Characterization of a Galactosynthase Derived from Bacillus circulans β‐Galactosidase: Facile Synthesis of D‐Lacto‐ and D‐Galacto‐N‐bioside

Glycosynthases—retaining glycosidases mutated at their catalytic nucleophile—catalyze the formation of glycosidic bonds from glycosyl fluorides as donor sugars and various glycosides as acceptor sugars. Here the first glycosynthase derived from a family 35 β‐galactosidase is described. The Glu→Gly mutant of BgaC from Bacillus circulans (BgaC‐E233G) catalyzed regioselective galactosylation at the 3‐position of the sugar acceptors with α‐galactosyl fluoride as the donor. Transfer to 4‐nitophenyl α‐D ‐N‐acetyl‐glucosaminide and α‐D ‐N‐acetylgalactosaminide yielded 4‐nitophenyl α‐lacto‐N‐biose and α‐galacto‐N‐biose, respectively, in high yields (up to 98 %). Kinetic analysis revealed that the high affinity of the acceptors contributed mostly to the BgaC‐E233G‐catalyzed transglycosylation. BgaC‐E233G showed no activity with β‐(1,3)‐linked disaccharides as acceptors, thus suggesting that this enzyme can be used in “one‐pot synthesis” of LNB‐ or GNB‐containing glycans.     

变形量对TC18钛合金力学性能的影响

采用一种专门用于钛合金锻造工艺参数定量研究的专利技术研究了β区变形量(从10%到65%)对TC18钛合金关键力学性能、显微组织的影响。研究结果表明:β区变形时,变形量对合金抗拉强度影响不大,σb在1150MPa左右;但对合金伸长率、断面收缩率和断裂韧度均有显著影响。变形量每增加10%,伸长率可提高0.7%左右;断面收缩率提高4%左右;断裂韧度下降3MPa·m1/2左右。为获得TC18钛合金强度-塑性-韧性的最佳匹配,应将β区变形量控制在35%左右。     

High‐cycle fatigue properties of beta Ti alloy 55Ti–30Nb–10Ta–5Zr,gum metal

This paper describes the fatigue properties of the beta titanium alloy 55Ti–30Nb–10Ta–5Zr, generally referred to as ‘Gum Metal’. Rotating bending fatigue tests have been performed in laboratory air and in a 3% NaCl aqueous solution. The results obtained were compared with those of a conventional beta titanium alloy, Ti–22V–4Al. In tensile tests, 55Ti–30Nb–10Ta–5Zr indicated elasticity and microplasticity in the elastic region. Thus, the elastic modulus slightly decreased with an increasing strain, and the work hardening was minimal during plastic deformation. The mechanical properties of both of the alloys were comparable. The fatigue strength of 55Ti–30Nb–10Ta–5Zr in laboratory air was higher than that of Ti–22V–4Al, which could be attributed to the higher fatigue crack initiation resistance of 55Ti–30Nb–10Ta–5Zr than Ti–22V–4Al, while the resistance to small fatigue crack growth was similar. The fatigue strength of 55Ti–30Nb–10Ta–5Zr in laboratory air and in the 3% NaCl aqueous solution was analogous. In addition, corrosion pits were not observed in the run‐out specimen in the 3% NaCl aqueous solution, indicating a high resistance of 55Ti–30Nb–10Ta–5Zr against corrosion fatigue.     

Liquid Crystal Enabled Early Stage Detection of Beta Amyloid Formation on Lipid Monolayers

Liquid crystals (LCs) can serve as sensitive reporters of interfacial events, and this property has been used for sensing of synthetic or biological toxins. Here it is demonstrated that LCs can distinguish distinct molecular motifs and exhibit a specific response to beta‐sheet structures. That property is used to detect the formation of highly toxic protofibrils involved in neurodegenerative diseases, where it is crucial to develop methods that probe the early‐stage aggregation of amyloidogenic peptides in the vicinity of biological membranes. In the proposed method, the amyloid fibrils formed at the lipid–decorated LC interface can change the orientation of LCs and form elongated and branched structures that are amplified by the mesogenic medium; however, nonamyloidogenic peptides form ellipsoidal domains of tilted LCs. Moreover, a theoretical and computational analysis is used to reveal the underlying structure of the LC, thereby providing a detailed molecular‐level view of the interactions and mechanisms responsible for such motifs. The corresponding signatures can be detected at nanomolar concentrations of peptide by polarized light microscopy and much earlier than the ones that can be identified by fluorescence‐based techniques. As such, it offers the potential for early diagnoses of neurodegenerative diseases and for facile testing of inhibitors of amyloid formation.     

A Single Episode of Cortical Spreading Depolarization Increases mRNA Levels of Proinflammatory Cytokines,Calcitonin Gene-Related Peptide and Pannexin-1 Channels in the Cerebral Cortex

Cortical spreading depolarization (CSD) is the neuronal correlate of migraine aura and the reliable consequence of acute brain injury. The role of CSD in triggering headaches that follow migraine aura and brain injury remains to be uncertain. We examined whether a single CSD occurring in awake animals modified the expression of proinflammatory cytokines (Il1b, TNF, and Il6) and endogenous mediators of nociception/neuroinflammation-pannexin 1 (Panx1) channel and calcitonin gene-related peptide (CGRP), transforming growth factor beta (TGFb) in the cortex. Unilateral microinjury of the somatosensory cortex triggering a single CSD was produced in awake Wistar rats. Three hours later, tissue samples from the lesioned cortex, intact ipsilesional cortex invaded by CSD, and homologous areas of the contralateral sham-treated cortex were harvested and analyzed using qPCR. Three hours post-injury, intact CSD-exposed cortexes increased TNF, Il1b, Panx1, and CGRP mRNA levels. The strongest upregulation of proinflammatory cytokines was observed at the injury site, while CGRP and Panx1 were upregulated more strongly in the intact cortexes invaded by CSD. A single CSD is sufficient to produce low-grade parenchymal neuroinflammation with simultaneous overexpression of Panx1 and CGRP. The CSD-induced molecular changes may contribute to pathogenic mechanisms of migraine pain and post-injury headache.     

串道现象对测量结果的影响

为更加准确地评价低水平放射性样品的测量结果,利用低本底α/β测量仪研究了串道现象对测量结果的影响及其影响程度。利用239Pu和90Sr-90 Y电镀源测定了α通道与β通道之间的串道因子,结果表明:α通道对β通道的串道现象明显,在样品测量时应考虑扣除串道带来的计数;β通道对α通道的串道影响很小,但在β净计数率足够高时,仍会对α的测量结果带来明显影响。样品测量过程中,考虑到不同α核素导致的串道因子之间的差异,为避免单一核素刻度串道因子引入新的误差,使用合适的遮挡物完全屏蔽样品中的α射线,可确保测量结果更加准确。