Introduction There exist two categories of pharmaceutical drugs; agonist and antagonist. Agonist drugs acts on the principle that it binds itself to the receptor substance of the respective cell. Normally agonists exists in form of hormones or neurons a fact that makes them very popular in the human body. In this scenario the unknown B2 drug belongs to the agonist category. On the other hand antagonists operate on the reverse principle of the agonists in that they tend to block the receptors. In order to evaluate and asses the pharmacological properties of B2 it is vital to examine two unique properties; efficacy and potency. Efficacy refers to the overall capacity of a drug to produce the desired effects. Potency on its part refers to the level of response that is generated by a drug. The higher the potency the lower the response level of a particular drug. For instance in order to generate a 50% response value, the dosage of the drug being administered needs to quite high.
The experiment is composed of two distinct phases; phase2 and phase3. Phase2 focused on establishing the effect of administering a selective antagonist dosage on the two substances; chlorphenamine and Atropine. As a result Atropine appeared to be blocked primarily because it is exhibit antagonistic attributes towards muscurinic and nicotinic receptors. On the other hand chorphenamine appeared to inhibit the effects of histamine more because it blocks autocoid histamine receptors remain blocked. In order to determine the blockage effect of B2 it was necessary to thoroughly test the selective dosage. This will allows for easier identification of the actual receptors which not works with B2 but those that blocks it affects. Another aspect examined in phase2 is related with how other agonists mimic the effect of B2. In this case it was vital to evaluate and compare the behavior of log-dose curves with the sole aim of deriving both the efficacy and the potency values.
Phase 3 involved the use of pseudocholiesterase from horse blood and an esterase inhibitor known as physostigmine. Cholinesterase action involves hydrolyzing the ester bond found in acetylcholine. Basically there exists two categories of cholinesterase; acetyl-cholinesterase and pseudo-cholinesterase. Another substance used in this phase is carbachol which is rather resistant to the effect of esterase digestion. This means that its presence is used to protect or inhibit the digestion of acetycholine, histamine and B2. In addition an interaction between an antagonist like physostigmine and agonist substance will result in an increase in ED50. In some cases this can be attributed to the ever increasing potential of grugs by many people.
Methods An organ bath is initially setup in presence of an ileum tissue from a guinea pig. Prior to using the tissue, a Petri dish is first filled with ringer solution and then subjected to oxygen supply. It is paramount to note that the tissue lacks any spontaneous patterns but rather it is characterized by contractions. The ileum tissue contains substances such as 5Ht, H1, nicotinic and muscurinic receptors. These substances are easily affected by contraction. In addition ileum tissue experience relaxation probably due to the fact that it lacks both beta and alpha receptors.
In order to produce good result the tissue required to be attached to a transducer using a threading string. Additionally this tissue was submerged in ringerâ€™s solution at a room temperature of 37 degrees Celsius. In a normal scenario the addition of an agonist may cause the ileum to contract; this tension would be amplified by the transducer, which would then record the trace of response on a computer. Each test was preceded by a complete wash out of the drug. Oxygen supply needs to quite constant in order to sustain the life of the cell. Data from the races is used to plot the graph which shows the behavior of each agonist in response to the effect of log-dose.
Results For B2 laced with Chlorphenamine 1 in 10000 dilutions Emax was 98/% while ED50 was 1.0X10-6M.
For B2 laced with atropine 1 in 5000 dilutions, Emax and ED50 were 4.4 x 10^-6 and 72% respectively.
It is evident that competitive antagonism was dominant. It is as a result of Atropine blocking specific masculine receptors. It means that B2 is a cholinergic agonist, which might be either acetylcholine or Carbachol.
B2 Gave an Emax value of 90% and an ED50 value of 1.44 x 10^-6M. The values for Acetylcholine were 60% and ED50 value of3.1 x 10 ^-6 M. However. Carbachol gave a high efficacy 100% Emax value and an ED50 value of 3.0 x 10^-6M. Additionally Histamine gave Emax and ED50 50% and4.4 x 10 ^-6M respectively. The lowest point was recorded while using Serotonin which had an ED50 value of 7.5 x 10^-6 and an Emax value of 21%.
Acetylcholine in the presence of physostigmine
Tthe Emax was 100% and the ED50 1.3×10^-7 while Carbacho was 98.4% Emax and ED501.7×10^-6. However in the presence of physostigmine EMAX was 100% and the ED50 was 6.0×10^-7.
Conclusion Both the mimicry graphs of B2 and Carbachol exhibits similar characteristics hence the same ED50 values Despite this there is no enough evidence to establish what exactly what the receptors acts on. When antagonistic atropine was used the ED50 of the respective B2 was considerably reduced. This mainly occurred at both the selective and effective dosage levels. It can be concluded that B2 indeed acted on cholinergic receptors. This is given more strength by the increase in ED50 reduction in potency level. To get even more definite results chlorphenamine was used as the sole histaminergic antagonist. Results indicated that both the effective and selective dose of Chlorphenamine had no antagonistic effect on B2. Additionally the potency did not reduce. It is evident that B@ does not in any way acts on histaminergic receptors. Thus it is prudent to argue that B2 does indeed acts upon cholinergic receptors
Experiment 2 Purpose: To demonstrate the pharmacological properties of unknown drug B16
Experimental phases (phase 1 and phase 2) are essential in determining these properties.Key attributes investigated include selective and effective dose of Atropine, Atropine and B2, effective and selective dose of Chlorphenamine, Chlophenamine and B2, Mimicry of B2 , digestion by pseudo-cholinesterase on B2, protection by Physostigmine of B2, and potentiation of B2.
Acetylcholine is regarded as an acetic acid such as ester of choline. It acts on cholinergic synapses to propagate nerve impulses. Acetylcholine has high and equal potency for muscurinic and nicotinic receptors. It is also highly susceptible to breakdown by cholinesterase. Carbachol which is is agonist of the muscurinic and nicotinic receptors is more potent on nicotinic receptors. In addition it is not broken down by Cholinesterase. Health applications of Acetylcholine includes but not limited to the treatment of Glaucoma.Its treatment remedy is based on the contraction principle; causes contraction of circular muscle in the eye leading to an increase in output of aqueous humour.
Obtained from Atropa belladonna also known as deadly nightshade, Atropine which is alkaloid in nature serves to block the cholinergic receptors. Medical applications of Atropine involve dilation of the pupil which is most common during examinations of the eyes. Another substance Chlorphenamine is rather antihistamine in nature and thus it blocks histamine receptors. It clinical uses involve the treatment of allergic reactions such as itching. (Youngson, 1999) Physostigmine is regarded as being one of those substances that tends to bring reversible cholinesterase inhibition. Since Physostigmine normally interferes with the breakdown of Acetylcholine , its overall effects is significantly ppextended. Major medical use encompasses the boosting of the muscle tone of people with Myasthenia Gravis (Youngson, 1999).
Effective dose of atropine
The purpose of the first experiment was to identify the effective dose of Atropine. Three doses of atropine were added to Acetylcholine; Acetylcholine with atropine 1/1000, Acetylcholine with atropine 1/10000 and Acetylcholine with atropine 1/5000. The three concentrations of atropine (1.4 x 10^-10M, 2.88 x 10^-10M and 1.4 x 10^-11M) were first carried out on both carbachol and acetylcholine. The three specimens showed a shift in the dose response curves to the right. This makes the drugs to appear to be below potent as they tend to increase their ED50 values. The results prove that both acetylcholine and carbachol are blocked by atropine. After observing results from graphs used in the experiment, it is evident that there is a distinct shift in all the dose response curves to the right. This helps to lower the potency of the drug at all concentrations.
Selective dose Atropine
The aim of this section of experiment is to establish whether the effective dose of Atropine is also a selective dose. In this case histamine was titrated with the three concentrations of atropine to identify if histamine is actually blocked antagonist. In a normal scenario histamine ought not to be antagonized by atropine. Instead there should not be a significant shift in the dose response curve or reduction in potency. However at high dose concentration, atropine can indirectly block histamine.
To analyze the selective dose of atropine, three different concentrations of atropine were used on histamine. The 1/5000 and 1/1000 dilutions of atropine i.e.1.4 x 10^-10M and 1.4 x 10^-9M became the histamine to shift to the right. This shows that high concentrations of atropine can cause an indirect antagonistic affect to histamine. Despite this, the 1.4 x 10^-11M (1 in 10000 obtained was found to be 2.3×10-6M. Actually dilution does not reduce the efficacy or the potency of histamine. Additionally the dose of 1.4 x 10^-11M (1/10000 dilution of atropine) does not shift histamine to the right thus retaining its ED50 value. This dose of atropine is both effective and selective for cholinergic agonist such as acetylcholine and Carbachol. It effectively blocks acetylcholine and carbochol especially when the affect on histamine is not great. Consequently the effective and selective dose for Atropine was resolved to be 1.4 x 10^-11M. It means Atropine did not affect Histamine activity.
Atropine and B16
Aim of the experiment was to find the impact of both the effective and selective dose of Atropine (1×10-7M) on the unknown drug B16. The effective and the selective dose were obtained by testing different concentrations of atropine on acetylcholine, carbachol and histamine. A distinct shift in the dose response curve to the right was found when administering the 1.4 x 10^-11M of atropine to unknown drug B16 there was. Therefore this dose of atropine result in drug B2 appearing to be less potent by lowering its ED50 value. It is clear that drug B2 is capable of acting upon cholinergic receptors. This is primarily because the effective and selective dose of atropine that was determined previously blocked the actions of drug B2. In effect it makes it to appear to be less potent and reducing its ED50 value. This means that Atropine was blocking Cholinergic receptors, which B2 acts on. Hence it may be deduced that B2 is a cholinergic agonist, and it may be Acetylcholine, or Carbachol.
Effective dose of Chlorphenamine
Experiment aim was to find out an effective dose of Chlorphenamine-an antagonist of histamine receptors. An effective dose will decrease the potency of histamine; however the same dose should not affect the Emax of histamine. Histamine when free of antagonist Emax was 100% while ED50 was 3.5×10-6M. However histamine when added to Chlorphenamine 1/ 10000 dilutions an Emax became 96% and an ED50 became 1.0×10-5M. This means that with the lesser dose of the antagonist the efficacy will be increased, while the potency will be decreased. The remarkable shift to the right confirms a decrease in potency with only a 4% variance in Emax. This is evidence that the effective and selective dose has shifted histamines Log-dose response curve to the right thus decreasing potency.
Selective dose of Chlorphenamine
Acetylcholine was in two different concentrations of Atropine. Chlorphenamine on its part does not result in the shift of the graph to the right. Additionaly this shift does not result in the reduction of potency. In addition, there was a small shift of the curves to the left with the addition of Chlorphenamine which may be due to re-sensitization. On the other hand as there is no shift to the right of the dose response curves with the addition of Chlorphenamine. It will be possible to realize that it is not antagonist towards Acetylcholine
Effective and selective dose of Chlorphenamine on B2
The aim of experiment was to determine whether the effective and selective dose for Chlorphenamine was able to competitively antagonise the unknown drug B2. Results indicate three combinations; B2 only, B2with Chlorphenamine 1 in 10000 dilution, and B2with Chlorphenamine 1 in 5000 dilution. Consequently the display of Emax`s is 98%,92%, 100% and respectively.The respective ED50 values are 2.2 x10-6M, 1.0×10-5M, and 7.0×10-6M respectively. From the results it can be demonstrated that the effective and selective dose of Chlorphenamine did not have any considerable effect on the drug B2.This shows that B2 is not acting on the autocoid receptor H1.
Mimicry of B2 with other muscurinic agonists
Aims to study the mimicry effects of muscurinic agonists as wellas study parallel efficacy and potency of unknown drub B2. The mimicry data appears to express that B2 mimics Carbachol as it has a similar ED50 value. In essence, B2 gave ED50 90% and Emax 1.44 x 10^-6M while Carbachol was ED50 100% and Emax 1.00 x 10^-6M. That saids it is not enough proof to ascertain that B2 acts on receptors. The cholinergic antagonist Atropine was used because whenever it decreased the ED50 of B2 at the effective and selective dose then this would confirm the B2 acted upon cholinergic receptors. An affirmative result proved that B2 acted upon cholinergic receptors as the ED50 increased and the potency decreased. In order to confirm this, Chlorphenamine was used as a histaminergic antagonist. The effective and selective dose of Chlorphenamine had no antagonistic effect on B; it failed to reduce the potency. It means that B2 does not act upon histaminergic receptors. Thus it can be concluded that drug B2 acts upon cholinergic receptors
Digestion by pseudo-cholinesterase/protection by physostigmine
The effects of Acetylcholine explain that when presented alone a 100% response is guaranteed.. In another perspective, Acetylcholine by pseudo-esterase gave a 0% response. However with the addition of Acetycholine, esterase, and physostigmine 95% response was acquired. Basically it means that Acetycholine is prone to the digestion by Pseudo-Cholinesterase obtained from the horseâ€™s blood. Additionally it is protected from being digested by physostigmine. When carbachol was treated with both blood esterase and physostigmine each every response was almost identical yielding only a 10% discrepancy. Evidently is not in any way capable of being digested into blood esterase. As a result, physostigmine is not suitable to be used to block the digestive effects of the esterase.
Other results (from graphs 1.5,1.6 and 1.7) indicate that B2 was indeed broken down by blood esterase suggesting that it is potentially digestible by the former. Indeed if blood esterase were to be added to drug B2 alone, esterase would immediately digest drug B2 reducing its reaction to approximately 0%. However when an indirect agonist such as physostigmine is used, drug B2 is capable will be able to produce a significant. One thing to note is that the blood esterase virtually broke down all of drug B2. Relevant indications appear to reveal that the concentration of drug B2 is slightly low. This explains the minimal response of drug B2 to blood esterase.
Another substance that was broken down and digested by blood esterase was acetylcholine. Additionally, physostigmine effectively inhibited the effects of the blood esterase on both acetylcholine and drug B2. This result helps to explain the mimicry phenomenon; drug B2 mimics the procedures of acetycholine as well as acting upon the cholinergic receptors.
By studying graph 1.8, there is revelation of the effects of histamine when treated with both blood esterase and physostigmine. From the data available it is evident that all four responses appear to be quite identical with only a 5-10% discrepancy. Graph 1.7, reveals that blood esterase does not digest histamine. This means that histamine would need physostigmine in order to block the digestive effects of the esterase.
From graph 1.9 it appears that physostigmine is acting as an indirect agonist towards Acetylcholine. This is because there is an obvious potentiation;the Emax leaped from 86.2% to 100% while at the same time the ED50 increased slightly with a shift left from 1.3×10^-7M to 3.0×10^-7M
In graph 2.0 there is no potentiation of Emax or ED50. This helps to explain the fact that physostigmine does not work as an indirect agonist towards Carbachol. In essence the Emax for both trails are almost identical the same as for ED50 which runs very close
Physostigmine raises thee Emax but fails to lower the ED50. It is manifested by the fact that physostigmine acts as an indirect agonistThere is increased level of Emax to B2 mainly due to re-sensitisation occuring through-out the experiment as well as biological variance of the tissue
The antagonist Atropine appears to act on the unknown B2 drug which is associated with bringing about competition for inhibition factors. The same case applies to B2 cholinergic agonist. In another analysis Chlorphenamine appears to lack proper antagonistic effect on B2. Again B2 fails to directly act on autocoid H1 receptors. From these findings it is evident that B2 is a Cholinergic Agonist. The fact that carabcol and histamine were not digested in blood esterase while acetylcholine got digested means that B2 is indded acetylcholine. The two attributes provides some of the unique agonistic properties of a pharmacological drugs.
Applications of Seed Therapy and Su Jok Therapy
Seed Therapy deals with the application of seeds or other parts of plants and attaching it with a tape at a corresponding point in the hand or foot of a person feeling pain. Seed Therapy is based on Sujok Therapy, when broken down, means Su = hand and Jok = foot. These Korean words rely solely on a therapy that makes use of the hands and feet as areas of treatment for the whole body (see Figure 1). Professor Park Jae Woo was a Korean scientist and philosopher who originated and developed this therapy (Richmond, 2006). He urbanized an assortment of successful systems of treatment which have expanded all over the world, including physicians, practitioners and ordinary people alike. Su Jok therapy is indeed an instantaneous and effective healing therapy requiring no medication and is entirely safe without any accompanying side effects (Richmond, 2006).
Among countless illnesses, Su Jok helps in curing many diseases such as:
Arthritis, bronchitis, asthma, backache, joints pain, migraine, hypertension, sinusitis, deafness, constipation, acidity, obesity, diabetes, menstrual problems, and many more chronic diseases related to different organs of our body (Woo, 2009). Su Jok therapy cures and prevents diseases at a physical, mental, and emotional level using hands and feet as treatment areas. This therapy is regarded as a healing system whereby simple stimulation to the specific corresponding points on the hands and feet, most popularly used is the Su Jok probe, would be applied on and around this area in order to seek the most painful spots confirmed by the client. Healing is reported in 94% of five hundred and thirty subjects according to Woo (2009).
Seed Therapy is considered harmonious to Su Jok Therapy and utilizes the energy of specific seeds. Since seeds are regarded as natural stimulators, they are able to cause the body part to respond. The objective of this paper is to discuss and review the effects of Seed Therapy in relieving pain and alleviating illnesses.
Seed Therapy is one of the important natural stimulator therapies. This precise acupressure phenomenon is the reason why Seed Therapy is regarded as a major treatment pertaining to Su Jok Therapy. Post acupressure treatment, patients are encouraged to tie or adhere seeds using adhesive plaster on the painful points. The pulsations of the seeds deliver further energy to accelerate the progression of expedited healing when in direct contact to the treated point. Seed therapy is effective against chronic diseases and certain pains; especially joint pains. The seeds could be either placed singly over the effected area or may cover the entire painful section (Devitt, 2009).
Seeds and Their Effects When implementing Seed Therapy, any seed may be used; each seed brings its proper cure effect (see Table 1). The most important factor for treatment is the shape of the seeds or beans being used. The shape of the seed is the indicator to which body part the seed will do optimal advantage (Umbra, 2007). For example cranberry, cowberry and lentil seeds offer support to cough, cold, and flu. Moreover, mound and spherical shaped seeds of pea, cherry, and black pepper are known to offer relief to disorders related to eyes, breasts, the head, knee joints, and back problems. Kidney-shaped red beans are used to treat kidney and stomach related disorders. The elongated forms of seeds are used to resolve problems in the limbs, lips, nose and intestines. The walnut seed is enforced as a cure to cerebral disorders, while peach shaped seeds of millet are used to treat urinary tract and gall bladder problems (Umbra, 2007). Green pea seeds are used to treat various heart conditions, whereas cumin and pumpkin seeds help alleviate gastric irritation and constipation. Also grape seeds are effective in cases of diabetes and pancreatic problems, as well as flaccidity in the urinary bladder muscles. Arrow wood seeds are novel seeds that are being widely used for the relief of hypertension. Rice is used to relief swelling, redness, bronchial problems and loss of sensation in fingers and toes. Flax seeds aids in eliminating toxic body fluids that assist in inflammatory diseases while buckwheat seeds treat pain and chronic inflammation in the shoulder, tooth, head, throat, eyes and tonsils (Umbra, 2007).
Table 1. This table briefly displays the types of seeds used depending on the symptom or area of complaint.
Cranberry, Cowberry, Lentil
Cough, Cold, Flu
Pea, Cherry, Black Pepper
Eyes, Breast, Head, Knees, Back
Limbs, Lips, Nose, Intestines
Urinary tract, Gall bladder
Gastric irritation, Constipation
Diabetes, Pancreatic problems, Urinary bladder muscles
Swelling, Redness, Bronchial problems, Loss of sensation fingers/toes
Eliminating toxic fluids
Chronic inflammation, Throat, Tooth, Shoulder, Head, eyes, Tonsils
Treating Special Populations; Children/Elders Auricular -relating to the ear and hearing- Seed Therapy is also referred to as the seed-pressure method (Steinflow, 2010). It corresponds to applying a hard and smooth seed, herb, or a magnetic pellet on a tape to a detected auricular point and pressing it properly so as to stimulate the point to treat diseases. Auricular seed therapy, a popular therapy for the past 40 years, came into being on the basis of Su Jok Seed Therapy. Through clinical practice it has been confirmed that auricular seed therapy may also be indicated for many diseases and achieve significant therapeutic effects (Steinflow, 2010). This method, due to its simple application, constant stimulation, and safety is regarded more suitable for the elders; the weak, children and those who are very afraid of pain, or cannot receive treatment everyday (Steinflow, 2010).
Treatment of Allergies The main points for the treatment of allergy include allergic area, endocrine, adrenal gland and ear apex bleeding. The Allergy Area is the specific point for diagnosis and treatment of allergic diseases (Steinflow, 2010). It is used to improve the immunological functions of the entire body. Allergic diseases result from the combination of Anaphylactogen and Anaphylactic antibody, which may disturb the normal metabolism in cells and lead to dilation of capillaries, capillary hyper permeability, and spasms of the smooth muscles. The points in the endocrine and adrenal glands are used to increase the secretion of various hormones, such as adrenal-cortical hormone (ACTH). This prevents the release of histamine and inhibits the antigen-antibody reaction in mucous membrane and skin. Prevention of antibody formation also reduces exudates from capillaries (Steinflow, 2010)
Seed Therapy Uses in Cancer Other benefits of seed therapy involve prostate cancer (Vatkarma, 2008). One man in six will be diagnosed with prostate cancer during his lifetime, but only one man in 30 will die of this disease. While there are several treatment options, including surgery, many doctors choose prostate seed therapy because of its ability to treat cancer without affecting surrounding healthy tissue, helping to minimize the risk of impotence or incontinence. Though the technique is somewhat new, preliminary data show that 90 percent of patients treated with prostate seed therapy remain cancer free after five years (Vatkarma, 2008). Prostate seed implantation, also called interstitial radiation and brachytherapy, involves a surgical procedure to implant up to 130 low-dose radioactive “seeds” into the prostate through 30 to 40 long, slender needles. The procedure takes less than two hours and patients return home the same day, resuming normal activity in three to 14 days. The seeds continue delivering radiation for several weeks and remain in place permanently (Vatkarma, 2008).
An alternative Seed Therapy following breast cancer surgery may reduce treatment time and concentrates radiation where it is most needed (Geraldini, 2010). The MammoSite Radiation Therapy System contributes brachytherapy to females who have received a lumpectomy, or a tumor that is removed from the breast. Instead of the usual high energy radiation that enters from the surface of the breast inwards, brachytherapy acts from inwards out. After a patient recovers from her breast cancer surgery, a radiation oncologist threads a catheter through the skin until it reaches the cavity left by the tumor, usually about 2 or 3 centimeters wide. A balloon on the catheter’s tip inflates with liquid within the cavity, and a tiny bit of radioactive material is placed within the balloon. The patient then goes home (Geraldini, 2010). Four or five days later, patients return to the clinic, where the radiation oncology team removes the catheter and radiation source, ending the treatment. Because the radiation source is so tiny, there is no risk of radiation exposure to family members or friends at home during therapy. When the seed is placed in the MammoSite balloon, the seed emits X-rays in all directions-much like light emanates from the sun. The dose of radiation is most highly concentrated right at the edge of the tissue cavity, but declines further away from the radioactive seed. Within tissue that lies one centimeter away from the edge of the tissue cavity, for example, the dose of radiation already has shrunk by half, and it keeps getting lower and lower the further away the tissue is from the site of the former tumor (Vatkarma, 2008)(Geraldini, 2010).
Instead of the five-to-seven weeks’ worth of daily office visits required for external radiation treatments, patients receiving MammoSite can complete radiation after only four or five days of therapy, making it time efficient and cost effective. Due to the fact that the radiation source is placed at the site of the patient’s tumor, the rays reach the very tissues surrounding the tumor where cancer is most likely to return. With MammoSites, the source can enter the breast so quickly where minimal radiation is witnessed to the rest of the breast. The benefit with this fact is that radiation is focused mainly on the area most at risk, which is the local area around the tumor (Geraldini, 2010).
Two recent studies followed 200 women for five years suggest that brachytherapy is as effective as external beam radiation in preventing breast cancer from coming back in women who have had a lumpectomy. This said, the effectiveness of Seed Therapy – Su Jok Therapy in essence – is a beyond promising treatment for such an invasive disease as cancer. Patients will not only be cured, yet, will be able to live better, productive lives without pain and suffering (Vatkarma, 2008).
In conclusion, unconventional treatments are overshadowed by the recognition and universal acceptance of Seed Therapy. In fact, various numbers of patients, whether cancer patients or arthritis sufferers, are turning towards Seed Therapy as an alternative for traditional medicine (Lachmi, 2007). In India, where there is an abundance of Su Jok Therapists, physicians are estimated to see and treat a maximum of 300 patients per day; most of whom have traveled long distances seeking a miracle as their last hope of treatment (Lachmi, 2007) There, the novel therapies of Sujok and Seeds are indeed the future of contemporary medicine that can be extremely promising in the treatment of minor to severe ailments afflicting a vast number of patients worldwide.
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Geraldini, F. (2010). Engaging in sujok seed therapy. Mediks Blog. Retrieved March 25, 2011, from (http://www.mediks-bg.com/su_jok_eng).
Jae Woo, P. (2009). Su Jok Seed Therapy. New York: Random House.
Lachmi, C. F. (2007). Fundamentals of Seed Therapy. Journal of Omnuri Medicine, 55, 893-896.
Najmana, A. (2008). Su Jok Therapy: Seeds and Miracles. Journal of Indian Therapy, 113, 71-76.
Pakra, G. M. (2006). The Power of Seeds. New York: Random House.
Richmond, P. K. (2006). What Exactly is Su Jok Therapy?, England, Oxford: University Press.
Steinflow, D. (2010). If We All Just Believed in Seed Therapy. New York: Roland Incorporated.
Umbra, B. (2007). The real therapeutic seeds. Medi India Organization. Retrieved March 25, 2011, from (http://medi-india.org/umbra_b_seeds).
Vatkarma, R. (2008). The Healing Powers of Su Jok. Journal of Indian Therapy, 113, 124-128.