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This project aims to develop, through a multi-disciplinary, multi-institutional, innovative and cost-effective approach, new paradigms to prevent the disease progression and support the rapid evaluation of new therapies.
These findings indicate that catabolic enzymes play a significant role in OA progression and support the development of therapies targeting these enzymes as a strategy to decelerate articular cartilage degradation.
Most significantly, however, these data suggest that pro- and anti-fibrogenic macrophage functions co-exist during disease progression and support the notion that reprogramming macrophages or otherwise enhancing anti-fibrogenic pathways may be a viable therapeutic strategy to ameliorate fibrogenesis during chronic liver disease.
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This increase in the inflammatory cytokines also correlates well with the disease progression and supports the histopathological observations measured in case of arthritic control animals.
As an oncogene, Cav-1 protects prostate cancer epithelial cells from apoptotic stimuli, enhances prosurvival pathways mediated by multiple growth factors involved in prostate cancer progression, and supports castrate-resistant growth.
This result indicates proxy measures may be more reliable than self-reported ones in later stages of prodromal HD disease progression, and supports the DSM-5 recommendation of using proxy measures when individuals have impaired cognitive function.
We have previously shown that nesprin-2 βΔKASH1 depletion stimulated VSMC proliferation, suggesting that this complex may regulate cell cycle progression and in support of this notion, nesprin-2 depleted VSMCs displayed mitotic defects and micronuclei formation, indicative of a G2/M checkpoint defect.
Tumor marker carcinoembryonic antigen (CEA) as well as inflammatory biomarker C-reactive protein (CRP) did not show the independent association with lymph node metastasis, suggesting that hyperfibrinogenemia was not a simple result of cancer progression and might support the metastatic process by providing beneficial microenvironment around the tumor.
This is in line with the notion that the LTP cancer cell sub-population is associated to the ability of a population of cells to initiate and drive tumor progression and further supports a direct correlation between the rate LTP cancer cell expand in vitro and the aggressiveness of the tumor in vivo.
Many of the filtrated genes have been linked to tumor progression and malignancy, supporting the reliability of our array data.
Strategies to improve the efficacy of endocrine agents in breast cancer (BC) therapy and to delay the onset of resistance include concomitant targeting of the estrogen receptor alpha (ER) and the mammalian target of rapamycin complex 1 (mTORC1), which regulate cell-cycle progression and are supported by recent clinical results.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com