whats the history of muscular dystrophy?
92570
Until the 1980s, little was known about the cause of any kind of muscular dystrophy. In 1986, MDA-supported researchers identified the gene that, when flawed - a problem known as a mutation - causes DMD. In 1987, the protein associated with this gene was identified and named dystrophin.\nGenes contain codes, or recipes, for proteins, which are very important biological components in all forms of life. DMD occurs when a particular gene on the X chromosome fails to make the protein dystrophin. BMD results from different mutations in the same gene. People with BMD have some dystrophin, but it's not enough or it's poor in quality. Having some dystrophin protects the muscles of those with Becker from degenerating as badly or as quickly as those of people with Duchenne.
920632
try these:\n\nhttp://www.mda.org.au/\n\nhttp://www.myotonicdystrophy.org/\n\nhttp://ghr.nlm.nih.gov/condition=myotonicdystrophy
764179
I have CMT (charcot-marie-tooth), also a muscular disease. My case is very mild as well. I'm 36.\n\nI didn't find out until I was 15, but I played sports. I ran track and played basketball. I wasn't very good, but my disease is why. I didn't know that at the time. \n\nI would say try a sport that isn't too strenuous. Something like swimming (which is doctor recommended for most muscular diseases), baseball or anything he's capable of doing.\n\nKeep in mind the psychological aspects of trying harder than the others and not doing as well as this is possible. Then again, only you know his abilities.
688543
http://www.wheelchairnet.org/WCN_WCU/SlideLectures/Sawatzky/WC_history.html\n\nhttp://www.wheelchairnet.org/WCN_ProdServ/Docs/WCHistory.html
254453
Wernig Hoffman Disease, also termed hereditary spinal muscular atrophy, is a disease of infants and young children that resembles amyotrophic lateral sclerosis. (spinal disease)Pathological changes are confined to the anterior horn cells of the cord and the cranial nerve motor nuclei. The disease affects all muscles to a varying degree. \n\nInfants with Werdnig Hoffmann disease may lack head control, may be unable to roll over or support their weight, and tend to lie relatively still, with little or no movement (flaccid paralysis). In addition, they may develop difficulties sucking, swallowing, and breathing; have an increased susceptibility to respiratory infections; or develop other complications that may lead to potentially life-threatening abnormalities within the first months or years of life. Intelligence is normal. Most affected children die before 2 years of age but survival may be dependent on the degree of respiratory function. \n\nFor infants who appear to have normal development for several months prior to the onset of muscle weakness, the disorder may tend to have a more slowly progressive course. Muscles of the pelvic, trunk, and shoulder areas may initially appear to be disproportionately affected. All muscles, with the exception of the eyes, are affected
142992
Diseases of the myocardium\nThere has been increasing recognition of a type of heart disease characterized as primary myocardial disease. The cardiomyopathies are diseases involving the myocardium (heart muscle) itself. They are unique in that they are not the result of hypertensive, congenital, valvular, or pericardial diseases and are rarely the result of ischemic heart disease
189578
I could copy the answer, but I have some good links instead. \nSkeletal muscle fibers are multinucleated and fusiform, and basically contain myofibrills. See details at the link:\nhttp://training.seer.cancer.gov/module_anatomy/unit4_2_muscle_structure.html\n\nPay special attention to the myofibrils, the mitochondria and the sarcoplasmic reticulum :-)\n\nIllustrations of structure at different levels (I wish these pictures had been around years ago when I studied this!):\nhttp://www.agen.ufl.edu/~chyn/age2062/lect/lect_19/179.gif\nhttp://www.mhhe.com/biosci/esp/2001_gbio/folder_structure/an/m5/s5/assets/images/anm5s5_1.jpg
237114
Cardiomyopathy means a problem with the heart muscle.  The problem can lead to overgrowth of the muscle (hypertrophic cardiomyopathy), or its dilation (dilated cardiomyopathy).  Dilated muscle leads to heart enlargement and an overall decrease in efficiency of the pumping action of the heart.  Clinically, it is one of the causes of congestive heart failure (CHF).\n\nThe topic is bit complicated, but both the treatment and the prognosis hinge on one thing: etiology (or what is the underlying cause of the dilation).  Some common causes include ischemic heart disease (due to coronary blockages), hypertension, alcohol use, or genetics.  Some less common causes include peripartum cardiomyopathy in women, autoimmune problems (like celiac sprue) and infections (HIV or viral myocarditis for example).  I state these, because the corner stone of treatment of dilated cardiomyopathy is to address the underlying cardiac issue (by controlling hypertension, opening up the blockages, etc).  \n\nAside from the optimization of the underlying cardiac problems, dilated cardiomyopathy merits specific medication regimen.   I do not want to trivialize this question and would advise you to definitely work with your physician with respect to the exact nature of this regimen.  In general, treatment of dilated cardiomyopathy involves careful titration of ace inhibitors (like lisnopril), beta blockers (carvidelol is preferred), diuretics and in some cases digoxin (for people with particulary poor pumping action of the heart).  For blacks, hydralazine plus a nitrate drug combination has been shown more beneficial than for whites.  The goal of titration of these medications is to make the patient comfortable with respect to common heart failure symptoms.  The medicaitons also reduce mortality (with ACE inhibitors having most effect) Interestingly, cardiac rehabilitation program consisting of aerobicexcercise routines can also help.\n\nYou asked about prognosis.  It also depends on etiology, but the mortality due to ischemic causes (most common; again due to blocked arteries...usually associated with prior heart attacks) has been shown to be about 50% at 10 years in a study of 1230 patients.  Other etiologies carry other mortality percentages with some better and some (particularly HIV) worse prognosis.  Proper long-term treatment reduces mortality significantly.  \n\nOne final thought.  If ejection fraction (EF) is below 35%, one may need an internal defibrillator device.  That is a topic in itself...just ask your doctor about it.  Hope that helps!
825946
http://en.wikipedia.org/wiki/Muscle\n\nYour answer is described in detail on the above site, too long to paste here, but I am sure that you will get your answer from this site.
308446
http://www.lasers.org.uk/laser_welding/briefhistory.htm\nhttp://www.google.com/search?sourceid=navclient&ie=UTF-8&rls=HPID,HPID:2005-17,HPID:en&q=history+of+lasers
62467
try going to www.dmdsales.com or www.deleter.com.
177421
In 1993, Dr. Morris and collaborators discovered that Williams syndrome is the result of deletion of the elastin gene on one of the number 7 chromosomes. This deletion usually occurs sporadically. Individuals who have the deletion, however, have a 50% chance of passing that deletion on to their offspring.
182409
Also known as ALS (amyotrophic lateral sclerosis).
518250
Duchenne Muscular Dystrophy is one of a group of muscular dystrophy's characterized the enlargement of muscles DMD is one of the most prevalent types of muscular dystrophy and is characterized by rapid progression of muscle degeneration. Duchenne was a French Neurologist who was the first to describe several nervous and muscular disorders.
163101
Well the reason you didn't find anything is because the word is rhabdomyolsis. Not labdo. It's an expedited degeneration of the muscle tissue. Statin drugs like Lipitor in a small population are known to have this side effect although I've yet to witness it for myself.
601153
I'm not sure, but I can recommend a very interesting book about the history of Autism, including, as I recall, some of the early diagnosed cases. \n\n"Not Even Wrong: Adventures in Autism" by Paul Collins.\n\nHope this helps you!
819962
try alieveor ask your doc for soma,i use soma for my muscle disease..it works well,good luck and hope ya feel better soon