For individual studies in the protocol and assay methodology should be identical

Different assays were designed to detect certain types of TGF-b 1 complexes which made some TGF-b complexes undetected by this assay. Grainger et al. compared the TGF-b 1 levels in the plasma of healthy subjects from 16 studies and the reported mean level ranged from less than 0.1 ng/ml to more than 25 ng/ml. Till now,Displurigen there is no consensus on the plasma TGF-b 1 levels in normal humans, and no particular assay method was recommended for universal application. Although plasma TGF-b 1 was proposed as a biomarker for assessment of PE severity and significant associations were observed, heterogeneity between studies remains. Thus, it may not be suitable to be introduced as a biomarker before a better assay methodology and sample preparation protocol could be developed. To improve the comparability of results between studies, each study should provide details about the chosen assay methodology, the form of detected TGF-b 1, and the preparation procedure of plasma samples. Specific protocols designed to minimize contamination from platelets are available and can be adopted in further studies to reduce the variation in detected TGF-b 1 levels between studies. For individual studies in which the protocol and assay methodology should be identical in the PE group and the control group,RTC13 the detected differences between groups should reflect the real differences to some degree. The plasma TGF-b 1 levels during the third trimester were significantly higher in the PE group than in the control group in all five studies, but the other two studies investigating the second trimester showed an altered association, indicating that the circulating level of TGF-b 1 during pregnancy may change in a special trend in PE patients. If true, whether the decreased TGF-b 1 level during second trimester is responsible for the increased Th17/Tregs ratio and triggered the systemic inflammation in PE patients, and whether the elevated TGF-b 1 level during third trimester is one trigger or consequence of PE are unclear. Therefore, its role in the pathogenesis of PE remains intriguing and further research is needed to investigate the TGF-b 1 level throughout gestation, especially in first and second trimesters.