He-Ne激光预处理对镉胁迫下小麦幼苗生理特性的影响

用He-Ne激光（波长632.8 nm,辐射剂量5.43 mW/mm²）对萌动小麦种子辐照5 min,待幼苗长至一叶一心时,用150 μmol/L CdCl₂溶液进行胁迫处理,研究He-Ne激光预处理对镉（Cd²⁺）胁迫下小麦幼苗生长发育和生理特性的影响。结果显示:He-Ne激光预处理能显著降低Cd²⁺胁迫下小麦幼苗中丙二醛（MDA）、过氧化氢（H₂O₂）含量及超氧自由基（O^-·₂）产生速率,显著提高幼苗叶片超氧化物歧化酶(SOD)、过氧化物酶(POD)、过氧化氢酶(CAT)、抗坏血酸氧化酶（APX）活性,并使叶片抗氧化物质谷胱甘肽(GSH)和抗坏血酸(AsA)含量以及幼苗株高、根长和干重增加。研究表明,He-Ne激光预处理可有效缓解镉胁迫对小麦幼苗生长的抑制作用,并通过促进其幼苗中酶类和非酶类抗氧化剂的产生,有效减少镉胁迫产生的脂质过氧化物含量,从而提高其耐镉性。     

采收期对青皮核桃果实生理特性与耐贮性的影响

以‘中林5号’(早熟)、‘辽宁4号’(中熟)、‘西扶1号’(中晚熟)青皮核桃果实为试材,于8月上、中、下旬3个采收期采果,在0~1℃冷藏过程中测定贮期生理指标和保鲜效应。结果显示:(1)各采收期和各品种果实呼吸强度(RI)均呈双峰型变化;8月中旬采收的果实呼吸峰出现较早,其纤维素酶(Cx)活性较另2个采收期多1个高峰;多聚半乳糖醛酸酶(PG)活性增强最早,其贮后核仁酸价上升幅度最大,果实腐烂最快。(2)8月下旬同期采收的3个品种果实的贮期各生理指标变化趋于一致;贮藏54d时,果实腐烂率依次为‘辽宁4号’>‘中林5号’>‘西扶1号’。(3)‘辽宁4号’核仁可溶性蛋白质含量越高,贮后下降率最大。研究表明,青皮核桃果实采后生理代谢活性与耐贮性主要与采收时期有关,受品种影响较小,且8月中旬采收的果实采后生理代谢旺盛,耐贮藏性均最差;‘辽宁4号’果实在各采收期的耐贮性均小于其他品种果实。     

Response of Pyropia haitanensis to agaro-oligosaccharides evidenced mainly by the activation of the eicosanoid pathway

The marine red alga Pyropia haitanensis (Protoflorideophyceae, Bangiaceae) has a nonvascular and multicellular structure and emerged earlier in evolution than other cultivatable red algae. It has been reported that lipid mediators from both the eicosanoid and octadecanoid pathways are involved in the innate immunity of other marine algae. But the defense strategies of P. haitanensis are not clearly understood. Here, we investigated the lipid defense of P. haitanensis elicited by agaro-oligosaccharides. The results indicate that the resistance of P. haitanensis was elicited and hydrogen peroxide was released by agaro-oligosaccharides. In P. haitanensis, C20 fatty acids are the essential fatty acids. Phospholipase A₂ was activated, and the free fatty acids decreased 3 h after treatment with agaro-oligosaccharides. Gas chromatography–mass spectrometry analyses revealed that the contents of volatile organic compounds increased after treatment for 3 h, which indicated that these free fatty acids were metabolized to volatile organic compounds. In conclusion, the lipid metabolic defense pathway of P. haitanensis was mainly via the C20 metabolism pathway. The C20 fatty acid was rapidly metabolized to volatile organic compounds, but not oxidized to oxylipins in response to agaro-oligosaccharides.     

High Expression of Lewis y Antigen and CD44 Is Correlated with Resistance to Chemotherapy in Epithelial Ovarian Cancers

Objectives

To measure Lewis y antigen and CD44 antigen expression in epithelial ovarian carcinoma and to correlate the levels of these antigens with clinical response to chemotherapy.

Methods

The study cases included 34 cases of ovarian carcinoma with resistance to chemotherapeutic drugs, 6 partially drug-sensitive cases, and 52 drug-sensitive cases (92 total).

Results

The rates of expression of Lewis y antigen and CD44 antigen were significantly greater in the drug-resistant group than that in the partially-sensitive or sensitive groups. Surgical stage, residual tumor size and expression of CD44 and Lewis y antigen in ovarian carcinoma tissues were independent risk factors for chemotherapeutic drug resistance.

Conclusions

Over-expression of Lewis y and CD44 antigen are strong risk factors for chemotherapeutic drug resistance in ovarian carcinoma patients.     

A Simple and Computationally Efficient Approach to Multifactor Dimensionality Reduction Analysis of Gene-Gene Interactions for Quantitative Traits

We present an extension of the two-class multifactor dimensionality reduction (MDR) algorithm that enables detection and characterization of epistatic SNP-SNP interactions in the context of a quantitative trait. The proposed Quantitative MDR (QMDR) method handles continuous data by modifying MDR’s constructive induction algorithm to use a T-test. QMDR replaces the balanced accuracy metric with a T-test statistic as the score to determine the best interaction model. We used a simulation to identify the empirical distribution of QMDR’s testing score. We then applied QMDR to genetic data from the ongoing prospective Prevention of Renal and Vascular End-Stage Disease (PREVEND) study.     

Stress-Derived Corticotropin Releasing Factor Breaches Epithelial Endotoxin Tolerance

Background and aims

Loss of the endotoxin tolerance of intestinal epithelium contributes to a number of intestinal diseases. The etiology is not clear. Psychological stress is proposed to compromise the intestinal barrier function. The present study aims to elucidate the role of the stress-derived corticotropin releasing factor (CRF) in breaching the established intestinal epithelial endotoxin tolerance.

Methods

Epithelial cells of HT-29, T84 and MDCK were exposed to lipopolysaccharide to induce the endotoxin tolerance; the cells were then stimulated with CRF. The epithelial barrier function was determined using as indicators of the endotoxin tolerant status. A water-avoid stress mouse model was employed to test the role of CRF in breaching the established endotoxin tolerance in the intestine.

Results

The established endotoxin tolerance in the epithelial cell monolayers was broken down by a sequent exposure to CRF and LPS manifesting a marked drop of the transepithelial resistance (TER) and an increase in the permeability to a macromolecular tracer, horseradish peroxidase (HRP). The exposure to CRF also increased the expression of Cldn2 in the epithelial cells, which could be mimicked by over expression of TLR4 in epithelial cells. Over expression of Cldn2 resulted in low TER in epithelial monolayers and high permeability to HRP. After treating mice with the 10-day chronic stress, the intestinal epithelial barrier function was markedly compromised, which could be prevented by blocking either CRF, or TLR4, or Cldn2.

Conclusions

Psychological stress-derived CRF can breach the established endotoxin tolerance in the intestinal mucosa.