Die fisiese skepping is verdraai en 'n beledeging en verkragting van die oorspronklike Geestelike skepping!!!
Het julle geweet dat daar twee skeppings is? Die een is 'n Geestelike skepping gemaak van 'n Geestelike energie wat die mens nie ken nie. Elke gees wat in die fisiese ligaam gevange is, is afhanklik van 'n energie bron wat vrylik te vinde is in die geestelike skepping waar dit leef en wat ook hulle voedsel is. Dan is daar ook 'n soortgelyke weergawe van daardie Geestelike skepping hier waar ons tans is, 'n fisiese weergawe wat genoem word "Die Tuin van Eden". Anders as die Geestelike skepping wat van 'n energie bron leef wat niks skade doen nie en net die geestelike wesens voed, moet die fisiese skepping mekaar doodmaak en eet om te kan oorleef. En as mens nou gaan kyk na die samestelling van die fisiese skepping teenoor die van die Geestelike skepping sal jy sien dat die Geestelike skepping so gemaak is om pyn en lyding te vermy teenoor die fisiese skepping wat met die senuwee stelsel toegerus is wat aan alles wat hier leef gegee is om pyn en skok te kan voel en beleef. Daar in die Geestelike skepping wat Saron genoem word is totale vryheid van marteling pyn en lyding en word die dood nooit gevind nie. As jy daar is, het jy die ewige lewe elke dag in jou hande. En jou wil is jou eie jy word nie geforseer om enige dade teen jou sin te doen nie. Waar jy in jou vleeslike ligaam onderworpe is aan 'n onsigbare slawedrywer soos ek al voorheen verduidelik het met die pos in "Die tronk en slawerny" uit die Tuin van Eden.
Julle sien hier dat gifstowwe deur die senuweestelsel ervaar word ... dus is daar geweldige lyding onder die insekte of selfs ander wesens soos die plante en diere ens wat vergif word. hulle ervaar vergifting net soos die mens ... pyn en lyding!!!!
How Insecticides Poison Insects John I. Pratt, Jr., Frank H. Babers. Somebody has said that because insects are small an insecticide kills them all over. Our knowledge of the subject is incomplete, but it is enough to belie the statement. Poisons affect the normal functions of specific cells and tissues of insects just as they are known to do in humans and other higher animals. Basically some chemical process in the animal is affected so as to bring about changes in its functions. Those changes are secondary to the original process that was affected and are frequently mistaken for the initial action of the poison. A complete knowledge of the way a chemical poisons an insect would have great value in the formulation of insecticides. While preparing an insecticidal mixture, for example, we could add a substance that would help the poison reach the target the organ or tissue it acts upon. Chemicals could be added to weaken or destroy the mechanisms that protect the insect against the poison in question. If we know how one poison acts, we could select or synthesize other chemicals of similar action. Research is giving us that knowledge so that before too long such ideals should become realities. Insecticides have been classified according to the way they get into the insect's body cavity: Stomach poisons are eaten, contact poisons enter through the skin, and fumigants enter through the breathing tubes or the skin as gases. Some insecticides may enter by all three routes. But often such a classification is used wrongly to refer to the mode of action of an insecticide an entirely different term, which Means the way in which a chemical acts on an animal's system. In studying the mode of action of an insecticide, we often rely for clues on what we know of the action of the poison on man or other higher animals. Sometimes the mode of action may be similar in vertebrates and in insects, but without experimental evidence it is unwise to assume that such a similarity exists. The poisonous properties of the inorganic arsenic compounds (paris green, calcium and lead arsenate, sodium arsenite) are due to the formation of the water-soluble compounds, arsenious or arsenic acid, in the digestive tract. Arsenic is considered a general protoplasmic poison; that is, it poisons the contents of all types of cells. Most tissues and organs therefore are affected in arsenic poisoning. One well-known effect of arsenic on vertebrate animals is the abrasion and destruction of the lining of the intestine. A similar destruction occurs in the mid-intestine of insects. Often it is said that such destruction is the primary reason that arsenic insecticides kill insects. If that were true, it still would not explain what biochemical process is disturbed in order to bring about destruction of the intestinal cells. Investigations with vertebrate animals have shown that arsenic poisons unidentified enzymes, which function in the metabolism of carbohydrates by cells. Probably arsenic acts on the insect system in the same manner. Nicotine first stimulates and then depresses the nervous system of animals. Paralysis follows rapidly and results in the failure of organs to function. In insects, as in higher animals, the poisoning action of nicotine occurs in the nerve ganglia, which are clumps of nerve tissue at various places in the nervous system. Nicotine seems to have practically no effect on nerve fibers or on the junctions of nerves with muscles. The chemical process of nicotine poisoning in insects is not known. Pyrethrum powder, the ground flowers of certain species of the chrysanthemum, contains the chemicals, pyrethrin I and II and cinerin I and II, which are the main toxic principles. The rapid paralyzing action of pyrethrum is evident to anybody who has sprayed a room with a household fly spray and watched the flies drop almost immediately to the floor. The insects recover from the paralysis, however, unless a lethal amount of the poison gets on them. Pyrethrin acts directly on the central nervous system of insects. The paralysis is a result of the blocking of transmission of nerve impulses. We know that* destructive changes occur in the nervous tissue of insects poisoned with pyrethrin, but the reason for the changes is obscure. Rotenone causes paralysis of the breathing mechanism in mammals, possibly by acting on bronchial tissues. All we know now about the method by which rotenone kills insects is that it slows the rate of heart action and breathing. The symptoms may indicate disturbances in the functions of practically any tissues so they really tell us little of the fundamental basis for rotenone poisoning. Several theories have been advanced to explain how oils kill insects: Oils penetrate the insect's breathing tubes, thus causing suffocation; or they penetrate the tissues and poison them; or certain poisonous, volatile substances in the oils kill by penetrating the tissues as gases. None of the theories has been proved. Maybe each may have some merit, depending on the oil in question. Nonvolatile oils (such as mineral oil) that contain no poisonous compounds might kill an insect through suffocation. For oils (such as kerosene) that contain volatile, poisonous constituents, the second and third theories might account for the killing action. In vertebrates, such volatile petroleums as gasoline act first as stimulants then as depressants of the central nervous system. Death is due to respiratory failure if the animal is exposed to the oil for a long time. Work done by George D. Shafer many years ago at the Michigan Agricultural Experiment Station indicates that a similar action occurs in insects. E. H. Smith and G. W. Pearce of the New York State Agricultural Experiment Station demonstrated that oil does not kill eggs of the oriental fruit moth by depriving them of oxygen (suffocation). They obtained some evidence that the oil prevented unknown poisonous substances formed by the egg from passing outward through the eggshell. The dinitrophenols are used in several phases of insect control most commonly the sodium, calcium, and dicyclohexylamine salts of 2,4,dinitro-6-cyclohexylphenol and the sodium and calcium salts of 4,6,dinitro-o-cresol. Dinitrophenol increases the metabolic rate of warm-blooded animals. Perhaps the poison acts directly on cells, causing them to increase the rate at which they use oxygen. Fat metabolism is involved because the excess oxygen is used only for burning this body food. Dinitrophenol and dinitrocresol act in the same manner on insects and raise the oxygen requirements by as much as three times the normal amount. The mechanism by which the dinitrophenols cause cells to use abnormally high amounts of oxygen has not been determined. The characteristic tremors of DDT poisoning are symptoms of a disturbance of the nervous system. The sensory nerves which carry impulses to the central nervous system--are the most sensitive to DDT poisoning, the nerve ganglia the least sensitive. When DDT gets on an insect's body, it affects hundreds of sensory nerve endings. The nerves then produce impulses faster and stronger than normal. These cause the nerves responsible for moving muscles to produce the tremors typical of DDT poisoning. The capacity of the central nervous system to coordinate sensory impulses is also disrupted, as seen in the stumbling gait and general instability of the insect. We do not know why DDT poisons nervous tissue. It has been suspected that DDT poisons the enzymes cholinesterase, which is important in the proper functioning of nerves, but considerable research has failed to show that DDT affects the enzyme. Perhaps another enzyme system in nervous tissue is involved. One theory is that DDT causes a depletion of calcium in nervous tissue, which in turn causes spontaneous activity of the nerve. Promising leads are emerging from research on house flies that are resistant to DDT. Flies can change DDT in their bodies to a nonpoisonous substance and DDT-resistant flies can do this faster than susceptible flies can. The chemical processes involved in this breakdown of DDT are being elucidated and should tell us much about the mode of action of DDT. Other effects of DDT on the physiology of insects include an increase in the consumption of oxygen and a decrease in the amount of stored food substances in the body. Those are probably secondary effects of DDT poisoning. Benzene hexachloride occurs in several forms, or isomers, each of which has a slightly different molecular shape. Of the 16 possible isomers, 5 are known the alpha, beta, gamma, delta, and epsilon. The gamma isomer, commonly called lindane, is several hundred times more toxic to insects than the others are. In vertebrate animals, gamma benzene hexachloride causes stimulation of the central nervous system, but the beta and delta isomers cause depression. The external symptoms of poisoning in insects resemble those of DDT, except that they usually appear more rapidly. As in DDT poisoning, the tremors suggest an effect upon the nervous system, but whether the mechanism of poisoning is the same as that Of DDT remains for future research to explain. 'n Gruwel is alle gifstowwe wat die fisiese lewende wesens so erg laat ly!!
Bacillus thuringiensis by W.S. Cranshaw1 (12/08) Bacillus thuringiensis (Bt) is a naturally occurring bacterial disease of insects. These bacteria are the active ingredient in some insecticides. Bt insecticides are most commonly used against some leaf- and needle-feeding caterpillars. Recently, strains have been produced that affect certain fly larvae, such as mosquitoes, and larvae of leaf beetles. Bt is considered safe to people and nontarget species, such as wildlife. Some formulations can be used on essentially all food Crops. Bacillus thuringiensis (Bt) is an insecticide with unusual properties that make it useful for pest control in certain situations. Bt is a naturally occurring bacterium common in soils throughout the world. Several strains can infect and kill insects. Because of this property, Bt has been developed for insect control. At present, Bt is the only "microbial insecticide" in widespread use. The insecticidal activity of Bt was first discovered in 1911. However, it was not commercially available until the 1950s. In recent years, there has been tremendous renewed interest in Bt. Several new products have been developed, largely because of the safety associated with Bt-based insecticides. Properties Unlike typical nerve-poison insecticides, Bt acts by producing proteins (delta-endotoxin, the "toxic crystal") that reacts with the cells of the gut lining of susceptible insects. These Bt proteins paralyze the digestive system, and the infected insect stops feeding within hours. Bt-affected insects generally die from starvation, which can take several days. Occasionally, the bacteria enter the insect's blood and reproduce within the insect. However, in most insects it is the reaction of the protein crystal that is lethal to the insect. Even dead bacteria containing the proteins are effective insecticides. The most commonly used strain of Bt (kurstaki strain) will kill only leaf- and needle-feeding caterpillars. In the past decade, Bt strains have been developed that control certain types of fly larvae (israelensis strain, or Bti). These are widely used against larvae of mosquitoes, black flies and fungus gnats. More recently, strains have been developed with activity against some leaf beetles, such as the Colorado potato beetle and elm leaf beetle (san diego strain, tenebrionis strain). Among the various Bt strains, insecticidal activity is specific. That is, Bt strains developed for mosquito larvae do not affect caterpillars. Development of Bt products is an active area and many manufacturers produce a variety of products. Effectiveness of the various formulations may differ. Disadvantages Bt is susceptible to degradation by sunlight. Most formulations persist on foliage less than a week following application. Some of the newer strains developed for leaf beetle control become ineffective in about 24 hours. Manufacturers are experimenting with several techniques to increase its persistence. One involves inserting Bt toxic crystal genes into other species of bacteria that can better survive on leaf surfaces (e.g., the M-Trak formulation of san diego strain). The highly specific activity of Bt insecticides might limit their use on Crops where problems with several pests occur, including nonsusceptible insects (aphids, grasshoppers, etc.). As strictly a stomach poison insecticide, Bt must be eaten to be effective, and application coverage must be thorough. This further limits its usefulness against pests that are susceptible to Bt but rarely have an opportunity to eat it in field use, such as codling moth or corn earworm that tunnel into plants. Additives (sticking or wetting agents) often are useful in a Bt application to improve performance, allowing it to cover and resist washing. Since Bt does not kill rapidly, users may incorrectly assume that it is ineffective a day or two after treatment. This, however, is merely a perceptual problem, because Bt-affected insects eat little or nothing before they die. Bt-based products tend to have a shorter shelf life than other insecticides. Manufacturers generally indicate reduced effectiveness after two to three years of storage. Liquid formulations are more perishable than dry formulations. Shelf life is greatest when storage conditions are cool, dry and out of direct sunlight. Advantages The specific activity of Bt generally is considered highly beneficial. Unlike most insecticides, Bt insecticides do not have a broad spectrum of activity, so they do not kill beneficial insects. This includes the natural enemies of insects (predators and parasites), as well as beneficial pollinators, such as honeybees. Therefore, Bt integrates well with other natural controls. For example, in Colorado, Bt to control corn borers in field corn has been stimulated by its ability to often avoid later spider mite problems. Mite outbreaks commonly result following destruction of their natural enemies by less selective treatments. Perhaps the major advantage is that Bt is essentially nontoxic to people, pets and wildlife. This high margin of safety recommends its use on food Crops or in other sensitive sites where pesticide use can cause adverse effects. Application The greatest use of Bt involves the kurstaki strain used as a spray to control caterpillars on vegetable Crops. In addition, Bt is used in agriculture as a liquid applied through overhead irrigation systems or in a granular form for control of European corn borer. The treatments funnel down the corn whorl to where the feeding larvae occur. Many formulations (but not all) are exempt from pesticide tolerance restrictions and may be used up to harvest on a wide variety of Crops. This also makes Bt useful in applications where pesticide drift onto Gardens is likely to occur, such as treating trees and shrubs. The exceptional safety of Bt products also makes them useful where exposure to pesticides is likely during mixing and application. To control mosquito larvae, formulations containing the israelensis strain are placed into the standing water of mosquito breeding sites. For these applications, Bt usually is formulated as granules or solid, slow-release rings or brickettes to increase persistence. Rates of use are determined by the size of the water body. Make applications shortly after insect eggs are expected to hatch, such as after flooding due to rain or irrigation. Bt persistence in water is longer than on sun-exposed leaf surfaces, but reapply if favorable mosquito breeding conditions last for several weeks. Although the israelensis strain is quite specific in its activity, some types of nonbiting midges, which serve as food for fish and wildlife, also are susceptible and may be affected. For information on mosquito control, see fact sheet 5.526, Mosquito Management. Use of Bt (israelensis) for control of fungus gnat larvae involves drenching the soil. Bt applied for control of elm leaf beetle or Colorado potato beetle (san diego/tenebrionis strain) is sprayed onto leaves in a manner similar to the formulations used for caterpillars. Bt does not control shore flies, another common fly found in greenhouses. Insects Controlled by Bt Kurstaki strain (Biobit, Dipel, MVP, Steward, Thuricide, etc.): Vegetable insects Cabbage worm (cabbage looper, imported cabbageworm, diamondback moth, etc.). Tomato and tobacco hornworm. Field and forage crop insects European corn borer (granular formulations have given good control of first generation corn borers). Alfalfa caterpillar, alfalfa webworm. Fruit crop insects Leafroller. Achemon sphinx. Tree and shrub insects Tent caterpillar. Fall webworm. Leafroller. Red-humped caterpillar. Spiny elm caterpillar. Western spruce budworm. Pine budworm. Pine butterfly. Israelensis strains (Vectobac, Mosquito Dunks, Gnatrol, Bactimos, etc.) Mosquito. Black fly. Fungus gnat. San diego/tenebrionis strains (Trident, M-One, M-Trak, Foil, Novodor, etc.) Colorado potato beetle. Elm leaf beetle. Cottonwood leaf beetle. Nou wonder ek hoe voel elke mens nadat hy die insekte vergiftig het in en om hulle huise .. dink hulle dit was wonderlik dat hulle die insekte so laat ly?? Nee ... dit is nie wonderlik nie dit is afgryslik wat julle doen om julle fisiese besittings hier te beskerm. Vermoor die groep omdaardie ander groep te beskerm ... die mens is net so onregverdig soos die God wat onder hulle regeer en hulle ook beheer!!
