[Appointment system for outpatients].
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Japan↗
Biomedical subjects
K Yuge
Publications and source records attributed to K Yuge.
Refolding and purification of human papillomavirus type 16 E7-lacZ fusion protein expressed in Escherichia coli.
Human papillomavirus (HPV) type 16 E7-lacZ fusion protein was produced in Escherichia coli, extracted as inclusion bodies, refolded with reducing reagents, and subjected to gel filtration. The refolded protein was purified by ion-exchange column chromatography, resulting in a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. 1H nuclear magnetic resonance spectral changes were observed in the high field methyl region in the presence of Zn2+ ion, suggesting that the refolded form of the fusion protein is possibly renaturated into the putative zinc finger motif (C. Edmond and K. H. Vousden, 1989, J. Virol. 63, 2650-2656) and supporting the data of J. A. Rawls, R. Pusztai, and M. Green (1990, J. Virol. 64, 6121-6129) on zinc binding to E7 protein using radioisotopically labeled zinc ion.
Amino Acid Sequence↗
Treatment with bifemelane for optic nerve damage following high intraocular pressure in rat eyes.
This study found that pretreatment with 4-(o-benzylphenoxy)-N- methylbuty-lamine hydrochloride (bifemelane hydrochloride, Celeport) reduced ischemia-reperfusion injury in rat eyes. Bifemelane (25 mg/kg) was injected intraperitoneally 30 minutes before an ischemic insult, then acute ischemia of the retina and optic disc was induced by increasing intraocular pressure to 110 mmHg for 45 minutes. After one week, the axonal count of the optic nerve was investigated using electron microscopy. The control group consisted of vehicle-treated eyes which received normal saline. The axon count was 93.4 +/- 7.9 for the bifemelane treated group, and 79.2 +/- 6.4 for the controls. The axon count in the treated group was significantly higher. These results suggest that bifemelane, which prevents cerebral nerve cell damage from ischemia, can reduce ischemic retinal nerve cell injury.
Animals↗
N-methyl-N-nitrosourea-induced photoreceptor apoptosis in the mouse retina.
Retinal degeneration induced by a single intraperitoneal injection of N-methyl-N-nitrosourea (MNU) in male and female albino (GRS/A and DDD/1) and colored (C57BL) mice at 7 weeks of age was examined morphologically 1, 3, 7, 14 and 21 days after the treatment. A dose of 60 mg/kg body weight evoked progressive retinal degeneration in all mice. All albino and colored mice had a comparable progression of photoreceptor cell degeneration by an apoptotic mechanism, as confirmed by morphological and TUNEL methods. Apoptosis had already taken place 1 day after the treatment and was completed by Day 7. This process resulted in a thin remnant of retina with complete loss of photoreceptor cells-21 days after the treatment. During the course of apoptosis, the pigment epithelial cells were maintained in a continuous layer in all strains of mice. In colored mice, several layers of the swollen pigment-enriched cells were seen between the inner nuclear layer and the pigment epithelial layer 14 and 21 days after the treatment. In summary, the destruction of photoreceptor cells by the apoptotic process was the mechanism by which retinal degeneration was induced by MNU.
Animals↗