篇一：药学论文翻译点评(一)
药学论文翻译点评（一）
泛瑞翻译
药学翻译的专业性比较强，翻译过程中译者要在完全理解文章意思的基础上进行。下面列举一个翻译样例，来加以阐述。
MRI-Guided Monitoring of Thermal Dose and Targeted Drug Delivery for Cancer Therapy ABSTRACT
Application of localized hyperthermia treatment for solid tumor therapy is under active clinical investigation. The success of this treatment methodology, whether for tumor ablation or drug delivery, requires accurate target localization and real-time temperature mapping of the targeted region. Magnetic Resonance Imaging (MRI) can monitor temperature elevations in tissues in real-time during tumor therapy. MRI can also be applied in concert with methods such as High Intensity Focused Ultrasound (HIFU) to enable image-guided drug delivery (IGDD) from temperature sensitive nanocarriers, by exploiting not only its anatomic resolution, but its ability to detect and measure drug release using markers co-loaded with drugs within the nanocarriers. We review this rapidly emerging technology, providing an overview of MRI-guided tissue thermal dose monitoring for HIFU and Laser therapy, its role in targeted drug delivery and its future potential for clinical translation.
摘要
实体瘤局部高温治疗的临床应用还在调查研究中。不论是瘤体消融还是药物治疗，成功的治疗需要精确的靶向定位和对定位部位的温度实时描绘。磁共振成像可以实时监控治疗中组织的温度提升情况。磁共振成像也可以与其他方法一起使用，例如高强聚焦超声，通过分析热敏纳米载体的结构和运用载体内装载药物的时标检测药物释放，使其以影像为指导药物输送成为可能。我们回顾了这迅速出现的新技术，为以磁共振成像为指导的组织热中子剂量监控高强聚焦超声治疗和激光治疗，在靶向药物输送中的角色扮演和临床翻译的潜能提供了概述。 点评：
第一句的“还在调查研究中”不符合语言表达习惯，under active clinical investigation意思为开展了大量的临床研究。“成功的治疗需要精确的靶向定位和对定位部位的温度实时描绘”是错译，句子意思完全看不懂。可翻译为“欲实施有效地治疗需精确的靶向定位，并对靶向
部位进行实时温度测定”。另外，其他地方也存在问题。可参考以下样例：
目前，大量研究对实体瘤局部高温治疗的临床治疗进行了探讨。无论是瘤体消融还是药物治疗，欲实施有效地治疗需精确的靶向定位，并对靶向部位进行实时温度测定。磁共振成像（ＭＲＩ）可监测肿瘤治疗过程中组织内温度的升高情况。此外，ＭＲＩ也可与其他方法联用，例如高强聚焦超声（ＨＩＦＵ），可借助分析热敏纳米载体的结构，或通过测定药物欧联分子标记，实现影像学介导的药物释放（ＩＧＤＤ）。本文对该项新技术（MRI联合HIFU与激光治疗）进行综述，阐述其在靶向药物给药及临床转移方面的应用。
篇二：药学SCI论文翻译样例
药学SCI论文翻译样例
泛瑞翻译
在翻译药学SCI论文时，译者不能单纯依靠原文的意思进行死板的翻译，更多时候需要借助专业文献进行撰写及翻译。在进行该项工作时，要多阅读文献，并抓住主要信息，同时纠正作者原文中存在的不足，或加以完善。以下是一个样例：
原文
WHO 对药物不良反应（adverse drug reactions,简称 ADR）的定义为：一种有害的和非预期的反应，这种反应是在人类预防、诊断或治疗疾病，或调节生理机能时出现的有害的和与用药目的无关的反应。在美国的一项meta分析研究(综合了39项以医院为基础的前瞻性研究)表明有6.7％的住院患者有严重的药物副反应。其中0.32％有致死性。后者导致美国每年10万人死于药物不良反应。药品不良反应在临床上的主要表现有：过敏反应、毒性反应、特异性反应、二重感染等；涉及器官或系统主要为：皮肤及软组织、消化系统、神经系统、血液系统、泌尿系统、呼吸系统等。其中ADRs以皮肤及其附件损害最为多见，由于这类ADRs为药物变态反应，临床比较常见，也易于发现和观察。其次为消化系统，而肝、肾、血液系统等因为较为隐匿，报道较少。
译文
Adverse drug reactions (ADRs) refer to an expression that describes harm related with the use of given medications at a normal dosage. ADRs are a significant cause of morbidity and mortality and contribute to the incidence of adverse events, leading to increased health-care costs. According to our knowledge, the major clinical symptoms of ADRs included allergy, toxic reaction, specific reaction and double infection. Additionally, organ and system dysfunction, such as disorders of skin, soft tissue, digestive system, nervous system, hematological system, urinary system and respiratory system, have been reported by those with ADRs. Among them, skin and appendages disorders was the most frequently reported events, followed by disorders of digestive system. However, few reports about ADRs were available as the symptoms were hard to observe.
篇三：药学专业英语文章及翻译
Expression of livin in gastric cancer and induction of apoptosis in SGC-7901 cells by shRNA-mediated silencing of livin gene
Background-Because of increased resistance to apoptosis in tumor cells, inhibition of specific antiapoptotic factors may provide a rational approach for the development of novel therapeutic strategies.Livin, a novel inhibitor of apoptosis protein family, has been found to be expressed in various malignancies and is suggested to have poorly prognostic significance. However, no data are available concerning the significance of livin in gastric cancer. In this study, we detected the expression of livin in human gastric carcinoma and investigated the apoptotic susceptibility of SGC-7901 cell by shRNAmediated silencing of the livin gene.
Methods-The mRNA and protein expression of livin were analyzed by RT-PCR and western blot assay.The relationship between livin expression and clinical pathologic parameters was investigated. The small interfering RNA eukaryotic expression vector specific to livin was constructed by gene recombination, and the nucleic acid was sequenced. Then it was transfected into SGC-7901 cells by Lipofectamin 2000. RT-PCR and Western blot assay were used to validate gene-silencing efficiency of livin in SGC-7901 cells. Stable clones were obtained by G418 screening. The cell apoptosis was assessed by flow cytometry (FCM). Cell growth state and 50 % inhibition concentration (IC50) of 5-FU and cisplatin was determined by MTT method.
Results-The expression of livin mRNA and protein were detected in 19 of 40 gastric carcinoma cases (47.5%) and SGC-7901 cells. No expression of livin was detected in tumor adjacent tissues and benign gastric lesion. The positive correlation was found between livin expression and poor differentiation of tumors as well as lymph node metastases (P < 0.05). Four small interfering RNA eukaryotic expression vector specific to livin were constructed by gene recombination. And one of them can efficiently decrease the expression of livin, the inhibition of the gene was not less than 70% (P < 0.01). The recombinated plasmids were extracted and transfected gastric cancer cells. The stable clones were obtained by G418 screening, and were amplified and cultured. When livin gene was silenced, the reproductive activity of the gastric cancer cells was significantly lower than the control groups(P < 0.05). The study also showed that IC50 of 5-Fu and cisplatin on gastric cancer cells treated by shRNA was
decreased and the cells were more susceptible to proapoptotic stimuli (5-Fu and cisplatin) (P < 0.01).
Conclusions-C Livin is overexpressed in gastric carcinoma with a relationship to tumor differentiation and lymph node metastases, which is suggested to be one of the molecular prognostic factors for some cases of gastric cancer. ShRNA can inhibit livin expression in SGC-7901 cells and induce cell apoptosis.Livin may serve as a new target for apoptosis-inducing therapy of gastric cancer.
1. Introduction
Gastric cancer is one of the most common malignancies in the world. Most patients with this disease are diagnosed in advanced stages, and lose the chance of surgical eradication. Despite much progress in chemotherapy, the overall survival of the patients with gastric cancer in advanced stage is still poor. Resistance of cancer cells to chemoagents may contribute to failure of the treatment. Among the reasons of drug resistance, inhibited process of cell apoptosis may play an important role.
Cancer cells are often characterized by increased resistance to apoptosis [1], which mediates their increased resistance to various stimuli of cell apoptosis, such as DNA damage, hypoxia, nutrient-deprivation [2,3]. Moreover, apoptosis resistance is considered to be a major cause of therapeutic failure for tumors in clinical practice, since many chemo- and/or radiotherapeutic agents function through the induction of apoptotic tumor death [4].
Inhibitor of apoptosis protein (IAPs) is a novel family of intracellular proteins which suppress apoptosis induced by a variety of stimuli [5,6], including viral infection, chemotherapeutic drugs, staurosporin, growth factor withdrawal, and by components of the tumor necrosis factor-a (TNF-a)/Fas apoptotic signaling pathways [7¨C9]. The IAPs consists of a group of structurally related proteins with antiapoptotic properties
[10], and may play a substantial role in preventing tumor cell from apoptosis, and has become the focus of research in recent years. A novel member of this family is ML-IAP/livin/KIAP/BIRC7 (in the following termed livin) which has two isoforms, livin a and livin b [11¨C14]. It has been shown that over-expression of the livin can block apoptosis induced by a variety of proapoptotic stimuli [12]. Interestingly, livin gene has been found to be restrictively expressed in tumor cells, but not, or to lesser amounts in most normal adult tissues [11¨C15], and may contribute to tumorigenesis by allowing malignant cell to avoid apoptotic cell death. So inhibition of livin expression may represent an interesting therapeutic strategy.
In the present study, we investigated the expression of livin in gastric cancinomas and their adjacent tissues. The relationship between livin expression and clinical pathologic parameters was analyzed. Furthermore, we explored the feasibility of shRNA in inhibiting livin gene expression and the apoptotic susceptibility of gastric cancer cell by shRNA-mediated silencing of the livin gene.
2. Patients and methods
2.1. Patients and tumor samples
Forty samples of gastric carcinoma and 13 samples of paracancerous tissues were collected from the patients who received gastrectomy (age of patients ranging from 29-77 years). Thirteen samples of benign gastric lesion (chronic superficial gastritis) were gained from the patients undergoing gastric endoscopic examination (age of patients ranging from 33-77 years). These samples were collected from patients admitted to the First Affiliated Hospital of Nanjing Medical University. The patients with gastric cancer were diagnosed as being in stage I to IV based on TNM classification (UICC, 2002). Tumor specimens were immediately frozen in liquid nitrogen after surgery and stored at -80℃ until use. Informed consent was obtained from all patients.
2.2. RT-PCR procedure
Total RNA (2 mg) extracted from frozen tissues was reverse transcribed in a final volume of 25 ml with 100 pmol of oligo(dT)15 and 200U M-MLV reverse transcriptase (promega, USA), according to the manufacturer’s guidelines.
Aliquots corresponding to 2.5 ml cDNA were then amplified in PCR buffer containing 25pmol/ml each primer and 1 U Taq polymerase in a final volume of 50 ml. Each amplification was performed for 35 cycles, one cycle profile consisted of denaturationat 94 8C for 30 s, annealing at 59 8C (livin and b-actin) for 30 s and extension at 72 8C for 30 s. A sample without RNA was included in each RT¨CPCR as a negative control.
Sequences of livin and β-actin primers used are as follows:livina/b up stream,50-TCCACAGTGTGCAGGAGACT-30;livina/βdownstream,50-ACGGCACAAAGACGATGGAC-30;b-actinupstream,50-AGCGCAAGTACTCCGTGTG-30;β-actin downstream, 50-AAGCAATGCTATCACCTCCC-30.The size of the amplified products were312/258 bp for livina/b and 501 bp for b-actin respectively.
2.3. Western Blot Analysis
Tissues were homogenized with lysis buffer [50 mM Tris-HCl(pH 7.5), 250 mM
NaCl, 0.1% NP40, and 5 mM EGTA containing 50 mM sodium fluoride, 60 mM b-glycerol-phosphate, 0.5 mM sodium vanadate, 0.1 mM phenylmethylsulfonyl fluoride, 10 mg/ml aprotinin, and 10 mg/ml leupeptin. The total protein concentration was determined using Coomassie Brilliant Blue. Protein samples were electrophoresed in a 10% denaturing SDS gel and transferred to PVDF membrane (Roche, USA). The membranes were incubated with specific primary antibodies, reacted with a peroxidase-conjugated secondary antibody (Cell signaling technology,USA), and finally visualized by enhanced chemiluminescence (Cell signaling technology, USA). Monoclonal antibodies recognizing livin (1:250) and actin (1:400) were purchased from Alexesis Inc. (USA) and Santa Cruz Biotechnology (USA).
2.4. Cell lines and cell culture
We selected a human gastric adenocarcinoma cell lines for thisstudy. SGC-7901 (Shanghai Institute of Cell Research, Shanghai,China) is an adherent, moderately differentiated, human gastric adenocarcinoma cell line. The cell lines are gastric cancer epithelial cells and grow as adherent cells in RPMI 1640 (Hyclone Inc, USA)containing 10% FCS (Life Technologies, Inc.), 100 units/ml penicillin,and 100 mg/ml streptomycin (BioWhittaker). SGC-7901 cells were maintainedat37 8Cina humidified incubatorwithanatmosphere of 5% CO2. Cisplatin and 5-fluorouracil (Qilu pharmaceutical factory,China) were solublized in DMSO and stored at 4 8C.
2.5. ShRNA synthesis and construction of PGPU/GFP/Neo/livin plasmids
ShRNA sequences of livin were designed by software of siRNA Sequence-Selector and synthesized (Shanghai Biotech, Ltd.Corp., China). The sequences as following (Table 1)then were inserted into BbsI and BamH sites of the pGPU/GFP/Neo(Shanghai GenePharma Co. Ltd China) to generate pGPU/GFP/Neo/livin and pGPU/GFP/Neo/Control plasmids,respectively.
2.6. Establishment of SGC-7901 stable transfectants expressing pGPU/GFP/Neo/livin and pGPU/GFP/Neo/Control
For transfection experiments, SGC-7901 cells were plated into 6-well plates (3?á105 cells/well), 96-well plates (1×104 cells/well) and 12-well plates (1.5×105 cells/well) for 24 h before transfection
The cells were transfected with 4 mg/well of empty pGPU/GFP/Neo/vector, pGPU/GFP/Neo/livin or pGPU/GFP/Neo/Control plasmid using Li-pofectAMINE 2000 (Life Technologies, Inc., Grand Island,NY) according to the manufacturer?ˉs instructions. Forty-eight hours after transfection, the cells were passaged at 1:15 (v/v)
and cultured in mediumsupplemented with Geneticin (G418) at 1000 g/ml for 4 weeks. Stably transfected clones were picked and maintained in medium containing 400 g/ml G418 for additional studies.
2.7. Assay of anchorage-dependent cell growth
Parent cells and cells stably expressing empty pGPU/GFP/Neo vector, pGPU/GFP/Neo/livin or pGPU/GFP/Neo/Control were seeded into 6-well plates. Cells from triplicate wells were collected every other day. Cell numbers were determined using a Coulter counter (Coulter Electronics, Miami, FL). The number of cells per well is reported as the average SD at the indicated number of days after plating.
2.8. MTT assay
Cytotoxicity was measured by MTT assay. Cells growing exponentially were plated onto 96-well plates at a density of 10000 cells/well for 24 h. The cells were then treated with different concentrations of drugs for 48 h. One hundred microliters of MTT stock solution (1 mg/ml) were added to each well, and the cells were further incubated at 37℃ for 4 h. The supernatant was replaced with isopropyl alcohol to dissolve formazan production. The absorbance at wavelength 595 nm was measured with a micro-ELISA reader (ClinBio-128, SLT, Austria). The ratio of the absorbance of treated cells relative to that of the control cells was calculated and expressed as a percentage of cell death.
2.9. Flow cytometry
Cells were collected and fixed with ice-cold 70% ethanol in PBS and stored at -4℃ until use. After resuspension, cells were incubated with 100 ml of RNase I (1 mg/ml) and 100 ml of PI (400 mg/ml) at 37℃ and analyzed by flow cytometry (BD, USA).
2.10. Statistical analysis
Data were expressed as the means of at least three different experiments ?? SD. The results were analyzed by Student’s t-test, and P < 0.05 was considered statistically significant.
3. Results
3.1. Expression of livin in gastric carcinomas
In the present study, for the first time, we evaluated by RT¨CPCR and westen blot the presence of livin expression in 40 gastric cancinomas, 13 para-cancerous tissues and 13 benign lesions of gastric mucosa. In para-cancerous tissues and benign lesions of gastric mucosa, no detectable levels of either mRNA isoforms were revealed, while
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