2,416 research outputs found

    High-Throughput Sequencing of MicroRNAs in Adenovirus Type 3 Infected Human Laryngeal Epithelial Cells

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    Adenovirus infection can cause various illnesses depending on the infecting serotype, such as gastroenteritis, conjunctivitis, cystitis, and rash illness, but the infection mechanism is still unknown. MicroRNAs (miRNA) have been reported to play essential roles in cell proliferation, cell differentiation, and pathogenesis of human diseases including viral infections. We analyzed the miRNA expression profiles from adenovirus type 3 (AD3) infected Human laryngeal epithelial (Hep2) cells using a SOLiD deep sequencing. 492 precursor miRNAs were identified in the AD3 infected Hep2 cells, and 540 precursor miRNAs were identified in the control. A total of 44 miRNAs demonstrated high expression and 36 miRNAs showed lower expression in the AD3 infected cells than control. The biogenesis of miRNAs has been analyzed, and some of the SOLiD results were confirmed by Quantitative PCR analysis. The present studies may provide a useful clue for the biological function research into AD3 infection

    Polaron Rashba effect in an asymmetric quantum dot

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    We study the influence of polaron Rashba effect in an asymmetric quantum dot. Using variational method, we derive the expression of the polaron ground state energy. We also discuss the dependencies of the ground state energy on the wave vector and the transverse (longitudinal) effective confinement length. It is found that the ground state energy splits into two branches due to the Rashba effect. The spin splitting energy is an increasing function of the wave vector and the Rashba SO parameter

    Identification of microRNAs Involved in the Host Response to Enterovirus 71 Infection by a Deep Sequencing Approach

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    Role of microRNA (miRNA) has been highlighted in pathogen-host interactions recently. To identify cellular miRNAs involved in the host response to enterovirus 71 (EV71) infection, we performed a comprehensive miRNA profiling in EV71-infected Hep2 cells through deep sequencing. 64 miRNAs were found whose expression levels changed for more than 2-fold in response to EV71 infection. Gene ontology analysis revealed that many of these mRNAs play roles in neurological process, immune response, and cell death pathways, which are known to be associated with the extreme virulence of EV71. To our knowledge, this is the first study on host miRNAs expression alteration response to EV71 infection. Our findings supported the hypothesis that certain miRNAs might be essential in the host-pathogen interactions

    Critical Role of Leucine-Valine Change in Distinct Low pH Requirements for Membrane Fusion between Two Related Retrovirus Envelopes

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    Many viruses use a pH-dependent pathway for fusion with host cell membrane, the mechanism of which is still poorly understood. Here we report that a subtle leucine (Leu)-valine (Val) change at position 501 in the envelope glycoproteins (Envs) of two related retroviruses, jaagsiekte sheep retro-virus (JSRV) and enzootic nasal tumor virus (ENTV), is responsible for their distinct low pH requirements for membrane fusion and infection. The Leu and Val residues are predicted to reside within the C-terminal heptad repeat (HR2) region of JSRV and ENTV Envs, particularly proximal to the hairpin turn of the putative six-helix bundle (6HB). Substitution of the JSRV Leu with a Val blocked the Env-mediated membrane fusion at pH 5.0, whereas replacement of the ENTV Val with a Leu rendered the ENTV Env capable of fusing at pH 5.0. A Leu-Val change has no apparent effect on the stability of native Env but appears to stabilize an intermediate induced by receptor binding. These results are consistent with the existence of at least two metastable conformations of these viral glycoproteins, the native prefusion conformation and a receptor-induced metastable intermediate. Collectively, this work represents an interesting perhaps unique example whereby a simple Leu-Val change has critical impact on pH-dependent virus fusion and entry

    Effects of waterlogging and elevated salinity on the allocation of photosynthetic carbon in estuarine tidal marsh: a mesocosm experiment

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    Embargo until September 10, 2023Background and aim Coastal marshes and wetlands hosting blue carbon ecosystems have shown vulnerability to sea-level rise (SLR) and its consequent effects. In this study, we explored the effects of waterlogging and elevated salinity on the accumulation and allocation of photosynthetic carbon (C) in a widely distributed species in marsh lands. Methods The plant–soil mesocosms of Phragmites australis were grown under waterlogging and elevated salinity conditions to investigate the responses of photosynthetic C allocation in different C pools (plant organs and soils) based on 13CO2 pulse-labeling technology. Results Both waterlogging and elevated salinity treatments decreased photosynthetic C fixation. The hydrological treatments also reduced 13C transport to the plant organs of P. australis while significantly increased 13C allocation percentage in roots. Waterlogging and low salinity had no significant effects on 13C allocation to rhizosphere soils, while high salinity (15 and 30 ppt) significantly reduced 13C allocation to soils, indicating a decreased root C export in saline environments. Waterlogging enhanced the effects of salinity on the 13C allocation pattern, particularly during the late growing season. The responses of flooding and elevated salinity on C allocation in plant organs and rhizosphere soils can be related to changes in nutrient, ionic concentrations and microbial biomass. Conclusion The adaptation strategy of P. australis led to increased C allocation in belowground organs under changed hydrology. Expected global SLR projection might decrease total C stocks in P. australis and alter the C allocation pattern in marsh plant-soil systems, due to amplified effects of flooding and elevated salinities.acceptedVersio

    Protection effect of Emodin pretreatment on intestinal I-RI damage of intestinal mucosa in ratsa

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    AbstractObjectiveTo tinvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury.MethodsA total of 50 SD rats were randomly divided into control group, model group, emodin groups of low, medium and high dose, with 10 in each group. Ischemia-reperfusion injury (I-RI) mode was established by using noninvasive clamp on superior mesentericartery (SMA). Control group and model group were pretreated with 0.5% sodium carboxymethyl cellulose solution lavage 2 h before operation, emodin groups of low, medium and high dose were given emodin lavage with 20, 40, 60 mg/kg pretreatment, femoral venous blood before the lavage pretreatment (T0) and 1 h ischemia (T1), and inferior vena venous blood after 1 h of reperfusion (T2) were extracted from each group of rats for detection of serum level of intestinal fatty acid binding protein (I-FABP), tumor necrosis factor (TNF-α), endotoxin, interleukin 6 (IL-6), and the content of diamine oxidase (DAO); After model establishment, the rats were sacrificed, intestine homogenate was prepared by using blind intestinal tissue to detect intestinal tissue myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels. And upper small intestine tissue was retrieved, followed by fixation and conventional HE staining to observe intestinal tissue morphology under light microscopy.ResultsIn emodin groups of low, medium and high dose at T1 and T2, I-FABP, TNF-α, endotoxin, IL-6 and DAO level were significantly lower than that of model group (P<0.05); in emodin group of low, medium and high dose, MPO and MDA content in intestinal tissue homogenate was significantly lower than that in model group (P<0.05), SOD level was significantly higher than that of model group (P<0.05). Intestinal damage of emodin low, medium and high dose groups were significantly lighter than model group.ConclusionsEmodin pretreatment has certain protective effect on intestinal mucosa in ischemia reperfusion injury

    Geraniol attenuates virulence factors by inhibiting quorum sensing of Pseudomonas aeruginosa

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    Pseudomonas aeruginosa is a ubiquitous opportunistic pathogen that can cause severe respiratory tract infections. Geraniol, a chemical component of essential oils, has antimicrobial and anti-inflammatory activities, along with low toxicity. However, the effect and mechanism of geraniol against P. aeruginosa virulence factors are rarely studied. In this study, we investigated the quorum sensing (QS) inhibitory effects and mechanisms of geraniol against P. aeruginosa PAO1, using physiological and biochemical techniques, quantitative reverse transcription polymerase chain reaction, and transcriptomics. Geraniol slightly affected P. aeruginosa PAO1 growth, prolonged the lag phase, and delayed growth periods in a concentration-dependent manner. Geraniol inhibited three QS systems of P. aeruginosa, las, rhl, and pqs by suppressing the expression level of their key genes, including the three signal synthetase encoding genes of lasI, rhlI, and pqsABCDEH, and the corresponding signal receptor encoding genes of lasR, rhlR, and pqsR. Geraniol also suppressed certain virulence genes regulated by these three QS systems, including rhlABC, lasAB, lecAB, phzABMS, and pelABG, resulting in the attenuation of the related virulence factors, rhamnolipids, exoprotease LasA, elastase, lectin, pyocyanin, and biofilm. In conclusion, geraniol can suppress the virulence factors of P. aeruginosa PAO1 by inhibiting the three QS systems of las, rhl, and pqs. This study is significant for improving the treatment of bacterial infections caused by P. aeruginosa

    Enhancement of cisplatin sensitivity in lewis lung carcinoma by liposome-mediated delivery of a survivin mutant

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    <p>Abstract</p> <p>Background</p> <p>A high concentration of cisplatin (CDDP) induces apoptosis in many tumor cell lines. CDDP has been administered by infusion to avoid severe toxicity. Recently, it has been reported that changes in survivin expression or function may lead to tumor sensitization to chemical and physical agents. The aim of this study was to determine whether a dominant-negative mouse survivin mutant could enhance the anti-tumor activity of CDDP.</p> <p>Methods</p> <p>A plasmid encoding the phosphorylation-defective dominant-negative mouse survivin threonine 34→alanine mutant (survivin T34A) complexed to a DOTAP-chol liposome (Lip-mS) was administered with or without CDDP in Lewis Lung Carcinoma (LLC) cells and in mice bearing LLC tumors, and the effects on apoptosis, tumor growth and angiogenesis were assessed. Data were analyzed using one-way analysis of variance(ANOVA), and a value of <it>P </it>< 0.05 was considered to be statistically significant.</p> <p>Results</p> <p>LLC cells treated with a combination of Lip-mS and CDDP displayed increased apoptosis compared with those treated with Lip-mS or CDDP alone. In mice bearing LLC tumors and treated with intravenous injections of Lip-mS and/or CDDP, combination treatment significantly reduced the mean tumor volume compared with either treatment alone. Moreover, the antitumor effect of Lip-mS combined with CDDP was greater than their anticipated additive effects.</p> <p>Conclusion</p> <p>These data suggest that the dominant-negative survivin mutant, survivin T34A, sensitized LLC cells to chemotherapy of CDDP. The synergistic antitumor activity of the combination treatment may in part result from an increase in the apoptosis of tumor cells, inhibition of tumor angiogenesis and induction of a tumor-protective immune response.</p

    A comparison of the changes in serum lactate between surgical repair and transthoracic device closure of ventricular septal defects in pediatric patients

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    ObjectiveThe purpose of this study was to compare the changes in serum lactate between surgical repair and transthoracic device closure of ventricular septal defects (VSDs) in pediatric patients.MethodsThis study was a retrospective analysis, and 314 pediatric patients with simple VSD from October 2019 to October 2021 were selected. The patients were divided into the S group (surgical repair) and the D group (transthoracic device closure). The serum lactate value at ICU admission and 6 h after operation, as well as the highest serum lactate value were collected, and the 6-h serum lactate clearance rate was calculated.ResultThrough propensity score matching, 43 pairs of cases were successfully matched. Compared with the S group, the D group had a shorter operation duration, ventilation duration, and ICU duration, as well as a lower drainage volume and total hospitalization cost. There was no significant difference between the two groups in the initial and highest serum lactate values after VSD closure, while the 6-h serum lactate value in the D group was significantly lower than that in the S group, and the 6-h serum lactate clearance rate in the D group was five times faster than that in the S group. In addition, the 6-h serum lactate clearance rate in the S group was mainly related to the operation time, CPB time, and ventilation time, while the 6-h serum lactate clearance rate in the D group was only related to the operation time.ConclusionThe initial and highest serum lactate levels were not significantly different between surgical repair and transthoracic device closure of VSD, but the 6-h serum lactate clearance rate of device closure was five times faster than that of surgical repair
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