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The article analyzes user IR system interaction from the broad, socio-cognitive perspective of lessons we can learn about human brain evolution when we compare the Neanderthal brain to the human brain before and after a small human brain mutation is hypothesized to have occurred 35,000 75,000 years ago.
The receptor change caused by the PROGINS mutation is hypothesized to affect ligand-and hormone-binding properties, leading to inadequate control of estrogen-receptor-driven proliferation and estrogen overactivation.
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A high incidence of the C150T transition in centenarians' leukocytes was observed and a remodeling event of mtDNA replication origin associated with this mutation was hypothesized.
Structural consequences of this mutation are hypothesized in comparison to homologous enzyme human factor XIIIA accepted as valid in similar structural analysis and are projected as guidelines for future studies at an experimental level on TGM1 thus mutated.
Recently, a mild form of muscular dystrophy characterized by hypoglycosylated α-DG was associated with the compound heterozygous missense mutations (V74I and D111N) with both mutated sites located within the N-terminal domain of α-DG and a pathological molecular mechanism similar to the one described for the T192M mutation was hypothesized [ 22].
The accumulation of mitochondrial DNA mutations is hypothesized to cause age-related degenerative diseases such as ARHL [ 73].
Five predicted non-neutral mutations are hypothesized as putative drivers.
The driver mutations are hypothesized to be involved in either protein-protein interactions (in the case of Rad51D), protein-nucleic acid interaction (e.g., in CG33714), or allosteric regulation (e.g., in HDAC4).
The distribution of allele frequencies of causal mutations is not known, but it is hypothesized that those mutations may have a low MAF [ 1].
It is hypothesized that the mutation was maternally inherited, since the proband's mother and maternal uncle deceased from generalized cancer at the age of 52 and 56, respectively and therefore, there is no available genetic material to confirm this.
Decreased functioning of DNA repair mechanisms under stress is hypothesized to enhance mutation rates as an adaptive strategy in bacteria and yeast (Foster 2007; Galhardo et al. 2007).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com