i AM LOOKING FOR THE SITE OF MYOTONIC DYSTROPHY.I T STARTS WITH CONTACT US?
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try these:\n\nhttp://www.mda.org.au/\n\nhttp://www.myotonicdystrophy.org/\n\nhttp://ghr.nlm.nih.gov/condition=myotonicdystrophy
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www.mda.org\nwww.mdausa.org\nwww.ninds.nih.gov\nwww.muscular-dystrophy\n\nWikipedia info \nGenetics\n\n\n\nDuchenne dystrophy is a type of dystrophinopathy which includes a spectrum of muscle disease caused by mutations in the DMD gene, which encodes the protein dystrophin. Becker's muscular dystrophy is a milder type of dystrophinopathy. Although it is caused by a defective gene, it often occurs in people from families without a known family history of the condition.\n\nDuchenne muscular dystrophy is inherited in an X-linked recessive pattern. Because of random X inactivation, some women carriers can actually be partially affected by this disease, despite its recessive nature. X inactivation leads to women being in a state of X0, not XX as is usually thought (see below). Women who carry the defective gene can pass an abnormal X on to their sons. Since boys have an X from their mother and a Y from father, there is no second X to make up for the defective gene from the carrier mother. The sons of carrier females each have a 50% chance of having the disease, and the daughters each have a 50% chance of being carriers. Daughters of men with Duchenne will always be carriers, since they will inherit an affected X chromosome from their father (note that the diagram only shows the results from an unnaffected father). Some females will also have very mild degrees of muscular dystrophy, and this is known as being a manifesting carrier.\n\nPrenatal testing, such as amniocentesis, for pregnancies at risk is possible if the DMD disease-causing mutation has been identified in a family member or if informative linked markers have been identified.\n\nIn 30% of the cases, the disease is a result of a spontaneous mutation.\n\nIn some female cases, DMD is caused by skewed x inactivation. In these cases, two copies of the x chromosome exist, but for reasons currently unknown, the flawed x chromosome manifests instead of the unflawed copy. In these cases, a mosaic form of DMD is seen, in which some muscle cells are completely normal while others exhibit classic DMD findings. The effects of a mosaic form of DMD on long-term outlook is not known.\n\n[edit]\nPatho-mechanism\nDuchenne muscular dystrophy is caused by a mutation of the dystrophin gene whose protein product is responsible for linking the actin filaments of muscle fibres to the extracellular matrix through a protein complex containing many subunits. As a result, the sarcolemma is damaged through shearing forces and muscle fibres undergo necrosis and are ultimately replaced with adipose and connective tissue.\n\n\n\n\n[edit]\nSymptoms\nMuscle weakness \nRapidly progressive \nFrequent falls \nDifficulty with motor skills (running, hopping, jumping) \nProgressive difficulty walking \nAbility to walk can be lost by age 11 \nFatigue \nIntellectual impairment (in approx. 30% of Duchenne's patients) \nSkeletal deformities \nChest and back (scoliosis) \nMuscle deformities \nContractures of heels, legs \nPseudohypertrophy of tongue and calf muscles \nMild mental retardation in some cases \nScoliosis in some cases \n\nSymptoms usually appear before age 6 and may appear as early as infancy. There is progressive muscle weakness of the legs and pelvis, which is associated with a loss of muscle mass (wasting). Muscle weakness also occurs in the arms, neck, and other areas, but not as severely or as early as in the lower half of the body. Calf muscles initially enlarge -- the enlarged muscle tissue is eventually replaced by fat and connective tissue (pseudohypertrophy). Muscle contractures occur in the legs, rendering the muscles unusable because the muscle fibers shorten and fibrosis occurs in connective tissue.\n\n[edit]\nSigns and tests\nThe pattern of symptom development resembles that of Duchenne's muscular dystrophy, but with a much slower rate of progression. Muscle wasting begins in the legs and pelvis, then progresses to the muscles of the shoulders and neck, followed by loss of arm
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Go to there website it should have the adress under the heading contacts.
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http://cancer.about.com
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(m)\n\nThere is no known cure for myotonia congenita, and treatment is supportive as needed. The use of anticonvulsant drugs (quinine, phenytoin) can relieve some symptoms of the disease along with physical therapy and other rehabilitative measures to assist in muscle function. Genetic counseling may be valuable. \n\nProgression: This disorder causes discomfort but is not life-threatening. In Thomsen type myotonia congenita, symptoms stabilize after onset and do not progress with age. Becker type is a progressive disorder that tends to initially affect muscles in the legs. Within a few years, muscles of the arms are affected, and, eventually, the muscles of the jaw (masticatory) and face become involved.
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mapquest.com they will give u suggestions if you have a partial address
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http://dendrites.com/contacts/dacnb_1.html\n\nGo to the 12th line and I think it has a doctor's name and contact info.  Hope that helps.\n\nI also found this:\nhttp://www.goodhope.org.uk/outpatients/neurology/default.asp
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None of the available resources are great.  You can use Merck Medicus or WebMD or medicinenet.com or medical-library.org or myelectronicmd.com
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yahoo is good. have you tried mIrc or ICQ? www.mirc.com or www.icq.com
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Try contacting the Fybromyalgia Network \n800-853-2929 Of what I understand they have a state by state listing.
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check their website. you might wanna check the contact section.
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Try contacting the webmaster on the site...
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Try the national contact center
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Check out http://disabilities-r-us.com
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http://www.doctormurray.com/conditions/Fibromyalgia.asp
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Muscle Media Magazine\n\nFor more information, call (800) 967-3462
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Try www.medlineplus.com