pain formalin is formaldehyde!
holy crap................ THE TRPA1 is supposed to mediate it.
but this attenuates it? attenuate? mmmm to make thin, reduce force etc?======= Definition of ATTENUATE1 : reduced especially in thickness, density, or force 2 : tapering gradually usually to a long slender point <attenuate leaves> Origin of ATTENUATE Middle English attenuat, from Latin attenuatus, past participle of attenuare to make thin, from ad- + tenuis thin — more at thin www.merriam-webster.com/dictionary/attenuate=================== formalin in vaccines? how do we get it?============= another look at TRP1 or TRPA1, one and the same? I don't think so.
TRP1 has the 23, the number of chromosomes we have paired............
while TRPA1 is for formalin induced pain, etc............ the cold/hot temp controlled, methyl vs capsacian...................... so temp of source of pain in nerve is issue.
! TRP1 Tyrosinase-Related Protein 1 TRPA1 TRPA1 Transient Receptor Potential Ankyrin 1 ==============Abstract A number of prostaglandins (PGs) sensitize dorsal root ganglion (DRG) neurons and contribute to inflammatory hyperalgesia by signaling through specific G protein-coupled receptors (GPCRs). One mechanism whereby PGs sensitize these neurons is through modulation of "thermoTRPs," a subset of ion channels activated by temperature belonging to the Transient Receptor Potential ion channel superfamily. Acrid, electrophilic chemicals including cinnamaldehyde (CA) and allyl isothiocyanate (AITC), derivatives of cinnamon and mustard oil respectively, activate thermoTRP member TRPA1 via direct modification of channel cysteine residues. preview.molecularpain.com/content/4/1/30=========================== TRPA1 Desensitization in Sensory Neurons is Agonist- Dependent and Regulated by TRPV1-DireThe pharmacological desensitization of receptors is a fundamental mechanism for regulating the activity of neuronal systems. The TRPA1 channel plays a key role in the processing of noxious information and can undergo functional desensitization by unknown mechanisms. Here we show that TRPA1 is desensitized by homologous (mustard oil; a TRPA1 agonist) and heterologous (capsaicin; a TRPV1 agonist) agonists via Ca2+-independent and Ca2+-dependent pathways, respectively, in sensory neurons. The pharmacological desensitization of TRPA1 by capsaicin and mustard oil is not influenced by activation of protein phosphatase 2B. However, it is regulated by phosphatidylinositol-4,5-bisphosphate depletion after capsaicin, but not mustard oil, application. Using a biosensor, we establish that capsaicin, unlike mustard oil, consistently activates phospholipase C in sensory neurons. We next demonstrate that TRPA1 desensitization is regulated by TRPV1, and it appears that MO-induced TRPA1 internalization is prevented by co-expression with TRPV1 in a heterologous expression system and in sensory neurons. In conclusion, we propose novel mechanisms whereby TRPA1 activity undergoes pharmacological desensitization through multiple cellular pathways that are agonist-dependent and modulated by TRPV1. www.ionchannels.org/showabstract.php?pmid=17584831===== S
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Post by skyship on Dec 28, 2010 0:35:21 GMT -5
Mustard oil? Ah yes, if we but have the "faith of a mustard seed"! interesting called Crucifera plants. =========================== mustard - any of several cruciferous plants of the genus Brassica crucifer, cruciferous plant - any of various plants of the family Cruciferae Brassica, genus Brassica - mustards: cabbages; cauliflowers; turnips; etc. Brassica juncea, chinese mustard, gai choi, indian mustard, leaf mustard - Asiatic mustard used as a potherb black mustard, Brassica nigra - widespread Eurasian annual plant cultivated for its pungent seeds; a principal source of table mustard Brassica napus, colza, rape - Eurasian plant cultivated for its seed and as a forage crop Brassica hirta, Sinapis alba, white mustard - Eurasian mustard cultivated for its pungent seeds; a source of table mustard and mustard oil Brassica kaber, chadlock, charlock, field mustard, Sinapis arvensis, wild mustard - weedy Eurasian plant often a pest in grain fields isothiocyanate - a family of compounds derived from horseradish and radishes and onions and mustards; source of the hotness of those plants and preparations 2. mustardmustard - pungent powder or paste prepared from ground mustard seeds table mustard dry mustard, powdered mustard - a substance such that one to three tablespoons dissolved in a glass of warm water is a homemade emetic condiment - a preparation (a sauce or relish or spice) to enhance flavor or enjoyment; "mustard and ketchup are condiments" mustard seed - black or white seeds ground to make mustard pastes or powders Chinese mustard - very hot prepared mustard isothiocyanate - a family of compounds derived from horseradish and radishes and onions and mustards; source of the hotness of those plants and preparations 3. mustard - leaves eaten as cooked greens mustard greens, Indian mustard, leaf mustard cruciferous vegetable - a vegetable of the mustard family: especially mustard greens; various cabbages; broccoli; cauliflower; brussels sprouts www.thefreedictionary.com/mustard+oil+glucosinolatescruciferous according to wiki: "Etymology of "cruciferous": having flowers with four equal petals arranged crosswise." good ole mustard greens..................... ============================ Arabidopsis thaliana is a small flowering plant that is widely used as a model organism in plant biology. Arabidopsis is a member of the mustard (Brassicaceae) family, which includes cultivated species such as cabbage and radish. Arabidopsis is not of major agronomic significance, but it offers important advantages for basic research in genetics and molecular biology. www.arabidopsis.org/portals/education/aboutarabidopsis.jsp
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Post by skyship on Dec 28, 2010 0:36:43 GMT -5
It is hard to see if this is being done for good, to heal, or to alter genetics through molecular models.
skyship
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Post by lilsissy on Dec 28, 2010 0:42:04 GMT -5
I was thinking about how it could be utilized the hot cold receptors and wonder could this translate to the modulations of frequencies? but look a new opsin in the eye found www.biomedsearch.com/nih/influence-intrinsically-photosensitive-retinal-ganglion/19850061.htmlAlso I keep seeing this over and over budding yeast and cancer the giberrlic acid is put on plants to bring on the bud and is used to kill pancreas cancer. Has me wondering if P.C. is not a yeast growth arrested before the bud stage? If they grew poly , pedot in our cells then maybe things like yeast can lie dormant in the comparments OH that's it I bet it breaks open compartments like the buds are in and the high energy sacs of morgs. Yeast buds comparmentalized sacs?
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Post by lilsissy on Dec 28, 2010 1:36:44 GMT -5
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Post by MonteWhero on May 1, 2020 3:54:22 GMT -5
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