Lenses of weakly deformed metagranitoid and coesite-bearing eclogite are both found within mylonitic orthogneiss of the Jiaodong Group in the Su-Lu ultrahigh pressure (UHP) province, eastern China. In the metagranitoid, omphacite overgrowing host clinopyroxene, and garnet coronas developed along the grain boundaries between igneous plagioclase and mafic phases suggest that the metagranitoid suffered an eclogite facies metamorphism. Quartz aggregates after igneous quartz in the metagranitoid show a distinctive polycrystalline, granoblastic texture. This texture is similar to quartz aggregates of the Dora-Maira metagranite which suffered coesite-eclogite facies metamorphism, but is dissimilar to the Mount Mucrone metagranite which recrystallized under the less extreme quartz eclogite facies. These features of the Su-Lu metagranitoid suggest that the UHP metamorphism may have affected not only the eclogite but also the surrounding metagranitoid.
This study focused on the purification and characterization of chitinase from alfalfa (Medicago sativa L.) infected by CP-MLO. Chitinase (EC 3.2.1 14) was purified from leaves and shoots of MLO-infected alfalfa plants by ammonium sulfate precipitation, chitin affinity chromatography and Sephadex column chromatography. Three chitinase isoenzymes were identified and shown to have molecular masses of approximately 40, 35 and 30 kilodaltons as determined by SDS-polyacrylamide gel electrophoresis, while only one chitinase isoenzyme was detected in healthy plants. The endochitinase activity in CP-MLO infected plants was 24 times higher than that in healthy plants. The optimum temperature range of the enzyme activity was from 35°C to 50°C. Ag and Hg ions significantly inhibited the enzyme activity.
We have immunocytochemically shown a significant reduction in the amount of laminin M (or merosin; a tissue-restricted basal lamina protein expressed in striated muscle, Schwann cells, and placental trophoblast) in the skeletal muscle of Fukuyama type congenital muscular dystrophy (FCMD).1) To inquire into the role of laminin M in the process of muscular dystrophies, we examined laminin M in several animal models that cause muscular dystrophy. Immunofluorescent, immunoblotting, and electron microscopic analyses have revealed that laminin M is missing from skeletal and cardiac muscles and peripheral nerve in the affected homozygous C57BL/6J-dy/dy mice, but not in the non-affected heterozygous Dy/dy and the other dystrophic animal models including mdx mice, BIO 14.6 hamsters, and line 413 chickens. In the dy/dy mice, laminin M mRNA is not detected by Northern blotting, but becomes detectable by RT-PCR amplification. Other components of the basal lamina such as laminin B, beta-integrin, type IV collagen, and fibronectin are normally expressed in all animals examined, including the dy/dy mice. These observations strongly suggest that laminin M defect is primarily responsible for the pathogenesis of muscle fiber damage and dysmyelination of the dystrophic dy/dy mice.