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To verify whether the antineoplastic activity of ribonucleases was exerted on malignant cells independently from their specific genetic lesions, we performed a systematic study of the effects of BS-RNase and HHP2-RNase against genetically well-defined systems of thyroid tumour cells.
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The availability of a genetically well-defined system of thyroid normal and tumour cells in our laboratory allowed us to perform a systematic study of the activities of BS-RNase and HHP2-RNase in comparison with the known chemotherapeutic drug doxorubicin.
However, to date, our understanding of the roles of the oxidative/antioxidative systems in the carcinogenesis of thyroid cancer and their relationships to thyroid profiles is limited.
However, there have been few reports concerning the effects of DBP and MBP on metamorphosis of X. laevis and the molecular mechanisms of thyroid system disruption.
Rodent models of thyroid system dysfunction were presented.
One previously suggested mechanism involves phthalate alteration of thyroid system function (Engel et al. 2010).
We then applied the expanded system on a corpus of thyroid cancer and generated interactions involving both genes and pathways.
The fact that considerable numbers of compounds have the potential to interfere with different aspects of thyroid system function and TH action raises an urgent need for the development of an in vivo assay for detection of thyroid-axis disrupting molecules.
Novel techniques and genetically engineered mouse model systems have increased our understanding of thyroid hormone receptor (TR) action, and shed new light on the underlying molecular mechanisms for RTH.
Hashimoto's thyroiditis is an autoimmune disorder in which the immune system reacts against a variety of thyroid antigens.
We developed a large-scale text mining system to generate a molecular profiling of thyroid cancer subtypes.
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