What is Bioactive Paper?
Envision paper towels that immediately signal contamination on kitchen counters, strips of paper that remove pathogens from water while confirming that the water is safe to drink, and medical masks that actively remove viruses. With the research being done through Canada’s Sentinel Bioactive Paper Network this technology could be coming to the world soon…
Drop a tablet of AchE into the sample, followed by a tablet of indoxyl acetate, and wait for the sample to turn faint blue or remain colourless if malathion is present.
Acetylcholinesterase, also known as AChE or acetylhydrolase, is ahydrolase that hydrolyzes the neurotransmitter acetylcholine. AChE is found at mainly neuromuscular junctions and cholinergic brain synapses, where its activity serves to terminate synaptic transmission. It belongs tocarboxylesterase family of enzymes. It is the primary target of inhibition by organophosphorus compounds such as nerve agents and pesticides....
Biological function[edit]
During neurotransmission, ACh is released from the nerve into the synaptic cleft and binds to ACh receptors on the post-synaptic membrane, relaying the signal from the nerve. AChE, also located on the post-synaptic membrane, terminates the signal transmission by hydrolyzing ACh. The liberated choline is taken up again by the pre-synaptic nerve and ACh is synthetized by combining with acetyl-CoA through the action of choline acetyltransferase.
Cholinesterase (ko-li-nes-ter-ace) is one of many important enzymes needed for the proper functioning of the nervous systems of humans, other vertebrates, and insects. Certain chemical classes of pesticides, such as organophosphates (OPs) and carbamates (CMs) work against undesirable bugs by interfering with, or 'inhibiting' cholinesterase. While the effects of cholinesterase inhibiting products are intended for insect pests, these chemicals can also be poisonous, or toxic, to humans in some situations.
Human exposure to cholinesterase inhibiting chemicals can result from inhalation, ingestion, or eye or skin contact during the manufacture, mixing, or applications of these pesticides.
http://extoxnet.orst.edu/tibs/cholines.htm
This video really explains the types, the actions and the dangers really well.
This is a playlist where I found the videos
https://www.youtube.com/watch?v=w1KlXOQuhhs&list=PL2839613ACB0F39F7
Electrical switching centers, called 'synapses' are found throughout the nervous systems of humans, other vertebrates, and insects. Muscles, glands, and nerve fibers called 'neurons' are stimulated or inhibited by the constant firing of signals across these synapses. Stimulating signals are usually carried by a chemical called 'acetylcholine' (a-see-till-ko-leen). Stimulating signals are discontinued by a specific type of cholinesterase enzyme, acetylcholinesterase, which breaks down the acetylcholine. These important chemical reactions are usually going on all the time at a very fast rate, with acetylcholine causing stimulation and acetylcholinesterase ending the signal. If cholinesterase-affecting insecticides are presentin the synapses, however, this situation is thrown out of balance. The presence of cholinesterase inhibiting chemicals prevents the breakdown of acetylcholine. Acetylcholine can then build up, causing a "jam" in the nervous system. Thus, when a person receives to great an exposure to cholinesterase inhibiting compounds, the body is unable to break down the acetylcholine.
WHAT IS THE CHOLINESTERASE TEST?
Humans have three types of cholinesterase: red blood cell (RBC) cholinesterase, called "true cholinesterase;" plasma cholinesterase, called "pseudocholinesterase;" and brain cholinesterase. Red blood cell cholinesterase is the same enzyme that is found in the nervous system, while plasma cholinesterase is made in the liver.
When a cholinesterase blood test is taken, two types of cholinesterase can be detected. Physicians find plasma cholinesterase readings helpful for detecting the early, acute effects of organophosphate poisoning, while red blood cell readings are useful in evaluating long-term, or chronic, exposure (8).
The cholinesterase test is a blood test used to measure the effect of exposure to certain or cholinesterase-affected insecticides. Both plasma (or serum) and red blood cell (RBC) cholinesterase should be tested.
http://extoxnet.orst.edu/tibs/cholines.htm
Improving Blood Monitoring of Enzymes as Biomarkers of Risk From Anticholinergic Pesticides and Chemical Warfare Agents
http://oai.dtic.mil/oai/oai?verb=getRecord&metadataPrefix=html&identifier=ADA429514
Medication Summary
The mainstays of medical therapy in organophosphate (OP) poisoning include atropine, pralidoxime (2-PAM), and benzodiazepines (eg, diazepam). A novel route of administration of intraosseous (bone injection gun, BIG) midazolam demonstrated rapid peak concentrations in swine compared with intravenous and intramuscular routes; the authors concluded this may play a role in quickly terminating seizures, especially in the prehospital arena.[13] Initial management must focus on adequate use of atropine. Optimizing oxygenation prior to the use of atropine is recommended to minimize the potential for dysrhythmias.
de Silva et al studied the treatment of organophosphate poisoning with atropine and 2-PAM and, later the same year, with atropine alone.[14] They found that atropine seemed to be as effective as atropine plus 2-PAM in the treatment of acute organophosphate poisoning. The controversy continued when other authors observed more respiratory complications and higher mortality rates with use of high-dose 2-PAM. Low-dose (1-2 g slow IV) 2-PAM is the current recommendation. Studies are underway to assess the role of low-dose 2-PAM. Improved survival has been shown in moderately severe OP poisoned patients who received early, continuous 2-PAM infusion compared with those who received intermittent boluses.[15]
A meta-analysis and review of the literature performed by Peter et al emphasized optimal supportive care along with discriminate use of 2-PAM, especially early in the course of treatment of moderately to severely OP poisoned patients, are the hallmarks of treatment.[16] More prospective data are required.
Because large amounts of atropine may be required for patients with organophosphate poisoning, reconstitution of powdered atropine is a viable option, especially in mass-casualty settings.[17] Recently, Rajpal et al demonstrated the clinical safety and efficacy of sublingual atropine to healthy volunteers. This may offer another route of administration for the OP poisoned patient, especially in a mass-casualty scenario.[18]
Intravenous glycopyrrolate or diphenhydramine may provide an alternative centrally acting anticholinergic agent used to treat muscarinic toxicity if atropine is unavailable or in limited supply. Additionally, Yavuz et al demonstrated reduced myocardial injury and troponin leak in fenthion-poisoned rats treated with diphenhydramine.[19]
In a single-center, randomized, single-blind study by Pajoumand et al found a benefit to magnesium therapy in addition to standard oxime and atropine therapy in reducing hospitalization days and mortality rate in patients with organophosphate poisoning.[20] The mechanisms appear to be inhibition of acetylcholine (ACh) and organophosphate antagonism. Larger randomized studies are needed to demonstrate magnesium efficacy in organophosphate (OP) poisoning.
Possible future interventions include neuroprotective agents used to prevent nerve damage and bioscavengers aimed to prevent AChE inhibition by nerve agents or organophosphate. Investigations into adjunctive and alternative therapies have mostly used animal models and have resulted in variable conclusions.[21, 22]
Envision paper towels that immediately signal contamination on kitchen counters, strips of paper that remove pathogens from water while confirming that the water is safe to drink, and medical masks that actively remove viruses. With the research being done through Canada’s Sentinel Bioactive Paper Network this technology could be coming to the world soon…
Acetylcholinesterase, also known as AChE or acetylhydrolase, is ahydrolase that hydrolyzes the neurotransmitter acetylcholine. AChE is found at mainly neuromuscular junctions and cholinergic brain synapses, where its activity serves to terminate synaptic transmission. It belongs tocarboxylesterase family of enzymes. It is the primary target of inhibition by organophosphorus compounds such as nerve agents and pesticides....
Biological function[edit]
During neurotransmission, ACh is released from the nerve into the synaptic cleft and binds to ACh receptors on the post-synaptic membrane, relaying the signal from the nerve. AChE, also located on the post-synaptic membrane, terminates the signal transmission by hydrolyzing ACh. The liberated choline is taken up again by the pre-synaptic nerve and ACh is synthetized by combining with acetyl-CoA through the action of choline acetyltransferase.
Cholinesterase (ko-li-nes-ter-ace) is one of many important enzymes needed for the proper functioning of the nervous systems of humans, other vertebrates, and insects. Certain chemical classes of pesticides, such as organophosphates (OPs) and carbamates (CMs) work against undesirable bugs by interfering with, or 'inhibiting' cholinesterase. While the effects of cholinesterase inhibiting products are intended for insect pests, these chemicals can also be poisonous, or toxic, to humans in some situations.
Human exposure to cholinesterase inhibiting chemicals can result from inhalation, ingestion, or eye or skin contact during the manufacture, mixing, or applications of these pesticides.
http://extoxnet.orst.edu/tibs/cholines.htm
Sodium channel receptors are on the cell membranes to trade sodium (cell salts) between the cell and the body. It's like a door. The cell membrane is call the phospholipid...Antiphospholipid means the channel doesn't work. SIMPLE!
This video really explains the types, the actions and the dangers really well.
This is a playlist where I found the videos
https://www.youtube.com/watch?v=w1KlXOQuhhs&list=PL2839613ACB0F39F7
Electrical switching centers, called 'synapses' are found throughout the nervous systems of humans, other vertebrates, and insects. Muscles, glands, and nerve fibers called 'neurons' are stimulated or inhibited by the constant firing of signals across these synapses. Stimulating signals are usually carried by a chemical called 'acetylcholine' (a-see-till-ko-leen). Stimulating signals are discontinued by a specific type of cholinesterase enzyme, acetylcholinesterase, which breaks down the acetylcholine. These important chemical reactions are usually going on all the time at a very fast rate, with acetylcholine causing stimulation and acetylcholinesterase ending the signal. If cholinesterase-affecting insecticides are presentin the synapses, however, this situation is thrown out of balance. The presence of cholinesterase inhibiting chemicals prevents the breakdown of acetylcholine. Acetylcholine can then build up, causing a "jam" in the nervous system. Thus, when a person receives to great an exposure to cholinesterase inhibiting compounds, the body is unable to break down the acetylcholine.
WHAT IS THE CHOLINESTERASE TEST?
Humans have three types of cholinesterase: red blood cell (RBC) cholinesterase, called "true cholinesterase;" plasma cholinesterase, called "pseudocholinesterase;" and brain cholinesterase. Red blood cell cholinesterase is the same enzyme that is found in the nervous system, while plasma cholinesterase is made in the liver.
When a cholinesterase blood test is taken, two types of cholinesterase can be detected. Physicians find plasma cholinesterase readings helpful for detecting the early, acute effects of organophosphate poisoning, while red blood cell readings are useful in evaluating long-term, or chronic, exposure (8).
The cholinesterase test is a blood test used to measure the effect of exposure to certain or cholinesterase-affected insecticides. Both plasma (or serum) and red blood cell (RBC) cholinesterase should be tested.
http://extoxnet.orst.edu/tibs/cholines.htm
Improving Blood Monitoring of Enzymes as Biomarkers of Risk From Anticholinergic Pesticides and Chemical Warfare Agents
http://oai.dtic.mil/oai/oai?verb=getRecord&metadataPrefix=html&identifier=ADA429514
Medication Summary
The mainstays of medical therapy in organophosphate (OP) poisoning include atropine, pralidoxime (2-PAM), and benzodiazepines (eg, diazepam). A novel route of administration of intraosseous (bone injection gun, BIG) midazolam demonstrated rapid peak concentrations in swine compared with intravenous and intramuscular routes; the authors concluded this may play a role in quickly terminating seizures, especially in the prehospital arena.[13] Initial management must focus on adequate use of atropine. Optimizing oxygenation prior to the use of atropine is recommended to minimize the potential for dysrhythmias.
de Silva et al studied the treatment of organophosphate poisoning with atropine and 2-PAM and, later the same year, with atropine alone.[14] They found that atropine seemed to be as effective as atropine plus 2-PAM in the treatment of acute organophosphate poisoning. The controversy continued when other authors observed more respiratory complications and higher mortality rates with use of high-dose 2-PAM. Low-dose (1-2 g slow IV) 2-PAM is the current recommendation. Studies are underway to assess the role of low-dose 2-PAM. Improved survival has been shown in moderately severe OP poisoned patients who received early, continuous 2-PAM infusion compared with those who received intermittent boluses.[15]
A meta-analysis and review of the literature performed by Peter et al emphasized optimal supportive care along with discriminate use of 2-PAM, especially early in the course of treatment of moderately to severely OP poisoned patients, are the hallmarks of treatment.[16] More prospective data are required.
Because large amounts of atropine may be required for patients with organophosphate poisoning, reconstitution of powdered atropine is a viable option, especially in mass-casualty settings.[17] Recently, Rajpal et al demonstrated the clinical safety and efficacy of sublingual atropine to healthy volunteers. This may offer another route of administration for the OP poisoned patient, especially in a mass-casualty scenario.[18]
Intravenous glycopyrrolate or diphenhydramine may provide an alternative centrally acting anticholinergic agent used to treat muscarinic toxicity if atropine is unavailable or in limited supply. Additionally, Yavuz et al demonstrated reduced myocardial injury and troponin leak in fenthion-poisoned rats treated with diphenhydramine.[19]
In a single-center, randomized, single-blind study by Pajoumand et al found a benefit to magnesium therapy in addition to standard oxime and atropine therapy in reducing hospitalization days and mortality rate in patients with organophosphate poisoning.[20] The mechanisms appear to be inhibition of acetylcholine (ACh) and organophosphate antagonism. Larger randomized studies are needed to demonstrate magnesium efficacy in organophosphate (OP) poisoning.
Possible future interventions include neuroprotective agents used to prevent nerve damage and bioscavengers aimed to prevent AChE inhibition by nerve agents or organophosphate. Investigations into adjunctive and alternative therapies have mostly used animal models and have resulted in variable conclusions.[21, 22]
http://emedicine.medscape.com/article/167726-medication
And in conclusion; there is no cure for pesticide poison.
But, from my own experience and what I have read those who drink organic carrot juice have a better outcome.
Pesticide, herbicide and insecticide are all the same thing.
And in conclusion; there is no cure for pesticide poison.
But, from my own experience and what I have read those who drink organic carrot juice have a better outcome.
Pesticide, herbicide and insecticide are all the same thing.
Drop This Tiny Pill Into a Glass of Water to See If You're Drinking PesticidesResearchers have been experimenting with an unlikely drugstore buy: dissolvable minty breath strips. A team from McMaster University in Canada discovered that pullulan, the same slimy fungus used to make the breath freshener strips, could also be used to make pills that contain pesticide-detecting enzymes. Just drop the pill in a glass of water, let it dissolve, and watch for any color changes.
http://asheepnomore.net/2013/12/31/soft-killing-american-people-using-toxic-food-toxic-water-toxic-vaccines/#sthash.RAl8ISRv.dpuf
“If the water doesn’t have any pesticides, [the water] actually forms a very strong blue. If it’s transparent at the end, it’s very contaminated,” Carlos Felipe, the chemical engineering professor who led the study, told Fast Company.
He said that testing water this way is a much cheaper alternative than other contamination screening processes. According to Felipe, producing 1,000 pills in one day would only cost a dollar. Countries such as India, where a large pesticide market compromises the water supply, could benefit from this quick and affordable technology.
Right now, it is estimated that approximately 70,000 chemicals are being used for commercial purposes, and as a result of our “modern lifestyles” we are literally being endlessly bombarded with toxins. This has resulted in a massive tsunami of death, disease and chronic illness in America. But very few people actually understand what is being done to all of us. The following are just a few of the ways that the “soft killing” of the American people is taking place…http://asheepnomore.net/2013/12/31/soft-killing-american-people-using-toxic-food-toxic-water-toxic-vaccines/#sthash.RAl8ISRv.dpuf
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