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The PCNA and 9 1 1 clamps play a crucial role during DNA replication and repair, serving as platforms capable of enabling access to the DNA by various proteins.
Before deployment of resident health workers, Kadawawa clinic was in a generally poor state of repair, serving only as a base for male CHEWs to provide immunization and related services on weekly visits to the community.
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The clinical application of a magnetic device for targeted cell delivery in cartilage repair serves as a suitable example of how data from animal models are directly translated into clinical cartilage repair (Cucchiarini et al. 2014).
Our results support a model whereby p53 mediated cell-cycle-arrest/DNA repair serves as a barrier to optimal chemotherapeutic treatment of ovarian and perhaps other carcinomas and suggest that inhibition of p53 during chemotherapy may enhance clinical outcome.
Our findings indicate that p53 mediated cell-cycle-arrest/DNA repair serves as a barrier to optimal chemotherapeutic treatment of ovarian and perhaps other carcinomas and suggest that inhibition of p53 during chemotherapy may enhance the long-term survivorship of ovarian cancer patients.
The genes involved in DNA repair serve a key function during G2 phase of the cell cycle, including that of chondrocytes (Kim et al. 2010).
These observations would be expected if DSB repair served as a prominent contributor to the rapid evolution rate of plant mitochondrial genomes.
Animals operated for previous [ 15, 16] or unpublished studies of experimental articular cartilage repair served as subjects to describe the surgical approaches.
We suggest that whereas some MN can be reunited with the main nucleus (through interactions with envelope-limited chromatin sheets) and participate in DNA repair, failure of repair serves as a signal for the chromatin autophagy of MN.
Around 1200 classrooms have been built and 54 schools repaired, serving 170,000 children.
While it has been reported that p53 may enhance chemotherapeutic treatment in some cellular contexts [35], [36], our results suggest that p53-mediated cell cycle arrest/DNA damage repair is serving as a barrier to the desired clinical outcome of DNA damaging chemotherapy in ovarian cancer.
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