To systemically evaluate the accuracy of pleth variability index to predict fluid responsiveness in mechanically ventilated patients. A literature search of PUBMED, OVID, CBM, CNKI and Wanfang Data for clinical studies in which the accuracy of pleth variability index to predict fluid responsiveness was performed (last update 5 April 2015). Related journals were also searched manually. Two reviewers independently assessed trial quality according to the modified QUADAS items. Heterogeneous studies and meta-analysis were conducted by Meta-Disc 1.4 software. A subgroup analysis in the operating room (OR) and in intensive care unit (ICU) was also performed. Differences between subgroups were analyzed using the interaction test. A total of 18 studies involving 665 subjects were included. The pooled area under the receiver operating characteristic curve (AUC) to predict fluid responsiveness in mechanically ventilated patients was 0.88 [95 % confidence interval (CI) 0.84-0.91]. The pooled sensitivity and specificity were 0.73 (95 % CI 0.68-0.78) and 0.82 (95 % CI 0.77-0.86), respectively. No heterogeneity was found within studies nor between studies. And there was no significant heterogeneity within each subgroup. No statistical differences were found between OR subgroup and ICU subgroup in the AUC [0.89 (95 % CI 0.85-0.92) versus 0.90 (95 % CI 0.82-0.94); P = 0.97], and in the specificity [0.84 (95 % CI 0.75-0.86) vs. 0.84 (95 % CI 0.75-0.91); P = 1.00]. Sensitivity was higher in the OR subgroup than the ICU subgroup [0.84 (95 % CI 0.78-0.88) vs. 0.56 (95 % CI 0.47-0.64); P = 0.00004]. The pleth variability index has a reasonable ability to predict fluid responsiveness.

Preeclampsia (PE), a common obstetrical disorder, is characterized by impaired migration and invasion abilities of trophoblastic cells. MicroRNA-183-5p (miR-183) was reported to regulate cell migration and invasion in various types of human cancers; however, its role in the pathogenesis of PE remains elusive. Herein, we investigated the role of miR-183 in HTR-8/SVneo trophoblast cells invasion and migration and explored the underlying mechanism. Our results showed that miR-183 was significantly up-regulated in placental tissues from pregnant women compared with that in normal pregnant women. Overexpression of miR-183 inhibited proliferation, migration and invasion, as well as induced apoptosis in HTR-8/SVneo cells. Otherwise, down-regulation of miR-183 achieved the opposite effects. Bioinformatics prediction and luciferase reporter assay confirmed that matrix metalloproteinase-9 (MMP-9) is a target of miR-183. In addition, MMP-9 expression was significantly down-regulated, and inversely correlated with the miR-183 level in placental tissues from pregnant women with severe PE. Down-regulation of MMP-9 suppressed the trophoblast cell invasion and migration, whereas overexpression of MMP-9 promoted cell invasion and migration in HTR-8/SVneo cells. More importantly, up-regulation of MMP-9 reversed the inhibitory effects of miR-183 on cell invasion and migration in trophoblast cells. Collectively, our findings suggested that miR-183 may play critical roles in the pathogenesis of PE and serve as a potential biomarker for severe PE.

Lung adenocarcinoma (LUAD) has been considered as the most common cause of cancer-associated mortality. Radiotherapy resistance is one of the main reasons for LUAD treatment failure. The microRNA (miR)-101-3p has been previously reported to function as a tumor suppressor in several types of cancer, including LUAD. The present study aimed to explore the role and mechanism of miR-101-3p on radioresistance of lung adenocarcinoma cells through bioinformatics analysis and biological experiments. Based on the analysis of Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) data, it was demonstrated that the expression of miR-101-3p was low in LUAD tissues compared with normal lung tissues and was associated with poor prognosis of patients with LUAD. The results of the CCK-8 assay, colony formation assay, immunofluorescence staining, caspase-3 activity assay and western blotting demonstrated that miR-101-3p overexpression sensitized LUAD cells to ionizing radiation by decreasing the abilities of LUAD cell proliferation, colony formation, DNA damage repair and increasing caspase-3 activity and apoptosis of LUAD cells following ionizing radiation. Furthermore, according to bioinformatics analysis and luciferase assay, baculoviral IAP repeat containing 5 (BIRC5) was identified as a direct target of miR-101-3p. Increased BIRC5 expression reversed the miR-101-3p-mediated increase in LUAD cell radiotherapy sensitivity. Taken together, the results of the present study demonstrated that miR-101-3p may be considered as a potential target that can enhance LUAD cell sensitivity to radiotherapy, which may provide a new strategy to improve therapy in patients with LUAD.