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Athletes who are more advanced or weigh more than 220 pounds can increase the dosage to 150 mg/day in the third week. This dosage, however, should not be taken for periods longer than two to three weeks. Following, the dose should be reduced by one tablet every week. Since Anadrol 50 quickly saturates the receptors, its intake should not exceed six weeks. The dramatic mass build up which often occurs shortly after administration rapidly decreases, so that either the dosage must be increased (which the athlete should avoid due to the considerable side effects) or, even better, another product should be used. Those who take Anadrol 50 for more than 5-6 weeks should be able to gain 20 – 25 pounds. These should be satisfying results and thus encourage the athlete to discontinue using the compound.

Education Dr. Gedikolu had his high school education in Isik Lisesi (Istanbul) and thereafter, he entered the Istanbul Faculty of Medicine in Istanbul University. After obtaining the medical doctor degree, he did his military service in the Field Officer School of the Sixth Army in Smyrna; and he had the first position while finishing the military service. He was accepted to the Baylor University in Houston to perform a residency in pediatrics. He did his subspecialty in Pediatric Hematology and Oncology in St. Paul Hospital and in the Wadley Research Center. Studies in Genetics He was accepted into the Cardiff University to perform research in genetics with the grand of the British Council. He transferred his experience in Cardiff to perform research in Istanbul Faculty of Medicine. Heterochromasy in Human Chromosomes Until 1966, existence of the heterochromatic regions in the chromosomes was well known in plants and animals, yet there was no information regarding to their presence in human chromosomes. First in 1966, Dr. Gedikolu observed such regions in chromosomes of a 22-years old Caucasian male bearing Wilson disease independent of the disease and published these observations in Lancet. New Observations in Kartagener's Disease In 1933, Kartagener described a new syndrome comprised of a symptoms trio of dextrocardia, bronchiectasis and sinusitis; and therefore, this syndrome is named as Kartagener's triad or syndrome. New research confirmed that this disease phenotype may associate with multiple chromosomal regions. Most frequently, the dynein axonemal intermediate chain protein locus (9p21-p13) exerts mutations; yet 5p and 19q anomalies are also linked with the similar disease phenotypes. In 1967, Dr. Gedikolu described new findings in a sibling born from nephew-parents with Kartagener symptoms. While documenting the existence of fibrocystic lung disease in both patients, and the eosinophilic infiltration in the sinonasal epithelium as a novel finding; he also described isolated green color blindness (deuteranopia) in one of the siblings and published these clinical data again in Lancet (3). Isolated color blindness could be the first sign of degenerative eye diseases with progressive rode-cone injury (64) and one gene causing one of such diseases, the retinitis pigmentosa is localized also in 19q similar to the gene of Kartagener's (65, 66). Only very recently, it is found that the motile flagellum and the immotile sensory cilia can bear the same structural proteins (67); and in 2001 Kartagener's syndrome-accompanying retinitis pigmentosa is described (68).

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