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Interestingly, the analysis of renal tissue gene expression associated with aging MMP-7 has been found among the genes significantly up-regulated in very old kidneys that showed higher rates of histopathological changes including glomerulosclerosis and interstitial fibrosis [ 33].
Quantitative morphological analysis of renal tissue revealed a preventive effect of EPL on the progressive development of fibrosis and tubular loss relevant for the clinical setting [ 4- 6, 8].
To elucidate the molecular mechanisms involved in renal inflammation during the progression, remission and relapse of nephritis we performed a transcriptome analysis of renal tissue from two murine lupus models, NZB/WF1 mice that develop proliferative glomerulonephritis and NZM2410 mice that develop glomerulosclerosis with minimal inflammation.
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It is interesting to note that the immunohistochemistry analysis of renal tissues in the present study demonstrated that CGL was mainly located in renal vasculature as well distal nephron segments while CBS was located only in the proximal tubules.
In this study, renal tissue consisted specifically of renal cortex as mRNA is differentially expressed dependant on the type of renal tissue [34].
Renal oxygen consumption per gram of renal tissue was calculated as VO2 (mL/min/g) = RBF × (AOC − RVOC).
Renal oxygen delivery per gram of renal tissue was calculated as DO2 (mL/min/g) = RBF × AOC.
Heterogeneous enhancement of renal tissue can also be seen with MR imaging.
Renal cortical fibroblasts have key roles in mediating intercellular communication with neighboring/infiltrating cells and extracellular matrix (ECM) and maintenance of renal tissue architecture.
Acute kidney damage (AKD) refers to renal parenchymal damage that may be evidenced via histological samples or by biomarkers of renal tissue damage but not by measures of renal function.
Renal cell isolation took place within 30 minutes of renal tissue collection.
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