Investigation of the Performance of Hastelloy X as Potential Bipolar Plate Materials in Proton Exchange Membrane Fuel Cells.

The phase, mechanical properties, corrosion resistance, hydrophobicity, and interfacial contact resistance of Hastelloy X were investigated to evaluate its performance in proton exchange membrane fuel cells (PEMFCs). For comparison, the corresponding performance of 304 stainless steel (304SS) was also tested. Hastelloy X exhibited a single-phase face-centered cubic structure with a yield strength of 445.5 MPa and a hardness of 262.7 HV. Both Hastelloy X and 304SS exhibited poor hydrophobicity because the water contact angles were all below 80°. In a simulated PEMFC working environment (0.5 M H2SO4 + 2 ppm HF, 80 °C, H2), Hastelloy X exhibited better corrosion resistance than 304SS. At 140 N·cm-2, the interfacial contact resistance of Hastelloy X can reach as low as 7.4 mΩ·cm2. Considering its overall performance, Hastelloy X has better potential application than 304SS as bipolar plate material in PEMFCs.

Characteristics of the pulmonary microbiota in patients with mild and severe pulmonary infection.

Background: Lung infection is a global health problem associated with high morbidity and mortality and increasing rates of hospitalization. The correlation between pulmonary microecology and infection severity remains unclear. Therefore, the purpose of this study was to investigate the differences in lung microecology and potential biomarkers in patients with mild and severe pulmonary infection. Method: Patients with pulmonary infection or suspected infection were divided into the mild group (140 cases) and the severe group (80 cases) according to pneomonia severity index (PSI) scores. Here, we used metagenomic next-generation sequencing (mNGS) to detect DNA mainly from bronchoalveolar lavage fluid (BALF) collected from patients to analyze changes in the lung microbiome of patients with different disease severity. Result: We used the mNGS to analyze the pulmonary microecological composition in patients with pulmonary infection. The results of alpha diversity and beta diversity analysis showed that the microbial composition between mild and severe groups was similar on the whole. The dominant bacteria were Acinetobacter, Bacillus, Mycobacterium, Staphylococcus, and Prevotella, among others. Linear discriminant analysis effect size (LEfSe) results showed that there were significant differences in virus composition between the mild and severe patients, especially Simplexvirus and Cytomegalovirus, which were prominent in the severe group. The random forest model screened 14 kinds of pulmonary infection-related pathogens including Corynebacterium, Mycobacterium, Streptococcus, Klebsiella, and Acinetobacter. In addition, it was found that Rothia was negatively correlated with Acinetobacter, Mycobacterium, Bacillus, Enterococcus, and Klebsiella in the mild group through co-occurrence network, while no significant correlation was found in the severe group. Conclusion: Here, we describe the composition and diversity of the pulmonary microbiome in patients with pulmonary infection. A significant increase in viral replication was found in the severe group, as well as a significant difference in microbial interactions between patients with mild and severe lung infections, particularly the association between the common pathogenic bacteria and Rothia. This suggests that both pathogen co-viral infection and microbial interactions may influence the course of disease. Of course, more research is needed to further explore the specific mechanisms by which microbial interactions influence disease severity.

PCMT1 regulates the migration, invasion, and apoptosis of prostate cancer through modulating the PI3K/AKT/GSK-3ß pathway.

Protein L-isoaspartate (D-aspartate) O-methyltransferase (PCMT1) is a repair enzyme that catalyzes the conversion of isomerized aspartic acid (iso-Asp) residues into their normal structure, thereby restoring the configuration and function of proteins. Studies have shown that PCMT1 is overexpressed in several tumors and affects patients' prognosis. However, there are few reports on the role of PCMT1 in prostate cancer (PCa). In the present research, with the assistance of The Cancer Genome Atlas Program (TCGA) database, we found that PCMT1 was overexpressed in PCa tissues. The results of quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blot and immunohistochemistry staining also showed that PCMT1 expression was significantly increased in PCa tissues and cell lines. In PCa clinical samples, PCMT1 expression was closely related to Gleason score, clinical stage, lymph node metastasis and bone metastasis. The experiments of overexpression and knockdown of PCMT1 in vitro or in vivo showed that PCMT1 can significantly promote the proliferation, migration and invasion of PCa cells, inhibit cell apoptosis, and promote the growth of PCa. We furthermore confirmed that PCMT1 regulated the migration, invasion and apoptosis of PCa cells by modulating the phosphatidylinositol 3-kinase/AKT kinase/glycogen-synthase kinase-3ß (PI3K/AKT/GSK-3ß) signaling pathway. Collectively, PCMT1 plays a cancer-facilitative role in PCa by promoting the proliferation, migration and invasion of PCa cells, and inhibiting apoptosis. Therefore, PCMT1 is considered to represent a novel target for treating PCa.

LncRNA LNC-565686 Promotes Proliferation of Prostate Cancer by Inhibiting Apoptosis through Stabilizing SND1.

Long non-coding RNAs (lncRNAs), typically more than 200 nt long, cannot encode proteins, but can regulate gene expression. They play an indispensable role in the occurrence and progression of various cancers. The main purpose of this study is to discuss the role and mechanism of LNC-565686 in prostate cancer. First, we found an increased expression of LNC-565686 in prostate cancer cells using RNA sequencing, which was further verified using qRT-PCR. Then, catRAPID was used to find that LNC-565686 might regulate SND1. Furthermore, a protein half-life experiment was performed to verify that LNC-565686 could stabilize the expression of SND1. In order to further explore the effects of LNC-565686 and SND1 on prostate cancer cells, we knocked down LNC-565686 and SND1 in prostate cancer cells, and verified using CCK8 and flow cytometry and western blot for the detection of apoptosis-related indicators. Collectively, we have found that LNC-565686 can promote the proliferation of prostate cancer cells and inhibit apoptosis by stabilizing the expression of SND1. Therefore, targeting LNC-565686 might be a new treatment for prostate cancer.

High Hardness, Excellent Hydrophobicity, and Favorable Corrosion Resistance of Plasma-Sprayed FeCrMoSi Amorphous Coatings on 304 Stainless Steel.

The FeCrMoSi amorphous coatings were fabricated on the surface of a 304 stainless steel (SS) base material using atmospheric plasma spraying. A comprehensive investigation was carried out to evaluate the structure, morphology, adhesion to base material, hardness, hydrophobicity, interfacial contact resistance, and corrosion resistance of the coatings. The results show a remarkable hardness of 1180.1 HV, a strong bond strength of up to 64.3 N/mm2, and excellent hydrophobicity with a water contact angle reaching 141.2°. Additionally, in an acidic environment with fluoride ions (0.5 M H2SO4 + 2 ppm HF, 80 °C), the FeCrMoSi amorphous coating demonstrated superior corrosion resistance compared with 304 SS while maintaining similar electroconductibility. Detailed analysis of the structural characteristics and corrosion resistance of FeCrMoSi amorphous coatings provided valuable insights into their mechanics. These promising results signify a bright future for FeCrMoSi amorphous coatings in various industrial sectors, including transportation, petroleum, and electric power industries.

Puerarin alleviated oxidative stress and ferroptosis during renal fibrosis induced by ischemia/reperfusion injury via TLR4/Nox4 pathway in rats.

PURPOSE: To investigate the role of puerarin on renal fibrosis and the underlying mechanism in renal ischemia and reperfusion (I/R) model. METHODS: Rats were intraperitoneally injected with puerarin (50 or 100 mg/kg) per day for one week before renal I/R. The level of renal collagen deposition and interstitial fibrosis were observed by hematoxylin and eosin and Sirius Red staining, and the expression of α-smooth muscle actin (α-SMA) was examined by immunohistochemical staining. The ferroptosis related factors and TLR4/Nox4-pathway-associated proteins were detected by Western blotting. RESULTS: Puerarin was observed to alleviate renal collagen deposition, interstitial fibrosis and the α-SMA expression induced by I/R. Superoxide dismutase (SOD) activities and glutathione (GSH) level were decreased in I/R and hypoxia/reoxygenation (H/R), whereas malondialdehyde (MDA) and Fe2+ level increased. However, puerarin reversed SOD, MDA, GSH and Fe2+ level changes induced by I/R and H/R. Besides, Western blot indicated that puerarin inhibited the expression of ferroptosis related factors in a dose-dependent manner, which further demonstrated that puerarin had the effect to attenuate ferroptosis. Moreover, the increased expression of TLR/Nox4-pathway-associated proteins were observed in I/R and H/R group, but puerarin alleviated the elevated TLR/Nox4 expression. CONCLUSIONS: Our results suggested that puerarin inhibited oxidative stress and ferroptosis induced by I/R and, thus, delayed the progression of renal fibrosis, providing a new target for the treatment of renal fibrosis.

Single-cell multi-omics sequencing reveals the immunological disturbance underlying STAT3-V637M Hyper-IgE syndrome.

Hyper-IgE syndrome (HIES) is a primary immunodeficiency characterized by, among others, the excessive production of IgE and repetitive bacterial/fungal infections. Mutations in STAT3, a transcription factor that orchestrates immune responses, may cause HIES, but the underlying mechanisms are not fully understood. Here, we used multi-omic approaches to comprehensively decipher the immune disturbance in a male HIES patient harboring STAT3-V637M. In his peripheral blood mononuclear cell (PBMC) we found significant clonal expansion of CD8 T cells (with increased CD8 subunits expression, potentially enhancing responsiveness to MHC I molecules), but not in his CD4 T cells and B cells. Although his B cells exhibited a higher potential in producing immunoglobulin, elevated SPIC binding might bias the products toward IgE isotype. Immune checkpoint inhibitors, including CTLA4, LAG3, were overexpressed in his PBMC-CD4 T cells, accompanied by reduced CD28 and IL6ST (gp130) expression. In his CD4 T cells, integrative analyses predicted upstream transcription factors (including ETV6, KLF13, and RORA) for LAG3, IL6ST, and CD28, respectively. The down-regulation of phagocytosis and nitric oxide synthesis-related genes in his PBMC-monocytes seem to be the culprit of his disseminated bacterial/fungal infection. Counterintuitively, in his PBMC we predicted increased STAT3 binding in both naïve and mature CD4 compartments, although this was not observed in most of his PBMC. In his bronchoalveolar lavage fluid (BALF), we found two macrophage subtypes with anti-bacterial properties, which were identified by CXCL8/S100A8/S100A9, or SOD2, respectively. Together, we described how the immune cell landscape was disturbed in STAT3-V637M HIES, providing a resource for further studies.

Investigation on the physical and electrochemical properties of typical Ni-based alloys used for the bipolar plates of proton exchange membrane fuel cells.

The phase, mechanical properties, corrosion resistance, hydrophobicity, and interface contact resistance of three typical Ni-based alloys (Hastelloy B, Hastelloy C-276, and Monel 400) and 304 stainless steels were experimentally studied to evaluate their service performances as bipolar plate materials of proton exchange membrane fuel cells. All four alloys exhibit single-phase face-centered cubic structure, high strength, good ductility, and high hardness. Hastelloy C-276 has the best ductility with an uniform elongation of 72.5% and highest hardness of 363.7 HV. Hastelloy B has the highest ultimate tensile strength of 913.6 MPa. The hydrophobicity of all four alloys is not good, although Monel 400 has the highest water contact angle of 84.2°. Hastelloy B, Hastelloy C-276, and 304 stainless steel exhibit unsatisfying corrosion resistance in a simulated acidic work environment of proton exchange membrane fuel cell (0.5 M H2SO4+2 ppm HF, 80 °C, H2) and high interface contact resistance. By contrast, Monel 400 demonstrates excellent corrosion resistance with a corrosion current density of 5.9 × 10-7 A cm-2 and a low interface contact resistance of 7.2 mΩ cm2 at 140 N/cm2. In terms of comprehensive performance, Monel 400 is the best uncoated material for the bipolar plates of proton exchange membrane fuel cells among typical Ni-based alloys.

System analysis based on the migration- and invasion-related gene sets identifies the infiltration-related genes of glioma.

The current database has no information on the infiltration of glioma samples. Here, we assessed the glioma samples' infiltration in The Cancer Gene Atlas (TCGA) through the single-sample Gene Set Enrichment Analysis (ssGSEA) with migration and invasion gene sets. The Weighted Gene Co-expression Network Analysis (WGCNA) and the differentially expressed genes (DEGs) were used to identify the genes most associated with infiltration. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to analyze the major biological processes and pathways. Protein-protein interaction (PPI) network analysis and the least absolute shrinkage and selection operator (LASSO) were used to screen the key genes. Furthermore, the nomograms and receiver operating characteristic (ROC) curve were used to evaluate the prognostic and predictive accuracy of this clinical model in patients in TCGA and the Chinese Glioma Genome Atlas (CGGA). The results showed that turquoise was selected as the hub module, and with the intersection of DEGs, we screened 104 common genes. Through LASSO regression, TIMP1, EMP3, IGFBP2, and the other nine genes were screened mostly in correlation with infiltration and prognosis. EMP3 was selected to be verified in vitro. These findings could help researchers better understand the infiltration of gliomas and provide novel therapeutic targets for the treatment of gliomas.

Long term exposure of saxitoxin induced cognitive deficits and YAP1 cytoplasmic retention.

While most studies assessed the acute toxicity of saxitoxin (STX), fewer studies focus on the long-term degenerative effects of STX on the central nervous system. We investigated the cognitive impairment and hippocampal damages of 6 months' exposure of low-dose STX to C57BL/6NJ mice with behavioral tests, H&E staining, and Western blots, and the possible mechanism (Ppp1C, YAP1, tau-phosphorylation) underlies the pathological changes. Furthermore, we discussed the specific localization of YAP1 in N2a cells induced by STX and the effect of inactivated Ppp1C on its downstream protein YAP1 in the Hippo signal pathway. We found STX intoxicated mice showed declined cognitive performance in both NOR test and MWM test, degenerations in the CA1 area of hippocampi. STX induced up-regulation expression of Ppp1C and YAP1 in hippocampus and N2a cells. Meanwhile, STX treatment induced cell apoptosis and Tau protein hyperphosphorylation. In addition, STX treatment promoted YAP1 cytoplasmic retention that indicates the activation of Hippo pathway, while depletion of Ppp1C inactivate YAP1 during the treatment of STX. Our results highlight the role of Ppp1C and YAP1 cytoplasmic retention in chronic low-dose STX intoxication.

A Rare Case of Post-Primary Tuberculosis Which Was Pathologically Diagnosed as Lipoid Pneumonia.

Case Presentation: The patient was a middle-aged housewife who had been using the household spray for a long time, and the main symptoms were cough and sputum production. Chest CT showed lobar ground-glass opacities (GGOs) with small patchy consolidation in the right middle lobe (RML), specifically, lung tissue pathology showed a large number of foamy cells and scattered multinucleated giant cells. The patient received empirical anti-infective treatment, but no clinical improvement was observed. Laboratory tests, including smears and cultures of sputum, blood and bronchoalveolar lavage fluid (BALF), did not provide clear evidence for pathogenic microorganisms. Therefore, the presumptive diagnosis was exogenous LP (ExLP). After 28 days of prednisone treatment, her symptoms improved, but 2 months later, she presented with a worsening cough, and the GGOs had progressed into lobar consolidation. Transbronchial lung biopsy (TBLB) culture showed mycobacterium tuberculosis (MTB), and lung tissue pathology showed granulomatous inflammation. After anti-tuberculosis treatment, the consolidation in the right middle lobe was gradually absorbed, along with a considerable symptom improvement. The final diagnosis of the patient was MTB infection with an endogenous lipoid pneumonia (EnLP)-like presentation. Conclusion: The current case highlights that the MTB infection should be considered when pathology shows LP accompanied by scattered multinucleated giant cells.

Weighted Gene Co-Expression Network Analysis (WGCNA) Reveals the Functions of Syndecan-1 to Regulate Immune Infiltration by Influenced T Cells in Glioma.

Our previous studies shown that syndecan-1 (SDC1) may be a novel class of biomarkers for the diagnosis and treatment of glioma, but its specific roles and the in-depth molecular mechanism remain elusive. Here, we used Estimation of STromal and Immune cells in Malignant Tumor tissues using Expression data (ESTIMATE) algorithms and single-sample Gene Set Enrichment Analysis (ssGSEA) algorithms to evaluate the immune score of tumor samples and quantify the relative infiltration of immune cells in the tumor microenvironment (TME), respectively, in different data sets obtained from the Chinese Glioma Genome Atlas and The Cancer Gene Atlas. Next, we calculate the correlation of the immune score and immune cells with SDC1, respectively. To identify the specific process regulated by SDC1, the differentially expressed genes (DEGs) analysis between the high and low expression of SDC1 of glioma samples were used to discover the hub genes through Weighted Gene Coexpression Network Analysis (WGCNA). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed cardinal biological processes and pathways involved in genes and tumor grade correlation and survival analysis verified its significance in glioma. The results show that SDC1 is associated with the immune infiltration of glioma in the TME, especially activated CD4+T cells and CD8+T cells. The three data sets filter 8,887 DEGs, the genes in the blue modules were selected as hub genes in WGCNA. GO and KEGG analysis found eight genes in the blue modules involved in antigen processing and presentation in T cells in glioma. Kaplan-Meier estimator and log-rank test statistic determined that the introduced genes are associated with poor prognosis in glioma. Protein-protein network interaction analysis showed that SDC1 may regulate antigen processing and presentation through CTSL or CD4 in glioma. Finally, this study provided insights and clues for the next research direction of SDC1 and identified the key pathways and genes that might participate in the immune escape of glioma. These results might provide a new insight on the study of immune infiltration of glioma in the future.

CBX3 accelerates the malignant progression of glioblastoma multiforme by stabilizing EGFR expression.

CBX3, also known as HP1γ, is a major isoform of heterochromatin protein 1, whose deregulation has been reported to promote the development of human cancers. However, the molecular mechanism of CBX3 in glioblastoma multiforme (GBM) are unclear. Our study reported the identification of CBX3 as a potential therapeutic target for GBM. Briefly, we found that, CBX3 is significantly upregulated in GBM and reduces patient survival. In addition, functional assays demonstrated that CBX3 significantly promote the proliferation, invasion and tumorigenesis of GBM cells in vitro and in vivo. Mechanistically, Erlotinib, a small molecule targeting epidermal growth factor receptor (EGFR) tyrosine kinase, was used to demonstrate that CBX3 direct the malignant progression of GBM are EGFR dependent. Previous studies have shown that PARK2(Parkin) and STUB1(Carboxy Terminus of Hsp70-Interacting Protein) are EGFR-specific E3 ligases. Notably, we verified that CBX3 directly suppressed PARK2 and STUB1 at the transcriptional level through its CD domain to reduce the ubiquitination of EGFR. Moreover, the CSD domain of CBX3 interacted with PARK2 and regulated its ubiquitination to further reduce its protein level. Collectively, these results revealed an unknown mechanism underlying the pathogenesis of GBM and confirmed that CBX3 is a promising therapeutic target.

Discovery of Novel Markers for Identifying Cognitive Decline Using Neuron-Derived Exosomes.

Alzheimer's disease (AD), the predominant cause of late-life dementia, has a multifactorial etiology. Since there are few therapeutic options for symptomatic AD, research is increasingly focused on the identification of pre-symptomatic biomarkers. Recently, evaluation of neuron-derived exosomal markers has emerged as a promising novel approach for determining neuronal dysfunction. We aimed to identify novel neuron-derived exosomal markers that signify a transition from normal aging to Mild Cognitive Impairment (MCI) and then to clinically established AD, a sequence we refer to as AD progression. By using a Tandem Mass Tag-based quantitative proteomic approach, we identified a total of 360 neuron-derived exosomal proteins. Subsequent fuzzy c-means clustering revealed two clusters of proteins displaying trends of gradually increasing/decreasing expression over the period of AD progression (normal to MCI to AD), both of which were mainly involved in immune response-associated pathways, proteins within these clusters were defined as bridge proteins. Several differentially expressed proteins (DEPs) were identified in the progression of AD. The intersections of bridge proteins and DEPs were defined as key proteins, including C7 (Complement component 7), FERMT3 (Fermitin Family Member 3), CAP1 (Adenylyl cyclase-associated protein 1), ENO1 (Enolase 1), and ZYX (Zyxin), among which the expression patterns of C7 and ZYX were almost consistent with the proteomic results. Collectively, we propose that C7 and ZYX might be two novel neuron-derived exosomal protein markers, expression of which might be used to evaluate cognitive decline before a clinical diagnosis of AD is warranted.

Involvement of a novel regulatory cascade consisting of SET-H3K18ac/H3K27ac-53BP1 in Cr(VI)-induced malignant transformation of 16HBE cells.

Hexavalent chromium (Cr(VI)) is a well-established human carcinogen with DNA damaging effects. Recently we established a Cr(VI)-induced malignant transformation model from a human bronchial epithelial (16HBE) cell line, and in the transformed (16HBE-T) cells reduced levels of 53BP1 (critical for DNA repair) and the acetylated histone H3K18/27 (H3K18/27ac) were observed. In 16HBE-T cells SET (a multifunctional protein) was elevated by Cr(VI) through quantitative proteomics analysis. In the present study, we further explore the involvement of SET in the H3K18/27ac/53BP1 cascade in the 16HBE-T model, primarily by knockdown of SET. Bioinformatic analysis of the differentially expressed proteins indicated enrichment in histone modifications, in which SET was a major regulator. In 16HBE cells SET expression was enhanced by Cr(VI) in a concentration- and exposure duration-dependent manner. In 16HBE-T cells, SET knockdown showed the following effects: reversal of H3K18/27ac and 53BP1 levels, enhanced enrichment H3K18/27ac in 53BP1's promotor region, increase rate of apoptosis and cell cycle G0/G1 arrest (with or without Cr(VI) treatment), and reduced colony-forming efficiency. Finally, In comparison with benzo(a)pyrene-transformed (malignant, 16HBE-B) cells from 16HBE where no changes in H3K18/27ac, 53BP1 or SET were observed, while the H3K18/27ac/53BP1 cascade was downregulated and SET upregulated in 16HBE-T cells, as compared with the parental 16HBE cells; thus the changes in 16HBE-T might be a specific effect of Cr(VI). In conclusion, our results suggest that SET may be involved in the malignant cell transformation, through inhibiting the H3K18/27ac/53BP1 cascade, at least in the 16HBE cell model.

The Prevalence, Coinfection, and Evolutionary and Molecular Characteristics of Prevalent Goose Circovirus in Guangdong, China.

To understand the prevalence, coinfection with other viruses, underlying genetic evolution, recombination, and molecular biological characteristics of goose circovirus (GoCV) in Guangdong, China, from December 2019 to August 2020, 310 tissue samples of geese showing stunted growth and feather disorder syndrome were collected from this region and analyzed. GoCV, Tembusu virus, waterfowl paramyxovirus, avian influenza virus, fowl adenovirus type 4, and duck plague virus were detected with PCR or real-time PCR. Thirty-one complete GoCV viral genomes were obtained from 164 PCR-verified GoCV nucleotide-positive samples and subjected to phylogenetic analysis, gene recombination analysis, and genome secondary structure prediction. The results showed that more than half of the samples were GoCV positive, and 31.1% of the GoCV-positive samples were from coinfections with at least one of the other viruses. The phylogenetic analysis showed that the GoCVs could be divided into three genome types. The genes of most main epidemic strains now circulating in Guangdong belonged to the Ia subtype, and some strains gradually formed a new Ib subtype. The secondary structure of the viral genome was similar to that of other known circoviruses. Furthermore, B cell linear epitope prediction and protein structure homology modeling of the viral capsid protein were performed based on the viral amino acid sequences. The results showed that the spatial structure of the capsid protein of the 31 sequenced strains was similar to that of duck circovirus and consisted of two ß-sandwich conformations. A total of five B cell linear epitopes were predicted, and four of them were mapped on the predicted model of the capsid protein of GoCVs. This report provides a reference for the epidemiology of GoCV in Guangdong, understanding the elemental composition of the virus genes and proteins, selecting representative vaccine strains, constructing targeted immune preparations for GoCV, and strengthening prevention and control of the disease.

Prevalencia, coinfección y características evolutivas y moleculares del circovirus del ganso prevalente en Guangdong, China. Para comprender la prevalencia, la coinfección con otros virus, su evolución genética subyacente, la recombinación y las características biológicas moleculares del circovirus del ganso (GoCV) en Guangdong, China, de diciembre de 2019 a agosto de 2020, 310 se recolectaron muestras de tejido de gansos que presentaban retraso en el crecimiento y síndrome del trastorno de las plumas en esta región y fueron analizadas. Se detectaron mediante PCR o por PCR en tiempo real el circovirus del ganso, el virus Tembusu (TMUV), el paramixovirus de aves acuáticas (WFPV), el virus de la influenza aviar (AIV), el adenovirus del pollo tipo 4 (Fadv-4) y el virus de la enteritis viral del pato (DPV). Se obtuvieron 31 genomas virales completos del circovirus del ganso de 164 muestras positivas de nucleótidos de circovirus del ganso verificadas por PCR y se sometieron a análisis filogenético, a análisis de recombinación de genes y predicción de la estructura secundaria del genoma. Los resultados mostraron que más de la mitad de las muestras eran positivas para circovirus del ganso y el 31.1% de las muestras positivas para circovirus del ganso eran de coinfecciones con al menos uno de los otros virus. El análisis filogenético mostró que los circovirus del ganso podrían dividirse en tres tipos de genomas. Los genes de la mayoría de las principales cepas epidémicas que ahora circulan en Guangdong pertenecían al subtipo Ia, y algunas cepas formaron gradualmente un nuevo subtipo Ib. La estructura secundaria del genoma viral era similar a la de otros circovirus conocidos. Además, la predicción del epítope lineal de células B y el modelo de la homología de la estructura de la proteína de la cápside viral se realizaron basándose en las secuencias de aminoácidos virales. Los resultados mostraron que la estructura espacial de la proteína de la cápside de las 31 cepas secuenciadas era similar a la del circovirus de pato y consistía de dos conformaciones de tipo sándwich ß. Se predijo un total de cinco epítopes lineales de células B y cuatro de ellos se mapearon en el modelo predicho de la proteína de la cápside del circovirus del ganso. Este informe proporciona una referencia para la epidemiología de circovirus del ganso en Guangdong, entendiendo la composición elemental de los genes y proteínas del virus, seleccionando cepas de vacunas representativas, construyendo preparaciones de blancos inmunitarios para circovirus del ganso y fortaleciendo la prevención y el control de la enfermedad.

miR-21-5p promotes lung adenocarcinoma progression partially through targeting SET/TAF-Iα.

OBJECTIVE: Although SET(I2PP2A) and miRNAs are reported to play a pivotal role in lung cancer, the underlying mechanisms have remained obscure. To address this issue, we investigated how miRNAs and SET participate in the progression of lung cancer. METHODS: miRNAs that target SET were predicted from multiple miRNA databases. Three human NSCLC cell lines and two normal lung cell lines were used to evaluate aberrant miRNA and SET expressions. A dual luciferase reporter assay system was employed to verify the interaction between miRNA and SET. Stable miRNA knockdown and SET overexpression in A549 cells were achieved through lentivirus transfection; the corresponding influences on lung cancer progression were also examined. RESULTS: In this study, A549 was the sole cell line to lack SET/TAF-Iα expression, which was inversely correlated with the up-regulation of miR-21-5p. SET was subsequently revealed as the direct target site of miR-21-5p in A549 cells. The stable miR-21-5p knockdown and SET/TAF-Iα overexpression were shown to markedly enhance the expression of SET/TAF-Iα and to inhibit the migration, invasion, proliferation as well as the in vivo tumorigenicity of A549 cells. CONCLUSION: We suggest that SET/TAF-Iα might be a tumor suppressing factor regulated by miR-21-5p in lung adenocarcinoma. This might provide a target for lung adenocarcinoma therapy.

Trichloroethylene-induced downregulation of miR-199b-5p contributes to SET-mediated apoptosis in hepatocytes.

Trichloroethylene (TCE) is a ubiquitous toxicant widespread in our environment. Exposure to TCE can cause severe liver damage. In previous studies, we detected an abnormal elevation of SET (a protein encoded by the SETgene in humans) which was observed in human HL-7702 cells (L-02 hepatocytes) under the treatment of TCE. Moreover, further study indicated that SET acts as an important mediator in TCE-induced hepatocyte apoptosis. The major functions of SET have been elucidated, while the regulatory mechanism responsible for modulation of SET remains unclear. In this study, four major microRNA-related databases were used to screen and identify 6 candidate microRNAs involved in the regulation of SET. Subsequent verification indicated that miR-21 and miR-199b-5p were decreased in TCE-treated L-02 cells, suggesting that miR-21 and miR-199b-5p (miR199b for short) miR199b potentially regulate SET expression. Additionally, the dual-luciferase system revealed that only miR199b could directly bind to untranslated region (3'-UTR) of the SETgene. Modulation of SET by miR199b was verified through overexpression and knockdown of miR199b in L-02 cells. Assessment of apoptosis indicated that elevated miR199b attenuated TCE-induced apoptosis, while reduced miR199b enhanced it. In summary, this study suggests that in cultured hepatocytes, TCE-induced suppression of miR199b drives SET induction, which further mediates the response to TCE.