Specific binding of antigenic peptides to cell-associated MHC class I molecules

T lymphocytes recognize antigen in the form of peptides that associate with specific alleles of class I or class II major histocompatibility (MHC) molecules. By contrast with the clear MHC allele-specific binding of peptides to purified class II molecules purified solubilized class I molecules either bind relatively poorly or show degenerate specificity. Using photo-affinity labelling, we demonstrate here the specific interaction of peptides with cell-associated MHC class I molecules and show that this involves metabolically active processes.     

有机铵表面修饰型针铁矿萃淋材料萃CrO_4~（2－）研究

利用不同取代基有机按的正电性，对控制等电点条件下合成的针铁矿电负性表面进行修饰负载。采用红外光谱，热分析与扫描电镜研究材料的一些基本物性；考查了材料在以铬酸根为代表的二价阴离子萃取体系中有机铵不同取代基和体系中酸碱性对萃取性能的影响规律及其解释，萃取过程动力学因素。该萃淋材料对ＣｒＯ单级提取率大于百分之九十，萃取速度快，半萃取率所需时间仅１分钟左右。     

Presynaptic release probability influences the locus of long-term potentiation.

The quantal hypothesis proposes that chemical synaptic transmission involves the probabilistic release of multimolecular packets of transmitter. Analysis of the resulting trial-to-trial fluctuations in postsynaptic response can provide estimates both of the number of quanta released and of the size of their postsynaptic effect. This in turn permits the quantification of the relative contributions of pre- and postsynaptic factors to the strength of a given synapse. Quantal analysis of excitatory synapses in the hippocampus has proved difficult and has led to contradictory conclusions when applied to long-term potentiation. Here we report the use of a combination of quantal analysis procedures to provide evidence that both pre- and postsynaptic changes can contribute substantially to the maintenance of long-term potentiation in the CA1 region of the hippocampus. The initial setting of the presynaptic release mechanism seems to determine their relative importance.     

Exocytotic fusion is activated by Rab3a peptides.

Studies of intracellular traffic in yeast and mammalian systems have implicated members of the Rab family of small GTP-binding proteins as regulators of membrane fusion. We have used the patch clamp technique to measure exocytotic fusion events directly and investigate the role of GTP-binding proteins in regulating exocytosis in mast cells. Intracellular perfusion of mast cells with GTP-gamma S is sufficient to trigger complete exocytotic degranulation in the absence of other intracellular messengers. Here we show that GTP is a potent inhibitor of GTP-gamma S-induced degranulation, indicating that sustained activation of a GTP-binding protein is sufficient for membrane fusion. We have found that synthetic oligopeptides, corresponding to part of the effector domain of Rab3a, stimulate complete exocytotic degranulation, similar to that induced by GTP-gamma S. The response is selective for Rab3a sequence and is strictly dependent on Mg2+ and ATP. This suggests that sustained activation of a Rab3 protein causes exocytotic fusion. The peptide response can be accelerated by GDP-beta S, suggesting that Rab3a peptides compete with endogenous Rab3 proteins for a binding site on a target effector protein, which causes fusion on activation.