Background and purpose MicroRNAs (miRNAs) have been demonstrated to play crucial roles in the early stage of acute ischaemic stroke (AIS). The purpose of this study was to investigate the expression patterns of miRNAs in peripheral blood mononuclear cells (PBMCs) from AIS patients and further explore related molecular mechanisms in stroke‐induced immunodeficiency syndrome (SIDS). Methods The miRNA expression patterns of PBMCs were detected by miRNA microarray and validated by quantitative real‐time polymerase chain reaction (qRT‐PCR) in AIS patients and healthy controls. Bioinformatics methods and luciferase reporter assays were used to detect the downstream target genes. Following stimulation with lipopolysaccharide and interleukin‐4, the expression of miR‐4443, tumor necrosis factor receptor associated factor 4 (TRAF4) and the nuclear factor kappa B (NF‐κB) pathway were evaluated. Furthermore, transfection with miR‐4443 mimic or inhibitor in the monocytes was carried out to gain insight into the mechanisms in SIDS. Results Interleukin‐10 in AIS patients was significantly higher than that of healthy controls. The miRNA microarray analysis and qRTPCR validation showed that only miR‐4443 was upregulated expressed in PBMCs from AIS patients, especially in monocytes. miR‐4443 was shown to directly interact with the 3′ untranslated regions of TRAF4, resulting in suppression of TRAF4 protein expression. Furthermore, the expression of miR‐4443 and TRAF4 was regulated by stimulation with lipopolysaccharide or interleukin‐4. Additionally, overexpression of miR‐4443 suppressed the TRAF4/Iκα/NF‐κB signaling pathway to activate the expression of anti‐inflammatory cytokines in monocytes. Conclusions The increased expression of miR‐4443 induced monocyte dysfunction by targeting TRAF4, which may function as a crucial mediator in SIDS.

Mesenchymal stem cells (MSCs) have been isolated from a variety of human tissues (eg, bone marrow, peripheral blood, muscle, fat, umbilical blood, amniotic fluid, embryonic tissues, and placenta). Placenta-derived MSCs (PDMSCs) have received considerable interest because of their wide availability and absence of ethical concerns. The authors characterized the biological properties, ultrastructure, growth factor production, and osteoblastic differentiation of PDMSCs and investigated their potential as seed cells for bone tissue engineering.

Alzheimer’s disease (AD) is the most common cause of dementia. Despite numerous studies on the subject, the pathologies for AD are still unclear and there is still no ideal biomarker for diagnosis. The present study aimed to investigate clinical significance of human complement factor H (CFH) in patients with late-onset AD. Methods: The present prospective study included 187 late-onset AD patients who went to our hospital from January 2015 to December 2017. One hundred patients with mild cognitive impairment (MCI) and 80 healthy individuals who were age and gender matched to AD patients were enrolled as controls. Demographic data such as age, gender, and education duration were recorded. Blood samples were collected and serum levels of C-reactive protein (CRP), CFH, and brain-derived neurotrophic factor (BDNF) were determined by Enzyme-linked immunosorbent assay (ELISA). The mini-mental state examination (MMSE) score was measured for all patients. Results: No significant difference was found in age, gender, and education duration for all participants. The MMSE scores showed AD patients had lower MMES scores than the other two groups. All factors of CFH, CRP, and BDNF were dramatically decreased in AD patients compared with the MCI and the ealthy control. Levels of CFH were found to be positively correlated with levels of CRP; however, no significant correlation was found between CFH and BDNF, nor CFH and MMSE. Conclusion: CFH was decreased in late-onset AD patients, and serum levels of CFH was correlated with serum levels of CRP, but not MMSE and BDNF. These results may provide more clinical evidences for the role of CFH in AD patients.

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