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Article Evaluation"Henrietta Lacks and family was not compensated for creation of HeLa line (cells obtained without consent). Wiki Article is clear and seems accurate, with no bias. No citations regarding Lack's (or her families) consent."Article Selection"Brody Myopathy/Brody disease -- Wiki page needs a lot of work. Background, inheritance, distinction from Brody syndrome, molecular characteristics, treatment, and prognosis sections. A lot of literature exists on the topic""Crisscross Heart -- lots of information missing from Wiki page. Needs anatomy, detection, and treatment sections. Lots of research papers available.""Juvenile Huntingtons Disease -- not much information out there. Doesn't differ significantly from regular HD."Article Drafting

= Brody myopathy = Brody myopathy, also known as Brody disease (BD), is a rare disorder that affects skeletal muscle function. BD was first characterized in 1969 by Dr. Irwin A. Brody at Duke University Medical Center. Individuals with BD have difficulty relaxing their muscles after exercise. This difficulty in relaxation leads to symptoms including cramps, stiffness, and discomfort in the muscles of the limbs and face. Symptoms are heightened by exercise and usually begin in childhood and progress in severity throughout adulthood.

Most cases of BD are inherited through an autosomal recessive mutation in ATP2A1, where each copy of the affected individual's gene contain the mutation. The gene involved in BD encodes the fast-twitch skeletal muscle ATPase, SERCA1. SERCA1 is a protein pump that uses ATP to pump Ca2+ ions from the cytosol to the sarcoplasmic reticulum in skeletal muscle. In those with BD, SERCA1 pumps are unable to effectively move Ca2+ across the membrane, leading to increased levels of cytoplasmic Ca2+. Increases in cytoplasmic Ca2+ levels interfere with muscle contraction, leading to the characteristic symptoms of BD.

In some cases of BD, no mutations in ATP2A1 have been observed. Disease transmission in cases of non-ATP2A1 BD has been characterized as an autosomal dominant inheritance pattern. These cases have revealed that the cause of the disease is likely heterogenous, meaning the disease involves multiple genes.

Diagnosis
Diagnosis of BD begins with clinical evaluation of individuals for characteristic symptoms of cramping and stiffness of exercised muscles. Blood testing may be used to measure serum creatine kinase, which ranges from normal to slightly elevated in those with BD. Skeletal muscle biopsies are used to examine muscle fibers. Biopsies in individuals with BD often show variation in muscle fiber size, atrophied fast-twitch muscle fibers, and increased nuclei number. Electromyography can be used in diagnosis to rule out myotonia, a similar musculo-skelatal disease. If the individual has BD, no myotonic discharges will be detected by electromyography. Genetic testing may also be used in the diagnosis of BD to look for mutations in ATP2A1. Since only some forms of the disease are associated with ATP2A1, results of genetic testing do not always confirm a diagnosis of BD, but are useful to rule out other similar disorders.

Treatment
There is no cure for BD, although treatment options are available for reducing the negative symptoms of BD. The drugs Dantrolene and verapamil are used in BD treatment due to their effects on Ca2+. Dantrolene is a muscle relaxer that decreases the symptoms of BD by inhibiting Ca2+ release channels in the sarcoplasmic reticulum, therefore reducing the intracellular Ca2+ concentration. Verapamil sequesters Ca2+ in the sarcoplasmic reticulum of muscle cells by functioning as a Ca2+ channel blocker.