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Larger quantities of air in the fire compartment result in lower concentrations of carbon monoxide, higher concentrations of carbon dioxide, and smoke dilution.
Acute myeloid leukaemia (AML) represents a group of clonal haematopoietic stem cell disorders in which both failure to differentiate and overproliferation in the stem cell compartment result in the accumulation of non-functional myeloid cells termed myeloblasts and loss of normal haematopoietic function.
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Specific deletion of Notch2 in the DC compartment resulted in decreased numbers of CD11b+ DCs.
Transient removal of oxygen and glucose in the axon compartment resulted in irreversible loss of axon length and neurofilament labeling.
Significant fracturing of the central compartment results in enhanced hydrodynamic properties of the aquifer and an inverse relationship between electrical resistivity and transmissivity.
For example, a conditional mouse model for TET2 loss in the hematopoietic compartment resulted in increased HSC self-renewal and myeloproliferation including splenomegaly, monocytosis, and extramedullary hematopoiesis (Moran-Crusio et al., 2011).
Similar to simultaneous ablation of Notch1 and Notch2 or RBP-J (Dumortier et al., 2010), ADAM17 inactivation in the keratinocyte compartment resulted in increased epidermal TSLP expression and spontaneous onset of AD and MPD in mice (Murthy et al., 2012).
Subsequent remodeling and thinning of the mesenchymal compartment results in a convergence of capillaries and lung epithelium and triggers septation of the sacs into mature alveoli (alveolar stage, secondary septa).
The sedimentary response (erosion and/or aggradation) of each compartment to a triggering event, such as cyclonic rainfall and/or seasonal rise of water discharge, is controlled both by the magnitude of the climatic event and by the state of the compartment resulting from previous evolution.
In addition, TBM may stimulate increased HIV replication in the CNS compartment, resulting in destruction of CSF lymphocytes.
However, absence of TNF receptors in either compartment resulted in deficient lymphocyte recruitment and thus protection from the development of fibrosis (Fig. 9A,C,E).
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