代写论文：三氯乙酸化合物
在该测试中，分离物从六名患者获得，这些患者确定来自患有用5-氟胞嘧啶（5-FC）治疗未成功治疗的患者的新生隐球菌。发现治疗后，这些分离物显示出大量且稳定的5-FC抗性。提取的六种分离物中的五种表明对5-氟尿嘧啶（5-FU）的巨大抗性。认为该化合物是基于尿苷-5′-单磷酸焦磷酸化酶引起耐药性的突变。对5-氟胞嘧啶敏感的第6个分离物表明化合物CyH3或5-FC1的吸收或掺入没有减少。该化合物的抗性机制尚未完全理解。但根据研究数据，存在几种可能性。这些类似于之前研究报道的upstype 2突变体。后者分离了5-FC和5-FU两种化合物的抗性。这些表明了研究的原因。它在三氯乙酸不溶性部分中掺入4C标记的胞嘧啶时没有任何损害。尿苷激酶内部强调了综合缺陷。这是一种催化尿苷转化为UMP的酶。 UMPase解释了在ups-type 2突变体中观察到的抗性模式。
代写论文：三氯乙酸化合物
另一种解释是基于5-FC在52R中转化为5 – 氟-2′ – 脱氧尿苷-5′-单磷酸（5F-dUMP）的事实。它们选择性结合胸苷酸合成酶（TS）酶。这不与核苷酸连接内的RNA结合。 5F-dUMP是一种非竞争性抑制剂，可以使脱氧尿苷酸甲基化为胸苷酸。这抑制了DNA合成。称为三氯乙酸的5F-dUMP-酶复合物用于刺激TS的从头合成。这些允许DNA合成进行。这发生在一个较低的速度。这阻止了5-FC的行动。该假设基于5-FC存在下52R的减少的增长率得到支持。第三种解释是考虑到5-FC 52R中的耐药性。根据分析，发现它被掺入到RNA或52R化合物中。这些不会引起细胞功能的显着改变。这些情况很可能。 5-FC或5-FU化合物可以被52R除氟，并且可以解释三氯乙酸部分中的药物抗性和放射性标记的出现。这些机制很遥远，没有微生物系统的先例。该研究表明，基于病原体和抗真菌剂之间的相互作用，细胞中可能出现的可能影响。必须了解的是，在6个分离株中，有5个分离株已经确定了具体影响。第六个孤立文件还解释了这些关系的影响。实际上，结构形成无法确定。在研究的基础上可以开发广泛的视角。
代写论文：三氯乙酸化合物
In the test, the isolates were obtained from six patients determined the Cryptococcus neoformans from patients who had an unsuccessful therapy with the treatment of 5-fluorocytosine (5-FC). It was found that after the therapy, the isolates were exhibiting massive and stable 5-FC resistance. The five of the six isolates that was extracted indicated that the massive resistance to the 5-fluorouracil (5-FU). It was deemed that the compound was the mutation was based on the uridine-5′-monophosphate pyrophosphorylase were responsible for the drug resistance. The 6th isolate that was susceptible to the 5-fluorocytosine indicated that there was no reduction in the uptake or incorporation of the compound CyH3 or 5-FC1. This mechanism of the resistance of the compound was not completely comprehended. However, several possibilities exist according to the research data. These resemble the upstype 2 mutant that was reported in previous research. The latter isolated the resistance of both the compounds of 5-FC and 5-FU. These indicated the reason for the research. It did not have any impairment in the incorporation of the 4C-labeled cytosine within the trichloroacetic acidinsoluble fraction. The combined deficiencies were emphasized inside the uridine kinase. This was an enzyme that was catalyzing the conversion of the uridine to UMP. The UMPase was accounting for the pattern of the resistance that was viewed in the ups-type 2 mutant.
代写论文：三氯乙酸化合物
Another explanation was based on the fact that 5-FC was converted into to 5 – fluoro – 2′ – deoxyuridine – 5′ – monophosphate (5F-dUMP) in the 52R. They selectively bind to the thymidylate synthetase (TS) enzyme. This does not incorporate with the RNA within the nucleotide linkage. The 5F-dUMP is a noncompetitive inhibitor that catlysis the methylation process of deoxyuridylic acid to thymidylic acid. This inhibits the DNA synthesis. The 5F-dUMP-enzyme complex known as the trichloroacetic acid is used to stimulate the de novo synthesis of TS. These permit the DNA synthesis to proceed. This occurs at a lower rate. This blocks the actions of the 5-FC. The hypothesis is supported based on the reduced growth rate of the 52R within the presence of the 5-FC. The third explanation is taking into account the drug resistance in the 52R of the 5-FC. From analysis, it is found to be incorporated into the RNA or the 52R compound. These did not cause significant alteration to the cell functions. These situations are probable. 5-FC or 5-FU compound can be defluorinated by 52R and can be accounted for the drug resistance and appearing of the radiolabel in the tricholroacetic acid fraction. These mechanisms are remote and do not have the precedent for the microbiological system. The research indicated the plausible impacts that would arise in the cells based on the interaction between the pathogen and the anti-fungal agent. It is imperative to understand that out of the 6 isolates, 5 isolates had determined in a specific impact. The sixth isolate also explained about the impacts of these relationships. In reality, the structural formation cannot be determined. A broad perspective can be developed based on the research.
