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The change in momentum due to the collision is usually easy to calculate buy generic cialis sublingual from india, but the duration of the collision t is difficult to determine precisely order discount cialis sublingual online. If the colliding objects are hard buy cialis sublingual 20mg otc, the collision time is very short, a few milliseconds. If one of the objects is soft and yields during the collision, the duration of the collision is lengthened, and as a result the impulsive force is reduced. Thus, falling into soft sand is less damaging than falling on a hard concrete surface. When a person falls from a height h, his/her velocity on impact with the ground, neglecting air friction (see Eq. If the impact surface is hard, such as concrete, and if the person falls with his/her joints rigidly locked, the collision time is estimated to be about 10−2 sec. The collision time is considerably longer if the person bends his/her knees or falls on a soft surface. Note, however, that the assumption of a 2-cm2 impact area is reasonable but some- what arbitrary. The area may be smaller or larger depending on the nature of the landing; furthermore, we have assumed that the person lands with legs rigidly straight. Exercises 5-2 and 5-3 provide further examples of calculating the injurious effect of impulsive forces. This is illustrated by examining the inflatable safety device used in automobiles (see Fig. In a collision, the bag expands suddenly and cushions the impact of the passenger. The forward motion of the passenger must be stopped in about 30 cm of motion if contact with the hard surfaces of the car is to be avoided. For a 70-kg person with a 30-cm allowed stopping distance, the average force is 70 × 103v2 3 2 F 1. If this force is uniformly distributed over a 1000-cm2 area of the passenger’s body, the applied force per cm2 is 4. At a 105-km impact speed, the average stopping force is 1010 dyn and the force per cm2 is 107 dyn. In the design of this safety system, the possibility has been considered that the bag may be triggered during normal driving. If the bag were to remain expanded, it would impede the ability of the driver to control the vehicle; therefore, the bag is designed to remain expanded for only the short time necessary to cushion the collision. If, however, the impact is sudden, as in a rear-end collision, the body is accelerated in the forward direction by the back of the seat, and the unsupported neck is then suddenly yanked back at full speed. Here the muscles do not respond fast enough and all the energy is absorbed by the neck bones, causing the well-known whiplash injury (see Fig. It was found in these cases that the body made about a 1-m-deep depression in the surface of the snow on impact. The credibility of these reports can be verified by calculating the impact force that acts on the body during the landing. It is shown in Exercise 5-6 that if the decelerating impact force acts over a distance of about 1 m, the average value of this force remains below the magnitude for serious injury even at the terminal falling velocity of 62. In the normal course of daily activities our bodies are subject mostly to smaller repetitive forces such as the impact of feet with the ground in walking and running. A still not fully resolved question is to what extent are such smaller repetitive forces particularly those encountered in exercise and sport, damaging. Osteoarthritis is the commonly suspected damage resulting from such repetitive impact. Chapter 5 Exercises 71 Osteoarthritis is a joint disease characterized by a degenerative wearing out of the components of the joint among them the synovial membrane and cartilage tissue. As a result of such wear and tear the joint loses flexibility and strength accompanied by pain and stiffness. After the age of 65, about 60% of men and 75% of women are to some extent affected by this condition. Over the past several years a number of studies have been conducted to determine the link between exercise and osteoarthritis. The emerging conclu- sion is that joint injury is most strongly correlated with subsequent develop- ment of osteoarthritis. Most likely this is the reason why people engaged in high impact injury-prone sports are at a significantly greater risk of osteo- arthritis. Further, there appears to be little risk associated with recreational running 20 to 40 km a week (∼13 to 25 miles). It is not surprising that an injured joint is more likely to be subsequently subject to wear and tear. A joint injury usually com- promises to some extent the lubricating ability of the joint leading to increased frictional wear and osteoarthritis. This simple picture would lead one to expect that the progress of osteoarthritis would be more rapidly in the joints of peo- ple who are regular runners than in a control group of non-runners. Osteoarthritis seems to progress at about the same rate in both groups, indicating that the joints possess some ability to self- repair. If the bones of one arm absorb all the kinetic energy (neglecting the energy of the fall), what is the minimum speed of the runner that will cause a fracture of the arm bone? Assume that the object is hard, that the area of contact with the skull is 1cm2, and that the duration of impact is 10−3 sec. Calculate the duration of the collision between the passenger and the inflated bag of the collision protection device discussed in this chapter. In a rear-end collision the automobile that is hit is accelerated to a veloc- ity v in 10−2/sec. What is the minimum velocity at which there is danger of neck fracture from whiplash? Use the data provided in the text, and assume that the area of the cervical vertebra is 1 cm2 and the mass of the head is 5 kg. Calculate the average decelerating impact force if a person falling with a terminal velocity of 62. Assume that the person’s mass is 70 kg and that she lands flat on her back so that the area of impact is 0. Assuming that the moving part of his hand weighs 5 kg, calculate the rebound velocity and kinetic energy of the bag. In particular, we will consider the hovering flight of insects, using in our calculations many of the concepts introduced in the previous chapters. The parameters required for the computations were in most cases obtained from the literature, but some had to be estimated because they were not readily available. A complete discussion of flight would take into account aerodynamics as well as the changing shape of the wings at the various stages of flight. Differences in wing movements between large and small insects have only recently been demonstrated.

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Even though you regain your tolerance toward minute bits of filth in dairy products 20mg cialis sublingual sale, do not go back to unsterilized milk products generic cialis sublingual 20 mg visa. Appendicitis The lower abdomen on the right side has the valve that sepa- rates the small intestine (ileum) from the large intestine 9 Sherwood L generic cialis sublingual 20 mg fast delivery. It is a common trouble spot because large parasites can attach themselves behind it and keep themselves safe from elimination. It is near this point where the appendix attaches and this, too, is a favorite location of pinworms. With an appendix full of pinworms and their bacteria, is it any wonder when it gets inflamed and causes pain? If there are any suspicions of appen- dicitis, zap pinworms and all enteric parasites and bacteria im- mediately. Because the current does not penetrate the bowel contents very well, zap every day for two weeks and take 2 tsp. Make sure bowel movements are regular after this (see the Bowel Program, page 546, for hints) and hands are washed after bathroom use and before eating. If appendicitis does not clear up it can lead to a burst appen- dix, spewing the dreadful contents into the abdomen. Kill pin- worms and roundworms and enteric parasites regularly (once a week) in children. Urinary Tract Pain Urinary tract infections, including bladder, kidney, and ure- thral infections, are easier to clear up than to test for. Make sure both of you clean up the urinary tract by zapping and doing the Kidney Cleanse. If dairy foods trigger yours, you can guess it is not allergic at all but simply Salmonella or Shigella infection. Boil all dairy foods, stop eating ice cream, cheese and yogurt which you cannot boil. If eating lettuce triggers your intestinal attack, but other roughage does not, it may be a true allergen and cleaning the liver will eventually cure it. Wheat “allergy” is due to the pancreas being full of pancreatic flukes, wood alcohol, Kojic acid (a mycotoxin), and gold. All these bowel diseases are quite easily cured by killing all parasites, bacteria, and viruses. Since reinfection is such a big problem, give your pet away until you are completely cured. For this reason, too, I recommend the Bowel Program (page 546) and Black Walnut Hull Tincture Extra Strength even though you may have gotten immediate relief from zapping alone. This is because sheep liver fluke and pancre- atic fluke are commonly the main parasites and these live in the pancreas and liver. Salmonella and Shigella are always part of the picture, too, as are various amoebae and fungi. The treatment is the same, kill all parasites and remove all pollutants, especially wood alcohol in commercial beverages. Reinfection is very quick too, if the rule about cooking dairy foods is not observed. Michelle Whorton had stomach pain at the middle of her abdomen, not related to eating. We found she had Ascaris (probably in her stomach where they cause indigestion and in- flammation). She was to be very careful with sanitation since they owned a number of farm dogs. Next seen after six weeks, she stated that all her previous problems were gone but she had a different pain in the mid-lower abdomen that got worse during her period and sent pain shooting down both legs. Her uterus was full of asbestos, arsenic, gold, silver, titanium, propyl alcohol, benzene, styrene, toluene and carbon tetrachloride. Mark Lippman, age 51, came in for his irritable bowel syndrome, hop- ing we would find Giardia and put an end to it quickly. He also had propyl alcohol built up in his body giving him a precancerous con- dition that needed immediate attention. The flukes were killed in twenty minutes, along with Ascaris (he had swollen eyelids). His young body also had a buildup of benzene, moth balls and carbon tetrachloride that he was eating, drinking, and breathing. His other problems recurred until he was older and could stop licking his fingers when eating. Tom Ochs, age 36, had chronic stomach problems, alternating consti- pation and diarrhea, was labeled “lactose intolerant” after an elaborate test, and finally had been diagnosed with irritable bowel syndrome. He was also toxic with cesium from drinking beverages out of clear plastic bottles. This frequently causes depression and he was happy to understand his mood changes. After changing to purer food and products and killing his parasites, he did not need to come back. Rex Callahan, age 5, had dark circles under his eyes, numerous ear infections until tonsils were removed and tubes put in, and many strep throat infections. We found he had sheep liver flukes and all their developmental stages in his blood and intestine. Nevertheless, in three months his bowel was nearly normal and the pain in his intestine much less. His parasites were quickly killed with a frequency gen- erator and he was put on the herbal parasite program. One month later his stomach felt much better, but he still had an occasional stomach ache. She had to be back on antibiotics and a few months ago the doctor began discussing tube implants with her since she was still on antibiotics (six months). Another ear, nose and throat doctor agreed with this opinion, but was willing to wait until Autumn. Our test showed pancreatic fluke infestation; this would easily lead to bad digestion, especially of milk and gluten in wheat. Simply killing the parasites (in both mother and baby) solved both problems and she did not need to come back. The ear infections were probably caused by bacteria and viruses brought in by the parasites. They all, including herself, had stomach problems, a lot of allergies, asthma, ear infections, and milk intolerance. His sister, Nola, had itching legs and headaches besides; she was toxic with bismuth and antimony (from shampoo fragrance and laundry fragrance). We found she had the three large flukes plus Chilomastix, dog whip worm, and amoebas in her intestine (but not in body organs). Her stomach and intestines were much too sensitive to accept parasite herbs, or in fact, anything— anything except slippery elm powder. Her blood test showed high phosphate levels since she was dissolving her bones to get cal- cium.

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In fact 20mg cialis sublingual free shipping, there appears to be a synergistic interaction between these two transmitter systems purchase genuine cialis sublingual line. Using doses of these drugs that were ineffective on either measure when given alone generic 20mg cialis sublingual free shipping, they did increase both satiety (Jackson et al. Petty, F, Kramer, G, Wilson, L and Jordan, S (1994) In vivo serotonin release and learned helplessness. Rouch, C, Nicolaidis, S and Orosco, M (1999) Determination, using microdialysis, of hypothalamic serotonin variations in response to different macronutrients. Samanin, R and Grignaschi, G (1996) Role of 5-hydroxytryptamine receptor subtypes in satiety and animal models of eating disorders. Takahashi, H, Takada, Y, Nagai, N, Urano, T and Takada, A (1998) Extracellular serotonin in the striatum is increased after immobilisation stress only in the nighttime. Uphouse, L (1997) Multiple serotonin receptors: too many, not enough, or just the right number? In fact,of the billions of long-axon neurons in the central nervous system,the majority use glutamate as their principal transmitter as do excitatory intrinsic neurons. A large proportion of peripheral sensory fibres conveying touch- and pain-related information contain glutamate and aspartate as do visual, auditory and other sensory afferent fibres. However,both release studies and,more importantly,electrophysiological recordings have shown that glutamate functions as a transmitter at many synapses. Here the coincident actions of glutamate in concert with peptides have a functional importance that is discussed later. It may be that the transmitter pool of glutamate uses the amino acid from any source given that it can be produced from such diverse origins as glucose,aspartate,glutamine and oxoglutarate. Once release occurs there are high-affinity uptake sites in both terminals and glia that remove the transmitter from the synaptic cleft (Fig. While neuronal glutamate may come from glucose via pyruvate,the Krebs cycle and transamination of alpha- oxoglutamate,it seems likely that most of the transmitter originates from the deamination of glutamine. After release,the high-affinity uptake sites (transporters) Neurotransmitters, Drugs and Brain Function. Here it is deaminated to neurotransmitter available glutamate by mitochondrial glutaminase. This complex but very general biochemical process provides very little opportunity for drug modification of glutamate synthesis or metabolism. Unlike other transmitter systems,there are no obvious mechanisms for dampening glutamate release. Presynaptic autoreceptors for glutamate are mostly of the kainate type (see below) and appear to act as positive rather than negative influences on further release of the amino acid. Although poorly characterised at present,inhibitory autoreceptors of the metabotropic type of receptors may act to inhibit release of glutamate. Thus despite any knowledge at that time of the receptors or the availability of selective antagonists,important roles were proposed for these transmitters in neuronal function. The receptor has a complicated structure and this is highlighted by the presence of many pharmacologically distinct binding sites through which the receptor activity can be modulated. The channel associated with the receptor is blocked by Mg2‡ at resting potential (770 mV). Receptor activation requires the removal of this Mg2‡ block (voltage-gated) as well as the binding of glutamate and the co-agonist,glycine (ligand-gated). The different binding sites (glutamate,phencyclidine,polyamine,glycine) are illustrated,and together with antagonists which act at the various sites (in parentheses). Kainate receptors are therefore thought to be excitatory autoreceptors that enhance the release of glutamate. By contrast,the kainate receptor might be an interesting target since its functional role will be linked to the level of glutamate release. Thus,antagonists at this receptor should reduce excessive glutamate release while having less effect on more normal functional synapses. The role of the kainate receptor system in the brain is at an early stage since there are as yet few pharmacological tools to study its function. However,mutations in the kainate receptor genes have been made in mice and there is a GluR6 kainate receptor knock-out mouse. Kainate binding is absent in areas of the brain which normally have high levels such as the hippocampus. Here,in normal animals kainate receptors mediate a postsynaptic current which is absent in the GluR6 knock-out mouse. Mechanisms of central amplification of a nociceptive input have been suggested to underlie aspects of the enhanced spinal transmission of nociceptive messages in protracted pain states,and in this case there is good clinical evidence to support the concepts that have arisen from animal studies. This is not simply due to the large amounts of calcium that enter neurons and thus the degree of excitability that ensues but also simply that many intracellular pathways are calcium dependent. Numerous studies have investigated the potential use of antagonists acting through the different recognition sites. However,due to the ubiquitous nature of the receptor,it has often been difficult to achieve therapeutic effects at the target organ,in the absence of adverse side-effects. The latter condition would appear to be ever present,due to the levels of glycine available in the brain and spinal cord. Finally,an induced depolarisation of the neuron to relieve the resting voltage-dependent magnesium block of the channel is a prerequisite for activation of the complex. The channel is blocked in a voltage-dependent manner so the receptor can only operate after sufficient repeated depolarisation. In the spinal cord,the removal of the Mg2‡ block is mediated by peptides,including tachykinins,which are co-released with glutamate. These events underlie central hyperexcitability and result in a significant amplification of the response. Thus regional specific conditions may control the receptor and determine its properties. The poor understanding of this class of receptor stems from the fact that there are eight receptors in the class which fall into three groups,divided by sequence homology,effector mechanisms and,to some extent,their pharmacology. We are presently lacking sufficiently potent and selective antagonists at all these metabotropic glutamate receptors to probe their roles. There is some evidence for both pre- and postsynaptic locations of all groups of receptors. Functionally,the mGluRs have been implicated in memory,pain,anxiety and neurodegeneration with few specific details due to the lack of antagonists. Thus the activation of this class of receptors brings about a marked increase in neuronal excitability and is responsible for the amplification and prolongation of neuronal responses in the spinal cord. The consensus would be that synaptic activation during high-frequency stimulation triggers a series of intracellular events that lead to the expression of synaptic potentiation with the release of glutamate being the first step. This persistent increase in synaptic efficacy is thought then to be critical for memory,presumably the acquisition. From a large clinical literature,the hippocampus appears to be a key structure in memory,and blocking glutamate receptors causes reduced memory-like behaviour in animals. Briefly, the depolarisation may drive neurons into a state where large quantities of calcium enter the neuron. For this to occur,the release of glutamate would have to be excessive and in this context,cerebral ischaemic episodes are thought to disrupte the reuptake of glutamate into neurons and glia.

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