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Exacerbation of STAT signaling pathway and chemokine production in USP18-silenced beta cells is accompanied by exacerbation of cell death.
Several studies have evidenced the pivotal role of ERS as a major contributor to the increase in apoptosis and the exacerbation of cell damage following IRI.
Several studies have evidenced the pivotal role of endoplasmic reticulum stress (ERS) as a major contributor to the increase in apoptosis and the exacerbation of cell damage after IRI [ 6, 7].
Thus, it is possible that alterations of receptor-mediated signaling pathways could contribute to protection or exacerbation of cell death cascades in the symptomatic and/or presymptomatic phases of HD [ 67].
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Therefore, identification of key components of this signaling pathway selectively involved in LID would be highly advantageous since the repeated use of available MEK inhibitors in PD patients may result in intolerable side effects, including an exacerbation of dopamine cell loss in the SN.
The EDP-dependent Hsp90 secretion by cancer cells, combined with the protease release, could explain the exacerbation of the cancer cells' invasive power in the presence of EDPs.
In the last follow-up (20 months after transplantation), Patient 1 described improvement of dyspnea, improvement of exercise capacity, less productive cough and less times of exacerbation after cell therapy; Patient 2 described less productive cough and less times of exacerbation after cell therapy.
Peripheral blood neutrophils show altered activity in both stable COPD and during exacerbations, including increased expression of cell surface adhesion molecules [16] [18], upregulation of genes relating to inflammation [19] and enhanced respiratory burst [17].
Reorganization of gene expression in stressed cells may disrupt maintenance of dosage compensation, leading to the exacerbation of cellular stress and cell death in males.
However, if an individual had a defect in the number of CD5+ B cells, in the expression of FasL by CD5+ B cells, or in the T-cell response to death signals, then this mechanism of peripheral tolerance could be ineffective, and interaction of CD5+ B cells with T cells might lead to exacerbation of disease by increasing the T-cell response to autoantigens.
In corroboration, we observed an increased fraction of senescent cells with exacerbation of defects in neurogenesis when CSB-suppressed neural progenitor cells are grown under hypoxic conditions (Supplementary data 1).
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