Der mit der Versuchsdauer anwachsende Resistenzfaktor

Abstract

Pseudomonas spp. strains capable of inducing systemic resistance were applied to sugarcane by sett treatment followed by soil applications in the field. Later the fungal pathogen Colletotrichum falcatum causing red rot disease of sugarcane was inoculated in the treated canes and its colonization was assessed by ELISA at different nodal positions above the point of inoculation. Studies with three cvs showed a significant variation in pathogen colonization only in disease susceptible cv CoC 671 and not with cvs Co 8021 and BO 91, moderately susceptible and moderately resistant to the disease, respectively. In further studies when pathogen colonization was assessed on the entire stalks of cv CoC 671, the pathogen titre was significantly reduced from three nodes upwards in the treated canes. In the upper nodes no pathogen colonization was noticed in bacteria-treated canes, whereas in the control all the nodes recorded higher titre for pathogen infection. Incorporation of chitin in the talc formulation caused further reduction in fungal colonization in the stalks.     

Interactions of three eco-types of Acidithiobacillus ferrooxidans with U(VI)

The interaction of uranium with cells of three recently described eco-types of Acidithiobacillus ferrooxidans recovered from uranium mining wastes was studied. The uranium sorption studies demonstrated that the strains from these types possess different capabilities to accumulate and tolerate uranium. The amount of uranium biosorbed by all A. ferrooxidans strains increased with considerable concentrations. We have found that the representatives of type II accumulate significantly higher amounts of uranium in comparison to the other A. ferrooxidans strains. The investigations of the tolerance to uranium showed that the types I and III are resistant to 8 and 9 mM of uranium respectively, whereas the type II does not tolerate more than 2 mM of uranium. The recovery of the accumulated uranium by desorption was investigated using various desorbing agents as sodium carbonate, sodium citrate and EDTA at different concentrations. Sodium carbonate was the most efficient desorbing agent, removing 97% of the uranium sorbed from the cells of A. ferrooxidans type III, and 88.33 and 88.50% from the cells of the types I and II, respectively.     

Effects of leaf shape plasticity on leaf surface temperature

干旱区植物叶片形态可塑性是植物适应高温干旱环境的重要生存策略, 但目前仍缺乏直观的数据予以证明。该研究应用热成像技术和图像分析技术, 同步测定真实叶片与模拟叶片的叶温、形态及风速、辐射和温度等环境参数。研究结果显示: 在干旱、高温环境下, 除了蒸腾, 叶片形态变化也是调控叶温的重要因子。干旱区植物叶片变小, 有利于加速叶片与环境的物质及热量交换, 从而达到降低叶温的目的。样地数据显示, 在高温、低风速环境下, 叶片宽度每减少1 cm, 叶片表面温度降低约2.1 ℃, 而模拟叶片叶宽度每减少1 cm, 叶片表面温度降低0.60-0.86 ℃。该研究对深入理解植物生存策略与环境适能力具有重要意义。     

Induction of vancomycin resistance in Enterococcus faecium by non-glycopeptide antibiotics

Abstract Bacitracin and other antibiotics that inhibit late stages in peptidoglycan biosynthesis induce vancomycin resistance in a high-level, inducibly vancomycin-resistant strain of Enterococcus faecium . Exposure to bacitracin led to synthesis of the lactate-containing UDP-MurNAc-pentadepsipeptide precursor required for vancomycin resistance. These findings indicate that inhibition of peptidoglycan biosynthesis can lead to induction of vancomycin resistance and raise the possibility that multiple signals may serve to induce resistance.     

Antibodies in the study of multiple drug resistance

Multidrug resistance (MDR) is a major problem in cancer chemotherapy. As P-glycoprotein is the key molecule in MDR, many investigators have constructed anti-P-glycoprotein monoclonal antibodies (MAbs). Those antibodies, including MRK16 and C219, were used for elucidation of the mechanism of MDR and for overcoming of MDR. This article describes the characterization of the antibodies against the P-glycoprotein and other proteins of multidrug-resistant tumor cells, and discusses the therapeutic implication of the antibodies.Abbreviation ADCC antibody-dependent cell-mediated cytotoxicity     

Psoralen reverses docetaxel-induced multidrug resistance in A549/D16 human lung cancer cells lines

Chemotherapy is the recommended treatment for advanced-stage cancers. However, the emergence of multidrug resistance (MDR), the ability of cancer cells to become simultaneously resistant to different drugs, limits the efficacy of chemotherapy. Previous studies have shown that herbal medicine or natural food may be feasible for various cancers as potent chemopreventive drug. This study aims to explore the capablility of reversing the multidrug resistance of docetaxel (DOC)-resistant A549 cells (A549/D16) of psoralen and the underlying mechanisms. In this study, results showed that the cell viability of A549/D16 subline is decreased when treated with psoralen plus DOC, while psoralen has no effect on the cell proliferation on A549 and A549/D16 cells. Furthermore, mRNA and proteins levels of ABCB1 were decreased in the presence of psoralen, while decreased ABCB1 activity was also revealed by flow cytometry. Based on these results, we believe that psoralen may be feasible for reversing the multidrug resistance by inhibiting ABCB1 gene and protein expression. Such inhibition will lead to a decrease in ABCB1 activity and anti-cancer drug efflux, which eventually result in drug resistance reversal and therefore, sensitizing drug-resistant cells to death in combination with chemotherapeutic drugs.     

Cloning and sequencing of a plasmid-mediated erythromycin resistance determinant from Staphylococcus xylosus

A 2.3-kb DNA fragment cloned from plasmid pCH200, the largest (52 kb) of four plasmids detected in Staphylococcus xylosus, was found to confer resistance to 14-membered ring macrolides in Bacillus subtilis and Staphylococcus aureus. DNA-sequence analysis of the fragment revealed the presence of an open-reading frame, the deduced product of which was identical to one of the two ATP-binding domains encoded by the macrolide/streptogramin-B-resistance gene msrA of Staphylococcus epidermidis. The observation that a polypeptide homologous to the C-terminus of MsrA is capable of mediating erythromycin resistance in the absence of the N-terminal region is of significance both to the evolution and functional activity of members of the ATP-binding transport super-gene family.     

Cellular resistance to the antimelanoma immunotoxin ZME-gelonin and strategies to target resistant cells

 The development of cellular resistance to immunotoxins has been demonstrated in a variety of models and can involve a number of mechanisms. For the present study, an immunotoxin was utilized composed of an antimelanoma antibody ZME-018 recognizing a 240-kDa surface glycoprotein (gp 240) and the plant toxin gelonin. Human melanoma cells (A375-M) were grown in the presence of increasing amounts of ZME-gelonin and a clonal variant (A-375-ZR) was developed that was 100-fold resistant to ZME-gelonin compared to parental cells. Scatchard analysis showed that the A375-M parental cells had 260×10³ ZME-gelonin-binding sites/cell with relatively low affinity (5 nM). In contrast, resistant A375-ZR cells demonstrated a reduced number of low-affinity sites (160×10³/cell), but showed a small number (47×10³) of higher-affinity sites (0.8 nM). Internalization rates and degradation rates of ¹²⁵I-labeled ZME-gelonin were identical in both the parental and resistant cells. A375-ZR cells were found to be more resistant to vincristine and doxorubicin than were parental cells. Both cell lines were almost equally sensitive to native gelonin, 5-fluorouracil (5-FU), cisplatin, melphalan, carmustine, interferon γ (IFNγ) and IFNα. In addition, both cell lines were equally sensitive to another gelonin-antibody conjugate that binds to cell-surface, GD₂ (antibody 14G₂A). However, resistant cells were twice as sensitive to the cytotoxic effects of etoposide than were parental cells. Finally, a variety of agents were tested in combination with ZME-gelonin against A375-ZR cells in an attempt to identify agents to augment immunotoxin cytotoxic effects against resistant cells. The agents 5-FU, cisplatin, IFNγ, IFNα, and etoposide were the most effective in augmenting the cytotoxicity of ZME-gelonin against resistant cells. These studies suggest that development of resistance to one immunotoxin does not cause development of cross-resistance to other gelonin immunotoxins. Further, specific biological response modifiers and chemotherapeutic agents may be effective in augmenting the effectiveness of immunotoxins and specifically targeting or reducing the emergence of immunotoxin-resistant cells. Received: 15 March 1995 / Accepted: 28 November 1995