Lack of platelet factor-3 activation after incubation of platelet-rich plasma with kaolin in the rat

Summary Stypven times, measured in rat platelet-rich plasma (P. R. P.) after incubation with kaolin, did not shorten as incubation proceeded, thus reflecting the lack of development of platelet factor-3 (PF₃) availability in this test system. Repeated freezing and thawing of P. R. P. or aggregation with collagen did result in PF-3 availability. Aggregation and PF-3 availability were inhibited by the compound VK774. These findings add another aspect to the list of species differences in platelet function.This study was partly supported by a grant from I. W. O. N. L.     

大连市银杏叶斑病病原菌鉴定

银杏(Ginkgo biloba L.)是常见的城市园林观赏绿化树种,并具有极高的材用、食用和药用价值.近年来,大连市银杏树发生了一种不明病因且较为严重的叶斑病,查明病因、为病害防治提供理论依据迫在眉睫.从病害发生严重区域采集叶斑病病叶样本,采用感病叶片单斑分离法,对分离菌株进行致病性测定、形态学鉴定及分子生物学鉴定等,对大连市银杏树发生的叶斑病进行了病原菌鉴定.结果表明,大连银杏叶斑病致病菌有2种,分别为链格孢属细极链格孢(Alternaria tenuissima)和链格孢(Alternaria alternata).迄今为止,细极链格孢(Alternaria tenuissima)侵染银杏导致其发生叶斑病鲜有报道.     

A new gene, encoding an anion transporter, is mutated in sialic acid storage diseases

Sialic acid storage diseases (SASD, MIM 269920) are autosomal recessive neurodegenerative disorders that may present as a severe infantile form (ISSD) or a slowly progressive adult form, which is prevalent in Finland (Salla disease). The main symptoms are hypotonia, cerebellar ataxia and mental retardation; visceromegaly and coarse features are also present in infantile cases. Progressive cerebellar atrophy and dysmyelination have been documented by magnetic resonance imaging (ref. 4). Enlarged lysosomes are seen on electron microscopic studies and patients excrete large amounts of free sialic acid in urine. A H+/anionic sugar symporter mechanism for sialic acid and glucuronic acid is impaired in lysosomal membranes from Salla and ISSD patients. The locus for Salla disease was assigned to a region of approximately 200 kb on chromosome 6q14-q15 in a linkage study using Finnish families. Salla disease and ISSD were further shown to be allelic disorders. A physical map with P1 and PAC clones was constructed to cover the 200-kb area flanked by the loci D6S280 and D6S1622, providing the basis for precise physical positioning of the gene. Here we describe a new gene, SLC17A5 (also known as AST), encoding a protein (sialin) with a predicted transport function that belongs to a family of anion/cation symporters (ACS). We found a homozygous SLC17A5 mutation (R39C) in five Finnish patients with Salla disease and six different SLC17A5 mutations in six ISSD patients of different ethnic origins. Our observations suggest that mutations in SLC17A5 are the primary cause of lysosomal sialic acid storage diseases.     

Lack of platelet factor-3 activation after incubation of platelet-rich plasma with kaolin in the rat.

Stypven times, measured in rat platelet-rich plasma (P.R.P.) after incubation with kaolin, did not shorten as incubation proceeded, thus reflecting the lack of development of platelet factor-3 (PF3) availability in this test system. Repeated freezing and thawing of P.R.P. or aggregation with collegan did result in PF-3 availability. Aggregation and PF-3 availability were inhibited by the compound VK774. These findings add another aspect to the list of species differences in platelet function.