Carrier mobility and optical properties of a type-II GaSe/ZnS heterostructure as a photocatalyst: a first-principles study.

In this paper, a new GaSe/ZnS van der Waals heterostructure (vdWH) was constructed and a systematic analysis of the electronic structure, interfacial properties, and transport and photocatalytic capacity of the GaSe/ZnS vdWH was performed by using first-principles calculations. It was found that the heterostructure exhibited excellent photocatalytic performance for water splitting. The direct band gap of the heterostructure calculated using the hybrid HSE06 functional was 2.19 eV, which had a good visible light absorption ability. The electronic structure of the type-II band arrangement effectively reduced the recombination of electron-hole pairs. The heterostructure also showed excellent transport ability, and the carrier mobility of electrons and holes along different directions was greatly improved. Additionally, as the electric field strength increased, the band gap width of the GaSe/ZnS vdWH narrowed and the heterostructure characteristics transitioned from semiconductor to metal properties, which were attributed to the appearance of near-free electronic (NFE) states induced by the strong electric field. Meanwhile, the optical absorption capacity of the heterostructure was greatly improved compared to the ZnS monolayer, reaching 1.44 × 105 cm-1 at an incident photon energy of 8.65 eV. Therefore, the GaSe/ZnS vdWH was proved to be an excellent photocatalytic material for water splitting in the present study.

Usefulness of magnetic resonance imaging characteristics in discriminating H3 K27M-mutant gliomas from wildtype gliomas in spinal cord.

AIM: The aim of this study was to determine the usefulness of magnetic resonance imaging (MRI) characteristics in discriminating H3 K27M-mutant gliomas from wildtype gliomas in the spinal cord. MATERIALS AND METHODS: Fifty-eight patients with spinal cord gliomas were enrolled in this study. The H3 K27 gene status was identified by Sanger sequencing or immunohistochemistry test of resection tumor specimens. The MR imaging characteristics were evaluated and compared between H3 K27M-mutant and wildtype gliomas using the χ2 test and the Mann-Whitney U test. RESULTS: Of 58 recruited patients, 23 (39.7%) were diagnosed with H3 K27M-mutant glioma. The H3 K27M-mutant gliomas were found to more likely occur in men compared with wildtype gliomas (87.0% vs. 42.9%, p = 0.001). On T2-weighted MR images, the signal-to-noise ratio (SNR) of H3 K27M-mutant gliomas was significantly lower than that of wildtype gliomas (103.9 ± 72.0 vs. 168.9 ± 86.8, p < 0.001). Of 35 wildtype tumors, 60% showed well-defined margin but this feature was not found in all mutant tumors (p < 0.001). The SNR of tumors on contrast-enhanced T1-weighted images of the H3 K27M-mutant gliomas was significantly lower than that of wildtype gliomas (187.7 ± 160.4 vs. 295.1 ± 207.8, p = 0.006). Receiver operating-characteristic analysis revealed that area under curve (AUC) of combination of 1/SNR on T2-weighted images, 1/SNR on contrast-enhanced T1-weighted images, ill-defined margin, and sex reached 0.937 (95% CI, 0.873-1.000) in discriminating H3 K27M-mutant gliomas. CONCLUSIONS: The MR imaging characteristics are valuable in discriminating H3 K27M-mutant from wildtype gliomas in the spinal cord and the combination of these imaging features with sex had a high strength in this discrimination.

An Effective Docking-Guided Strategy for Rational Tailoring of Fluorescent Aptamer Switches of Dimethylindole Red Analogue.

The light-up aptamer-dimethylindole red (DIR) complexes have been applied in biochemistry analysis as promising signal transduction tools. However, the unfavorable repulsions between DIR and the long-sequence aptamer switch hinder the complex's further development, and it is urgent to engineer a feasible and efficient strategy for synchronously and rationally adjusting the DIR chemical structure and the DIR aptamer performance. Herein, we communicate a versatile docking-guided rational tailoring strategy to effectively upgrade a DNA aptamer which specifically turns on the fluorescence of a synthesized amino-functionalized DIR analogue (NH2-DIR). After optimizing with three-level tailoring strategies including molecule docking-guided tailoring, coarse tailoring, and fine tailoring, the NH2-DIR aptamer switch with higher binding affinity and specificity, considerable fluorescence-activation ability, and 40% shortened length was obtained. Integrating the experimental and docking results, the binding mechanism between NH2-DIR and the tailored aptamer was deciphered via three types of interactions.

The Application of Probe-Based Confocal Laser Endomicroscopy as a Diagnostic Tool in Choledochoscopic Gallbladder-Preserving Surgery.

BACKGROUND AND AIMS: Choledochoscopic gallbladder-preserving surgery (CGPS) has the advantage of treating benign gallbladder diseases on the premise of gallbladder preservation. However, it has no reliable preoperative diagnosis if the gallbladder is benign. Probe-based confocal laser endomicroscopy (pCLE) can obtain real-time and clear endoscopic images at the cell level in vivo. It is widely used in the diagnosis of digestive system diseases, but not in gallbladder diseases yet. We applied these two technologies in a complementary way into the diagnosis of gallbladder diseases and thereby lifted the reliability of CGPS. METHODS: We retrospectively analyzed the total 28 patients with the indication of CGPS with intraoperative pCLE scan referred to the Second Affiliated Hospital of Baotou Medical College between October 2019 and July 2020. The intraoperative pCLE results were compared with the postoperative pathology in various gallbladder diseases. RESULTS: We compared the intraoperative pCLE diagnosis with the postoperative pathological diagnosis and found a complete match without exception in both sensitivity and specificity. CONCLUSIONS: Based on our investigation, pCLE can provide the same accuracy as the traditional pathology in the diagnosis of gallbladder diseases with the additional advantages like noninvasive, real time, and instancy. This study serves to validate the correlation between CLE and histology. It holds a broad prospect in the application of pCLE as an intraoperative diagnosis in CGPS.

Effect of Steam Flash-Explosion on Physicochemical Properties and Structure of High-Temperature Denatured Defatted Rice Bran Protein Isolate.

The effects of Steam Flash-Explosion (SFE) on the physicochemical properties and molecular structure of high-temperature denatured defatted rice bran protein isolate (RBPI) were investigated. The mechanism of SFE treatment on high-temperature denatured defatted RBPI was revealed. The analysis of the physical and chemical properties of RBPI showed that the surface hydrophobicity, characteristic viscosity, and thermal stability of rice bran protein isolate were significantly affected by the pressure of saturated steam and pressure holding time. Under the conditions of 2.1 MPa and 210 s, the surface hydrophobicity index decreased significantly from 137.5 to 17.5, and the characteristic viscosity increased significantly. The peak temperature of denaturation decreases from 114.2 to 106.7 °C, and the enthalpy of denaturation decreases from 356.3 to 231.4 J/g. The higher structure (circular dichroic spectrum and endogenous fluorescence spectrum) of rice bran protein isolate was analyzed by volume rejection chromatography (SEC). The results showed that steam flash treatment could depolymerize and aggregate RBPI, and the relative molecular weight distribution changed greatly. The decrease in small molecules with poor solubility was accompanied by the increase in macromolecules (>550 kDa) soluble aggregates, which were the products of a Maillard reaction. The contents of free sulfhydryl and disulfide bonds in high-temperature rice bran meal protein isolate were significantly increased, which resulted in the increase in soluble aggregates containing disulfide bonds. Circular dichroism (CD) analysis showed that the α-helix content of the isolated protein was significantly decreased, the random curl content was increased, and the secondary structure of the isolated protein changed from order to disorder. The results of endogenous fluorescence spectroscopy showed that the high-temperature rice bran meal protein isolate was more extended, tryptophan was in a more hydrophilic microenvironment, the fluorescence intensity was reduced, and the tertiary structure was changed. In addition, the mean particle size and net surface charge of protein isolate increased in the aqueous solution, which was conducive to the development of the functional properties of the protein.

Structural Characterization, In Vitro Digestion Property, and Biological Activity of Sweet Corn Cob Polysaccharide Iron (III) Complexes.

This study aimed to enhance the utilization value of sweet corn cob, an agricultural cereal byproduct. Sweet corn cob polysaccharide-ron (III) complexes were prepared at four different temperatures (40 °C, 50 °C, 60 °C, and 70 °C). It was demonstrated that the complexes prepared at different temperatures were successfully bound to iron (III), and there was no significant difference in chemical composition; and SCCP-Fe-C demonstrated the highest iron content. The structural characterization suggested that sweet corn cob polysaccharide (SCCP) formed stable ß-FeOOH iron nuclei with -OH and -OOH. All the four complexes' thermal stability was enhanced, especially in SCCP-Fe-C. In vitro iron (III) release experiments revealed that all four complexes were rapidly released and acted as iron (III) supplements. Moreover, in vitro antioxidant, α-glucosidase, and α-amylase inhibition studies revealed that the biological activities of all four complexes were enhanced compared with those of SCCP. SCCP-Fe-B and SCCP-Fe-C exhibited the highest in vitro antioxidant, α-glucosidase, and α-amylase inhibition abilities. This study will suggest using sweet corn cobs, a natural agricultural cereal byproduct, in functional foods. Furthermore, we proposed that the complexes prepared from agricultural byproducts can be used as a potential iron supplement.

Spontaneous In-Source Fragmentation Reaction Mechanism and Highly Sensitive Analysis of Dicofol by Electrospray Ionization Mass Spectrometry.

Although dicofol has been widely banned all over the world as a kind of organochlorine contaminant, it still exists in the environment. This study developed a high-performance liquid chromatography coupled with mass spectrometry (HPLC-MS/MS) detection technique for dicofol, an environmental pollutant, for the first time using in-source fragmentation. The results confirmed that m/z 251 was the only precursor ion of dicofol after in-source fragmentation, and m/z 139 and m/z 111 were reasonable product ions. The main factors triggering the in-source fragmentation were the H+ content and solution conductivity when dicofol entered the mass spectrometer. Density functional theory can be used to analyze and interpret the mechanism of dicofol fragmentation reaction in ESI source. Dicofol reduced the molecular energy from 8.8 ± 0.05 kcal/mol to 1.0 ± 0.05 kcal/mol, indicating that the internal energy release from high to low was the key driving force of in-source fragmentation. A method based on HPLC-MS/MS was developed to analyze dicofol residues in environmental water. The LOQ was 0.1 µg/L, which was better than the previous GC or GC-MS methods. This study not only proposed an HPLC-MS/MS analysis method for dicofol for the first time but also explained the in-source fragmentation mechanism of compounds in ESI source, which has positive significance for the study of compounds with unconventional mass spectrometry behavior in the field of organic pollutant analysis and metabonomics.

Transcriptomic analysis reveals a novel regulatory factor of ECHDC1 involved in lipid metabolism of non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is the highest incidence of chronic liver disease worldwide characterized by lipid accumulation in the liver. The full understanding of the lipogenesis of NAFLD is extreme importance. Here, whole-genome transcriptome analysis was performed on liver tissues of NAFLD patients and healthy controls to identify the differentially expressed genes and find new pathways and target genes related to the lipogenesis of NAFLD. Combined with the Gene Expression Omnibus (GEO) database, we found 86 overlapping genes, many of which are related to lipid metabolism of NAFLD. ECHDC1 is one of 86 overlapping genes, and its role in NAFLD has not been reported. The expression of ECHDC1 was significantly increased in liver tissue of patients with NAFLD than that of healthy controls, and oil Red O intensity was positively correlated with the expression levels of ECHDC1. Inhibition of ECHDC1 expression in HepG2 cells by RNAi significantly reduced intracellular lipid droplet number in vitro. In summary, this study analyzed pathogenic factors related to NAFLD at the whole-genome level and demonstrated that ECHDC1 may be involved in the occurrence and development of NAFLD by regulating hepatic lipid metabolism.

Identification of MAP3K4 as a novel regulation factor of hepatic lipid metabolism in non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a metabolic disorder with abnormal lipid metabolism. The present study was to identify regulatory genes related to lipid droplets (LDs) abnormal accumulation in NAFLD. METHODS: transcriptomic analysis and bioinformatics analysis (GEO database) were used to identify potential genes in abnormal lipid metabolism of NAFLD. A candidate gene MAP3K4 expression were detected by immunohistochemistry staining in NAFLD and controls. RNA interference and immunoblotting were used to verify the roles of MAP3K4 in the formation of hepatic LDs. RESULTS: A total of 134 candidate genes were screened, including 44 up-regulated genes and 90 down-regulated genes. 29 genes in the protein-protein interaction (PPI) were selected as hub genes, including MAP3K4. The expression levels of MAP3K4 were positively correlated with NAFLD activity score (r = 0.702, p = 0.002). Furthermore, we found a positive correlation of MAP3K4 expression with serum total cholesterol (r = 0.564, p = 0.023), uric acid levels (r = 0.520, p = 0.039), and body mass index (r = 0.574, p = 0.020). Downregulation of MAP3K4 decreased LDs accumulation in HepG2 cells and reduced the expression of CGI-58 and Plin-2 by imbibition of JNK and group IVA cytosolic phospholipase A2 (cPLA2) activation. CONCLUSION: The study revealed a number of regulatory genes related to hepatic lipid metabolism of NAFLD, and demonstrated that MAP3K4 played a pivotal role in the hepatic lipogenesis of NAFLD.

Structural characterization of a novel polysaccharide from sweet corncob that inhibits glycosylase in STZ-induced diabetic rats : Structural characterization of a novel polysaccharide.

In the current study, we extracted a polysaccharide from sweet corncob and evaluated its hypoglycemic function. After collection in water, alcohol precipitation, and purification by DEAE-52 and Sephadex G-100 columns, we obtained a polysaccharide (SCP50) that was composed primarily of mannose and glucose (9.73:190.27), with a molecular weight of 9280.33 Da. We demonstrated that SCP50 exhibited significant inhibition of α-glucosidase activity, with an IC50 of 4.866 mg/mL, Km of 1.297 × 10-3, and Vmax of 0.076 mol/L·min-1 in vitro. We also observed that SCP50 markedly attenuated disaccharidase (maltase, sucrase, and lactase) activity in a rat model of T2DM. We conclude that SCP50 exerts a hypoglycemic effect via inhibition of intestinal glycosylase. These results thus provide new insight into the hypoglycemic action underlying sweet corncob polysaccharide's effects.

Expression stability of internal reference gene in response to Trichoderma polysporum infection in Avena fatua L.

Trichoderma polysporum was a pathogenic fungi which showed strong pathogenicity to Avena fatua L. in recent study. The stress response of A. fatua to T. polysporum is mediated by the regulation of gene expression. Quantification of the expression of genes requires normalizing RT-qPCR data using reference genes with stable expression in the system studied as internal standards. To construct a RT-qPCR system suitable for response of A. fatua to T. polysporum, and screen stable internal reference genes, GeNorm, NormFinder, BestKeeper and RefFinde were used to perform SYBR Green-based RT-qPCR analysis on eight candidate internal reference genes (18S, 28S, TUA, UBC, ACT, GAPDH, TBP and EF-1α) in A. fatua samples after inoculation of T. polysporum Strain HZ-31. The results showed that TBP, 18S and UBC were the most stable internal reference genes, TBP and TUA, TBP and GAPDH, 18S and TBP, UBC and 18S were the most suitable combination of the two internal reference genes, which could be used as internal reference genes for functional gene expression analysis during the interaction between T. polysporum and A. fatua. This is the first study describing a set of reference genes with a stable expression under fungi stress in A. fatua. These genes are also candidate reference genes of choice for studies seeking to identify stress-responsive genes in A. fatua.

Graphene-Based Environmental Sensors: Electrical and Optical Devices.

In this review paper, we summarized the recent progress of using graphene as a sensing platform for environmental applications. Especially, we highlight the electrical and optical sensing devices developed based on graphene and its derivatives. We discussed the role of graphene in these devices, the sensing mechanisms, and the advantages and disadvantages of specific devices. The approaches to improve the sensitivity and selectivity are also discussed.

A Flexible Acetylcholinesterase-Modified Graphene for Chiral Pesticide Sensor.

Sensors based on graphene are promising devices for chemical and biological detection owing to their high sensitivity, biocompatibility, and low costs. However, for chiral recognition, which is very important in biological systems, graphene sensors remain unable to discriminate enantiomers. Here, using chiral pesticide molecules as an example, we realized a highly sensitive graphene chiral sensor by modification with acetylcholinesterase (AChE). Quantum chemical simulations indicate that the inhibition effect of the enantiomer on AChE was transferred to graphene, which allowed for the electrical detection of chiral molecules. Under an operating voltage of 1 V, the sensitivity of the device reached 0.34 µg/L and 0.32 µg/L for (+)/(-)-methamidophos, respectively, which is much higher than by circular dichroism (6.90 mg/L and 5.16 mg/L, respectively). Furthermore, real-time, rapid detection was realized by combining with smartphones and wireless transmission.

Potential of C1QTNF1-AS1 regulation in human hepatocellular carcinoma.

The aim of our study is to explore the regulation of C1QTNF1-AS1 on its target miR-221-3p/SOCS3 in human hepatocellular carcinoma (HCC). To explore the underlying molecular regulation of non-coding RNA for HCC, differentially expressed patterns of lncRNAs and genes were examined by RNA-seq. GO and KEGG pathway analysis were done based on the function of mRNAs that mediated by differentially expressed lncRNAs. RT-qPCR and western blot were conducted to detect the mRNA and protein level expression of C1QTNF1-AS1, miR-221-3p, SOCS3 and key proteins in JAK/STAT signaling pathway in HCC tissues and cells. The target miRNA of differentially expressed C1QTNF1-AS1 and SOCS3 was miR-221-3p predicted by bioinformatics analysis. C1QTNF1-AS1 and SOCS3 was downregulated and miR-221-3p was upregulated in HCC tissues and cells. In HepG2 and Huh-7 cells, the overexpression of C1QTNF1-AS1 or SOCS3, and silencing of miR-221-3p inhibited proliferation, migration, invasion and JAK/STAT signaling pathway, while promoted cell apoptosis. The results of dual-luciferase assay indicated that C1QTNF1-AS1 regulated miR-221-3p and miR-221-3p targeted SOCS3 by directly binding. And the growth of HCC in vivo was impeded when C1QTNF1-AS1 was upregulated. Overexpression of C1QTNF1-AS1 could downregulate miR-221-3p thereby inhibited the proliferation, migration and invasion of HCC cells.

Systemic Evaluation of Vascular Dysfunction by High-Resolution Sonography in an Nω -Nitro-l-Arginine Methyl Ester Hydrochloride-Induced Mouse Model of Preeclampsia-Like Symptoms.

OBJECTIVES: The purpose of this study was to evaluate vascular function, including arterial resistance and endothelial function, by high-resolution sonography in an Nω -nitro-l-arginine methyl ester hydrochloride (l-NAME)-induced mouse model of preeclampsia-like symptoms. METHODS: Pregnant mice were subcutaneously injected with a saline solution (control; n = 10) or l-NAME (n = 10) between the 7th and 18th days of gestation. The resistive index and pulsatility index (RI and PI, indicators of arterial resistance) of the uteroplacental, umbilical, femoral, and common carotid arteries and the flow-mediated dilatation (index of endothelial function) of the femoral artery were measured by high-frequency sonography in both groups. RESULTS: We noted significant increases in the RI and PI of the uteroplacental and umbilical arteries and a decrease in the flow-mediated dilatation of the femoral artery in the l-NAME group compared with the control group. We also found that the RI and PI of the uteroplacental and umbilical arteries were negatively correlated with fetal weight and crown-rump length. The results of the multivariate analysis using a logistic regression model indicated that the flow-mediated dilatation at 120 seconds was an independent diagnostic criterion for the l-NAME-induced preeclampsia-like model. A receiver operating characteristic analysis showed that flow-mediated dilatation at 120 seconds had the greatest area under the curve of 0.934, with an optimal cutoff point of 11.1%, yielding sensitivity of 100% and specificity of 84.6%. CONCLUSIONS: The PI and RI of the fetomaternal vasculature can identify fetuses in "high-risk" pregnancies, and flow-mediated dilatation is a reliable indicator for predicting preeclampsia. Assessment of vascular function by high-resolution sonography provides a useful platform for preeclampsia-related basic research with high reproducibility.

Genetic and Pharmacologic Inhibition of the Chemokine Receptor CXCR2 Prevents Experimental Hypertension and Vascular Dysfunction.

BACKGROUND: The recruitment of leukocytes to the vascular wall is a key step in hypertension development. Chemokine receptor CXCR2 mediates inflammatory cell chemotaxis in several diseases. However, the role of CXCR2 in hypertension development and the underlying mechanisms remain unknown. METHODS: Angiotensin II (490 ng·kg-1·min-1) or deoxycorticosterone acetate (DOCA) salt-induced mouse hypertensive models in genetic ablation, pharmacologic inhibition of CXCR2, and adoptive bone marrow transfer mice were used to determine the role of CXCR2 in hypertension (measured by radiotelemetry and tail-cuff system), inflammation (verified by flow cytometry and quantitative real-time polymerase chain reaction [PCR] analysis), vascular remodeling (studied by haematoxylin and eosin and Masson's trichrome staining), vascular dysfunction (assessed by aortic ring), and oxidative stress (indicated by nicotinamide adenine dinucleotide phosphate [NADPH] oxidase activity, dihydroethidium staining, and quantitative real-time PCR analysis). Moreover, the blood CXCR2+ cells in normotensive controls and hypertension patients were analyzed by flow cytometry. RESULTS: Angiotensin II significantly upregulated the expression of CXCR2 mRNA and protein and increased the number of CD45+ CXCR2+ cells in mouse aorta (n=8 per group). Selective CXCR2 knockout (CXCR2-/-) or pharmacological inhibition of CXCR2 markedly reduced angiotensin II- or DOCA-salt-induced blood pressure elevation, aortic thickness and collagen deposition, accumulation of proinflammatory cells into the vascular wall, and expression of cytokines (n=8 per group). CXCR2 inhibition also ameliorated angiotensin II-induced vascular dysfunction and reduced vascular superoxide formation, NADPH activity, and expression of NADPH oxidase subunits (n=6 per group). Bone marrow reconstitution of wild-type mice with CXCR2-/- bone marrow cells also significantly abolished angiotensin II-induced responses (n=6 per group). It is important to note that CXCR2 blockade reversed established hypertension induced by angiotensin II or DOCA-salt challenge (n=10 per group). Furthermore, we demonstrated that CXCR2+ proinflammatory cells were higher in hypertensive patients (n=30) compared with normotensive individuals (n=20). CONCLUSIONS: Infiltration of CXCR2+ cells plays a pathogenic role in arterial hypertension and vascular dysfunction. Inhibition of CXCR2 pathway may represent a novel therapeutic approach to treat hypertension.

Proteomics analysis of human placenta reveals glutathione metabolism dysfunction as the underlying pathogenesis for preeclampsia.

Hypertensive disorder in pregnancy (HDP) refers to a series of diseases that cause the hypertension during pregnancy, including HDP, preeclampsia (PE) and eclampsia. This study screens differentially expressed proteins of placenta tissues in PE cases using 2D LC-MS/MS quantitative proteomics strategy. A total of 2281 proteins are quantified, of these, 145 altering expression proteins are successfully screened between PE and control cases (p<0.05). Bioinformatics analysis suggests that these proteins are mainly involved in many biological processes, such as oxidation reduction, mitochondrion organization, and acute inflammatory response. Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFκB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process. Results of this study revealed that glutathione metabolism disorder of placenta tissues may contribute to the occurrence of PE disease.

Dynamic changes of mononuclear phagocytes in circulating, pulmonary alveolar and interstitial compartments in a mouse model of experimental silicosis.

CONTEXT: Silicosis is a devastating, irreversible lung fibrosis condition exposed to crystalline silica. The mononuclear phagocyte system plays an important role in the pathogenesis of silicosis. OBJECTIVE: The present study was aimed to explore the dynamic changes of mononuclear phagocytes in circulating, pulmonary alveolar and interstitial compartments in experimental silicosis model. MATERIALS AND METHODS: A mouse model of lung fibrosis was developed with crystalline silica particles (2 mg/40 µL via oropharyngeal instillation) using male C57BL/6 mice, and were killed on days 1, 3, 7, 14, and 28. The lung inflammation and fibrosis was investigated using hematoxylin-eosin staining and bronchoalveolar lavage fluid (BALF) analysis, Masson's trichrome staining, and immunofluorescence. Circulating monocyte subsets (Ly6C(hi) and Ly6C(lo)), polarization state of BALF-derived alveolar macrophages (AMϕ) and lung interstitial macrophages (IMϕ, derived from enzymatically digested lung tissue) were analyzed by flow cytometry. RESULTS: The percentage of Ly6C(hi) monocytes significantly increased on day 1 after silica exposure, which reached the peak level from day 7 till day 28. Moreover, M2 (alternative activation) AMϕ (PI - CD64 + CD206+) was dramatically and progressively increased from day 1 to day 28. A parallel increase in IMϕ with M2 polarization (PI-CD64 + CD11b + CD206+) was also observed from day 1 to day 28. CONCLUSION: Our data demonstrate a dynamic view of mononuclear phagocyte change in three compartments after silica challenge, which highlights the remodeling of mononuclear phagocyte system as a potential therapeutic target for silicosis.

Neutrophil extracellular traps in ischemia-reperfusion injury-induced myocardial no-reflow: therapeutic potential of DNase-based reperfusion strategy.

Emerging evidence suggests a potential role of neutrophil extracellular traps (NETs) in linking sterile inflammation and thrombosis. We hypothesized that NETs would be induced during myocardial ischemia-reperfusion (I/R), and NET-mediated microthrombosis may contribute to myocardial "no-reflow". Male Wistar rats were randomly divided into I/R control, DNase (DNase I, 20 µg/rat), recombinant tissue-type plasminogen activator (rt-PA, 420 µg/rat), DNase + rt-PA, and sham control groups after 45-min myocardial ischemia. In situ NET formation, the anatomic "no re-flow" area, and infarct size were evaluated immediately after 3 h of reperfusion. Long-term left ventricular (LV) functional and histological analyses were performed 45 days after operation. Compared with the I/R controls, the DNase + rt-PA group exhibited reduced NET density [8.38 ± 1.98 vs. 26.86 ± 3.07 (per 200 × field), P < 0.001] and "no-flow" area (15.22 ± 0.06 vs. 34.6 ± 0.05%, P < 0.05) in the ischemic region, as well as reduced infarct size (38.39 ± 0.05 vs. 71.00 ± 0.03%, P < 0.001). Additionally, compared with the I/R controls, DNase + rt-PA treatment significantly ameliorated I/R injury-induced LV remodeling (LV ejection fraction: 64.22 ± 3.37 vs. 33.81 ± 2.98%, P < 0.05; LV maximal slope of the LV systolic pressure increment: 3,785 ± 216 vs. 2,596 ± 299 mmHg/s, P < 0.05). The beneficial effect was not observed in rats treated with DNase I or rt-PA alone. Our study provides evidence for the existence of NETs in I/R-challenged myocardium and confirms the long-term benefit of a novel DNase-based reperfusion strategy (DNase I + rt-PA), which might be a promising option for the treatment of myocardial I/R injury and coronary no-reflow.

Hierarchical Bayesian Causality Network to Extract High-Level Semantic Information in Visual Cortex.

Functional MRI (fMRI) is a brain signal with high spatial resolution, and visual cognitive processes and semantic information in the brain can be represented and obtained through fMRI. In this paper, we design single-graphic and matched/unmatched double-graphic visual stimulus experiments and collect 12 subjects' fMRI data to explore the brain's visual perception processes. In the double-graphic stimulus experiment, we focus on the high-level semantic information as "matching", and remove tail-to-tail conjunction by designing a model to screen the matching-related voxels. Then, we perform Bayesian causal learning between fMRI voxels based on the transfer entropy, establish a hierarchical Bayesian causal network (HBcausalNet) of the visual cortex, and use the model for visual stimulus image reconstruction. HBcausalNet achieves an average accuracy of 70.57% and 53.70% in single- and double-graphic stimulus image reconstruction tasks, respectively, higher than HcorrNet and HcasaulNet. The results show that the matching-related voxel screening and causality analysis method in this paper can extract the "matching" information in fMRI, obtain a direct causal relationship between matching information and fMRI, and explore the causal inference process in the brain. It suggests that our model can effectively extract high-level semantic information in brain signals and model effective connections and visual perception processes in the visual cortex of the brain.