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The study of the ancient Luanhe alluvial fan has focused more on the Holocene, and no systematic study has been conducted on its Pleistocene evolution and variation. We studied the magnetic stratigraphy, chronostratigraphy, sedimentology, logging sedimentology, and core color of the boreholes PZK10 and PZK20 in the ancient Luanshe alluvial fan. Based on that, we carried out a comprehensive study of the Quaternary three-dimensional geological structure, the scale of the alluvial fan body, and the migration pattern of the ancient Luanshe alluvial plain. The borehole PZK10 recorded Brunches, Matuyama, and Gauss polarity chrons; the boundaries between them are 77.42 m and 71.50 m, respectively. The borehole PZK10 also revealed a set of diluvial “mud-gravel” layers deposited in the Pliocene, with two alluvial fan-lake phase cycles in the Early Pleistocene, braided river deposits in the Middle Pleistocene, and lake, alluvial fan and braided river facies in the late Pleistocene. A set of highly thick “mud-gravel” layers was deposited in the Pliocene of the borehole PZK20. The early Pleistocene is the fan-front–plain-braided river facies deposition, the middle Pleistocene is the braided river–alluvial fan facies deposition, and the late Pleistocene is the braided river deposition. Early Pleistocene, the ancient Luanhe River out of the mountain formed a large-scale alluvial fan in Shaliuhe town, which is the first stage of the ancient Luanhe alluvial fan. In the middle of the early Pleistocene, the ancient Luanhe River diverged in the current Qiuzhuang reservoir, and the alluvial fan formed in the Fengrun area, namely the second stage alluvial fan. In the middle Pleistocene, the first alluvial fan began to shrink, while the second alluvial fan continued to develop, forming a vast thick gravel layer. Late Pleistocene, the ancient Luanhe river was captured north of Qianxi county. It flowed eastwards and migrated out of the research area into the Qian’an basin in Xixiakou village, forming the alluvial fan with Xixiakou village as its apex.

Objective To explore the role and mechanism of RNA demethylase FTO in the apoptosis of mouse spermatocyte GC-2 cells induced by bisphenol S (BPS). Methods GC-2 cells were treated with BPS at a final concentration of 0 (DMSO control group), 20, 40, 80, 160, and 320 μmol/L for 72 h. The cell morphology changes were observed with microscopy. CCK-8 assay was utilized to detect cell viability, and flow cytometry was used to detect cell apoptosis and cycle changes. Colorimetric assay was adopted to measure the global level of m6A RNA methylation. Western blotting was employed to detect the protein levels of RNA methyltransferase METTL3, RNA demethylase FTO, RNA binding protein, YTHDF1, apoptosis-related molecules P53, P21, BCL2, Caspase9, Caspase3, BAX and cell cycle-related molecules CyclinD1, CDK4, CDK2. After FTO gene interference cell model was established, CCK-8 assay was used to measure cell survival and flow cytometry to detect cell apoptosis. The protein levels of FTO, P53, BCL2 and BAX were detected by Western blotting. Results Compared with the control group, the number of GC-2 cells was significantly reduced and more vacuole cells appeared in the BPS exposure group. The cell survival rate was significantly decreased and the apoptotic rate was markedly increased at 160 and 320 μmol/L of BPS (P < 0.05). The protein levels of apoptosis-related molecules P53, P21, Caspase9 and Caspase3 were increased significantly, and that of BCL2 was decreased significantly (P < 0.05). When the BPS concentration was 80, 160 and 320 μmol/L, cell cycle was arrested at G1/S phase (P < 0.05). The protein levels of G1/S phase related molecules CyclinD1, CDK4, and CDK2 were significantly down-regulated (P < 0.05). When the dose of BPS increased to 80~320 μmol/L, the global RNA methylation level was relatively increased (P < 0.01). The protein levels of RNA methyltransferase METTL3 and RNA binding protein YTHDF1 did not change obviously, while that of RNA demethylase FTO decreased sharply (P < 0.05). Compared with the control group, after interference with FTO expression, the number and viability of GC-2 cells were significantly reduced, and the apoptotic rate was notably increased (P < 0.05). The protein level of P53 was remarkably up-regulated, and that of BCL2 down-regulated when FTO expression was knocked down (P < 0.05). Conclusion RNA demethylase FTO may play an important role in BPS-induced apoptosis of GC-2 cells through regulating P53-P21 and BCL2 mitochondrial pathway

Objective To explore the possible key pathways in the male reproductive toxicity induced by exposure to low-dose bisphenol A (BPA). Methods BPA-related genes were screened based on Comparative Toxicogenomics Database (CTD). Functional enrichment analysis was used for these genes to explore the possible pathways and identify the key genes in related pathways. Mouse spermatogonia cell line GC-2 cells were treated with BPA at a final concentration of 0 (DMSO control group), 20, 40 and 80 μmol/L for 72 h. Then the changes of cell morphology and apoptotic rate were observed. The mRNA and protein expression levels of the obtained key genes were detected by RT-qPCR and Western blotting, respectively. Results A total of 1 460 BPA-related genes were screened out from the CTD database. Gene Ontology (GO) enrichment analysis showed that these genes were significantly enriched in molecular biological processes, such as reproductive system development and reproductive structure development, and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis found that they were significantly enriched in HIF-1 and PI3K-Akt signaling pathways (P < 0.01). Visual analysis showed that the key genes in the pathway were HIF-1α, PKC and P300/CBP, and PI3K, JAK, P53 and BCL-2. The apoptotic rate of GC-2 cells exposed to BPA was significantly increased in a dose-dependent manner (P < 0.05). Compared with the control cells, the mRNA expression levels of PI3K and JAK were significantly down-regulated, while those of P53 and BCL-2 were up-regulated (P < 0.05). The protein levels of PI3K and BCL-2 were obviously down-regulated, while that of P53 up-regulated (P < 0.05). Conclusion The PI3K-Akt signaling pathway may play an important role in the process of GC-2 cell apoptosis induced by low-dose BPA exposure.

Objective To explore the effect of ten-eleven translocation family 1 (TET1) gene expression on the migration and invasion of lung cancer cells and investigate its underlying mechanism. Methods The expression level of TET1 gene in normal human bronchial epithelial (HBE) cells and lung cancer cell lines (H460, H358, 95D and LTEP-a-2) was detected by quantitative RT-PCR. The effects of different expression level (overexpression and knockdown) of TET1 gene on the migration and invasion ability in lung cancer cells was analyzed by wound healing experiment and Transwell assay. The mRNA and protein expression levels of downstream regulatory gene β-catenin (CTNNB1) and MMP7 were detected by quantitative RT-PCR and Western blotting to determine the possible signal pathway. Results The expression level of TET1 gene was decreased in lung cancer cells compared with normal HBE cells (P < 0.01). Overexpression of TET1 gene significantly inhibited the migration and invasion of lung cancer cells, while its knockdown enhanced the invasion and migration abilities of lung cancer cells (P < 0.01). The mRNA and protein expression levels of CTNNB1 and MMP7 were decreased after TET1 overexpression, while the mRNA and protein levels of the 2 molecules were increased after knockdown (P < 0.01). Blockade of CTNNB1 by its inhibitor significantly diminished the effect of TET1 on the migration and invasion of lung cancer cell lines. Conclusion The expression level of TET1 is down-regulated in lung cancer cell lines. TET1 gene may inhibit the migration and invasion of lung cancer cells mainly through Wnt/β-catenin signaling pathway and its key downstream genes CTNNB1 and MMP7.

Objective To investigate the mRNA expression of SMAD9 in lung adenocarcinoma, and its relationship with clinicopathological parameters, survival and prognosis, so as to provide some valuable references for the screening and postoperative survival. Methods The expression of SMAD9 in tumor tissues (510 cases) and adjacent normal tissues (59 cases) of lung adenocarcinoma patients and its relationship with clinicopathological parameters and postoperative survival were analyzed based on the Cancer Genome Atlas (TCGA) database. The expression of SMAD9 in tumor tissues and adjacent normal tissues of lung adenocarcinoma patients, HBE malignant transformed cells induced by 3-MCA and lung adenocarcinoma cells were detected by quantitative real-time RT-PCR (qRT-PCR) and Western blotting. The effect of SMAD9 overexpression and interference on cell proliferation was detected by CCK-8 assay. Results The mRNA expression analysis of SMAD9 in TCGA database showed that the expression of SMAD9 was significantly lower in lung adenocarcinoma than adjacent normal tissues (P < 0.01). The results of qRT-PCR and Western blotting also showed that the expression of SMAD9 was significantly down-regulated in 3-MCA-induced HBE malignant transformed cells and lung adenocarcinoma tissues and cell lines (P < 0.05). The down-regulation of SMAD9 expression was closely correlated with N grade and tumor grade (P < 0.05). ROC curve analysis indicated that the mRNA expression of SMAD9 was a sensitive indicator of lung adenocarcinoma (AUC=0.903, 95%CI=0.868~0.938, P < 0.001). Kaplan-Meier analysis displayed that the survival time of patients with low expression of SMAD9 was significantly shorter than those with high expression (P < 0.05). Overexpression of SMAD9 inhibited the proliferation of lung adenocarcinoma cells (P < 0.01), and the proliferation of HBE cells was significantly enhanced after interfering with SMAD9 expression as compared with the control cells (P < 0.01). Conclusion SMAD9 gene expression is down-regulated in the incidence and development of lung adenocarcinoma. The expression of SMAD9 may be of great value for the screening and postoperative survival of lung adenocarcinoma patients.

Low density parity check code (LDPC) is the most popular error correction code (ECC) for current nand flash memory controllers. Next generation flash memory, such as triple-level cell (TLC) and quad-level cell (QLC) with a higher bit error rate, bring up the demand for superior ECC algorithms providing excellent performance and acceptable hardware overhead. This letter proposes turbo product code (TPC) as an alternative to LDPC by exploring embedding of a TPC engine into a solid-state drive (SSD) controller architecture. The implementation of this TPC engine uses 2-D error coding and applies the Bose-Chaudhuri–Hocquenghem (BCH) code in each dimension. The algorithm is further improved by flipping the dedicated bit matrix when the basic TPC decoding algorithm terminates with uncorrectable conditions. This bit-flipping enhanced TPC (BFE-TPC) module is finally integrated into a nonvolatile memory express (NVMe) SSD controller driving eight flash memory channels. This BFE-TPC module illustrates the potential of 2D-TPCs as a replacement for LDPCs due to its high throughput and low hardware overhead. [ABSTRACT FROM AUTHOR]