METHODS: The Web of Science, SCOPUS, and PUBMED databases were searched to find eligible studies. The standardized mean difference (SMD) and 95% confidence interval (CI) were used to evaluate the differences in NLR, MLR, and PLR levels between SAP and non-SAP patients. The meta-analysis was conducted using the software "Review Manager" (RevMan, version 5.4.1, September 2020). The random-effect model was used for the pooling analysis if there was substantial heterogeneity. Otherwise, the fixed-effect model was adopted.

RESULTS: Twelve studies comprising 6302 stroke patients were included. The pooled analyses revealed that patients with SAP had significantly higher levels of NLR, MLR, and PLR than the non-SAP group. The SMD, 95% CI, p-value, and I2 for them were respectively reported as (0.88, 0.70-1.07, .00001, 77%); (0.94, 0.43-1.46, .0003, 93%); and (0.61, 0.47-0.75, .001, 0%). Subgroup analysis of NLR studies showed no significant differences in the effect size index between the severity of the stroke, the sample size, and the period between the stroke onset and the blood sampling.

METHODS: EMA detection was performed by flow cytometry in monocytes and monoblasts. EMA expression was compared with other known markers of monocytic-macrophage lineage (CD11c, CD14 and intracellular CD68). Samples of purified monocytes were obtained from 20 healthy volunteers. Twenty-two cases of monocytic AML (M4 and M5) were studied and controls were selected from 20 cases of acute lymphoblastic leukaemia (ALL) and 18 cases of non-monocytic AML (M0, M1, M2, M3, and M7).

RESULTS: EMA was shown to be expressed strongly on the surface of all purified monocytes. EMA expression was observed on blast cells in 18/22 (81.8%) cases of AML M4 and M5, but not in that of non-monocytic AML or ALL. In this study EMA monoclonal antibody has demonstrated a strong association (P<0.001) with all the other known markers of monocytic-macrophage lineage in acute leukaemia subtypes. EMA had also shown 100% specificity and 81.8% sensitivity in the diagnosis of AML M4 and M5.

MATERIALS AND METHODS: An in vitro monocyte recruitment model utilizing THP-1 and HUVECs was developed to evaluate TNF-α-induced monocyte adhesion and trans-endothelial migration. To study the role of Nrf2 for MA-mediated anti-inflammatory effects, Nrf2 inhibitor ML385 was used as the pharmacological inhibitor. The expression of Nrf2, monocyte chemoattractant protein-1 (MCP-1), vascular cell adhesion molecule 1 (VCAM-1), cluster of differentiation 36 (CD36), and scavenger receptor type A (SR-A) in HUVECs and THP-1 macrophages were investigated using RT-qPCR and Western blotting. The NF-κB activity was determined using NF-κB (p65) Transcription Factor Assay Kit.

KEY FINDINGS: The results showed opposing effects of MA on Nrf2 expression in HUVECs and THP-1 macrophages. MA suppressed TNF-α-induced Nrf2 expression in HUVECs, but enhanced its expression in THP-1 macrophages. Combined effects of MA and ML385 suppressed MCP-1, VCAM-1, and SR-A expressions. Intriguingly, at the protein level, ML385 selectively inhibited SR-A but enhanced CD36 expression. Meanwhile, ML385 further enhanced MA-mediated inhibition of NF-κB activity in HUVECs. This effect, however, was not observed in THP-1 macrophages.