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This cerebellar network oscillation has also been documented in mouse models of human conditions with complex developmental cerebellar dysfunction, such as Angelman syndrome and fetal alcohol syndrome.
Taken together we conclude that whole-cell [Ca2+]i transients in hiPSC-CMs depend on both Ca2+ influx via L-type Ca2+ channels and intracellular Ca2+ store release, as previously documented in mouse [25], [26] and human ESC-CMs [18], [19].
The deficiency was documented in mouse ES cells, mouse neural progenitors, and human CD34+ haematopoietic progenitors.
Such heterosubtypic immunity is well documented in mouse models [ 35, 36], while the evidence from human studies, although inferential, is supportive.
Our extensive literature search indicates that this is the first time that the Hsp70 secretion is documented in mouse and human prostate cancer cells.
The nuclear gene mutations documented in mouse brain tumors and melanomas were also detected in the normal embryonic tissues of the mice derived from the tumor nuclei (47, 48).
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Furthermore, H5N1 virus infections in the laboratory have been documented in mice, ferrets, monkeys, pigs, and cats [23] [28].
This cycling is under the control of molecular signals, which have been documented in mice and inferred in humans from clinical observations.
Injuries that possibly stimulated chronic inflammation in ageing MPSIIIB mice are the alteration of the blood-brain barrier, as documented in mice with GM1 or GM2 gangliosidosis [20], the secondary accumulation of GM2 and GM3 ganglisosides [33] and the cell death.
While it remains unclear if the ability of satellite cells to contribute to muscle repair is indeed impaired in old age [18], an age-associated decline in the number of satellite cells was certainly documented in mice and rats, at least in some limb muscles [19], [20], [21], [22].
To further address the possible expansion of Treg cells upon exposure to TCDD as documented in mice [8], [9], we assessed the frequency of CD4+ T cells simultaneously expressing high levels of the IL-2 receptor subunit CD25 and the Treg-specific transcription factor FoxP3 in resting conditions [32].
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