Exploring Google Translate-friendly strategies for optimizing the quality of Google Translate in academic writing contexts.

The present study explored the types of errors found in Google Translate (GT) Chinese-to-English translations and, based on those error types, proposes strategies for optimizing the performance of GT. Seven abstracts written in both Chinese and English from seven articles published in English Teaching and Learning in 2017 were selected as the materials. The researchers compared the GT translations to the English abstracts written by the original author(s) and analyzed the problems in the translations. The problematic translations consisted of grammatical errors (35%) and lexical errors (65%). Relatedly, we propose nine specific strategies to employ when writing Chinese abstracts to be translated into English using GT. According to the strategies, we suggest that users (1) avoid native language-specific expressions, (2) maintain the use of original English terminologies in composing Chinese abstracts, and (3) enhance logical relations and expressions for the discipline-specific discourse community. Further analyses revealed that 99% of the 69 identified problems in the GT translations of the seven abstracts could be avoided by using the proposed strategies. A conceptual framework for the collaboration between GT and GT users is proposed and pedagogical implications are discussed.

The SnRK1A protein kinase plays a key role in sugar signaling during germination and seedling growth of rice.

Sugars repress alpha-amylase expression in germinating embryos and cell cultures of rice (Oryza sativa) through a sugar response complex (SRC) in alpha-amylase gene promoters and its interacting transcription factor MYBS1. The Snf1 protein kinase is required for the derepression of glucose-repressible genes in yeast. In this study, we explored the role of the yeast Snf1 ortholog in rice, SnRK1, in sugar signaling and plant growth. Rice embryo transient expression assays indicated that SnRK1A and SnRK1B act upstream and relieve glucose repression of MYBS1 and alphaAmy3 SRC promoters. Both SnRK1s contain N-terminal kinase domains serving as activators and C-terminal regulatory domains as dominant negative regulators of SRC. The accumulation and activity of SnRK1A was regulated by sugars posttranscriptionally, and SnRK1A relieved glucose repression specifically through the TA box in SRC. A transgenic RNA interference approach indicated that SnRK1A is also necessary for the activation of MYBS1 and alphaAmy3 expression under glucose starvation. Two mutants of SnRK1s, snrk1a and snrk1b, were obtained, and the functions of both SnRK1s were further studied. Our studies demonstrated that SnRK1A is an important intermediate in the sugar signaling cascade, functioning upstream from the interaction between MYBS1 and alphaAmy3 SRC and playing a key role in regulating seed germination and seedling growth in rice.

Induction of tubulin by docetaxel is associated with p53 status in human non small cell lung cancer cell lines.

Docetaxel (DOC), a member of the taxane family of anticancer drugs, binds to tubulin and produces unnaturally stable microtubules that induce cell death. DOC is used clinically alone or in combination with other compounds to treat advanced stages of cancer. We have treated the human lung cancer cell lines A549 and H1299 and human cervical cancer HeLa cells with low concentrations of DOC to characterize the response of beta-tubulin isotypes and p53 genes. The relationship between p53 function and DOC, acting through a microtubule-based mechanism, was examined. We found that after 18-hr treatment with DOC, beta-tubulin gene transcription was enhanced in p53-null H1299 cells but not in A549 cells. Also, p53 RNA was strongly induced in the A549 cells. In addition, beta-tubulin levels also increased in the H1299 cells after the DOC treatment. Further demonstrating an association of DOC treatment with p53 and beta-tubulin, inhibition of p53 expression by interference RNA in A549 cells showed increasing beta-tubulin gene expression with DOC treatment. We also selected a clone from the H1299 cells that stably expressed p53, examined the beta-tubulin expression after DOC treatment and found an inhibition of beta-tubulin induction in these p53-expressing cells. Our data suggest that the initial response of cells to DOC treatment involves p53; alternatively, in the absence of p53, tubulins may be transactivated. Selection of the DOC-resistant A549 cells showed beta-tubulin expression was increased, in contrast to the initial response to the DOC treatment. From the initial and selection responses of beta-tubulin in cancer cells, it appears that there is a p53-associated beta-tubulin expression as a result of the DOC treatment.