• Journal of the Korea Academia-Industrial cooperation Society
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• v.18 no.9
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• pp.418-424
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• 2017

Magnesium has a higher specific strength than other metals and is widely used industry wide due to its excellent vibration absorption ability and electromagnetic wave shielding property.For example, it is used for automobile parts such as car seat frames and cylinder heads, and is widely used in electronic products such as notebook cases and mobile phone cases. In addition, it is in the spotlight as a bone-implant material used to assist in the treatment of damaged bones when the bones are cracked or broken. Currently, Ti alloy, stainless steel and Co-Cr-Mo alloy are used as the implant material, and the Mg alloy remains in research stage. The current problem with bone implant implants is that the patients must undergo reoperation to remove the implants after joint surgery. Magnesium, however, can achieve sufficient strength compared to current materials. In addition, since it is self-decomposed after the recovery, reoperation is not necessary. In this paper, Mg alloys were designed by adding harmless Ca and Zn to the human body. In order to improve the strength and corrosion resistance, the final alloy was designed by adding a small amount of Sr as a grain refiner. The radioactive elements of Sr are harmful to the human body, but other naturally occurring Sr elements are harmless. Microstructure analysis of the alloys was performed by optical microscopy and scanning electron microscopy. The mechanical properties and corrosion characteristics were evaluated by tensile test, potentiodynamic test and immersion test.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.29-34
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• 2015

Citrullinemia type1 is an autosomal recessive disorder of the urea cycle characterized by neonatal or late onset of hyperammonemia caused by a deficiency of the enzyme argininosuccinate synthetase (ASS). An ASS1 deficiency demonstrates fatal clinical manifestations that are characterized by the neonatal metabolic coma and early death when untreated. It causes a broad spectrum of effects, ranging from a mild disorder to a severe mental retardation, epilepsy, neurologic deficits. An acute neonatal form is the most common. Infants are normal at birth followed by an acute illness characterized by vomiting, lethargy, seizures and coma. These medical problems are life-threatening in many cases. A later onset form is less frequent and may be milder than the neonatal form. This later-onset form is associated with severe headaches, visual dysfunction, motor dysfunction, and lack of energy. Citrullinemia type1 is caused by mutations in the ASS1 gene located on chromosome 9q34.1 that encodes argininosuccinate synthetase, the third enzyme of the urea cycle catalyzing the formation of argininosuccinic acid from citrulline and aspartic acid. The enzyme is distributed in tissues including liver and fibroblasts. This mutation leads to hyperammonemia, arginine deficiency and elevated citrulline level. In the urea cycle, argininosuccinate synthetase catalyses the conversion of citrulline and aspartate to argininosuccinate.. Here, we describe a female newborn patient with lethargy, rigidity and hyperammonemia who was diagnosed as citrullinemia type1 with a c.[421-2A>G], c.[1128-6_1188dup] mutation.