Toward Predicting Interfacial Tension of Impure and Pure CO2-Brine Systems Using Robust Correlative Approaches.

In the context of global climate change, significant attention is being directed toward renewable energy and the pivotal role of carbon capture and storage (CCS) technologies. These innovations involve secure CO2 storage in deep saline aquifers through structural and capillary processes, with the interfacial tension (IFT) of the CO2-brine system influencing the storage capacity of formations. In this study, an extensive data set of 2811 experimental data points was compiled to model the IFT of impure and pure CO2-brine systems. Three white-box machine learning (ML) methods, namely, genetic programming (GP), gene expression programming (GEP), and group method of data handling (GMDH) were employed to establish accurate mathematical correlations. Notably, the study utilized two distinct modeling approaches: one focused on impurity compositions and the other incorporating a pseudocritical temperature variable (Tcm) offering a versatile predictive tool suitable for various gas mixtures. Among the correlation methods explored, GMDH, employing five inputs, exhibited exceptional accuracy and reliability across all metrics. Its mean absolute percentage error (MAPE) values for testing, training, and complete data sets stood at 7.63, 7.31, and 7.38%, respectively. In the case of six-input models, the GEP correlation displayed the highest precision, with MAPE values of 9.30, 8.06, and 8.31% for the testing, training, and total data sets, respectively. The sensitivity and trend analyses revealed that pressure exerted the most significant impact on the IFT of CO2-brine, showcasing an adverse effect. Moreover, an impurity possessing a critical temperature below that of CO2 resulted in an elevated IFT. Consequently, this relationship leads to higher impurity concentrations aligning with lower Tcm values and subsequently elevated IFT. Also, monovalent and divalent cation molalities exhibited a growing influence on the IFT, with divalent cations exerting approximately double the influence of monovalent cations. Finally, the Leverage approach confirmed both the reliability of the experimental data and the robust statistical validity of the best correlations established in this study.

Temperature-Responsive Separation Membrane with High Antifouling Performance for Efficient Separation.

Temperature-responsive separation membranes can significantly change their permeability and separation properties in response to changes in their surrounding temperature, improving efficiency and reducing membrane costs. This study focuses on the modification of polyvinylidene fluoride (PVDF) membranes with amphiphilic temperature-responsive copolymer and inorganic nanoparticles. We prepared an amphiphilic temperature-responsive copolymer in which the hydrophilic poly(N-isopropyl acrylamide) (PNIPAAm) was side-linked to a hydrophobic polyvinylidene fluoride (PVDF) skeleton. Subsequently, PVDF-g-PNIPAAm polymer and graphene oxide (GO) were blended with PVDF to prepare temperature-responsive separation membranes. The results showed that temperature-responsive polymers with different NIPAAm grafting ratios were successfully prepared by adjusting the material ratio of NIPAAm to PVDF. PVDF-g-PNIPAAm was blended with PVDF with different grafting ratios to obtain separate membranes with different temperature responses. GO and PVDF-g-PNIPAAm formed a relatively stable hydrogen bond network, which improved the internal structure and antifouling performance of the membrane without affecting the temperature response, thus extending the service life of the membrane.

Modeling of large-scale hoxbb cluster deletions in zebrafish uncovers a role for segmentation pathways in atrioventricular boundary specification.

Hox genes orchestrate the segmental specification of the muscular circulatory system in invertebrates but it has not proven straightforward to decipher segmental parallels in the vertebrate heart. Recently, patients with HOXB gene cluster deletion were found to exhibit abnormalities including atrioventricular canal defects. Using CRISPR, we established a mutant with the orthologous hoxbb cluster deletion in zebrafish. The mutant exhibited heart failure and atrioventricular regurgitation at 5 days. Analyzing the four genes in the hoxbb cluster, isolated deletion of hoxb1b-/- recapitulated the cardiac abnormalities, supporting hoxb1b as the causal gene. Both in situ and in vitro data indicated that hoxb1b regulates gata5 to inhibit hand2 expression and ultimately is required to pattern the vertebrate atrioventricular boundary. Together, these data reveal a role for segmental specification in vertebrate cardiac development and highlight the utility of CRISPR techniques for efficiently exploring the function of large structural genomic lesions.

Do you like it or not? Identifying preference using an electroencephalogram during the viewing of short videos.

Accurately predicting whether a short video will be liked by viewers is a topic of interest to media researchers. This study used an electroencephalogram (EEG) to record neural activity in 109 participants as they watched short videos (16 clips per person) to see which neural signals reflected viewers' preferences. The results showed that, compared with the short videos they disliked, individuals would experience positive emotions [indexed by a higher theta power, lower (beta - theta)/(beta + theta) score], more relaxed states (indexed by a lower beta power), lower levels of mental engagement and alertness [indexed by a lower beta/(alpha + theta) score], and devote more attention (indexed by lower alpha/theta) when watching short videos they liked. We further used artificial neural networks to classify the neural signals of different preferences induced by short videos. The classification accuracy was the highest when using data from bands over the whole brain, which was 75.78%. These results may indicate the potential of EEG measurement to evaluate the subjective preferences of individuals for short videos.

Erratum: IRS-1 regulates proliferation, invasion and metastasis of pancreatic cancer cells through MAPK and PI3K signaling pathways.

[This corrects the article on p. 5185 in vol. 11, PMID: 31949598.].

Sanguisorba parviflora (Maxim.) Takeda alleviates cyclophosphamide-induced leukopenia by regulating haematopoietic cell-specific protein 1-associated protein X-1 gene expression.

WHAT IS KNOWN AND OBJECTIVE: We have previously shown that the saponins of Sanguisorba parviflora (Maxim.) Takeda (Sp. T) relieved cyclophosphamide-induced myelosuppression in leukopenic mice. Haematopoietic cell-specific protein 1-associated protein X-1 (HAX-1) participated in the survival of neutrophils through the regulation of mitochondrial function. The aim of the present study was to comprehensively identify the role of HAX-1 in the mechanism of leukopenia alleviation by Sp. T. METHODS: HAX-1 gene and protein expression levels in peripheral blood neutrophils were examined using real-time quantitative reverse transcription-polymerase chain reaction, western blot and immunohistochemical assays. Neutrophil apoptosis was measured using flow cytometry. Mitochondrial function was determined via assessments of the reactive oxygen species (ROS) generation and mitochondrial membrane potential (ΔΨm) integrity levels. RESULTS AND DISCUSSION: The HAX-1 gene expression level in the peripheral blood neutrophils was significantly lower in patients with leukopenia than in healthy donors. The saponins of Sp. T induced HAX-1 expression and promoted myeloid progenitor cell (mEB8-ER cell) viability. HAX-1 overexpression reduced the production of ROS and maintained ΔΨm integrity. Cyclophosphamide-induced mitochondrial dysfunction and apoptosis could be abrogated by treatment with Sp. T or metformin. WHAT IS NEW AND CONCLUSION: Our data suggest a mechanism through which Sp. T protects against chemotherapy-induced leukopenia by regulating HAX-1 gene expression in a mitochondrial-dependent manner.

Sanguisorba parviflora (Maxim) Takeda alleviates cyclophosphamide-induced leukopenia via regulating the hematopoietic cell-specific protein 1-associated protein X-1 gene.

WHAT IS KNOWN AND THE OBJECTIVE: Our previous studies have shown that saponins of Sanguisorba parviflora (Maxim) Takeda (Sp. T) relieved cyclophosphamide-induced myelosuppression in mice with leukopenia. The hematopoietic cell-specific protein 1-associated protein X-1 (HAX-1) participated in the survival of neutrophils through the regulation of mitochondrial function. This study aimed to comprehensively identify the role of HAX-1 in Sp. T to alleviate leukopenia. METHODS: HAX-1 expression was examined in the peripheral blood neutrophils using real-time polymerase chain reaction (PCR), Western blot analysis and immunohistochemical staining. Neutrophil apoptosis was measured by flow cytometry. Mitochondrial function was evaluated via reactive oxygen species (ROS) generation and mitochondrial membrane potential (ΔΨm) integrity. RESULTS AND DISCUSSION: Our study indicated that the expression of the HAX-1 gene was significantly decreased in the peripheral blood neutrophils of leukopenia patients compared with healthy donors. The saponins of Sp. T induced HAX-1 expression and promoted myeloid progenitor cell (mEB8-ER cell) viability, while overexpression of HAX-1 reduced the production of reactive oxygen species (ROS) and maintained the integrity of the mitochondrial membrane potential. Cyclophosphamide-induced mitochondrial dysfunction and apoptosis could be abrogated by treatment with Sp. T or the addition of metformin. WHAT IS NEW AND OUR CONCLUSION: Our data support a mechanism where Sp. T protects against chemotherapy-induced leukopenia by regulating HAX-1 gene expression in a mitochondrial-dependent manner.

Aortic dissection during pregnancy and postpartum.

BACKGROUND: Patients with aortic dissection during pregnancy and postpartum period exhibit a high mortality. At present, a complete overview of aortic dissection during pregnancy and postpartum period is lacking. ​Methods: This systematic review included 80 reports published from 2000 to 2020, comprising a total study population of 103 patients with aortic dissection. ​Results: We found that Stanford Type A aortic dissection was more common in prepartum cases, especially in the third trimester, while postpartum cases of aortic dissection were more common in Stanford Type B. The most common risk factor was connective tissue disease, with no other known risk factors. The mode of delivery had no significant effect on the type of postpartum aortic dissection. Reduced maternal and fetal mortality was observed when patients with Stanford Type A aortic dissection occurring after 28 gestational weeks underwent cesarean section followed by aortic replacement. Patients with Stanford Type B aortic dissection were treated mainly with medication and/or endovascular repair. ​Conclusion: Contemporary management of patients during pregnancy and within 12 weeks postpartum requires multidisciplinary cooperation and includes serial, noninvasive imaging, biomarker testing, and genetic risk profiling for aortopathy. Early diagnosis and accurate treatment are essential to reduce maternal and fetal mortality.

Trichinella spiralis infection decreases the diversity of the intestinal flora in the infected mouse.

BACKGROUND: Trichinella spiralis is a kind of intestinal nematode that can strongly modulate the host immune system. However, the effects of T. spiralis infection on the intestinal flora are poorly understood. This study aimed to explore the effect of T. spiralis infection on the intestinal flora. METHODS: The intestinal contents of T. spiralis infected mice were examined through high-throughput sequencing (Illumina) of the V3-V4 hypervariable region in bacterial 16S rRNA gene. The sequences were analyzed using the QIIME software package and other bioinformatics methods. RESULTS: Altogether 2,899,062 sequences were generated from the samples collected from different intestinal regions at various infection time points; the 44,843 Operational Taxonomic Unit (OTUs) analysis showed that T. spiralis infection would decrease the diversity of intestinal flora in the infected mice relative to that in the uninfected ones, especially in the large intestine and feces. Further analysis indicated that, the genera Oscillospira from the phylum Firmicutes showed a higher abundance in the helminth-infected small and larger intestines; the genera Bacteroides from the phyla Bacteroides, the genera Lactobacillus from the phyla Firmicutes, the genera Escherichia from the phyla Proteobacteria, and the genera Akkermansia from the phyla Verrucomicrobia displayed increased abundances in the T. spiralis positive fecal samples compared with those in the negative samples. CONCLUSIONS: T. spiralis infection decreases the diversity of the intestinal flora in the infected mouse. However, it remains unclear about the association between the changes in intestinal flora caused by T. spiralis infection and the parasite pathogenesis, which should be further examined.

MiR-126 promotes esophageal squamous cell carcinoma via inhibition of apoptosis and autophagy.

MiRNA-126 (miR-126) has been shown to be involved in various malignancies as well as other biological processes. However, currently, its role in esophageal squamous cell carcinoma (ESCC) is not well understood. The present study is focused on the mechanisms that underlie the effect of miR-126 on cell survival and death (apoptosis and autophagy) in ESCC cells. MiR-126 expression was found to be enhanced in ESCC cells and tissues. Downregulation of miR-126 suppressed cell survival, and TUNEL staining indicated that miR-126 inhibition promoted ESCC cell death. In addition, the production of LC3B and p62 proteins, two autophagy signals, was reduced following miR-126 inhibition. A dual luciferase reporter assay demonstrated that the STAT3 3'-UTR is a direct target of miR-126. Furthermore, STAT3 knock-down rescued the effects on autophagy and apoptosis caused by miR-126 inhibition in ESCC cells. The results of this study may provide some insight into the molecular and biological mechanisms underlying ESCC generation and contribute to the development of novel therapeutic approaches for ESCC.

Role of exosomal microRNA-125b-5p in conferring the metastatic phenotype among pancreatic cancer cells with different potential of metastasis.

AIMS: To explore the pro-metastatic role of exosomes derived from highly invasive pancreatic cancer cell and the associated aberrant expression of exosomal microRNAs (miRNAs). MAIN METHODS: Weakly invasive PC-1 cells were treated with exosomes of highly invasive PC-1.0 cells to determine the pro-metastatic effect of PC-1.0 derived exosomes. The exosomal miRNA profile was further investigated using high-throughput sequencing. The level of miR-125b-5p in highly and weakly invasive pancreatic cancer cells was further determined. Pancreatic cancer cells transfected with miR-125b-5p mimic and inhibitor were used to explore the effect of miR-125b-5p on migration, invasion and epithelial-to-mesenchymal transition (EMT). Treatment with PC-1.0 derived exosome and Western blot assay were performed to validate STARD13 as a target of exosomal miR-125b-5p in pancreatic cancer. KEY FINDINGS: PC-1.0 derived exosomes promoted the migration and invasion of weakly invasive PC-1 cells. miRNA sequencing revealed 62 miRNAs upregulated in PC-1.0 derived exosomes. miR-125b-5p most significantly promoted migration and invasion and was associated with metastasis in pancreatic cancer. Further, miR-125b-5p was upregulated in highly invasive pancreatic cancer cells and increased migration, invasion, and EMT. Moreover, its upregulation was associated with activation of MEK2/ERK2 signaling. The tumor suppressor STARD13 was directly targeted by miR-125b-5p in pancreatic cancer, which was associated with good prognosis and was suppressed by exosomes derived from highly invasive cancer cells. SIGNIFICANCE: This study explored the pro-metastatic role of exosomes derived from highly invasive pancreatic cancer cells and the associated aberrant expression of exosomal miRNAs, which may help to elucidate the metastatic mechanism of pancreatic cancer.

Integrin beta 4 (ITGB4) and its tyrosine-1510 phosphorylation promote pancreatic tumorigenesis and regulate the MEK1-ERK1/2 signaling pathway.

Pancreatic cancer is the fourth leading cause of cancer death, with a 5-year survival rate of only 1-4%. Integrin-mediated cell adhesion is critical for the initiation, progression, and metastasis of cancer. In this study we investigated the role of integrin b4 (ITGB4) and its phosphorylation at tyrosine Y1510 (p-ITGB4-Y1510) in the tumorigenesis of pancreatic cancer. We analyzed the expression of ITGB4 and p-ITGB4-Y1510 in pancreatic cancer tissue and cell lines using immunohistochemistry, Western blot, or semi-quantitative reverse transcription PCR. ITGB4 and p-ITGB4-Y1510 were highly expressed in pancreatic cancer (n = 176) compared with normal pancreatic tissue (n = 171). High p-ITGB4-Y1510 expression correlated with local invasion and distant metastasis of pancreatic cancer, and high ITGB4 was significantly associated with poor survival of patients. Inhibition of ITGB4 by siRNA significantly reduced migration and invasion of PC-1.0 and AsPC-1 cells. Overexpression of the mutant ITGB4-Y1510A (a mutation of tyrosine to alanine at 1510 position) in PC-1.0 and AsPC-1 cells not only blocked the ITGB4 phosphorylation at Y1510 but also suppressed the expression of ITGB4 (p < 0.05 vs. wild-type ITGB4). The transfection of PC-1.0 and AsPC-1 cells with ITGB4-Y1510A significantly decreased the level of p-mitogen-activated protein kinase kinase (MEK)1 (T292) and p-extracellular signal-regulated kinase (ERK)1/2 but did not affect the level of p-MEK1 (T386) and p-MEK2 (T394). Overall, our study showed that ITGB4 and its phosphorylated form promote cell migration and invasion in pancreatic cancer and that p-ITGB4-Y1510 regulates the downstream MEK1-ERK1/2 signaling cascades. Targeting ITGB4 or its phosphorylation at Y1510 may be a novel therapeutic option for pancreatic cancer.

Primary glioblastoma transcriptome data analysis for screening survival-related genes.

PURPOSE: The aim of this study was to screen survival-related genes for glioblastoma (GBM). METHODS: GSE53733 was downloaded from Gene Expression Omnibus (GEO) database, including 16 short-term (ST), 31 intermediate (IM), and 23 long-term (LT) survivors. Analysis of variance was used to analyze the expression in three groups. The genes with P < .01 were screened as differentially expressed genes (DEGs). Soft clustering was performed using Mfuzz to mine the expression patterns of differential genes in three groups of overall survival (OS) classification. The cytoscape plugin clueGO was used for functional enrichment analysis. The protein interaction between differential genes was extracted from the STRING V10 database, and the protein-protein interaction (PPI) network was constructed and displayed with cytoscape. The hub genes were verified by quantitative reverse-transcription polymerase chain reaction. RESULTS: Total 662 DEGs were obtained among three groups and enriched in 12 clusters. The overlap analysis between clusters could classify these 12 clusters Cluster A and B. Total 264 OS.DEGs were contained in Cluter A and Cluster B, and enriched in 28 Gene Ontology terms, such as trophoblast giant cell differentiation (P value = 6.18E-04), muscle fiber development (P value = 9.09E-04), and negative regulation of stem cell differentiation (P value = 1.76E-03). The top five nodes with highest degree in OS.PPI were HDAC1, DECR1, RASL11A, PDIA3, and POLR2F. The expression of DECR1 and POLR2F was significantly lower, while the levels of HDAC1 and PDIA3 were highly expressed in GBM tissues. CONCLUSION: DECR1, POLR2F, HDAC1, and PDIA3 might be potential key genes affected the overall survival time of patients with GBM.

Actinomyces lilanjuaniae sp. nov., isolated from the faeces of Tibetan antelope (Pantholops hodgsonii) on the Qinghai-Tibet Plateau.

Two novel, Gram-stain-positive, non-motile, facultatively anaerobic, rod-shaped bacteria (strains 2129T and 2119) were isolated from the faeces of Tibetan antelopes (Pantholops hodgsonii) on the Qinghai-Tibet Plateau, PR China. The 16S rRNA gene sequences of the strains showed highest similarity values to Actinomyces timonensis DSM 23838T (92.9 and 92.8 %, respectively), and phylogenetic analysis based on 16S rRNA gene and genomic sequences indicated that strains 2129T and 2119 represent a new lineage. Strains 2129T and 2119 could ferment d-adonitol and d-xylose, but were unable to utilize d-mannose and d-melibiose nor produce esterase (C4) and proline arylamidase. The G+C contents of the two strains were both 69.0 mol%. Their genomes exhibited less than 40.4 % relatedness in DNA-DNA hybridization tests (below 70 % as the recommended threshold for new species) with all available genomes of the genus Actinomyces in the NCBI database. The major fatty acids of the two strains were C18 : 1ω9c and C16 : 0, and the major polar lipids were diphosphatidylglycerol, glycolipid, phosphatidylinositol, phosphatidyl inositol mannoside and phosphoglycolipid. Based on the results of genotypic, phenotypic and biochemical analyses, it is proposed that the two unidentified bacteria be classified as representing a novel species, Actinomyces lilanjuaniae sp. nov. The type strain is 2129T (=CGMCC 4.7483T=DSM 106426T).

Genomic and molecular characterisation of Escherichia marmotae from wild rodents in Qinghai-Tibet plateau as a potential pathogen.

Wildlife is a reservoir of emerging infectious diseases of humans and domestic animals. Marmota himalayana mainly resides 2800-4000 m above sea level in the Qinghai-Tibetan Plateau, and is the primary animal reservoir of plague pathogen Yersinia pestis. Recently we isolated a new species, Escherichia marmotae from the faeces of M. himalayana. In this study we characterised E. marmotae by genomic analysis and in vitro virulence testing to determine its potential as a human pathogen. We sequenced the genomes of the seven E. marmotae strains and found that they contained a plasmid that carried a Shigella-like type III secretion system (T3SS) and their effectors, and shared the same O antigen gene cluster as Shigella dysenterae 8 and E. coli O38. We also showed that E. marmotae was invasive to HEp-2 cells although it was much less invasive than Shigella. Thus E. marmotae is likely to be an invasive pathogen. However, E. marmotae has a truncated IpaA invasin, and lacks the environmental response regulator VirF and the IcsA-actin based intracellular motility, rendering it far less invasive in comparison to Shigella. E. marmotae also carried a diverse set of virulence factors in addition to the T3SS, including an IS1414 encoded enterotoxin gene astA with 37 copies, E. coli virulence genes lifA/efa, cif, and epeA, and the sfp gene cluster, Yersinia T3SS effector yopJ, one Type II secretion system and two Type VI secretion systems. Therefore, E. marmotae is a potential invasive pathogen.

Baicalin ameliorates lipopolysaccharide-induced acute lung injury in mice by suppressing oxidative stress and inflammation via the activation of the Nrf2-mediated HO-1 signaling pathway.

This research aims to investigate the ameliorative potential of baicalin on lipopolysaccharide-induced acute lung injury by the suppression of oxidative stress and inflammation via the activation of the nuclear erythroid factor 2 (Nrf2)-mediated heme oxygenase-1 (HO-1) signaling pathway. Specific pathogen-free male mice, weighing between 25 and 30 g, were divided into the following four groups of 10 mice each: the control group, LPS group, LPS + baicalin group, and baicalin group. Bronchoalveolar lavage fluid (BALF), blood, and tissue were collected on the 16th day and used for hematological (total leukocyte, macrophage, neutrophil, and lymphocyte counts in both blood and BALF, biochemical (antioxidant enzymes, MDA, Nrf2, and HO-1), and histological analyses. The protective effect of baicalin on lipopolysaccharide-induced acute lung injury is based on its antioxidative stress capabilities that are mediated partly by the Nrf2/HO-1 signaling pathway. Baicalin pretreatment significantly decreased the rise in the lung injury score; total leukocyte, neutrophil, lymphocyte, and macrophage counts; pro-inflammatory mediators, tumor necrosis factor (TNF-α), interleukins (IL-6 and IL-1ß); biosynthesis of oxidative products, e.g., malondialdehyde (MDA); and restoration of antioxidative enzyme (superoxide dismutase and catalase) activities by improving the expression of nuclear Nrf2 and cytosolic HO-1 in lipopolysaccharide-induced acute lung injury. The protective effects of baicalin are partly due to its antioxidant and anti-inflammatory effects. Our findings indicate that baicalin protects against lipopolysaccharide-induced severe lung injury by enhancing antioxidant systems and significantly reducing both inflammatory cells and mediators via the Nrf2-mediated HO-1 signaling pathway.

LncRNA DLX6-AS1 promotes the proliferation, invasion, and migration of non-small cell lung cancer cells by targeting the miR-27b-3p/GSPT1 axis.

Background: Non-small cell lung cancer (NSCLC) has a significant impact on human health. The aim of this study was to explore the role of long non-coding RNA DLX6-AS1 in the proliferation, migration, and invasion of NSCLC cells. Methods: The expression of DLX6-AS1 in NSCLC tumor tissues and cell lines was examined by qRT-PCR. The effects of DLX6-AS1 knockdown on cell proliferation, migration, and invasion were assessed by Cell Counting Kit-8, wound healing, and transwell assays, respectively. Bioinformatics analyses, luciferase reporter assays, and RNA pull-down assays were employed to examine the mechanism by which DLX6-AS1 exerted its oncogenesis effects in NSCLC. The anti-tumor effect of silencing DLX6-AS1 in vivo was also evaluated. Results: DLX6-AS1 was over-expressed in NSCLC tumor tissues and cell lines and its level of expression was found to be associated with tumor size and advanced clinical stage in patients with NSCLC. Downregulation of DLX6-AS1 inhibited cell proliferation, cell clone formation, migration, and invasion of NSCLC cells. DLX6-AS1 was found to interact with miR-27b-3p/GSPT1. DLX6-AS1 expression was negatively correlated with miR-27b-3p expression, but positively correlated with GSPT1 expression in NSCLC samples. DLX6-AS1 knockdown also effectively suppressed tumor growth in an in vivo xenograft model. Conclusion: DLX6-AS1 regulated NSCLC progression by targeting the miR-27b-3p/GSPT1 axis, which may provide novel insights for NSCLC prognosis and therapy.

Preparation and Properties of Polyvinylidene Fluoride Nanocomposited Membranes based on Poly(N-Isopropylacrylamide) Modified Graphene Oxide Nanosheets.

The nanomaterial of graphene oxide grafting poly (N-isopropylacrylamide) (GO-g-PNIPAAm) was synthesized and PVDF/GO-g-PNIPAAm blended membranes were fabricated by wet phase inversion. In this work, a hydrophilic nanomaterial GO-g-PNIPAAm with poly(N-isopropylacrylamide) (PNIPAAm) grafted on GO, was synthesized by the atom transfer radical polymerization (ATRP) method. The resulting nanomaterial was confirmed by scanning electron microscope (SEM), Fourier transform infrared spectroscopy (FTIR), Raman spectrum, and X-ray photoelectron spectroscopy (XPS) analysis. The synthesized GO-g-PNIPAAm was incorporated with polyvinylidene fluoride (PVDF) via phase inversion, and investigated for its temperature sensitivity, porosity, contact angle, scanning electron microscopy, and permeate properties. The water contact angle measurements confirmed that GO-g-PNIPAAm nanomaterial-endowed PVDF membranes with better hydrophilicity and thermo-responsive properties compared with those of the pristine PVDF membranes. Bovine serum albumin (BSA) adsorption experiments suggested that excellent antifouling properties of membranes were acquired after adding GO-g-PNIPAAm. The modified membranes showed good performance when the doping amount of GO-g-PNIPAAm was 0.2 wt %.

ITGA6 and RPSA synergistically promote pancreatic cancer invasion and metastasis via PI3K and MAPK signaling pathways.

Pancreatic cancer is one of the most malignant tumors. Invasion and metastasis can occur in the early stage of pancreatic cancer, contributing to the poor prognosis. Accordingly, in this study, we evaluated the molecular mechanisms underlying invasion and metastasis. Using mass spectrometry, we found that Integrin alpha 6 (ITGA6) was more highly expressed in a highly invasive pancreatic cancer cell line (PC-1.0) than in a less invasive cell line (PC-1). Through in vitro and in vivo experiments, we observed significant decreases in invasion and metastasis in pancreatic cancer cells after inhibiting ITGA6. Based on data in TCGA, high ITGA6 expression significantly predicted poor prognosis. By using Co-IP combined mass spectrometry, we found that ribosomal protein SA (RPSA), which was also highly expressed in PC-1.0, interacted with ITGA6. Similar to ITGA6, high RPSA expression promoted invasion and metastasis and indicated poor prognosis. Interestingly, although ITGA6 and RPSA interacted, they did not mutually regulate each other. ITGA6 and RPSA affected invasion and metastasis via the PI3K and MAPK signaling pathways, respectively. Inhibiting ITGA6 significantly reduced the expression of p-AKT, while inhibiting RPSA led to the downregulation of p-ERK1/2. Compared with the inhibition of ITGA6 or RPSA alone, the downregulation of both ITGA6 and RPSA weakened invasion and metastasis to a greater extent and led to the simultaneous downregulation of p-AKT and p-ERK1/2. Our research indicates that the development of drugs targeting both ITGA6 and RPSA may be an effective strategy for the treatment of pancreatic cancer.