几种有机酸对牙釉面作用的体外研究

用扫描电镜、光学显微镜和化学分析等方法,观察了在不同条件下醋酸、乳酸、柠檬酸,酒石酸、EDTA 等几种有机酸对牙釉面的脱矿作用,分析和比较了这些有机酸的化学性质,浓度、作用时间与釉面损伤形态学变化关系.     

用DTA法对环氧树脂固化条件的研究

用热分析方法来研究环氧树脂与乙二胺、二乙烯三胺、三乙醇胺、六次甲基四胺、邻苯二甲酸酐和顺丁烯二酸酐的固化条件．     

林语堂代人受过──从鲁迅《论“费厄泼赖”应该缓行》的一条注释谈起

鲁迅《论“费厄泼赖”应该缓行》一文后的第二条注释给读者三点印象：一、林语堂是“费厄泼赖”的倡导者；二、鲁迅写作此文是专门批判林语堂的；三、二三十年代林语堂始终站在进步文学的对立面。事实并非如此。“费厄泼赖”的始作俑者是周作人，而不是林语堂。鲁迅对“费厄泼赖”的批评，表面上对着林语堂．其实瞄准的是周作人。准确地讲，是针对当时一些善良人们姑息养奸的错误倾向而言的。二十年代的林语堂作为语丝派叱咤风云的一员战将，伴随着鲁迅的步伐，在反抗封建势力和现代评论派的攻城劫寨中立下了汗马功劳。林语堂是代人受过的。这场围绕“费厄泼赖”问题的讨论，是语丝派内部人之间不同意见的磋商，长期以来人们把它定格在“两个阶级”、“两条路线”斗争的档次上是不科学的。     

Structure of pre-pro-von Willebrand factor and its expression in heterologous cells

Von Willebrand factor (vWF), a multifunctional haemostatic glycoprotein derived from endothelial cells and megakaryocytes, mediates platelet adhesion to injured subendothelium and binds coagulation factor VIII in the circulation. Native vWF is a disulphide-bonded homopolymer; the monomeric subunits, of apparent relative molecular mass (Mr) 220,000 (220K) are derived from an intracellular precursor estimated at 260-275K. Multimer assembly is preceded by the formation of dimers, linked near their C-termini, which then assemble into filamentous polymers. The importance of the removal of the large vWF pro-polypeptide during multimer assembly, and whether this or other stages of the complex post-translational processing require components specific to endothelial cells or megakaryocytes, is unknown. Here we report an analysis of the complete sequence of pre-pro-vWF and expression of the molecule in heterologous cells. The vWF precursor is composed of several repeated subdomains. When expressed in COS and CHO cells, it is cleaved and assembled into biologically active high relative molecular mass disulphide bonded multimers. This suggests that the information for assembly of this complex molecule resides largely within its primary structure.     

Long-range colour-generating interactions across the retina

The existence of colour-generating interactions across the corpus callosum has recently been suggested from observations with a 'split-brain' patient, thus indicating long-range colour computations at the cortical level. Observations on induced colours described here suggest long-range colour computations at the retinal level. If a white surface surrounded by a particular colour is fixated for some time, the resulting after-image has two colours: the surround appears in complementary colour, whereas the white centre takes on the colour of the surround. The question of whether such colour induction is located in the retina or more centrally was tested in a brain-injured patient with hemianopia. It could be demonstrated that areas of the visual field that are no longer represented in the geniculo-striatal pathway still contribute to colour induction, suggesting that colour induction is a retinal phenomenon.     

Implications of fragile X expression in normal males for the nature of the mutation

The fragile site at Xq27, associated with a common form of X-linked mental retardation (XLMR), is expressed in a variable proportion of the peripheral lymphocytes of affected males when the cells are cultured under thymidylate stress (Td stress) produced by folate or thymidylate deprivation. Some clinically normal males--transmitting males--are known to carry and transmit the fragile X mutation and yet show no cytogenetic expression in lymphocytes. Normal males with no family history of X-linked mental retardation express the site only rarely. When the fragile X chromosome from affected males is isolated in a rodent genetic background by somatic cell hybridization, the level of expression is similar to that seen in lymphocytes under Td stress. Here we show that X chromosomes from two transmitting males and two normal control males, all of which were fragile X negative in lymphocytes or lymphoblasts, could be made to express the fragile site in hybrids, although at levels that were below those seen in hybrids from affected males. Furthermore, transmitting males could be differentiated from normal males by their significantly higher expression rates when hybrids were exposed to caffeine before cytogenetic harvest. One male chimpanzee also showed low level expression in hybrid cells. These data suggest that the hybrid system lowers the threshold for fragile X expression, a fragile site at Xq27 may be present on all human and chimpanzee X chromosomes and constitutes a previously unrecognized common fragile site and the hybrid system with caffeine post-treatment can distinguish between the common Xq27 fragile site of control males, the occult mutant fragile site of a transmitting male, and the fully expressed fragile site of an affected male with XLMR. Thus the mutation producing XLMR may represent a multi-step alteration of a naturally occurring DNA sequence producing a continuum of cytogenetic expression and a threshold for clinical manifestation.     

HLA-D region beta-chain DNA endonuclease fragments differ between HLA-DR identical healthy and insulin-dependent diabetic individuals

The human HLA-D histocompatibility region encodes class II antigens each of which consists of two polypeptide chains (alpha and beta) inserted in the plasma membrane. These molecules are implicated in the regulation of the immune response but several human diseases are also found to be associated with certain HLA-DR antigens. The occurrence of insulin-dependent (type I) diabetes (IDDM) is strongly associated with HLA-DR3 and/or 4 (ref. 5). The class II antigens, however, show a marked genetic polymorphism associated with the beta-chains which seem, from hybridization studies, to be encoded by several genes. We have therefore used the beta-chain cDNA probe, pDR-beta-1 (refs 8, 10) to test whether there are differences in hybridization pattern between DNA from healthy individuals and diabetic patients, after digestion with restriction endonucleases. Among the HLA-DR 4 and 3/4 individuals, the IDDM patients showed an increased frequency of a PstI 18 kilobase (kb) fragment. A BamHI 3.7 kb fragment, frequent among controls (30-40%), was rarely detected in the IDDM patients (0-2%). These differences may be related to susceptibility to develop the disease.