why muscular dystrophies affect some muscles and not others?
91572
There are VAST amount of different types of MD. Each one attacks its own set of muscles. Check out the link from the source.
322067
Have you checked w/your doctor?  For complete details, click here:  \nhttp://en.wikipedia.org/wiki/Muscle_contraction
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.
638973
I don't understand the question, are you asking what muscles make what work?
702949
The contraction phenomenon in muscular cells are mostly due to interaction of two elements, ie, Actin and Myosin. Their interaction are powered by some molecules called ATP. The ATP is produced in some cellular structures called mitochondria. The role of food for human is to produce energy. Energy is produced by hydrolyzing of ATP.
931657
Cardiac and skeletal muscles are both highly organized and contract in a single direction, uniformly. Smooth muscle, on the other hand is much more loosely organized. This probably leads to confusion about the order of contraction, etc.
429735
Type IIB and type IIX are different subtypes of skeletal muscle. They are not the same thing.
651667
It's tough to put an exact figure on, but it's rare.  It's exact rarity is tough to peg; because it's so rare, it's not a well known illness to diagnose.  Mild forms of it are often written off as muscular dystrophy.  There's likely instances of MM that weren't diagnosed as MM because the infant died before a correct diagnosis was made.  The rarest variants of MM have a estimate of affecting 1 in about a billion people.
100814
myotonin protein kinase: gene product of myotonic dystrophy is localized in the sarcoplasmic reticulum of skeletal muscle. Also, may be located at the intercalated discs and have a different isoform in cardiac tissue.\n\nIt is quite important to know the exact localization and function of myotonin protein kinase (MtPK), identified as the gene product of myotonic dystrophy, the most prevalent disease with multisystem disorders among muscular dystrophies. To investigate the localization of MtPK, we raised a polyclonal antibody against a synthetic peptide chosen within the deduced sequence of MtPK. This antibody detected both a membrane-bound 70-kd protein and a soluble 55-kd protein on Western blots of human muscles. By using this antibody for immunohistochemical studies of both biopsied human skeletal muscle fibers and mature innervated cultured muscle fibers, we can now demonstrate by confocal laser scanning microscopy that MtPK is localized mainly in the I-band. By immunoelectron microscopy, it was determined that MtPK is a membrane-bound protein localized mainly in the terminal cisternae of the sarcoplasmic reticulum. To our knowledge, this is the first documentation of the ultrastructural localization of MtPK. This finding is quite important for clarifying the pathophysiological basis of myotonic dystrophy, which might be due to a dysregulation of calcium metabolism.
295139
"All muscles within the human body are composed of a COMBINATION of these three fiber types.  This allows our muscles to be adaptable in different situations.  The distribution of fibers within a certain muscle varies from individual to individual".\n\nThe three fibre types mentioned above contain differing amounts of mitochondria.  Therefore, everyone's muscles would have a different amount of mitochondria.
139576
Although differentiated cells have the entire genome of the organism (yes, there are exceptions, but don't worry about that now), many parts of it are inactived, and this inactivation is hard to undo. Thus, a muscle cell has the genes for a neuron, but it can't use them, and we can't figure out how to undo this programing.\n\nAs for HIV, it is a virus, and it just uses our genes for lipid synthesis.
274204
creatine just causes your body to put water into the muscle....which makes muscles look bigger, but doesn't truely do anything for strength.
282411
It's all to do with the action potential of the muscle cell. We have different sorts of them in our body...eg cardiac, smooth muscle..etc.
722254
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
1157941
The contraction of a skeletal muscle is caused by the movement of actin and myosin fibers resulting from influx of exracelluar calcium caused by surface depolarization of the cell initiated by presynaptic discharge of a motor neuron. If this is a homework question, I suppose a one word answer would depend on the nature of the course discussion to which this question is addressed.
354452
process of elimination. of the 3 muscle types, smooth muscle is the only type withou cross-straitions. these stripes contribute to the fact that cardiac muscle and skeletal muscle contract in the same way. however the heart muscle, intimately interconnected continuous fabric,  has its characteristic intercalated discs which connect adjacent myocardial cells mechanically and electrically. the latter being, when one cell is stimulated it passes the electrical pulse throughout the heart and stimulates all cells (measured in ECG).
654478
FAT AND MUSCLE CELLS VARY IN COMPOSITION, AND 1 DOES NOT CONVERT TO THE OTHER. YOU CAN GET INCREASED BODY FAT AND DECREASED MUSCLE MASS IF YOU DONT EXERCISE LIKE YOU SHOULD.