If now and then one of them recovers, he certainly loses the little Reason he had, and turns Ideot...
French naval surgeon Marie-Théophile Griffon du Bellay treated and described cases while stationed aboard the hospital ship Caravane in Gabon in the late 1860s.In 1901, a devastating epidemic erupted in Uganda, killing more than 250,000 people, including about two-thirds of the population in the affected lakeshore areas. According to The Cambridge History of Africa, "It has been estimated that up to half the people died of sleeping-sickness and smallpox in the lands on either bank of the lower river Congo. "The causative agent and vector were identified in 1903 by David Bruce, and the subspecies of the protozoa were differentiated in 1910. Bruce had earlier shown that T. brucei was the cause of a similar disease in horses and cattle that was transmitted by the tsetse fly (Glossina morsitans).The first effective treatment, atoxyl, an arsenic-based drug developed by Paul Ehrlich and Kiyoshi Shiga, was introduced in 1910, but blindness was a serious side effect. Suramin was first synthesized by Oskar Dressel and Richard Kothe in 1916 for Bayer. It was introduced in 1920 to treat the first stage of the disease. By 1922, Suramin was generally combined with tryparsamide (another pentavalent organoarsenic drug), the first drug to enter the nervous system and be useful in the treatment of the second stage of the gambiense form.
Hypochondroplasia (HCH) is a developmental disorder caused by an autosomal dominant genetic defect in the fibroblast growth factor receptor 3 gene (FGFR3) that results in a disproportionately short stature, micromelia and a head that appears large in comparison with the underdeveloped portions of the body. It is classified as short-limbed dwarfism. Signs and symptoms
Individuals affected by this disorder appear normal at birth. As the infant grows, however, their arms and legs do not develop properly, and their body becomes thicker and shorter than normal. The following are characteristics consistent with this condition:
Brachydactyly
Short stature
Micromelia
Skeletal dysplasia
Abnormality of femur

Cause
Hypochondroplasia is transmitted as an autosomal dominant trait affecting the FGFR3 gene on chromosome 4p16.3. There is currently no cure for this condition. Pathophysiology
This disorder results from mutations in the proximal tyrosine kinase domain of the FGFR3 gene. This gene plays an important role in embryonic development, playing a part in regulating activities such as cell division, migration and differentiation.Hypochondroplasia can result from p. Lys650Asn as well. In FGFR3, some 20 different mutations have been associated to hypochondroplasia, and it seems to have a role in skeletal dysplasia. Diagnosis
The diagnosis of this condition can be done via X-rays (with lack of normal distance L1 to L5), and additionally genetic testing is available to ascertain hypochondroplasia. However, the physical characteristics are one of the most important in determining the condition. Treatment
Treatment of hypochondroplasia usually takes the form of orthopedic surgery and physical therapy. Genetic counseling is advised for individuals and their families.