With the outbreak of war appearing imminent in 1938, the War Office created the Army Blood Supply Depot (ABSD) in Bristol, headed by Lionel Whitby and in control of four large blood-depots around the country. British policy through the war was to supply military personnel with blood from centralized depots, in contrast to the approach taken by the Americans and Germans where troops at the front were bled to provide required blood. The British method proved more successful in adequately meeting all requirements, and over 700,000 donors were bled over the course of the war. This system evolved into the National Blood Transfusion Service established in 1946, the first national service to be implemented. Stories tell of Nazis in Eastern Europe during World War II using captive children as repeated involuntary blood-donors. Medical advances
A blood-collection program was initiated in the US in 1940 and Edwin Cohn pioneered the process of blood fractionation. He worked out the techniques for isolating the serum albumin fraction of blood plasma, which is essential for maintaining the osmotic pressure in the blood vessels, preventing their collapse. Gordon R. Ward, writing in the correspondence columns of the British Medical Journal, proposed the use of blood plasma as a substitute for whole blood and for transfusion purposes as early as 1918. At the onset of World War II, liquid plasma was used in Britain. A large project, known as "Blood for Britain", began in August 1940 to collect blood in New York City hospitals for the export of plasma to Britain.
Mitochondrial myopathies are types of myopathies associated with mitochondrial disease. On biopsy, the muscle tissue of patients with these diseases usually demonstrate "ragged red" muscle fibers. These ragged-red fibers contain mild accumulations of glycogen and neutral lipids, and may show an increased reactivity for succinate dehydrogenase and a decreased reactivity for cytochrome c oxidase. Inheritance was believed to be maternal (non-Mendelian extranuclear). It is now known that certain nuclear DNA deletions can also cause mitochondrial myopathy such as the OPA1 gene deletion. There are several subcategories of mitochondrial myopathies. Signs and symptoms
Signs and symptoms include (for each of the following causes):

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like syndrome (MELAS)
Varying degrees of cognitive impairment and dementia
Lactic acidosis
Strokes
Transient ischemic attacks
Hearing loss
Weight loss
Myoclonic epilepsy and ragged-red fibers (MERRF)
Progressive myoclonic epilepsy
Clumps of diseased mitochondria accumulate in muscle fibers and appear as "ragged-red fibers" when muscle is stained with modified Gömöri trichrome stain
Short stature
Kearns–Sayre syndrome (KSS)
External ophthalmoplegia
Cardiac conduction defects
Sensorineural hearing loss
Chronic progressive external ophthalmoplegia (CPEO)
Progressive ophthalmoparesis
Symptomatic overlap with other mitochondrial myopathies

Cause
Zidovudine, an HIV medication can cause red ragged fiber myopathy. Diagnosis
Muscle biopsy: ragged red fibers in Gömöri trichrome stain. Treatment
Although no cure currently exists, there is hope in treatment for this class of hereditary diseases with the use of an embryonic mitochondrial transplant. References


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