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PubMed2000

Facial prosthetics: techniques used in the retention of prostheses following ablative cancer surgery or trauma and for congenital defects.

The retention of facial prostheses is a major factor influencing the successful outcome of rehabilitative treatment following ablative cancer surgery or trauma and for the prosthetic replacement of congenitally absent tissue. Since the sixteenth century to the present day, facial prosthetic devices have been retained by methods including adhesives and spectacle frames. The introduction of the Branemark extra oral implant system enhanced the stability of life-like prostheses thus giving patients more confidence in their use. This paper outlines the retention systems commonly used at the authors unit and the benefits gained by the use of implants to retain facial prostheses. The use of a single stage surgical technique instead of the usual two stage procedure is detailed.

Adolescent↗
PubMed1979

Congenital defects in calves from maternal ingestion of Nicotiana glauca of high anabasine content.

Administration of Nicotiana glauca to four cows from the 50th to the 75th days of gestation induced congenital deformities in their calves. All four calves had arthrogryposis of forelimbs and one also had spinal curvature and rib cage deformity. The plant material contained 0.113% of the piperidine alkaloid anabasine as authenticated by gas chromatography and by infrared spectroscopy. Because of the presence of anabasine at a high concentration and because of its structural relationship to known teratogens, anabasine may be responsible teratogen.

Abnormalities, Drug-Induced↗
PubMed1983

Genetic patterns of transcobalamin II and the relationships with congenital defects.

The vitamin B12-binding protein, transcobalamin II, is a trace component of plasma with a rapid turnover. This protein is essential for absorption, transport, cellular uptake and for recycling of vitamin B12 (cobalamin). Congenital transcobalamin II deficiency, an inborn error of metabolism is inherited as a recessive trait. The homozygous form of the deficiency is accompanied by severe clinical, hematological and immunological disturbances in the first months of life. Analytical, genetic, biochemical and clinical aspects of transcobalamin II in man and in vertebrates have been reviewed here. A genetic polymorphism for the protein has been found in man, rabbits and mice. Family studies revealed that the genetic patterns in man are determined by four polymorphic and several rare alleles. This genetic variability has been applied in paternity testing and in population studies. Transcobalamin II typing in families of patients with the inherited functional deficiency has led to identification of various deficient alleles in heterozygous carriers of the defects. Applying transcobalamin II typing after bone marrow transplantation demonstrated that this protein originates partly in the bone marrow. Subsequent investigations in cell culture have shown that human skin fibroblasts and cultured bone marrow synthesize and secret isotypes of a transport protein corresponding to the genetic isotypes observed in plasma. Comparison of transcobalamin II types in umbilical cord serum with the maternal types, has proven that the transcobalamin II activity in the cord serum is derived from the fetus. This finding will be of crucial importance in the early diagnosis of the deficiency syndrome.

Alleles↗