Dutch Research on Beriberi: I. Christiaan Eijkman's Research and Evaluation of Kanehiro Takaki's Diet Reforms of the Japanese Navy.

Dutch researcher Christiaan Eijkman realized that a form of Polyneuritis closely resembling Beriberi occurred among chickens that were fed with cooked, instead of raw rice. He found that the cause of this illness lay in the nutritional differences between rice that still had its bran layer, and polished white rice. He also found that this bran layer had a therapeutic effect. He decided to investigate the incidence of Beriberi among humans by comparing a diet based on white rice with one based on unpolished, full-grain rice. In 1898, he published 'Beri-Beri en Voeding, Een Kritisch-Historische Studie' (Beri-beri and Feeding, An Important Historical Study), in which he discussed the diet reforms of Van Leent in the Dutch East Indian Navy, and of Kanehiro Takaki in the Japanese Navy. Notwithstanding the fact that Takaki's research was highly praised by the Lancet, Eijkman was very critical of his research methods. He was conscious, however, that a shift had occurred in the research of Beriberi from bacteria-based research to nutritional deficiencies, and discussed Takaki's findings insofar as he could.

Endothelial cells and the pathogenesis of lepromatous neuritis:insights from the armadillo model.

Selective infection of peripheral nerves is a unique property of Mycobacterium leprae that results in serious injury, but its basis is unexplained. Recent evidence from infected armadillos suggests that endothelial cells of peripheral nerve vasculature may be the gatekeepers by which M. leprae infects nerves. The pathogenesis of neuropathy in leprosy may thus entail a dynamic sequence of adhesion, immunologic, and inflammatory processes involving peripheral nerve endothelial cells.

From Horus the child to Hephaestus who limps: a romp through history.

The question of why Hephaestus, the Greek god of smiths, limped has been the subject of much debate, mainly on mythological grounds. This debate extended also into the field of medical diagnosis, with attempts at defining the nature of the deformity that made the crippled Hephaestus the buffoon of the other Olympic gods. One problem encountered in these debates was the changes to which the ugly young Hephaestus was subjected with the passing of time-from a limping deformed youth to the later dignified and normal man. While some authors, largely influenced by poetic Greek texts and vase paintings, attributed the limp to talipes (club-feet), others pointed to certain features suggestive of achondroplasia. Since the image of the early Hephaestus is based mainly on the much earlier concept of the Egyptian god Ptah, who as the triune god of the resurrection sometimes is depicted as an achondroplastic dwarf (Ptah-Pataikos), the suggestion of the possible achondroplastic dwarf-like nature of the early Hephaestus is not implausible. It is supported by similarities in the image of Hephaestus to some features in other Egyptian gods, such as the domestic god Bes, the guardian of the new-born, and the Horus the Child or Harpocrates (Greek), yet another protector of youth and "the symbol of everything that is young and vigorous" [Budge, 1969: The Gods of the Egyptians, or Studies in Egyptian Mythology. Volume I.]. The characteristic feature of this child-god is the "lock of Harpocrates" on the right side of his head. That this lock can sometimes also be seen not only on the head of Ptah-Pataikos and of Bes but also on the young Hephaestus is highly suggestive of the Egyptian influence on his image. Recently, however, another interesting explanation of Hephaestus's limp has been suggested that may explain why the Egyptian influenced image of the early achondroplastic Hephaestus changed to the later, more Grecian view of the smith-god who hobbled because of club-feet. Improvements in composition-analysis of samples from antique statues and various utensils have led to the suggestion that the introduction of new smelting techniques in antique times may have exposed ancient metal workers to the effects of various toxic metals causing, for instance, chronic lead poisoning or, more relevant here, chronic arsenic poisoning causing peripheral neuritis with weakness and lameness of one or both lower extremities. Later changes in smelting technique, and recognition or guess-work of a possible connection between these techniques and toxic effects, may explain the change from the buffoon-like achondroplastic walk to the club-footed limp and eventual normal behaviour of Hephaestus, the Smith. In other words: Did Hephaestus limp because of his arsen-neuritis?

[Roussy-Levy hereditary areflexic dysstasia. Its historical relation to Friedreich's disease, Charcot-Marie-Tooth atrophy and Dejerine-Sottas hypertrophic neuritis; the present status of the original family; the nosologic role of this entity]. / La dystasie aréflexique héréditaire de Roussy-Lévy. Ses rapports historiques avec la maladie de Friedreich, l'atrophie Charcot-Marie-Tooth et la névrite hypertrophique de Dejerine-Sottas; l'état actuel de la famille originale; la place nosologique de cette entité.

This survey of Roussy-Lévy disease begins with an historical account of the three neurological conditions from which this entity has been separated: Friedreich disease, described in 1861-1863, which proved with time to be a genuine anatomoclinical disorder: Charcot-Marie-Tooth atrophy, described in 1886, particular because of its morphology and evolution but due to various processes: Dejerine-Sottas hypertrophic neuritis, described in 1893, which was the first variant to be individualized within the heterogenous group of primary and familial hypertrophic neuritis. The initial description of Roussy-Lévy disease--in 1926, 1932, and 1934--and the controversies raised by this concept are recalled as well as the present state of the original family: five out of seven members have been examined since 1956 and it has been demonstrated that they are suffering from a form of hypertrophic neuritis. However it is this author's opinion that the concept of an autonomous Roussy-Lévy disease within hypertrophic neuritis is justified by the following criteria: dominant transmission, very precocious onset, extreme slowness of the evolution, remarkable benignity of the prognosis.