高胆固醇血症家兔红细胞在交、直流电场中的电泳行为

本文对高胆固醇血症家兔红细胞在交、直流电场中的电泳行为进行了多指标测定,结果显示,高脂组与正常组相比红细胞聚集能力增强,变形能力及膜流动性下降,表明高脂血症可能较易导致血栓形成。中药有效成分8501有对抗高脂引起的红细胞上述改变的作用,提示8501可能对血栓和动脉粥样硬化斑块形成有防治作用。     

大果木姜子的甘油三酯组成

采用光谱法和胰酯酶分解法对大果木姜子油酯中分得的结晶C—I组成进行了分析,结果表明C—I是由11种甘油三酯组成。其中2-位为月硅酸的甘油三酯占91.80％,1,3-位脂肪酸主要为癸酸和月桂酸,甘油三酯的组成中,CLC占62.24％,LLC占24.50％。     

浙江产蝮蛇毒(Agkistrodon halys pallas venom)凝血酶样酶的性质及其对血凝和血脂的影响

从浙江产蝮蛇毒中分离出一种凝血酶样酶,该酶能明显地延长全血凝固时间,白陶土部分凝血活酶时间(KPTT),并降低了血浆中的纤维蛋白原水平,同时全血的比粘度和血浆的比粘度及血清中的胆固醇和β脂蛋白均有所下降.该酶不激活凝血因子ⅩⅢ.     

Tyrosine mutations within the alpha platelet-derived growth factor receptor kinase insert domain abrogate receptor-associated phosphatidylinositol-3 kinase activity without affecting mitogenic or chemotactic signal transduction.

A phosphatidylinositol-3 (PI-3) kinase activity of unknown biological function associates with tyrosine kinase-containing proteins, including a number of growth factor receptors after ligand stimulation. In the beta platelet-derived growth factor (beta PDGF) receptor, phosphorylation of a specific tyrosine residue within the kinase insert domain was required for its interaction with this enzyme. We show that substitutions of phenylalanine for tyrosine residue 731 or 742 within the kinase insert domain of the alpha PDGF receptor do not impair PDGF-induced tyrosine phosphorylation of the receptor or of an in vivo substrate, phospholipase C-gamma. Moreover, phosphatidylinositol turnover in response to ligand stimulation is unaffected. However, both lesions markedly impair receptor association with PI-3 kinase. Antiphosphotyrosine antibody-recoverable PI-3 kinase was also dramatically reduced in PDGF-stimulated cells expressing either mutant receptor. Since neither mutation abolished PDGF-induced mitogenesis or chemotaxis, we conclude that alpha PDGF receptor-associated PI-3 kinase activity is not required for either of these major PDGF signalling functions.     

Identification and characterization of the ATP·Mg-dependent protein phosphatase activator (FA) as a microtubule protein kinase in the brain

The activating factor of ATP·Mg-dependent protein phosphatase (F _A) has been identified in brain microtubules. When using purified MAP-2 (microtubule associated protein 2) and tau proteins as substrates,F _A could phosphorylate MAP-2 to 16 moles of phosphates per mole of protein with aK _m value of 0.4 µM, and tau proteins to 4 moles of phosphates per mole of proteins with aK _m value of about 3 µM. When using microtubules as substrates,F _A could enhance many-fold the endogenous phosphorylation of many microtubule-associated proteins including MAP-2, tau proteins, and several low-molecular-weight MAPs. In contrast to other reported MAP kinases, such as cAMP-dependent protein kinase and Ca⁺²/phospholipid-dependent protein kinase, theF _A-catalyzed phosphorylation of tau proteins could cause an electrophoretic mobility shift on sodium dodecyl sulfate polyacrylamide gel electrophoresis, suggesting that a dramatic conformational change of tau proteins was produced byF _A. Peptide mapping analysis of the phosphopeptides derived from SV8 protease digestion revealed thatF _A could phosphorylate MAP-2 and tau proteins on at least four specific sites distinctly different from those phosphorylated by cAMP-dependent and Ca⁺²/phospholipid-dependent MAP kinases. Quantitative analysis further indicated that approximately 19% of the total endogenous kinase activity in brain microtubules was due toF _A. Taken together, the results provide initial evidence that the ATP·Mg-dependent protein phosphatase activating factor (F _A) is a potent and unique MAP kinase, and may represent one of the major factors involved in phosphorylation of brain microtubules.     

Utility of the hot-wire spirometer

A comparative study has been carried out to investigate the performance of the hot-wire spirometer and the Rollingseal spirometer; the reproducibility of the data generated by an individual examiner; and the validity of data obtained by an "inexperienced examiner" using the hot-wire spirometer. The following results were obtained: 1. The experimental data given by the hot-wire spirometer were about 5-6% higher for FVC and FEV1, and about 10-12% higher for PFR, V50, and V25, respectively, when compared to the data generated by the Rollingseal spirometer. 2. The reproducibility of the data produced by the hot-wire spirometer operated by an "experienced examiner" was good, as the percent difference was about +/- 3%. 3. Reliable data were obtained with the spirometer even by an "inexperienced examiner" if he/she has gone through an on-site training concerning instrumentation and measurement methods for spirography.     

Rat model of the human "Triton" tumor: direct genetic evidence for the myogenic differentiation capacity of schwannoma cells using the mutant neu gene as a cell lineage marker

Spontaneous myogenic differentiation was observed in 2 out of 15 cases when cells from schwannomas induced in the offspring of BDIX rats by transplacental exposure to N-ethyl-N-nitrosourea (EtNU) were grown in monolayer culture following fluorescence-activated cell sorting with monoclonal antibody (Mab) 217c. Myotubes and numerous mononucleated cells no longer expressed the Schwann cell antigens 217c and S-100 protein, but rather revealed the presence of desmin, the alpha-sarcomeric form (alpha-sr) of actin, and the cell surface antigen specified by Mab RB21-7, a 250 kD glycoprotein sharing an epitope with the neural cell adhesion molecule (N-CAM). Subcutaneous reimplantation of such cells into syngeneic animals led to the appearance of tumors composed of both S-100 positive Schwann cells and desmin and alpha-sr-actin positive rhabdomyoblasts, thus closely resembling the human "Triton" tumor. With the use of the polymerase chain reaction and allele-specific oligonucleotide hybridization, DNA isolated from individual myotubes was analyzed for the presence of a T----A transversion mutation at nucleotide 2012 of the neu gene, which is diagnostic of EtNU-induced rat schwannomas. All of the amplified DNA isolates contained the mutant neu allele, thus providing direct genetic proof for the capacity of mammalian neuroectodermal cells for myogenic differentiation.     

The U1 snRNA gene repeat from the sea urchin (Strongylocentrotus purpuratus): the 70 kilobase tandem repeat ends directly 3'' to a U1 gene.

Lambda phage clones containing multiple copies of the 1.1 kb tandemly repeated unit of the sea urchin (S. purpuratus) U1 RNA genes were isolated from a gene library. The 1.1 kb repeat unit encodes a single copy of the predominant U1 RNA expressed in oocytes and embryos prior to the blastula stage. The tandem repeat unit is about 80 kb in size and is probably present one time per haploid genome as judged by pulsed-field electrophoresis of sperm DNA digested with restriction enzymes which do not cut in the repeat unit. Two of the phage contained DNA flanking the repeat unit as well as several repeat units. The tandem repeat unit ends just 3' to the U1 coding region. There is only limited homology in the 5' flanking region with U1 snRNA genes from the sea urchin L. variegatus.