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Biomedical subjects

R Yagi

Publications and source records attributed to R Yagi.

44 records · Page 3Linked to original sources
PubMed1983

The effect of a high fat diet on pyruvate decarboxylase deficiency without central nervous system involvement.

A nine-year-old Japanese boy with low pyruvate decarboxylase activity in fibroblasts showed no central nervous symptoms except for muscle fatigue. The pyruvate decarboxylase activities in fibroblasts of the patient and two control subjects were 0.407 +/- 0.083, 1.029 +/- 0.137 and 1.607 +/- 0.096 mumoles/g protein/30 min, respectively. The Michaelis-Menten constant (Km) was the same in the patient and controls. There was no inhibitor of pyruvate decarboxylase in the patient's fibroblasts. A high fat diet has been given to the patient for five years. At present he does not complain of any kind of muscle fatigue, except after severe exercise. Mental and physiological development of the patient are within the normal ranges. However, trials of orally administered thiamine hydrochloride or thiamine hydrochloride combined with lipoamide did not improve his muscle fatigue.

Carboxy-Lyases↗
PubMedDate not supplied

Design and anti-HIV-1 activity of hammerhead and hairpin ribozymes containing a stable loop.

Three ribozymes, a hairpin ribozyme (HR112) and two hammerhead ribozymes (RZ115 and RZ119) containing a 5'C(UUCG)G3' loop were designed to cleave the U5 region in the long terminal repeat (LTR) of HIV-1 RNA. The t1/2 values of chemically synthesized substrates mediated by three ribozymes were measured. The transformed CEM cells possessing these three ribozyme-encoding genes were challenged with a HIV-1IIIB strain, and two of these three ribozymes, HR112 and RZ119, were shown to possess strong anti-HIV-1 activity.

Anti-HIV Agents↗
PubMedDate not supplied

Overview of studies comparing human normal cartilage with minimal and advanced osteoarthritic cartilage.

A major area under study in the osteoarthritis (OA) research field is the characterization of specific molecular and biochemical changes that distinguish advanced diseased cartilage from less involved or normal tissue. This information is important to better define the pathogenic mechanisms that are operating during OA progression and to identify disease-specific markers. This review describes recent studies that have addressed changes in chondrocyte gene expression, proliferation, and apoptosis in "experimental" (more advanced OA cartilage) versus "control" (less involved or non-OA cartilage). Included is a comprehensive listing of recently published studies in this area with general findings. The review also includes a discussion of study design and the strengths and weaknesses of the various approaches. In addition, specific strategies to deal with some of the important issues are discussed. One particular model utilizing minimal and advanced OA cartilage obtained from the same patient is described in more detail.

Apoptosis↗