Sentence examples for evolution of inflammation from inspiring English sources

Analysis of the evolution of inflammation and tissue damage showed initial infiltration of immune cells into the CNS in both groups as early as 10 days post EAE induction.

Although a MCD dietary model does not replicate in full measure the pathogenesis of NASH in humans, it represents one of the best-established methods to study the evolution of inflammation, oxidant stress, and fibrotic changes associated with NASH[12].

This study contributed to showing the concerted evolution of inflammation and angiogenesis in OA synovial membrane.

Our objective was to determine the evolution of inflammation in patients treated for infection on general wards and the impact of previous statin use.

We recently argued that currently used markers of systemic inflammation such as C-reactive protein and procalcitonin are substantially cleared during continuous renal replacement therapy (CRRT) and thus may lose sensitivity to evaluate the degree and evolution of inflammation [ 2].

Our primary outcome measures were the changes in the systemic inflammatory response syndrome (SIRS) during the follow-up period, defined as the proportion of patients who had at least one SIRS criterion on each day of follow-up, and the evolution of inflammation, as defined by trends in CRP and WCC.

In particular, it should lend itself well to the identification of genes that act at different time points in the evolution or resolution of inflammation, genes that are regulated in response to treatment with anti-inflammatory agents, or genes that reflect changes in the resident connective tissue cells in response to inflammation.

(C) Evolution of corneal inflammation (number of eyes).

Together, the accumulated evidence indicates that Treg cells may play an important role in maintaining peripheral tolerance and preventing the evolution of autoimmune inflammation.

Since most studies concerning the calcium status in IBD yielded contradictory data, in the most recent literature, the discussion has focused on the possible role of vitamin D as a risk factor for the onset and evolution of gut inflammation.

The evolution of islet inflammation, and its potential progression to clinical diabetes, probably depends on the interplay between the patient's genetic background and environmental triggers, such as viral infections and/or dietetic components (1– 4).