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Our understanding of the basis of severe disease in malaria is incomplete.
As with pregnancy-associated malaria, the aim now is to use this information to understand the basis of severe malaria and identify novel approaches to prevention or treatment.
A detailed understanding of endothelial activation and regulation during infection may provide new insights into the molecular basis of severe and fatal malaria.
In rather numerous cases where a presumptive mutant was identified initially on the basis of severe cardiac edema at E10.5, we did further isolations at E9.5, which often allowed more relevant observations on the specific nature of the phenotype and also to avoid possible loss of embryos due to resorption.
Although the pathophysiologic basis of severe malaria is complex and may likely include reduced deformability of [2], [3] as well as cytoadherence of [4] [6] parasitized red blood cells, convincing arguments have nevertheless been made for an important role of pro-inflammatory cytokines in many aspects of disease [7] [9].
The basis of severe respiratory involvement observed in pdm influenza during pregnancy may be related to the conjunction of immunologic and physiologic changes, including the switch from cell-mediated to antibody-mediated immune responses, respiratory compromise by mechanical effect, and heightened cardiopulmonary demand to compensate the raised blood volume [17] [21].
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However, little is known about the molecular basis of this severe growth defect.
On the basis of the severe harmful effects of fluorosis on human beings, some measures should be taken to control the occurrence and progress of fluorosis.
To understand the molecular basis of these severe in vivo defects, we studied these alleles in vitro using the biochemical assays detailed earlier (Figs 6 and 7 and Supplementary Material, Fig. S4).
No routine use of G-CSF was recommended, but G-CSF could be given on an individual basis in instances of severe neutropenia.
There is little evidence of the efficacy of other therapeutic alternatives, such as systemic corticosteroids, dapsone, omalizumab, intravenous immunoglobulins and plasmapheresis; these options should be evaluated on an individual basis in cases of severe refractory chronic urticaria [ 1, 7, 9, 113, 114].
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