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In many pathological conditions, including ischemia, epilepsy and multiple sclerosis, tissue acidosis is a common feature and contributes to brain injury [17] [20].
Control tissue (CON1 CON8, Table 1) was provided by the UK multiple sclerosis tissue resource, London.
Apoptosis inducing factor was present in the mitochondria of healthy neurons in control and multiple sclerosis tissue (Fig 3V).
So far, no systematic study has correlated axonal injury and destruction in multiple sclerosis tissue, including the NAWM, with inflammation.
Lesions were identified as regions of well-defined hyperintense signal, as previously described in post-mortem multiple sclerosis tissue (De Groot et al., 2001).
In multiple sclerosis tissue, additional staining was predominantly present in myelin sheaths in active lesions, which in many instances were fragmented.
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We categorized the multiple sclerosis tissues used in our studies based on the findings of pathological exams as active, based on evidence of monocyte infiltrates and inactive, if there were no infiltrates present.
In multiple sclerosis brain tissue, however, the results show major discrepancies.
In this study, we determined the composition and quantified the content of lipids and sterols in normal appearing white matter (NAWM) and normal appearing grey matter (NAGM) from control and multiple sclerosis brain tissues by electrospray ionization tandem mass spectrometry.
To test this hypothesis, (co -localization of DGco -localizationLC1 was analyzed by immunofistochemical stainings in gliotic brain tissue from a patient with multiple sclerosis, in glioblastoma tissue and in brain tissue from an MLC patient.
In multiple sclerosis (MS) brain tissue, gamma delta T cells co-localize with heat shock protein (hsp 65+ oligodendrocytes and are oligoclonally restricted in the V delta 2J delta 3 lineage.
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