The syndrome of caudal dysplasia (CDS) and the wide spectrum of associated skeletal and other anomalies are reviewed, and a further case of this disorder is presented. The syndrome of CDS should be distinguished from the familial forms of sacral dysgenesis, three forms of which are tentatively identified. Two of these usually involve some degree of "hemi-sacrum." The third is usually manifested as partial sacral agenesis with absent distal segments. All these familial types are probably genetic dominants, and none is associated with maternal diabetes. Usually CDS is not familial, but it often is associated with a tendency toward diabetes in the mother. The suggestion is advanced here that CDS is the result of a combination of two principal factors represented by (a) a maternal diabetic tendency and (b) separate nondiabetogenic genes. Determination of the human leucocyte antigen (HLA) haplotypes involved in CDS is suggested to investigate the possibility of genetically distinctive factors in this condition.
The current status of the much-debated question of the still-hypothetical stem cells of the liver is reviewed, with an emphasis on their role in hepatocarcinogenesis. The widely held view of the primacy of the hepatocyte, notably of the mononuclear diploid type, in this process--the "hepatocytic theory"--has been compared with variants of the "stem cell hypothesis" based on the "non-parenchymal epithelial cells" of the liver--the "oval" or biliary ductular cells, the "nondescript periductular" cells and the "primitive" bipotential epithelial cells. An attempt has been made to concentrate mainly on the more recent publications, in an effort to balance the conflicting opinions expressed by comparing results obtained by the newer procedures currently in use. Despite some interesting and relevant findings it appears that the evidence in favour of the stem-cell hypothesis is still circumstantial and that the hepatocytic theory has not been invalidated. Presumably the question of the hepatic stem cells will be answered when the riddle of hepatocarcinogenesis has been solved.
The historical development of the iodine-sulphuric acid reaction for amyloid is described. The reaction dates back to 1814 when Colin and Gaultier de Claubry, and independently Stromeyer, introduced the iodine reaction for starch. A variant of the acidified iodine reaction appears to have been used for printing paper by Gmelin in 1829, and in 1838 Schleiden used the iodine-sulphuric acid test on plants to demonstrate what he considered to be a transformation of the plant material into starch. Shortly afterwards Payen (1839) defined "cellulose", and the iodine-sulphuric acid reaction became a standard procedure used by botanists to demonstrate this plant component. In 1853 Virchow used Harting's (1847) procedure to demonstrate the reaction of Purkynĕ's corpora amylacea to this test, on the assumption that they might be cellulose derivatives, and applied it to what appeared to be similar corpuscles in a "waxy" spleen. The first histochemical reaction for amyloidosis had thus been introduced into pathology, and continued to exert from that time on an important influence on amyloid research, whose impact is felt to the present day.
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