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BackgroundPeroxiredoxin (Prx) protein family have been reported as important damage-associated molecular patterns (DAMPs) in ischemic stroke. Since peroxiredoxin 2 (Prx2) is the third most abundant protein in erythrocytes and the second most protein in the cerebrospinal fluid in traumatic brain injury and subarachnoid hemorrhage (SAH) patients, we assessed the role of extracellular Prx2 in the context of SAH.MethodsWe introduced a co-culture system of primary neurons and microglia. Prx2 was added to culture medium with oxyhemoglobin (OxyHb) to mimic SAH in vitro. Neuronal cell viability was assessed by lactate dehydrogenase (LDH) assay, and neuronal apoptosis was determined by TUNEL staining. Inflammatory factors in culture medium were measured by ELISA, and their mRNA levels in microglia were determined by qPCR. Toll-like receptor 4 knockout (TLR4-KO) mice were used to provide TLR4-KO microglia; ST-2825 was used to inhibit MyD88, and pyrrolidine dithiocarbamate (PDTC) was used to inhibit NF-κB. Related cellular signals were analyzed by Western blot. Furthermore, we detected the level of Prx2 in aneurysmal SAH patients’ cerebrospinal fluids (CSF) and compared its relationship with Hunt-Hess grades.ResultsPrx2 interacted with TLR4 on microglia after SAH and then activated microglia through TLR4/MyD88/NF-κB signaling pathway. Pro-inflammatory factors were expressed and released, eventually caused neuronal apoptosis. The levels of Prx2 in SAH patients positively correlated with Hunt-Hess grades.ConclusionsExtracellular Prx2 in CSF after SAH is a DAMP which resulted in microglial activation via TLR4/MyD88/NF-κB pathway and then neuronal apoptosis. Prx2 in patients’ CSF may be a potential indicator of brain injury and prognosis.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1118-4) contains supplementary material, which is available to authorized users.

Abundant and refined structural information under forest canopy can be obtained by using terrestrial laser scanning (TLS) technology. This study explores the methods of using TLS to obtain point cloud data and estimate individual tree height and diameter at breast height (DBH) at plot level in regions with complex terrain. Octree segmentation, connected component labeling and random Hough transform (RHT) are comprehensively used to identify trunks and extract DBH of trees in sample plots, and tree height is extracted based on the growth direction of the trees. The results show that the topography, undergrowth shrubs, and forest density influence the scanning range of the plots and the accuracy of feature extraction. There are differences in the accuracy of the results for different morphological forest species. The extraction accuracy of Yunnan pine forest is the highest (DBH: Root Mean Square Error (RMSE) = 1.17 cm, Tree Height: RMSE = 0.54 m), and that of Quercus semecarpifolia Sm. forest is the lowest (DBH: RMSE = 1.22 cm, Tree Height: RMSE = 1.23 m). At plot scale, with the increase of the mean DBH or tree height in plots, the estimation errors show slight increases, and both DBH and height tend to be underestimated.

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Background: Aucubin (Au), an iridoid glycoside from natural plants, has antioxidative and anti-inflammatory bioactivities; however, its effects on a traumatic brain injury (TBI) model remain unknown. We explored the potential role of Au in an H 2 O 2-induced oxidant damage in primary cortical neurons and weight-drop induced-TBI in a mouse model. Methods: In vitro experiments, the various concentrations of Au (50 μg/ml, 100 μg/ml, or 200 μg/ml) were added in culture medium at 0 h and 6 h after neurons stimulated by H 2 O 2 (100 μM). After exposed for 12 h, neurons were collected for western blot (WB), immunofluorescence, and M29,79-dichlorodihydrofluorescein diacetate (DCFH-DA) staining. In vivo experiments, Au (20 mg/kg or 40 mg/kg) was administrated intraperitoneally at 30 min, 12 h, 24 h, and 48 h after modeling. Brain water content, neurological deficits, and cognitive functions were measured at specific time, respectively. Cortical tissue around focal trauma was collected for WB, TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, Nissl staining, quantitative real time polymerase chain reaction (q-PCR), immunofluorescence/immunohistochemistry, and enzyme linked immunosorbent assay (ELISA) at 72 h after TBI. RNA interference experiments were performed to determine the effects of nuclear factor erythroid-2 related factor 2 (Nrf2) on TBI mice with Au (40 mg/kg) treatment. Mice were intracerebroventricularly administrated with lentivirus at 72 h before TBI establishment. The cortex was obtained at 72 h after TBI and used for WB and q-PCR.

Due to the widespread use of sophisticated imaging tools, digital image forgeries have already become a serious social problem. In this paper, we proposes an efficient and robust algorithm for detection of a specific category of digital image forgery known as region duplication forgery, which is done by copying a block of an image and pasting it on to some other block of the same image. The image is first reduced in dimension by Gaussian pyramid, and four features are adopted for each circle block. The feature vectors are lexicographically sorted. Then similar vectors will be matched by a certain threshold value. Finally, the area threshold value is proposed to remove the wrong similar blocks. Experimental results show that our method is robust to not only the post processing including noise adding, blurring, lossy compression, but also the copy region rotation. Meanwhile, the proposed method reduces the total number of blocks to narrow blockmatching searching space, which can improve the efficiency comparing with the exiting methods.

Background and Aim Gastric cancer (GC), a prevalent tumor, exerts a major economic burden, and we aimed to explore miR‐876‐3p's effects on GC and related mechanisms. Methods Cell viability was analyzed via CCK‐8 and colony formation assay. Stem cell‐like properties were examined via spheroid colony formation assay. mRNA abundance of key genes was analyzed via quantitative polymerase chain reaction. Protein level of TMED3 and stem cell markers was examined by western blot. TargetScan, luciferase, and biotin‐miRNA pulldown assay were used to identify miR‐876‐3p's target. Results MiR‐876‐3p was downregulated in GC, and its mRNA level had negative relationship with cisplatin resistance of GC. Moreover, decreased miR‐876‐3p expression level suggested poor prognosis of GC patients. MiR‐876‐3p inhibited drug resistance of cisplatin‐resistant cell line SGC‐7901/DDP and MKN‐45/DDP, as shown by decreased cell viability, IC50, and colony formation ability. MiR‐876‐3p inhibited stem cell‐like features and downregulated the expressions of Sox‐2, Oct‐4, CD133, and CD44 in GC cells. Luciferase and biotin‐miRNA pulldown assay confirmed that TMED3 was miR‐876‐3p's direct target. TMED3 siRNA inhibited miR‐876‐3p's effects on cisplatin resistance and stem cell‐like features of SGC‐7901/DDP cells. Conclusion MiR‐876‐3p enhanced cisplatin sensitivity and restricted stem cell‐like features of GC through targeting TMED3.