深容SCI写作助手：汉译英
例如，有下面这样一段原文（中国生物化学与分子生物学报，DOI：10.13865/ j.cnki.cjbmb. 2020.11.1395 ），怎样翻译成地道的科技英语呢？
糖尿病作为一种高血糖为主要特征的代谢性疾病，会引起中枢神经系统损伤，造成脑组织结构和功能改变，进而导致认知功能障碍。目前，糖尿病对认知功能障碍的影响及相关调控机制已成为国内外研究的热点和难点。磷酸肌醇3激酶/蛋白激酶B/叉头样转录因子（PI3K/AKT/FOXO）通路是自噬的重要上游调控机制。本文概述了PI3K/AKT/FOXO信号通路可调控Gs， Bnip3和Spk2等基因的表达；GS可以通过调控Gln-mTORC1通路，从而激活自噬；BNIP3促进LC3表达，上调自噬水平；此外，AMPK-FOXO3a-mTORC1也是自噬的重要上游调控机制。以上研究提示，FOXO3a可能是糖尿病认知功能障碍（DACD）治疗的重要靶点。通过本综述为临床上治疗DACD及其相关药物的研发提供更为深入的理论依据和分子靶点。
首先，我们提交中文原文，得到一段AI译文。
把AI译文复制到任意编辑器中，便于逐句润色——因为模块会逐句提示相似的SCI例句。
第1句AI译文：Diabetes mellitus, as a metabolic disease characterized by hyperglycemia, can cause damage to the central nervous system, cause changes in brain tissue structure and function, and then lead to cognitive dysfunction.
如图中高亮显示：例句中有非常相似的内容，据此进行润色，可见润色后的句子比AI译文要地道很多。
Diabetes mellitus, as a metabolic disease characterized by hyperglycemia, can cause damage to the central nervous system, cause changes in brain tissue structure and function, and then lead to cognitive dysfunction.
Diabetes mellitus is a metabolic disorder characterized by hyperglycemia and can cause damage to the central nervous system, which leads to structural and neurophysiological changes in the brain, and thus increases the risk of cognitive decline.
第2句AI译文：At present, the effects of diabetes on cognitive dysfunction and the related regulatory mechanisms have become hot and difficult points in domestic and foreign research.
原文说的是这个发病机制已经成为'国内外'的研究热点。注意，我们翻译成SCI论文的时候，面向的读者是全世界的，说国内外就很茫然了，所以应该改为“全世界范围的”。请比较AI译文，高亮的SCI例句和我们根据例句所做的润色。
At present, the effects of diabetes on cognitive dysfunction and the related regulatory mechanisms have become hot and difficult points in domestic and foreign research.
At present, the mechanism underlying the development of cognitive dysfunction in diabetes has become an important research domain, where substantial effort has been invested worldwide.
第3句AI译文：The phosphoinositide 3 kinase/protein kinase B/forkhead-like transcription factor (PI3K/AKT/FOXO) pathway is an important upstream regulatory mechanism of autophagy.
这个句子很简单，但AI译文的问题在于FOXO的全称不正确，我们根据SCI例句作了修改；另外，调控机制改为modulator更地道。
The phosphoinositide 3 kinase/protein kinase B/forkhead-like transcription factor (PI3K/AKT/FOXO) pathway is an important upstream regulatory mechanism of autophagy.
The phosphoinositide 3 kinase/protein kinase B/forkhead transcription factor (PI3K/AKT/FOXO) pathway is an important upstream modulator of autophagy.
第4句AI译文：This paper summarizes that PI3K/AKT/FOXO signaling pathway can regulate the expression of Gs, Bnip3 and Spk2; GS can activate autophagy by regulating Gln-mTORC1 pathway; BNIP3 promotes LC3 expression and upregulates autophagy level; in addition, AMPK-FOXO3a-mTORC1 is also an important upstream regulatory mechanism of autophagy.
这一句AI译文很长，AI翻译引擎把很长的一段中文翻译成了很长的一段英文，中文的封号译成了英文的封号。实践中，中文的一个封号往往要译成英文的一个句子，中文的一个长句，可以译成英文的若干个短句。
This paper summarizes that PI3K/AKT/FOXO signaling pathway can regulate the expression of Gs, Bnip3 and Spk2; GS can activate autophagy by regulating Gln-mTORC1 pathway; BNIP3 promotes LC3 expression and upregulates autophagy level; in addition, AMPK-FOXO3a-mTORC1 is also an important upstream regulatory mechanism of autophagy.
Here we summarize that PI3K/AKT/FOXO signaling pathway regulates the expression of Gs, Bnip3 and Spk2. Gs activates autophagy by regulating Gln-mTORC1 pathway. BNIP3 promotes LC3 expression and upregulates autophagy level. In addition, AMPK-FOXO3a-mTORC1 is an important upstream modulator of autophagy.
第5句AI译文：These studies suggest that FOXO3a may be an important target for the treatment of diabetic cognitive impairment (DACD).
这也是一个简单的句子，AI按字面翻译了“糖尿病认知功能障碍”这个词，但实际上DACD是一个专有名词，我们根据模块给出的SCI例句进行修改。
These studies suggest that FOXO3a may be an important target for the treatment of diabetic cognitive impairment (DACD).
These studies suggest that FOXO3a may be an important target for the treatment of diabetes-associated cognitive decline (DACD).
第6句AI译文：This review provides a more in-depth theoretical basis and molecular targets for the development of clinical therapies for DACD and related drugs.
综述本身并不产出新的知识，只是对现有研究的总结。根据模块给出的SCI例句进行润色，不仅语言更地道，语义也更准确。
This review provides a more in-depth theoretical basis and molecular targets for the development of clinical therapies for DACD and related drugs.
In this review, we describe the in-depth studies which provide theoretical basis and molecular targets for the development of clinical therapies for DACD.
综上，我们就通过深容SCI写作助手完成了一段论文的翻译和润色：
糖尿病作为一种高血糖为主要特征的代谢性疾病，会引起中枢神经系统损伤，造成脑组织结构和功能改变，进而导致认知功能障碍。目前，糖尿病对认知功能障碍的影响及相关调控机制已成为国内外研究的热点和难点。磷酸肌醇3激酶/蛋白激酶B/叉头样转录因子（PI3K/AKT/FOXO）通路是自噬的重要上游调控机制。本文概述了PI3K/AKT/FOXO信号通路可调控Gs， Bnip3和Spk2等基因的表达；GS可以通过调控Gln-mTORC1通路，从而激活自噬；BNIP3促进LC3表达，上调自噬水平；此外，AMPK-FOXO3a-mTORC1也是自噬的重要上游调控机制。以上研究提示，FOXO3a可能是糖尿病认知功能障碍（DACD）治疗的重要靶点。通过本综述为临床上治疗DACD及其相关药物的研发提供更为深入的理论依据和分子靶点。
Diabetes mellitus, as a metabolic disease characterized by hyperglycemia, can cause damage to the central nervous system, cause changes in brain tissue structure and function, and then lead to cognitive dysfunction. At present, the effects of diabetes on cognitive dysfunction and the related regulatory mechanisms have become hot and difficult points in domestic and foreign research. The phosphoinositide 3 kinase/protein kinase B/forkhead-like transcription factor (PI3K/AKT/FOXO) pathway is an important upstream regulatory mechanism of autophagy. This paper summarizes that PI3K/AKT/FOXO signaling pathway can regulate the expression of Gs, Bnip3 and Spk2; GS can activate autophagy by regulating Gln-mTORC1 pathway; BNIP3 promotes LC3 expression and upregulates autophagy level; in addition, AMPK-FOXO3a-mTORC1 is also an important upstream regulatory mechanism of autophagy. These studies suggest that FOXO3a may be an important target for the treatment of diabetic cognitive impairment (DACD). This review provides a more in-depth theoretical basis and molecular targets for the development of clinical therapies for DACD and related drugs.
Diabetes mellitus is a metabolic disorder characterized by hyperglycemia and can cause damage to the central nervous system, which leads to structural and neurophysiological changes in the brain, and thus increases the risk of cognitive decline. At present, the mechanism underlying the development of cognitive dysfunction in diabetes has become an important research domain, where substantial effort has been invested worldwide. The phosphoinositide 3 kinase/protein kinase B/forkhead transcription factor (PI3K/AKT/FOXO) pathway is an important upstream modulator of autophagy. Here we summerize that PI3K/AKT/FOXO signaling pathway regulates the expression of Gs, Bnip3 and Spk2. Gs activates autophagy by regulating Gln-mTORC1 pathway. BNIP3 promotes LC3 expression and upregulates autophagy level. In addition, AMPK-FOXO3a-mTORC1 is an important upstream modulator of autophagy. These studies suggest that FOXO3a may be an important target for the treatment of diabetes-associated cognitive decline (DACD). In this review, we describe the in-depth studies which provide theoretical basis and molecular targets for the development of clinical therapies for DACD.
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