Intravenously injected sialidase inactivates attachment sites for lymphocytes on high endothelial venules

Blood-borne lymphocytes initiate entry into secondary lymphoid organs, such as peripheral lymph nodes (PN) and gut-associated Peyer's patches (PP), by a highly specific adhesive interaction between the lymphocytes and the endothelium of specialized blood vessels known as a high endothelial venules (HEV). The selectivity with which functional subpopulations of lymphocytes migrate into particular lymphoid organs is believed to be regulated by the expression of cell adhesion receptors and complementary ligands on lymphocytes and HEV, respectively. The entry of lymphocytes into PN and PP has clearly been shown to involve distinct receptor-ligand pairs. Employing the Stamper-Woodruff in vitro adhesion assay, which measures lymphocyte attachment to HEV in cryostat-cut sections of lymphoid organs, we have previously shown that treatment of PN sections with two different sialidases inactivates HEV-adhesive ligands, whereas treatment of PP tissue sections has no effect on HEV-adhesive function. We now report that in vivo exposure of HEV to sialidase (after i.v. injection of the enzyme) also selectively prevents subsequent in vitro attachment of lymphocytes to PN HEV but not to PP HEV. Consistent with this organ-selective impairment of HEV-adhesive function by sialidase, i.v. injection of the enzyme is shown to prevent short term lymphocyte accumulation within peripheral lymph nodes while having no significant effect on accumulation in PP, blood, or nonlymphoid organs. Histologic examination with the sialic acid-specific lectin from Limax flavus verified that i.v. injected sialidase effectively removes stainable sialic acid moieties from HEV in both PN and PP. This study confirms that sialic acid is required for the adhesive function of PN HEV-ligands. A role for sialic acid as either a recognition determinant or as a regulatory molecule can be envisioned. In view of the fact that many pathogens release sialidase and cause substantially elevated serum levels of this enzyme, the present observations may have pathophysiologic significance. One mechanism by which such pathogens may avoid destruction is to inactivate susceptible HEV-ligands and disrupt the entry of lymphocytes into lymphoid organs where immune responses against the pathogens would normally be initiated.     

黄土高原地区提取植被信息方法的研究

研究评价了适于黄土高原地区植被信息提取的最佳植被指数和方法。该地区分布有落叶阔叶林、草原和荒漠,植被类型丰富多样。然而土壤背景对植被信息提取有较大影响。经对比分析,修正后的土壤调节植被指数（ＭＳＡＶＩ）, 不仅能增强植被信号,并能大大减小土壤背景的影响,同时又能宏观地反映该地区植被类型的分布状况。它是黄土高原地区目前提取植被信息较好的植被指数。标准化差值植被指数（ＮＤＶＩ）、土壤调节植被指数（ＳＡＶＩ）和垂直植被指数（ＰＶＩ）分别适用于高密度、中等密度和稀少植被地区植被信息的提取和监测。各种植被指数多时象累加产生的图像能较好地提取植被信息     

Substance P and neurokinin A metabolism by cultured human skeletal muscle myocytes and fibroblasts

A recent study determined that cultured human skeletal muscle adult myoblasts, myotubes, and fibroblasts degraded angiotensins and kinins via neutral endopeptidase-24.11 (NEP-24.11; EC 3.4.24.11) and aminopeptidase N (APN; EC 3.4.11.2). Due to the possible importance of other peptides to skeletal muscle blood flow and function, the present study looked specifically at the metabolism of the neurokinins substance P (SP) and neurokinin A (NKA) by skeletal muscle peptidases. The results show that SP is degraded not only by NEP-24.11, but also sequentially by dipeptidyl(amino)peptidase IV (DAP IV; EC 3.4.14.5)/APN. NKA is unaffected by DAP IV but is metabolized by NEP-24.11 and APN. NEP-24.11 was inhibited by phosphoramidon (IC₅₀ = 80 nM), thiorphan and ZINCOV, DAP IV by diprotin A (IC₅₀ = 8 μM), and APN by amastatin (IC₅₀ = 50 nM) and bestatin (IC₅₀ = 100 μM). Skeletal muscle myocyte and fibroblast metabolism of SP and NKA may regulate local skeletal muscle vascular and extravascular functions including SP- and NKA-mediated nerve-induced vasodilation. Inhibition of both NEP-24.11 and DAP IV/APN may increase skeletal muscle blood flow and decrease peripheral vascular resistance via potentiation of local neurokinin levels.     

Excess amino acid polymorphism in mitochondrial DNA: contrasts among genes from Drosophila, mice, and humans

Recent studies of mitochondrial DNA (mtDNA) variation in mammals and Drosophila have shown an excess of amino acid variation within species (replacement polymorphism) relative to the number of silent and replacement differences fixed between species. To examine further this pattern of nonneutral mtDNA evolution, we present sequence data for the ND3 and ND5 genes from 59 lines of Drosophila melanogaster and 29 lines of D. simulans. Of interest are the frequency spectra of silent and replacement polymorphisms, and potential variation among genes and taxa in the departures from neutral expectations. The Drosophila ND3 and ND5 data show no significant excess of replacement polymorphism using the McDonald-Kreitman test. These data are in contrast to significant departures from neutrality for the ND3 gene in mammals and other genes in Drosophila mtDNA (cytochrome b and ATPase 6). Pooled across genes, however, both Drosophila and human mtDNA show very significant excesses of amino acid polymorphism. Silent polymorphisms at ND5 show a significantly higher variance in frequency than replacement polymorphisms, and the latter show a significant skew toward low frequencies (Tajima's D = -1.954). These patterns are interpreted in light of the nearly neutral theory where mildly deleterious amino acid haplotypes are observed as ephemeral variants within species but do not contribute to divergence. The patterns of polymorphism and divergence at charge-altering amino acid sites are presented for the Drosophila ND5 gene to examine the evolution of functionally distinct mutations. Excess charge-altering polymorphism is observed at the carboxyl terminal and excess charge-altering divergence is detected at the amino terminal. While the mildly deleterious model fits as a net effect in the evolution of nonrecombining mitochondrial genomes, these data suggest that opposing evolutionary pressures may act on different regions of mitochondrial genes and genomes.      

Investigation of the role of the disulphide bond in the activity and structure of staphylococcal enterotoxin C1

The goal of this study was to Investigate the role of the disulphide bond of staphylococcal enterotoxin C1 (SEC1) in the structure and activity of the toxin. Mutants unable to form a disulphide bond were generated by substituting alanine or serine for cysteine at positions 93 and/or 110. Although we did not directly investigate the residues between the disulphide linkage, tryptic lability showed that significant native structure in the cystine loop is preserved in the absence of covalent bonding between residues 93 and 110. Since no correlation was observed between the behaviour of these mutants with regard to toxin stability, emesis and T cell proliferation, we conclude that SEC1 -induced emesis and T cell proliferation are dependent on separate regions of the molecule. The disulphide bond itself is not an absolute requirement for either activity. However, conformation within or adjacent to the loop is important for emesis. Although mutants with alanine substitutions were not emetic, those with serine substitutions retained this activity, suggesting that the disulphide linkage stabilizes a crucial conformation but can be replaced by residues which hydrogen bond.     

生淀粉高浓度酒精发酵的研究

本研究利用国内常用的糖化酶制剂糖化生玉米面中的淀粉,同时接种酵母菌,在30℃下,探讨了玉米淀粉的高浓度酒精发酵工艺。选择到了一株产高浓度酒精酵母菌,H0菌株。发酵温度为30℃、pH4一s、加糖化酶量为每克原料300单位、酵母接种量3％(v／v)和原料加量为33．0％(w／v)时,这株酵母菌在70小时内可产生17．5％(v／v)的乙醇。如果原料加量为36．0％(w／v)时,该菌株在96小时内可以产生18．O％(v／v)的乙醇。在前一种加料情况下,成熟发酵醪中的pH为5、残还原糖为O．19％、残总糖为3．5“。在后一种加料情况下,成熟发酵醪中的pH为5、残还原糖为0．81％、残总糖为5．1％。     

大鼠尾核痛反应神经元放电和甩尾反射关系的研究

用浅麻醉的Ｗｉｓｔａｒ大鼠４０只,以辐射热照尾作为伤害性刺激,经玻璃微电极引导尾核痛兴奋神经元（ＰＥＮ）和痛抑制神经元（ＰＩＮ）的放电,同时测量甩尾反射潜伏期（ＴＦＬ）作为甩尾痛阈的指标。结果表明：（１）自然状态下辐射热照尾引起尾核中ＰＥＮ放电频率增加和ＰＩＮ放电频率减少与甩尾反射（ＴＦ）相伴行。放电变化发生在ＴＦ之前,结束在ＴＦ之后,ＰＥＮ和ＰＩＮ放电变化与ＴＦＬ呈高度正相关。（２）辐射热照尾同时引起一侧尾核ＰＥＮ放电频率增加和另一侧ＰＩＮ放电频率减少,二者协同活动,并发生在ＴＦ之前,结束在ＴＦ之后。（３）侧脑室注射５５μｇ／１０μｌ吗啡呈镇痛作用时,尾核ＰＥＮ放电频率减少和ＰＩＮ放电频率增加,放电变化仍发生在ＴＦ之前,结束在ＴＦ之后。结果提示,尾核中ＰＥＮ、ＰＩＮ放电和ＴＦ是中枢不同水平同时对痛觉调制所产生的结果。     

Identification and characterization of glucocorticoid receptors in liver of nude mice

Glucocorticoids regulate the expression of many liver-specific genes via glucocorticoid receptors. The presence of glucocorticoid receptors in liver has been reported in many mammalian species but not in nude mice. In the present study, we demonstrate the presence of specific glucocorticoid receptors in nude mouse liver. The binding of ligands to these receptors could be completely inhibited by RU486, and partially blocked by hydrocortisone and progesterone, whereas estrogen and testosterone had no effect. Hydrocortisone down-regulated the level of glucocorticoid receptors in livers of nude mice and correspondingly enhanced the activities of tyrosine aminotransferase and -glutamyltransferase. Our results indicate that glucocorticoid receptors in nude mouse liver are specific, fully functional, and present at levels 28.5-fold higher than in the liver of normal inbred mice. We suggest that the nude mouse is a valuable model for studies of hepatic glucocorticoid action and may provide a clue to a putative hepatic-thymic interaction.