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In the southern thrust belt (STB) of Junggar Basin, hydrocarbon resources are abundant at ultradeep depths. The genesis of highly mature oil and gas is complex, with considerable geological implications, because of the burial depth of these resources and multiphase tectonic evolution. The deep–ultradeep oil and gas reservoir accumulation processes and the contribution of Permian source rocks are still unclear in the STB. In this study, using the ultradeep reservoirs of the middle section of the STB (MSTB) as an example, systematic evaluations were conducted on the hydrocarbon geochemical characteristics of the area. Additionally, this study detailed the accumulation and evolution processes of the reservoir in the lower play of the MSTB using various comprehensive technical analyses, such as those for the geochemical characteristics of crude oil, the genesis and source of crude oil and gas, inclusion observations, homogenization temperature, quantitative particle fluorescence, and basin simulation. The integrated analysis results showed that the oil and gas from Well HT-1 in Huxi Anticline (HXA) in the lower play was characterized by mixed sources from Permian argillaceous source rock and Jurassic coal-bearing source rocks. The pristane/phytane ratio (Pr/Ph) and biomarkers of the crude oil indicated the presence of Permian source crude oil. The natural gas drying coefficient and the carbon isotope of methane conveyed a typical coal-related gas from the Lower–Middle Jurassic epoch. In addition, three types of hydrocarbon inclusions (yellow–green fluorescence, blue–white fluorescence, and gaseous hydrocarbons) were developed in the MSTB. Oil and gas accumulation periods included Early Cretaceous, Eocene, and Miocene. Finally, substantial deviations were found for accumulation periods from different anticlines in the study area, which were controlled by the ancient structural background and tectonic evolution. The early anticlines, formed by Yanshanian tectonic movement (YSTM), controlled the early hydrocarbon migration as well as reservoir formation, and the newer anticlines, formed by Himalayan tectonic movement (HMTM), controlled the redistribution of hydrocarbons from ancient reservoirs. The oil and gas reservoir formed in Qingshuihe Formation (K1q) in HXA occurred during the Miocene. The ancient oil reservoirs to the south of HXA were damaged, and hydrocarbons were redistributed; the hydrocarbons migrated and accumulated in HXA and mixed with highly mature gas from Jurassic source rocks. The Permian hydrocarbons made a substantial contribution to the deep–ultradeep resources of MSTB and provided extremely rich hydrocarbon resources together with the Jurassic source rocks. Additionally, within MSTB, large anticlines were thoroughly developed in ultradeep strata, which provided superior trapping conditions for large-scale hydrocarbon accumulation. [ABSTRACT FROM AUTHOR]

Peste des petits ruminants virus (PPRV) is an important pathogen that seriously influences the productivity of small ruminants worldwide. PPRV is lymphotropic in nature and SLAM was identified as the primary receptor for PPRV and other Morbilliviruses. Many viruses have been demonstrated to engage extracellular vesicles (EVs) to facilitate their replication and pathogenesis. Here, we provide evidence that PPRV infection significantly induced the secretion levels of EVs from goat PBMC, and that PPRV-H protein carried in EVs can enhance SLAM receptor expression in the recipient cells via suppressing miR-218, a negative miRNA directly targeting SLAM gene. Importantly, EVs-mediated increased SLAM expression enhances PPRV infectivity as well as the expression of various cytokines related to SLAM signaling pathway in the recipient cells. Moreover, our data reveal that PPRV associate EVs rapidly entry into the recipient cells mainly through macropinocytosis pathway and cooperated with caveolin- and clathrin-mediated endocytosis. Taken together, our findings identify a new strategy by PPRV to enhance virus infection and escape innate immunity by engaging EVs pathway. Author summary: Peste des petitsruminants virus (PPRV) infection induces a transient but severe immunosuppression in the host, which threatens both small livestock and endangered susceptible wildlife populations in many countries. Despite extensive research, the mechanism underlying pathogenesis of PPRV infection remains elusive. Our data provide the first direct evidence that the EVs derived from PPRV-infected cells are involved in PPRV replication. In this study, the EVs derived from PPRV-infected goat PBMCs can enhance SLAM expression in the recipient cells, and more importantly, EVs-mediated increased SLAM expression enhances PPRV replication as well as the expression of various cytokines related to SLAM signaling pathway in the recipient cells. Taken together, our research has provided new insight into understanding the effect of EVs on PPRV replication and pathogenesis, and revealed a potential therapeutic target for antiviral intervention. [ABSTRACT FROM AUTHOR]

Hydropericardium-hepatitis syndrome (HHS) is caused by some strains of fowl adenovirus serotype 4 (FAdV-4). However, the mechanism of FAdV-4 entry is not well understood. Therefore, to investigate the changes in host cellular response at the early stage of FAdV-4 infection, a conjoint analysis of miRNA-seq and mRNA-seq was utilized with leghorn male hepatocellular (LMH) cells at 30, 60, and 120 min after FAdV-4 infection. In total, we identified 785 differentially expressed (DE) miRNAs and 725 DE mRNAs in FAdV-4-infected LMH cells. Most miRNAs and mRNAs, including gga-miR-148a-3p, gga-miR-148a-5p, gga-miR-15c-3p, CRK, SOCS3, and EGR1, have not previously been reported to be associated with FAdV-4 infection. The conjoint analysis of the obtained data identified 856 miRNA–mRNA pairs at three time points. The interaction network analysis showed that gga-miR-128-2-5p, gga-miR-7475-5p, novel_miR205, and TCF7L1 were located in the core of the network. Furthermore, the relationship between gga-miR-128-2-5p and its target OBSL1 was confirmed using a dual-luciferase reporter system and a real-time quantitative polymerase chain reaction assay. In vitro experiments revealed that both gga-miR-128-2-5p overexpression and OBSL1 loss of function inhibited FAdV-4 entry. These results suggested that gga-miR-128-2-5p plays an important role in FAdV-4 entry by targeting OBSL1. To the best of our knowledge, the present study is the first to analyze host miRNA and mRNA expression at the early stage of FAdV-4 infection; furthermore, the results of this study help to elucidate the molecular mechanisms of FAdV-4 entry. [ABSTRACT FROM AUTHOR]

Macroautophagy/autophagy is an essential cellular response in the fight against intracellular pathogens. Although some viruses can escape from or utilize autophagy to ensure their own replication, the responses of autophagy pathways to viral invasion remain poorly documented. Here, we show that peste des petits ruminants virus (PPRV) infection induces successive autophagic signalling in host cells via distinct and uncoupled molecular pathways. Immediately upon invasion, PPRV induced a first transient wave of autophagy via a mechanism involving the cellular pathogen receptor NECTIN4 and an AKT-MTOR-dependent pathway. Autophagic detection showed that early PPRV infection not only increased the amounts of autophagosomes and LC3-II but also downregulated the phosphorylation of AKT-MTOR. Subsequently, we found that the binding of viral protein H to NECTIN4 ultimately induced a wave of autophagy and inactivated the AKT-MTOR pathway, which is a critical step for the control of infection. Soon after infection, new autophagic signalling was initiated that required viral replication and protein expression. Interestingly, expression of IRGM and HSPA1A was significantly upregulated following PPRV replication. Strikingly, knockdown of IRGM and HSPA1A expression using small interfering RNAs impaired the PPRV-induced second autophagic wave and viral particle production. Moreover, IRGM-interacting PPRV-C and HSPA1A-interacting PPRV-N expression was sufficient to induce autophagy through an IRGM-HSPA1A-dependent pathway. Importantly, syncytia formation could facilitate sustained autophagy and the replication of PPRV. Overall, our work reveals distinct molecular pathways underlying the induction of self-beneficial sustained autophagy by attenuated PPRV, which will contribute to improving the use of vaccines for therapy. Abbreviations: ACTB: actin beta; ANOVA: analysis of variance; ATG: autophagy-related; BECN1: beclin 1; CDV: canine distemper virus; Co-IP: coimmunoprecipitation; FIP: fusion inhibitory peptide; GFP: green fluorescent protein; GST: glutathione S-transferase; HMOX1: heme oxygenase 1; hpi: hours post infection; HSPA1A: heat shock protein family A (Hsp70) member 1A; HSP90AA1: heat shock protein 90 kDa alpha (cytosolic), class A member 1; IFN: interferon; IgG: immunoglobulin G; INS: insulin; IRGM: immunity related GTPase M; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MeV: measles virus; MOI: multiplicity of infection; MTOR: mechanistic target of rapamycin kinase; PI3K: phosphoinositide-3 kinase; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; SDS: sodium dodecyl sulfate; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; UV: ultraviolet. [ABSTRACT FROM AUTHOR]

Peste des petits ruminants virus (PPRV) has emerged as a significant threat to the productivity of small ruminants worldwide. PPRV is lymphotropic in nature and induces in the hosts a transient but severe immunosuppression, especially innate immunity. However, it remains largely unknown how NK cells respond and are regulated at the earliest time points after an acute viral PPRV infection in goats. In this study, we revealed that multiple immune responses of goat peripheral NK cells were compromised during PPRV infection, including the cytolytic effector molecule expression and cytokine production. Importantly, we demonstrated that PPRV infection stimulated the expression of TWEAK, a negative regulator of cytotoxic function of NK cells, which may be involved in the suppression of cytotoxicity as well as cytokine production in infected goat NK cells. Furthermore, we found that PPRV infection induced TWEAK expression in goat NK cells involving post-transcription by suppressing miR-1, a novel negative miRNA directly targeting the TWEAK gene. Moreover, replication of virus is required for inhibition of miR-1 expression during PPRV infection, and the non-structural V protein of PPRV plays an important role in miR-1 mediated TWEAK upregulation. Additionally, we revealed that the regulation of NK cell immune responses by TWEAK is mediated by MyD88, SOCS1, and STAT3. Taken together, our results demonstrated that TWEAK may play a key role in regulating goat peripheral NK cell cytotoxicity and cytokine expression levels during PPRV infection. [ABSTRACT FROM AUTHOR]

Peste des petits ruminants virus (PPRV) causes an acute and highly contagious disease of sheep and goats and has spread with alarming speed around the world. The pathology of Peste des petits ruminants is linked to retrogressive changes and necrotic lesions in lymphoid tissues and epithelial cells. However, the process of PPRV entry into host epithelial cells remains largely unknown. Here, we performed a comprehensive study of the entry mechanism of PPRV into caprine endometrial epithelial cells (EECs). We clearly demonstrated that PPRV internalization was inhibited by chloroquine and ammonium chloride, which elevate the pH of various organelles. However, PPRV entry was not affected by chlorpromazine and knockdown of the clathrin heavy chain in EECs. In addition, we found that the internalization of PPRV was dependent on dynamin and membrane cholesterol and was suppressed by silencing of caveolin-1. Macropinocytosis did not play a role, but phosphatidylinositol 3-kinase (PI3K) was required for PPRV internalization. Cell type and receptor-dependent differences indicated that PPRV entry into caprine fetal fibroblast cells (FFCs) occurred via a different route. Taken together, our findings demonstrate that PPRV enters EECs through a cholesterol-dependent caveolae-mediated uptake mechanism that is pH-dependent and requires dynamin and PI3K but is independent of clathrin. This potentially provides insight into the entry mechanisms of other morbilliviruses. [ABSTRACT FROM AUTHOR]

Peste des petits ruminants virus (PPRV), the etiological agent of peste des petits ruminants (PPR), causes an acute or subacute disease in small ruminants. Although abortion is observed in an unusually large proportion of pregnant goats during outbreaks of PPR, the pathogenic mechanism underlying remains unclear. Here, the gene expression profile of caprine endometrial epithelial cells (EECs) infected with PPRV Nigeria 75/1 was determined by DNA microarray to investigate the cellular response immediately after viral entry. The microarray analysis revealed that a total of 146 genes were significantly dysregulated by PPRV internalization within 1 h post-infection (hpi). Of these, 85 genes were upregulated and 61 genes were downregulated. Most of these genes, including NFKB1A, JUNB, and IL1A, have not previously been reported in association with PPRV infection in goats. Following viral replication (24 hpi), the expression of 307 genes were significantly upregulated and that of 261 genes were downregulated. The data for the genes differentially expressed in EECs were subjected to a time sequence profile analysis, gene network analysis and pathway analysis. The gene network analysis showed that 13 genes (EIF2AK3, IL10, TLR4, ZO3, NFKBIB, RAC1, HSP90AA1, SMAD7, ARG2, JUNB, ZFP36, APP, and IL1A) were located in the core of the network. We clearly demonstrate that PPRV infection upregulates the expression of nectin-4 after 1 hpi, which peaked at 24 hpi in EECs. In conclusion, this study demonstrates the early cellular gene expression in the caprine endometrial epithelial cells after the binding and entry of PPRV. [ABSTRACT FROM AUTHOR]

Peste des petits ruminants (PPR) is an acute and highly contagious disease in small ruminants that causes significant economic losses in developing countries. An increasing number of studies have demonstrated that both autophagy and apoptosis are important cellular mechanisms for maintaining homeostasis, and they participate in the host response to pathogens. However, the crosstalk between apoptosis and autophagy in host cells during PPRV infection has not been clarified. In this study, autophagy was induced upon virus infection in caprine endometrial epithelial cells (EECs), as determined by the appearance of double- and single-membrane autophagy-like vesicles, LC3-I/LC3-II conversion, and p62 degradation. We also found that PPRV infection triggered a complete autophagic response, most likely mediated by the non-structural protein C and nucleoprotein N. Moreover, our results suggest that autophagy not only promotes the replication of PPRV in EECs but also provides a potential mechanism for inhibiting PPRV-induced apoptosis. Inhibiting autophagosome formation by wortmannin and knocking down the essential autophagic proteins Beclin-1 and ATG7 induces caspase-dependent apoptosis in EECs in PPRV infection. However, inhibiting autophagosome and lysosome fusion by NH4Cl and chloroquine did not increase the number of apoptotic cells. Collectively, these data are the first to indicate that PPRV-induced autophagy inhibits caspase-dependent apoptosis and thus contributes to the enhancement of viral replication and maturity in host cells. [ABSTRACT FROM AUTHOR]

The aim of this study was to determine the mechanism by which Newcastle disease virus (NDV) affects eggshell quality. Thirty-week-old specific pathogen free (SPF) egg-laying hens were inoculated with the velogenic genotype VIId NDV strain (infected group) or with inoculating media without virus (control group) by combined intraocular and intranasal routes. The levels of CaBP-D28k mRNA expression in the uterus, a gene related to eggshell quality, were examined by quantitative reverse transcriptase polymerase chain reaction (RT-PCR). The quality of eggshells was analyzed by scanning electron microscopy (SEM). The infected group showed a marked decline in egg production when compared to the control group. The NDV antigen was found more abundantly in the glandular epithelium of the infected hens' uteri from 1 to 15 d post-inoculation (dpi). The levels of CaBP-D28k mRNA expression in the uteri of infected hens were significantly lower than in the control hens from 3 to 15 dpi ( P < 0.05). The changes in the Ca concentrations in the eggshells were consistent with the expression of CaBP-D28k mRNA in the infected hens. Ultrastructural examination of eggshells showed significantly reduced shell thickness in the infected hens from 1 to 15 dpi ( P < 0.05). Furthermore, obvious changes in the structure of the external shell surface and shell membrane were detected in the infected hens compared with the control hens. In conclusion, the current study confirmed that velogenic genotype VIId NDV infection is associated with the deterioration of the eggshell quality of the laying hens. [ABSTRACT FROM AUTHOR]

The Balkhash–West Junggar remnant ocean is a conspicuous tectonic feature that had an important effect on the Paleozoic tectonic evolution of the Central Asian Orogenic Belt. How the Carboniferous Balkhash–West Junggar remnant ocean was filled and closed is poorly understood. In this study, we focus on the integrated tectonic–sedimentary evolution of the Tacheng Basin, which is located in the eastern part of the Balkhash–West Junggar remnant ocean, using high-resolution seismic reflection, well-line, geochronological and geochemical data to establish the filling of the basin by sediments and its evolution. The Carboniferous Balkhash–West Junggar remnant ocean basin was filled with Early Carboniferous deep marine mudstone and interbedded sandstone with minor andesite, basalt and tuff, and Late Carboniferous basalt, andesite, breccia and tuff and shallow marine mudstone and sandstone. The Carboniferous igneous assemblage mainly consists of basalt with high Nb content and (Nb/La) PM values and concomitant magnesian andesites with adakite geochemical characteristics of high Sr and low Y and Yb, suggesting a subduction-related tectonic setting. Zircons in the tuff that underlies the basalts and magnesian andesites were dated to ca. 315 Ma by LA–ICP–MS U–Pb. The identified unconformity between the Carboniferous and Lower Permian from seismic reflection profile in Well Tacan-1 subdivided the Carboniferous–Early Permian strata into two tectonostratigraphic units. The Lower Permian sequences overlap the Carboniferous strata and the facies transition from the submarine Carboniferous to the terrigenous Lower Permian indicates that the Balkhash–West Junggar remnant ocean closed during the Early Permian. These new data suggest that the sedimentary filling of the basin was in response to subduction and accretionary processes and that oceanic subduction was an important mechanism that led to the shrinking, filling and closure of the Balkhash–West Junggar remnant ocean because of compression. Therefore, lateral crust growth through subduction–accretionary processes still played an important role in the Carboniferous construction of western Junggar. [ABSTRACT FROM AUTHOR]

High rate of fetal mortality in ruminant somatic cell nuclear transfer (SCNT) pregnancies is due, at least in part, to immune-mediated abortion of fetuses. In the present study, goat uterine leukocytes were isolated by Dolichos biflorus agglutinin (DBA) coated magnetic beads, and with majority being were CD56+CD16- in phenotype with low levels of perforin and Granzyme B expression. The responses of the isolated cells to SCNT and in vitro fertilization (IVF) embryos conditioned mediums containing hormone steroids were compared by measuring their phenotype and cytokines expression. The results showed there was a 2-fold increase in the numbers of isolated uterine leukocytes after incubation with different conditioned mediums for 120 h. However, significantly lower percentage and absolute numbers of uterine CD56+CD16- leukocytes incubated with SCNT conditioned mediums were detected as compared with those incubated with IVF conditioned mediums (P < 0.05). The group treated with progesterone (P4) or the combination of P4 and 17β-estradiol (E2) were associated with significantly higher percentage and absolute numbers of CD56+CD16- cells as compared with those treated with E2 alone (P < 0.05). Furthermore, in the presence of steroids, the isolated leukocytes incubated with SCNT conditioned mediums associated with greater levels of IFN-γ secretion and expression, as well as lesser levels of VEGF, as compared with those treated with IVF conditioned mediums (P < 0.05). In conclusion, this study demonstrates that SCNT embryos have a profound effect on the phenotype expression of goat uterine DBA+ leukocytes, as well as the secretion and expression of IFN-γ and VEGF by these cells in vitro. [ABSTRACT FROM AUTHOR]

Hepatitis-hydropericardium syndrome (HHS) is caused by fowl adenovirus serotype 4 (FAdV-4) and has resulted in considerable economic losses to the poultry industry globally. FAdV-4 elicits apoptosis in host cells. Long noncoding RNAs (lncRNAs) have emerged as important regulatory RNAs with profound effects on various biological processes, including apoptosis. However, it remains unknown whether lncRNAs participate in FAdV-4-induced apoptosis. In this study, RNA sequencing was applied to determine the transcription of cellular lncRNA in leghorn male hepatocellular (LMH) cells infected with FAdV-4. Cellular RNA transcription analysis demonstrated that FAdV-4 infection elicited 1798 significantly differentially expressed (DE) lncRNAs in infected LMH cells at 24 h post-infection (hpi) compared to mock control infection. In addition, 2873 DE mRNAs were also found. Target prediction and analyses revealed that 775 DE lncRNAs whose 671 target mRNAs were among the DE mRNAs were involved in several signaling pathways, including the AMPK signaling pathway, p53 signaling pathway and insulin signaling pathway. From these 775 DE lncRNAs, we identified 71 DE lncRNAs related to apoptosis based on their target gene functions. Subsequently, lncRNA 54128 was selected from the 71 identified DE lncRNAs, and its role in FAdV-4-induced apoptosis was verified. LncRNA 54128 interference significantly suppressed the rate of apoptosis, which was accompanied by reduced BMP4 transcription levels. To the best of our knowledge, this is the first study to analyze host lncRNA transcription during FAdV-4 infection. Our findings provide a better understanding of host responses to FAdV-4 infection and provide new directions for understanding the potential association between lncRNAs and FAdV-4 pathogenesis. [ABSTRACT FROM AUTHOR]

The Bulonggoer paleo-oil reservoir (BPR) on the northwest Junggar Basin is the first Devonian paleo-oil reservoir discovered in North Xinjiang, China. Solid bitumens occur within sandstone pores and as veins filling fractures. Samples of both types were analyzed using stable carbon isotope and reflectance measurements, as well as molecular biomarker parameters. The extremely positive δ 13 C values and biomarker indicators of depositional environment/lithology, such as pristane/phytane (Pr/Ph), C 29 /C 30 hopane, diasteranes/regular steranes and dibenzothiophene/phenanthrene ratios, indicate a siliciclastic source for the BPR and their deposition in a highly reducing hypersaline environment. The presence of long chain n -alkanes and abundant tetracyclic diterpanes, C 20 –C 21 tricyclic terpanes and perylene are indicators of higher plant organic matter input. Moreover, the bimodal distribution of C 27 > C 28 < C 29 regular steranes and abundant methyltriaromatic steroids also support a contribution of microalgae as well as higher plants organic matter. The similar molecular composition and thermal maturity parameters indicate that the reservoir and veined solid bitumens were altered from a common paleo-petroleum, which originated from peak oil window matured source rocks. All solid bitumens from the BPR are characterized by relatively low bitumen reflectance values (Rb% < 0.7), suggesting that they were generated from low temperature processes rather than oil thermal cracking. Comparatively, the Rb% values for veined bitumens are higher than reservoir bitumens, indicating that the veined bitumens occurred earlier and experienced higher thermal conditions. [ABSTRACT FROM AUTHOR]

β-catenin is a key component of the Wnt/β-catenin signal transduction cascade which is a highly conserved signaling pathway in eukaryotes. Increasing evidence suggests that the Wnt/β-catenin signaling pathway is involved in the infection of many viruses. However, its role in fowl adenovirus serotype 4 (FAdV-4) replication remains unclear. In the present study, we showed that FAdV-4 infection increased the expression of β-catenin and promoted the nuclear translocation of β-catenin. Overexpression of β-catenin and LiCl treatment stimulated the accumulation of β-catenin in the nucleus, and then facilitated FAdV-4 replication. Conversely, repression of β-catenin by inhibitors and siRNA significantly inhibited FAdV-4 replication. Furthermore, inhibition of autophagy by 3-Methyladenine (3-MA) suppressed the FAdV-4 replication, and repression of β-catenin inhibited the FAdV-4-triggered autophagy. In conclusion, the nuclear translocation of β-catenin benefits FAdV-4 replication, and suppression of β-catenin limits FAdV-4 production by inhibiting FAdV-4-induced autophagy. These findings indicated that β-catenin is an important regulator of FAdV-4 replication which can serve as a potential target for anti-FAdV-4 agents. • FAdV-4 infection increases the expression of β-catenin and promotes the nuclear translocation of β-catenin. • The nuclear translocation of β-catenin facilitates FAdV-4 replication. • Suppression of β-catenin limits FAdV-4 production by inhibiting FAdV-4-induced autophagy. [ABSTRACT FROM AUTHOR]

Abstract: TiO2/Fe2O3 core–shell nanocomposition film has been fabricated via two-step method. TiO2 nanorod arrays are synthesized by a facile hydrothermal method, and followed by Fe2O3 nanoparticles deposited on TiO2 nanorod arrays through an ordinary chemical bath deposition. The phase structures, morphologies, particle size, chemical compositions of the composites have been characterized by X-ray diffraction (XRD), field emission scanning electron microscope (FESEM) and ultraviolet–visible (UV–vis) spectrophotometer. The results confirm that Fe2O3 nanoparticles of mean size ca. 10nm coated on the surface of TiO2 NRs. After depositing Fe2O3, UV–vis absorption property is induces the shift to the visible-light range, the annealing temperature of 600°C is the best condition for UV–vis absorption property of TiO2/Fe2O3 nanocomposite film, and increasing Fe content, optical activity are enhanced one by one. The photoelectrochemical (PEC) performances of the as-prepared composite nanorods are determined by measuring the photo-generated currents under illumination of UV–vis light. The TiO2 NRs modified by Fe2O3 show the photocurrent value of 1.36mA/cm2 at 0V vs Ag/AgCl, which is higher than those of unmodified TiO2 NRs. [Copyright &y& Elsevier]

Abstract: CdS quantum dots (QDs) coated TiO2 nanorod arrays have been prepared via a two-step method. TiO2 nanorod arrays were synthesized by a facile hydrothermal method, and CdS QDs were deposited on the nanorods by a sequential chemical bath deposition (S-CBD) technique. The surface morphology, structure, optical and photoelectrochemical behaviors of the core–shell nanorod array films are considered. A photocurrent of 2.5mA/cm2, an open circuit photovoltage of 1.10V, and a conversion efficiency of 1.91% were obtained under an illumination of 100mW/cm2, when the CdS QDs deposited on TiO2 nanorods film for about 7 cycles. The results demonstrate that the composite films are of excellence with respect to photovoltaic conversion. [ABSTRACT FROM AUTHOR]

Abstract: Large-quantity flower-like tubular ZnO coated with Fe3O4 nanoparticles were synthesized via a simple solution method at low temperature. The phase structures and morphologies of the composite had been characterized by XRD and FESEM. The results showed that Fe3O4 nanoparticles coating on flower-like tubular ZnO can be obtained at 90°C. The structure of flower-like tubular ZnO was not destroyed in the coating process. The test of electromagnetic wave absorption was carried out by the radar-absorbing materials (RAM) reflectivity far field radar cross-section (RCS) method. Magnetic measurements revealed the presence of magnetite nanoparticles in the composites. Measurements of the electromagnetic parameters of the samples showed that the flower-like tubular ZnO/Fe3O4 nanocomposites were much better than the pure ZnO or Fe3O4 with the efficiency of electromagnetic wave absorption. [ABSTRACT FROM AUTHOR]

Bovine viral diarrhea virus (BVDV) belongs to the family Flaviviridae and includes two biotypes in cell culture: cytopathic (CP) or non-cytopathic (NCP) effects. Ferroptosis is a non-apoptotic form of programmed cell death that contributes to inflammatory diseases. However, whether BVDV induces ferroptosis and the role of ferroptosis in viral infection remain unclear. Here, we provide evidence that both CP and NCP BVDV can induce ferroptosis in Madin-Darby bovine kidney cells at similar rate. Mechanistically, biotypes of BVDV infection downregulate cytoplasmic and mitochondrial GPX4 via Nrf2-GPX4 pathway, thereby resulting in lethal lipid peroxidation and promoting ferroptosis. In parallel, BVDV can degrade ferritin heavy chain and mitochondrial ferritin via NCOA4-mediated ferritinophagy to promote the accumulation of Fe 2+ and initiate ferroptosis. Importantly, CP BVDV-induced ferroptosis is tightly associated with serious damage of mitochondria and hyperactivation of inflammatory responses. In contrast, mild or unapparent damage of mitochondria and slight inflammatory responses were detected in NCP BVDV-infected cells. More importantly, different mitophagy pathways in response to mitochondria damage by both biotypes of BVDV are involved in inflammatory responses. Overall, this study is the first to show that mitochondria may play key roles in mediating ferroptosis and inflammatory responses induced by biotypes of BVDV in vitro .IMPORTANCEBovine viral diarrhea virus (BVDV) threatens a wide range of domestic and wild cattle population worldwide. BVDV causes great economic loss in cattle industry through its immunosuppression and persistent infection. Despite extensive research, the mechanism underlying the pathogenesis of BVDV remains elusive. Our data provide the first direct evidence that mitochondria-mediated ferroptosis and mitophagy are involved in inflammatory responses in both biotypes of BVDV-infected cells. Importantly, we demonstrate that the different degrees of injury of mitochondria and inflammatory responses may attribute to different mitophagy pathways induced by biotypes of BVDV. Overall, our findings uncover the interaction between BVDV infection and mitochondria-mediated ferroptosis, which shed novel light on the physiological impacts of ferroptosis on the pathogenesis of BVDV infection, and provide a promising therapeutic strategy to treat this important infectious disease with a worldwide distribution., Competing Interests: The authors declare no conflict of interest.

Mycoplasma synoviae ( M. synoviae ) is one of the major poultry pathogens causing infectious synovitis, airsacculitis, a high incidence of shell breakage, and egg production loss. However, the pathogenesis of M. synoviae remains unclear. Adhesion of mycoplasmas to host cells is a crucial step in infection and colonization. The purpose of this study was to determine the adhesive function of a putative P80 family lipoprotein (LP78) and evaluate its application in the detection of antibodies against M. synoviae . Recombinant LP78 (rLP78) was expressed in the supernatant component of Escherichia coli and mouse anti-rLP78 serum was prepared. Bioinformatic analysis and western blotting results revealed that LP78 was conservative among M. synoviae strains. It was distributed not only in the cytoplasm but also on the membrane of M. synoviae through western blotting and indirect immunofluorescence (IFA). The adherence of M. synoviae to DF-1 cells was significantly inhibited by mouse anti-rLP78 serum ( p  < 0.01). IFA revealed that rLP78 adhered to DF-1 cells, and this adherence was prevented by mouse anti-rLP78 serum. Furthermore, rLP78 was found to bind to the DF-1 cells membrane proteins in a dose-dependent manner by enzyme-linked immunosorbent assay (ELISA). Screening of DF-1 cells membrane proteins by western blotting showed that proteins with molecular weight of 35-40 kDa and 55-70 kDa bound to rLP78. Moreover, rLP78 was identified to be a fibronectin/plasminogen binding protein. The sensitivity and specificity of rLP78-based iELISA were 85.7 and 94.1%, respectively. The maximum dilution of positive serum (HI titer, 1:128) detected via rLP78-based iELISA was 1:6,400, whereas that detected using a commercial ELISA kit was 1:12,800-1:25,600. Both rLP78-based iELISA and the commercial ELISA kit detected seroconversion after 7 days of challenge and immunization. No cross-reactivity with positive sera against other avian pathogens was observed in rLP78-based iELISA. Collectively, these results indicate that LP78 is a fibronectin/plasminogen-binding adhesion protein of M. synoviae and a potential diagnostic antigen. The present study will facilitate a better understanding of the pathogenesis of M. synoviae and the development of new diagnostic., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Han, Wang, Wang, Chang, Wen, Fang, Hou, Qi and Wang.)

Introduction: African swine fever (ASF) is a highly contagious hemorrhagic fever disease in pigs caused by African swine fever virus (ASFV). It is very difficult to control and prevent ASF outbreaks due to the absence of safe and effective vaccines., Methods: In order to develop a safe and effective ASF vaccine for the control and prevention of ASF, two ASFV recombinant vesicular stomatitis virus (VSV) live vector vaccine prototypes, containing the gene of p72, and a chimera of p30 and p54, were developed based on the replication-competent VSV, and named VSV-p72 and VSV-p35. The immune potency of VSV-p72 or VSV-p35 alone and in combination was evaluated in BALB/c mice via intramuscular and intranasal vaccination., Results: The results indicated that whether administered alone or in combination, the two vaccine prototypes showed acceptable safety in mice and, more importantly, induced high-level specific antibodies against p72, p30, and p54 of ASFV and a strong cellular immune response 28 days after vaccination. The sera from mice vaccinated with the vaccine prototypes significantly inhibited ASFV from infecting porcine alveolar macrophages (PAMs) in vitro . Most notably, the immunized sera from a mixture of VSV-p35 and VSV-p72 inhibited ASFV from infecting PAMs, with an inhibition rate of up to 78.58%., Conclusion: Overall, our findings suggest that ASFV recombinant VSV live vector vaccine prototypes may become a promising candidate vaccine for the control and prevention of ASF., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Ma, Shao, Liu, Gao, Peng, Miao, Yang, Hou, Zhou, Qi and Chang.)

Mycoplasma synoviae ( MS ) is a primary avian pathogen prevalent worldwide that causes airsacculitis and synovitis in birds. Vaccination is recommended as the most cost-effective strategy in the control of MS infection. Novel alternative vaccines are needed for eradicating and controlling MS infection in flocks. DnaK, enolase, elongation factor Tu (EF-Tu), MSPB, NADH oxidase and LP78 are the major immunogenic antigens of MS and are promising targets for subunit vaccine candidates. In the present study, genes encoding DnaK, enolase, EF-Tu, MSPB, LP78, and NADH oxidase were cloned and expressed in Escherichia coli . Enzyme-linked immunosorbent assay showed that the six recombinant proteins were recognized by convalescent sera, indicating that they were expressed during infection. Two injections of the six subunit vaccines induced a robust antibody response and increased the concentrations of IFN-γ and IL-4, especially rEnolase and rEF-Tu. The proliferation of peripheral blood lymphocytes was enhanced in all of the immunized groups. Chickens immunized with rEnolase, rEF-Tu, rLP78, and rMSPB conferred significant protection against MS infection, as indicated by significantly lower DNA copies in the trachea, lower scores of air sac lesions, and lesser tracheal mucosal thickness than that in the challenge control. Especially, rEnolase provided the best protective efficacy, followed by rEF-Tu, rMSPB, and rLP78. Our finds demonstrate that the subunit vaccines and bacterin can only reduce the lesions caused by MS infection, but not prevent colonization of the organism. Our findings may contribute to the development of novel vaccine agents against MS infection., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Han, Wang, Chang, Wang, Fang, Han, Hou, Qi and Wang.)

Introduction: Oesophageal squamous cell carcinoma (OSCC) is one of the most commonly occurring devastating tumours worldwide, including in China. To date, the standard care of patients with stage IV OSCC is systemic chemotherapy and palliative care, which results in poor prognosis. However, no consensus has been established regarding the role of radiotherapy in targeting the primary tumour in patients with stage IVa OSCC. Thus, the aim of this study is to assess the effectiveness of primary radiotherapy combined with S-1 and nedaplatin (NPD) chemotherapy in the patients with stage IV OSCC., Methods and Analysis: The study is a multicentre, open-label, randomised controlled trial. A total of 180 eligible patients with stage IV OSCC will be randomised into a study group (90 patients) and a control group (90 patients). Patients in the study group will receive radiotherapy to the primary tumour at a dose of 50.4 Gy combined with 4-6 cycles of S-1 and NPD chemotherapy. In the control group, patients will only receive 4-6 cycles of S-1 and NPD chemotherapy. The primary and secondary outcomes will be measured. The differences between the two groups will be statistically analysed with regard to overall survival, the progression-free survival and safety. All outcomes will be ascertained before treatment, after treatment and after the follow-up period.The results of this study will provide evidence on the role of radiotherapy in patients with stage IV OSCC in China, which will show new options for patients with advanced oesophageal cancer., Ethics and Dissemination: This study was approved by the Institutional Ethics Committee of The First Hospital Affiliated of Zhengzhou University (approval number: SS-2018-04)., Trial Registration: The trial has been registered at the Chinese Clinical Trial Registry (ChiCTR1800015765) on 1 November 2018; retrospectively registered, http://www.chictr.org.cn/index.aspx., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)