Detection of an Actinobacillus pleuropneumoniae serotype 2 lipopolysaccharide (LPS) variant

Until now 12 serotypes of Actinobacillus pleuropneumoniae have been recognized. The specificity of the serotypes reside in the carbohydrate composition of the capsular polysaccharides and lipopolysaccharides (LPS). The LPS of A. pleuropneumoniae serotype 2 is a smooth type LPS with O-chains of linear repeating pentasaccharide units with an O-acetyl group linked to a glucose unit. A monoclonal antibody (MAb 102-G02) directed against A. pleuropneumoniae serotype 2 was characterized in enzyme linked immunosorbent assay (ELISA) and in sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). The MAb 102-G02 was directed against an epitope on the O-chain of the LPS and was used to define a new. LPS variant of A. pleuropneumoniae serotype 2 (referred to as A. pleuropneumoniae serotype 2X). Investigation of the reactivity of the MAb 102-G02 against an A. pleuropneumoniae serotype 2X, field isolate (9008) and the Danish App-2 strain 4226 in electron microscopy, confirmed the different binding patterns.     

Chronic expression of P-selectin on endothelial cells stimulated by the T-cell cytokine, interleukin-3

P-selectin expressed on the surface of endothelium mediates leukocyte adhesion in vitro and rolling in vivo. Several inducers of cell-surface P-selectin expression on endothelial cells (EC) have previously been identified, all of which yield transient cell-surface expression of P-selectin lasting minutes to a few hours. We now show that a T-lymphocyte product, interleukin-3 (IL-3), stimulates the long-term endothelial cells (HUVEC). IL-3 induced cell-surface P-selectin expression in two phases. An initial peak at 10 minutes was followed by a prolonged upregulation beginning 16 hours after IL-3 addition and lasting at least 4 days. The level of P-selectin expression induced by IL-3 added for 48 hours was similar to that induced by treatment of HUVEC for 10 minutes with thrombin, and the effect of adding IL-3 for 48 hours followed by thrombin for 10 minutes was additive. Induction of cell-surface P-selectin expression by IL-3 was blocked by pretreatment of EC with a blocking monoclonal antibody against the IL-3 receptor alpha-chain. Lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF alpha) and a mutant form of IL-3 with decreased potency did not induce cell-surface P-selectin expression after 48 hours' incubation with HUVEC, suggesting that the effect was specific to IL-3. The increase in cell-surface P-selectin expression occurring after 16 hours of incubation with IL-3 was accompanied by a similar prolonged increase in the steady-state mRNA level that was not observed at 10 minutes after IL-3 addition. As T-lymphocyte infiltration is a hallmark of chronic inflammation, our observations suggest that the secretion of IL-3 by T lymphocytes may serve to maintain the inflammatory state during chronic inflammation.     

高温焙烧高钛渣工艺的试验研究

以云南地区钛铁矿富集得到的高钛渣为原料,置于加热装置内焙烧,在1000℃下加热处理20min,利用XRD、SEM研究了高温焙烧对高钛渣相组成和微观结构的影响.结果表明:在高温条件下高钛渣中的锐铁型TiO2转化为金红石型TiO2.提出了一种高温焙烧高钛渣的新工艺,从生产源头消除了对环境的污染,实现钛资源的可持续发展.     

组合锥形液体贮罐的简化设计方法

组合圆锥-圆柱形壳形式的钢贮罐是一种常见的用于储存液体的压力罐。大部分此类压力罐的破坏都由于钢壳的失稳而引起。引起这些破坏的主要原因是没有适当的设计方法来对这类结构进行设计。在本次研究中,提出了简化的设计方法,以保证静水加载的组合钢罐在发生屈曲时的安全。应用非线性有限元模型进行数值模拟,对大变形和几何缺陷对钢罐稳定性的破坏作用进行分析。采用有限元计算结果与非线性回归分析建立函数,将壳的总应力与膜应力关联起来。采用算例说明了所提议设计方法的应用。     

Preventing expulsive hemorrhage using an anterior chamber maintainer to eliminate hypotony

We describe a method in which constant infusion inflow through an anterior chamber maintainer (ACM) is used to maintain positive intraocular pressure (IOP) during cataract extraction through a self-sealing tunnel incision. A retrospective review of patient records showed that the difference in the incidence of intraoperative suprachoroidal hemorrhage was significantly greater in eyes in which IOP was not constant throughout surgery than in eyes in which IOP was maintained using the ACM system.     

Oral malodor in beagles: association with indicators of periodontal disease

The study of oral malodor continues to receive attention. Most bad breath is of oral origin and can be corrected with proper oral hygiene. Studies performed with saliva from people with periodontal disease and from healthy individuals showed that saliva from diseased patients produced a more objectionable odor faster than that of healthy people, and that the volatile sulfur components (VSC) produced may actually play a role in the etiology of periodontal disease. However, not all people or animals with bad breath have periodontal disease. The objectives of this study were to determine if a trained panel could discriminate between 10 dogs with clinically defined periodontal disease and those with relatively healthy periodontium. Second, this study attempted to establish a correlation between odor intensity and six clinical parameters of oral health. The judges were able to differentiate between the two groups of dogs based only on oral malodor (p < 0.02). There were strong associations of the intensity of oral malodor with oral health index scores. The correlations established between odor and gingivitis (r = 0.81) and between odor and furcation exposure (r = 0.88) were very high and statistically significant. Similarly, probing depth (r = 0.73), plaque (r = 0.07) and tooth mobility (r = 0.66) showed clear, positive relationships with oral malodor.     

C1q augments platelet activation in response to aggregated Ig

Immune complexes and aggregated IgG (agg-IgG) induce platelet aggregation and the release reaction. Immune complexes also activate the complement system and interact with the complement component C1q. Since platelets possess both Fc and C1q receptors capable of signal transduction, the present study focused on the interaction between these binding sites and platelet activation. Subaggregating doses of agg-IgG (20-400 microg/ml) were identified for washed platelets from each of 11 healthy donors, and platelet aggregation was monitored in the presence or the absence of increasing concentrations of C1q (5-100 microg/ml). C1q produced a dose-dependent potentiation of platelet alphaIIb/beta3 integrin activation, platelet aggregation, and granule secretion when combined with low doses of agg-IgG. C1q alone was without effect. Maximal enhancement of agg-IgG-induced platelet activation was noted at C1q concentrations ranging from 50 to 100 microg/ml. The observed C1q-induced potentiation of platelet aggregation in response to agg-IgG was blocked by polyclonal antibody F(ab')2 directed against platelet binding sites recognizing the collagen-like domain of C1q (cC1qR) or by mAb Fab (IV.3) directed against platelet FcgammaRII receptors. These data suggest a cooperative interaction between platelet FcgammaRII and cC1q receptors and support a potential role for platelet cC1q receptors in pathologic platelet activation by circulating immune complexes often associated with in vivo thrombosis and thrombocytopenia.