Integrating iron metabolism-related gene signature to evaluate prognosis and immune infiltration in nasopharyngeal carcinoma.

BACKGROUND: Dysregulation of iron metabolism has been shown to have significant implications for cancer development. We aimed to investigate the prognostic and immunological significance of iron metabolism-related genes (IMRGs) in nasopharyngeal carcinoma (NPC). METHODS: Multiple Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) datasets were analyzed to identify key IMRGs associated with prognosis. Additionally, the immunological significance of IMRGs was explored. RESULTS: A novel risk model was established using the LASSO regression algorithm, incorporating three genes (TFRC, SLC39A14, and ATP6V0D1).This model categorized patients into low and high-risk groups, and Kaplan-Meier analysis revealed significantly shorter progression-free survival for the high-risk group (P < 0.0001). The prognostic model's accuracy was additionally confirmed by employing time-dependent Receiver Operating Characteristic (ROC) curves and conducting Decision Curve Analysis (DCA). High-risk patients were found to correlate with advanced clinical stages, specific tumor microenvironment subtypes, and distinct morphologies. ESTIMATE analysis demonstrated a significant inverse relationship between increased immune, stromal, and ESTIMATE scores and lowered risk score. Immune analysis indicated a negative correlation between high-risk score and the abundance of most tumor-infiltrating immune cells, including dendritic cells, CD8+ T cells, CD4+ T cells, and B cells. This correlation extended to immune checkpoint genes such as PDCD1, CTLA4, TIGIT, LAG3, and BTLA. The protein expression patterns of selected genes in clinical NPC samples were validated through immunohistochemistry. CONCLUSION: This study presents a prognostic model utilizing IMRGs in NPC, which could assist in assessing patient prognosis and provide insights into new therapeutic targets for NPC.

Biotransformation of HBCDs by the microbial communities enriched from mangrove sediments.

1,2,5,6,9,10-Hexabromocyclododecanes (HBCDs) are a sort of persistent organic pollutants (POPs). This research investigated 12 microbial communities enriched from sediments of four mangroves in China to transform HBCDs. Six microbial communities gained high transformation rates (27.5-97.7%) after 12 generations of serial transfer. Bacteria were the main contributors to transform HBCDs rather than fungi. Analyses on the bacterial compositions and binning genomes showed that Alcanivorax (55.246-84.942%) harboring haloalkane dehalogenase genes dadAH and dadBH dominated the microbial communities with high transformation rates. Moreover, expressions of dadAH and dadBH in the microbial communities and Alcanivorax isolate could be induced by HBCDs. Further, it was found that purified proteins DadAH and DadBH showed high conversion rates on HBCDs in 36 h (91.9 ± 7.4 and 101.0 ± 1.8%, respectively). The engineered Escherichia coli BL21 strains harbored two genes could convert 5.7 ± 0.4 and 35.1 ± 0.1% HBCDs, respectively, lower than their cell-free crude extracts (61.2 ± 5.2 and 56.5 ± 8.7%, respectively). The diastereoisomer-specific transforming trend by both microbial communities and enzymes were γ- > α- > ß-HBCD, differed from α- > ß- > Î³-HBCD by the Alcanivorax isolate. The identified transformation products indicated that HBCDs were dehalogenated via HBr elimination (dehydrobromination), hydrolytic and reductive debromination pathways in the enriched cultures. Two enzymes converted HBCDs via hydrolytic debromination. The present research provided theoretical bases for the biotransformation of HBCDs by microbial community and the bioremediation of HBCDs contamination in the environment.

Regulation of interstitial fluid flow in adventitia along vasculature by heartbeat and respiration.

Converging studies showed interstitial fluid (ISF) adjacent to blood vessels flows in adventitia along vasculature into heart and lungs. We aim to reveal circulatory pathways and regulatory mechanism of such adventitial ISF flow in rat model. By MRI, real-time fluorescent imaging, micro-CT, and histological analysis, ISF was found to flow in adventitial matrix surrounded by fascia and along systemic vessels into heart, then flow into lungs via pulmonary arteries and back to heart via pulmonary veins, which was neither perivascular tissues nor blood or lymphatic vessels. Under physiological conditions, speckle-like adventitial ISF flow rate was positively correlated with heart rate, increased when holding breath, became pulsative during heavy breathing. During cardiac or respiratory cycle, each dilation or contraction of heart or lungs can generate to-and-fro adventitial ISF flow along femoral veins. Discovered regulatory mechanisms of adventitial ISF flow along vasculature by heart and lungs will revolutionize understanding of cardiovascular system.

CD44-targeting hyaluronic acid-selenium nanoparticles boost functional recovery following spinal cord injury.

BACKGROUND: Therapeutic strategies based on scavenging reactive oxygen species (ROS) and suppressing inflammatory cascades are effective in improving functional recovery after spinal cord injury (SCI). However, the lack of targeting nanoparticles (NPs) with powerful antioxidant and anti-inflammatory properties hampers the clinical translation of these strategies. Here, CD44-targeting hyaluronic acid-selenium (HA-Se) NPs were designed and prepared for scavenging ROS and suppressing inflammatory responses in the injured spinal cord, enhancing functional recovery. RESULTS: The HA-Se NPs were easily prepared through direct reduction of seleninic acid in the presence of HA. The obtained HA-Se NPs exhibited a remarkable capacity to eliminate free radicals and CD44 receptor-facilitated internalization by astrocytes. Moreover, the HA-Se NPs effectively mitigated the secretion of proinflammatory cytokines (such as IL-1ß, TNF-α, and IL-6) by microglia cells (BV2) upon lipopolysaccharide-induced inflammation. In vivo experiments confirmed that HA-Se NPs could effectively accumulate within the lesion site through CD44 targeting. As a result, HA-Se NPs demonstrated superior protection of axons and neurons within the injury site, leading to enhanced functional recovery in a rat model of SCI. CONCLUSIONS: These results highlight the potential of CD44-targeting HA-Se NPs for SCI treatment.

Novel insights into aerobic 17ß-estradiol degradation by enriched microbial communities from mangrove sediments.

Various persistent organic pollutants (POPs) including estrogens are often enriched in mangrove regions. This research investigated the estrogens pollution levels in six mangroves located in the Southern China. The estrogen levels were found to be in the range of 5.3-24.9 ng/g dry weight, suggesting that these mangroves had been seriously contaminated. The bacterial communities under estrogen stress were further enriched by supplementing 17ß-estradiol (E2) as the sole carbon source. The enriched bacterial communities showed an excellent E2 degradation capacity > 95 %. These communities were able to transform E2 into estrone (E1), 4-hydroxy-estrone, and keto-estrone, etc. 16 S rDNA sequencing and metagenomics analysis revealed that bacterial taxa Oleiagrimonas, Pseudomonas, Terrimonas, and Nitratireductor etc. were the main contributors to estrogen degradation. Moreover, the genes involved in E2 degradation were enriched in the microbial communities, including the genes encoding 17ß-hydroxysteroid dehydrogenase, estrone 4-hydroxylase, etc. Finally, the analyses of functional genes and binning genomes demonstrated that E2 was degraded by bacterial communities via dehydrogenation into E1 by 17ß-hydroxysteroid dehydrogenase. E1 was then catabolically converted to 3aα-H-4α(3'-propanoate)- 7aß-methylhexahydro-1,5-indanedione via 4,5-seco pathway. Alternatively, E1 could also be hydroxylated to keto-estrone, followed by B-ring cleavage. This study provides novel insights into the biodegradation of E2 by the bacterial communities in estrogen-contaminated mangroves.

Root-centric ß diversity reveals functional homogeneity while phylogenetic heterogeneity in a subtropical forest.

Root-centric studies have revealed fast taxonomic turnover across root neighborhoods, but how such turnover is accompanied by changes in species functions and phylogeny (i.e., ß diversity) remains largely unknown. As ß diversity can reflect the degree of community-wide biotic homogenization, such information is crucial for better inference of below-ground assembly rules, community structuring, and ecosystem processes. We collected 2480 root segments from 625 0-30 cm soil profiles in a subtropical forest in China. Root segments were identified into 138 species with DNA-barcoding with six root morphological and architectural traits measured per species. By using the mean pairwise (Dpw ) and mean nearest neighbor distance (Dnn ) to quantify species ecological differences, we first tested the non-random functional and phylogenetic turnover of root neighborhoods that would lend more support to deterministic over stochastic community assembly processes. Additionally, we examined the distance-decay pattern of ß diversity, and finally partitioned ß diversity into geographical and environmental components to infer their potential drivers of environmental filtering, dispersal limitation, and biotic interactions. We found that functional turnover was often lower than expected given the taxonomic turnover, whereas phylogenetic turnover was often higher than expected. Phylogenetic Dpw (e.g., interfamily species) turnover exhibited a distance-decay pattern, likely reflecting limited dispersal or abiotic filtering that leads to the spatial aggregation of specific plant lineages. Conversely, both functional and phylogenetic Dnn (e.g., intrageneric species) exhibited an inverted distance-decay pattern, likely reflecting strong biotic interactions among spatially and phylogenetically close species leading to phylogenetic and functional divergence. While the spatial distance was generally a better predictor of ß diversity than environmental distance, the joint effect of environmental and spatial distance usually overrode their respective pure effects. These findings suggest that root neighborhood functional homogeneity may somewhat increase forest resilience after disturbance by exhibiting an insurance effect. Likewise, root neighborhood phylogenetic heterogeneity may enhance plant fitness by hindering the transmission of host-specific pathogens through root networks or by promoting interspecific niche complementarity not captured by species functions. Our study highlights the potential role of root-centric ß diversity in mediating community structures and functions largely ignored in previous studies.

Nanomaterials as therapeutic agents to modulate astrocyte-mediated inflammation in spinal cord injury.

Promoting the recovery of neurological function in patients with traumatic spinal cord injury (TSCI) remains challenging. The balance between astrocyte-mediated neurotrophic and pro-inflammatory responses is critical for TSCI repair. Recently, the utilization of nanomaterials has been considerably explored in immunological reconstructive techniques that specifically target astrocyte-mediated inflammation, yielding positive outcomes. In this review, we aim to condense the present knowledge regarding the astrocyte-mediated inflammation following TSCI. We then review the various categories of nanomaterials utilized in the management of astrocyte-mediated inflammation in TSCI and conclude by summarizing their functions and advantages to offer novel insights for the advancement of effective clinical strategies targeting TSCI.

Effect of Reactive Oxygen Scavenger N,N'-Dimethylthiourea (DMTU) on Seed Germination and Radicle Elongation of Maize.

Reactive oxygen species (ROS) are an important part of adaptation to biotic and abiotic stresses and regulate seed germination through positive or negative signaling. Seed adaptation to abiotic stress may be mediated by hydrogen peroxide (H2O2). The effects of the ROS scavenger N,N'-dimethylthiourea (DMTU) on maize seed germination through endogenous H2O2 regulation is unclear. In this study, we investigated the effects of different doses of DMTU on seed endogenous H2O2 and radicle development parameters using two maize varieties (ZD958 and DMY1). The inhibitory effect of DMTU on the germination rate and radicle growth was dose-dependent. The inhibitory effect of DMTU on radicle growth ceased after transferring maize seeds from DMTU to a water medium. Histochemical analyses showed that DMTU eliminated stable H2O2 accumulation in the radicle sheaths and radicles. The activity of antioxidant enzyme and the expression of antioxidant enzyme-related genes (ZmAPX2 and ZmCAT2) were reduced in maize seeds cultured with DMTU compared with normal culture conditions (0 mmol·dm-3 DMTU). We suggest the use of 200 mmol·dm-3 DMTU as an H2O2 scavenger to study the ROS equilibrium mechanisms during the germination of maize seeds, assisting in the future with the efficient development of plant growth regulators to enhance the seed germination performance of test maize varieties under abiotic stress.

Loss of ACOX1 in clear cell renal cell carcinoma and its correlation with clinical features.

Clear cell renal cell carcinoma (ccRCC) is a major pathological type of kidney cancer with a poor prognosis due to a lack of biomarkers for early diagnosis and prognosis prediction of ccRCC. In this study, we investigated the aberrant expression of Acyl-coenzyme A oxidase 1 (ACOX1) in ccRCC and evaluated its potential in diagnosis and prognosis. ACOX1 is the first rate-limiting enzyme in the peroxidation ß-oxidation pathway and is involved in the regulation of fatty acid oxidative catabolism. The mRNA and protein levels of ACOX1 were significantly downregulated in ccRCC, and its downregulation was closely associated with the tumor-node-metastasis stage of patients. The ROC curves showed that ACOX1 possesses a high diagnostic value for ccRCC. The OS analysis suggested that lower expression of ACOX1 was closely related to the worse outcome of patients. In addition, gene set enrichment analysis suggested that expression of ACOX1 was positively correlated with CDH1, CDH2, CDKL2, and EPCAM, while negatively correlated with MMP9 and VIM, which strongly indicated that ACOX1 may inhibit the invasion and migration of ccRCC by reversing epithelial-mesenchymal transition. Furthermore, we screened out that miR-16-5p is upregulated at the mRNA transcript level in ccRCC and negatively correlated with ACOX1. In conclusion, our results showed that ACOX1 is abnormally low expressed in ccRCC, suggesting that it could serve as a diagnostic and prognostic biomarker for ccRCC. Overexpression of miR-16-5p may be responsible for the inactivation of ACOX1.

The unimodal intransitivity-fertility relationship is not mediated by demographic trade-offs in a subtropical forest.

Intransitive competition has long been acknowledged as a potential mechanism favoring species coexistence. However, its prevalence, variance along environmental gradients, and possible underlying mechanisms (trade-offs) in plant communities (especially in forests) has seldom been examined. A recently developed "reverse-engineering" approach based on Markov Chain allowed us to estimate the competitive transition matrices and competitive intransitivity from observational abundance data. Using this approach, we estimated competitive intransitivity of five dominant species in a subtropical forest and then related it to soil fertility (soil organic matter and soil pH) and demographic trade-offs (growth-survival and stature-recruitment trade-offs). In our forest plot, intransitive competition was common among the dominant species and peaked at the intermediate level of soil organic matter. Neither the growth-survival trade-off nor the stature-recruitment trade-off was positively related to competitive intransitivity. Our study for the first time empirically supported the unimodal intransitivity-fertility relationship in forests, which, however, was not mediated by the two demographic trade-offs in our plot.

Recent advances in endogenous neural stem/progenitor cell manipulation for spinal cord injury repair.

Traumatic spinal cord injury (SCI) can cause severe neurological impairments. Clinically available treatments are quite limited, with unsatisfactory remediation effects. Residing endogenous neural stem/progenitor cells (eNSPCs) tend to differentiate towards astrocytes, leaving only a small fraction towards oligodendrocytes and even fewer towards neurons; this has been suggested as one of the reasons for the failure of autonomous neuronal regeneration. Thus, finding ways to recruit and facilitate the differentiation of eNSPCs towards neurons has been considered a promising strategy for the noninvasive and immune-compatible treatment of SCI. The present manuscript first introduces the responses of eNSPCs after exogenous interventions to boost endogenous neurogenesis in various SCI models. Then, we focus on state-of-art manipulation approaches that enhance the intrinsic neurogenesis capacity and reconstruct the hostile microenvironment, mainly consisting of pharmacological treatments, stem cell-derived exosome administration, gene therapy, functional scaffold implantation, inflammation regulation, and inhibitory element delineation. Facing the extremely complex situation of SCI, combined treatments are also highlighted to provide more clues for future relevant investigations.

Inactivation of epithelial sodium ion channel molecules serves as effective diagnostic biomarkers in clear cell renal cell carcinoma.

BACKGROUND: Non-voltage-gated sodium channel, also known as the epithelial sodium channel (ENaC), formed by heteromeric complexes consisting of SCNN1A, SCNN1B, and SCNN1G, is responsible for maintaining sodium ion and body fluid homeostasis in epithelial cells. However, no systematic study of SCNN1 family members has been conducted in renal clear cell carcinoma (ccRCC) to date. OBJECTIVE: To investigate the abnormal expression of SCNN1 family in ccRCC and its potential correlation with clinical parameters. METHODS: The transcription and protein expression levels of SCNN1 family members in ccRCC were analyzed based on the TCGA database, and were confirmed by quantitative RT-PCR and immunohistochemical staining assays, respectively. The area under curve (AUC) was used to evaluate the diagnostic value of SCNN1 family members for ccRCC patients. RESULTS: The mRNA and protein expression of SCNN1 family members was significantly downregulated in ccRCC compared with normal kidney tissues, which might be due to DNA hypermethylation in the promoter region. It is worth noting that the AUC of SCNN1A, SCNN1B, and SCNN1G were 0.965, 0.979, and 0.988 based on the TCGA database (p < 0.0001), respectively. The diagnostic value was even higher when combing these three members together (AUC = 0.997, p < 0.0001). Intriguingly, the mRNA level of SCNN1A was significantly lower in females compared with males, while SCNN1B and SCNN1G were increased with the progression of ccRCC and remarkably associated with a worse outcome for patients. CONCLUSION: The aberrantly decrease of SCNN1 family members might serve as valuable biomarkers for the diagnosis of ccRCC.

Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of ß-Catenin.

Epstein-Barr virus (EBV) infects host cells and establishes a latent infection that requires evasion of host innate immunity. A variety of EBV-encoded proteins that manipulate the innate immune system have been reported, but whether other EBV proteins participate in this process is unclear. EBV-encoded envelope glycoprotein gp110 is a late protein involved in virus entry into target cells and enhancement of infectivity. Here, we reported that gp110 inhibits RIG-I-like receptor pathway-mediated promoter activity of interferon-ß (IFN-ß) as well as the transcription of downstream antiviral genes to promote viral proliferation. Mechanistically, gp110 interacts with the inhibitor of NF-κB kinase (IKKi) and restrains its K63-linked polyubiquitination, leading to attenuation of IKKi-mediated activation of NF-κB and repression of the phosphorylation and nuclear translocation of p65. Additionally, gp110 interacts with an important regulator of the Wnt signaling pathway, ß-catenin, and induces its K48-linked polyubiquitination degradation via the proteasome system, resulting in the suppression of ß-catenin-mediated IFN-ß production. Taken together, these results suggest that gp110 is a negative regulator of antiviral immunity, revealing a novel mechanism of EBV immune evasion during lytic infection. IMPORTANCE Epstein-Barr virus (EBV) is a ubiquitous pathogen that infects almost all human beings, and the persistence of EBV in the host is largely due to immune escape mediated by its encoded products. Thus, elucidation of EBV's immune escape mechanisms will provide a new direction for the design of novel antiviral strategies and vaccine development. Here, we report that EBV-encoded gp110 serves as a novel viral immune evasion factor, which inhibits RIG-I-like receptor pathway-mediated interferon-ß (IFN-ß) production. Furthermore, we found that gp110 targeted two key proteins, inhibitor of NF-κB kinase (IKKi) and ß-catenin, which mediate antiviral activity and the production of IFN-ß. gp110 inhibited K63-linked polyubiquitination of IKKi and induced ß-catenin degradation via the proteasome, resulting in decreased IFN-ß production. In summary, our data provide new insights into the EBV-mediated immune evasion surveillance strategy.

HIGD1A inactivated by DNA hypermethylation promotes invasion of kidney renal clear cell carcinoma.

Hypoxia contributes to the tumorigenesis and metastasis of the tumor. However, the detailed mechanisms underlying hypoxia and kidney renal clear cell carcinoma (KIRC) development and progression remain unclear. Here, we investigated the role of the system HIG1 hypoxia inducible domain family member 1 A (HIGD1A) in the proliferation and metastasis of KIRC and elucidated the underlying molecular mechanisms. The expression of HIGD1A is significantly downregulated in KIRC due to promoter hypermethylation. HIGD1A could serve as a valuable diagnostic biomarker in KIRC. In addition, ectopic overexpression of HIGD1A significantly suppressed the growth and invasive capacity of KIRC cells in vitro under normal glucose conditions. Interestingly, the suppressive efficacy in invasion is much more significant when depleted glucose, but not in proliferation. Furthermore, mRNA expression of HIGD1A positively correlates with CDH1 and EPCAM, while negatively correlated with VIM and SPARC, indicating that HIGD1A impedes invasion of KIRC by regulating epithelial-mesenchymal transition (EMT). Our data suggest that HIGD1A is a potential diagnostic biomarker and tumor suppressor in KIRC.

Hierarchical structure design of sea urchin Shell-Based evaporator for efficient omnidirectional Solar-Driven steam generation.

Solar-driven steam generation (SSG) is regarded as a feasible solution to the problem of fresh water scarcity. Although several attempts have been devoted to increase the efficiency of solar-to-steam conversion, it remains difficult to fabricate cost-effective, steady, and multi-angle sunlight-absorbing evaporators from readily available biomass materials. Herein, a novel hierarchical structured SSG evaporator (PDA@Shell-NaClO) is developed through a simple, low-cost, and scalable etching treatment on discarded sea urchin (SU) shells. Attributing to the dedicatedly designed microneedles array structure and porous skeleton structure of the SU shell, this PDA@Shell-NaClO evaporator shows an outstanding average light absorption performance (>90%) in a broad range of angles from 0° to 60° and exceedingly high evaporation rate of 2.81 kg m-2 h-1 under one sun condition. Furthermore, the prepared evaporator also maintains an overall stable evaporation performance and exhibits an excellent durability for a long time of up to two weeks in actual seawater. This full-ocean biomass-based SSG evaporator with plentiful raw material availability offers innovative opportunities for large-scale fresh water production.

Community assembly and network structure of epiphytic and endophytic phyllosphere fungi in a subtropical mangrove ecosystem.

Microorganisms can influence plant growth and health, ecosystem functioning, and stability. Community and network structures of mangrove phyllosphere fungi have rarely been studied although mangroves have very important ecological and economical values. Here, we used high throughput sequencing of the internal transcribed spacer 2 (ITS2) to assess epiphytic and endophytic phyllosphere fungal communities of six true mangrove species and five mangrove associates. Totally, we obtained 1,391 fungal operational taxonomic units (OTUs), including 596 specific epiphytic fungi, 600 specific endophytic fungi, and 195 shared fungi. The richness and community composition differed significantly for epiphytes and endophytes. Phylogeny of the host plant had a significant constraint on epiphytes but not endophytes. Network analyses showed that plant-epiphyte and plant-endophyte networks exhibited strong specialization and modularity but low connectance and anti-nestedness. Compared to plant-endophyte network, plant-epiphyte network showed stronger specialization, modularity, and robustness but lower connectance and anti-nestedness. These differences in community and network structures of epiphytes and endophytes may be caused by spatial niche partitioning, indicating their underlying ecological and environmental drivers are inconsistent. We highlight the important role of plant phylogeny in the assembly of epiphytic but not endophytic fungal communities in mangrove ecosystems.

Case Report: The effective treatment of patients in advanced no-small cell lung cancer patients with EGFR G719X/S768I/L861Q and acquired MET amplification: A case series and literature review.

Preclinical cases suggest that EGFR tyrosine kinase inhibitors (TKIs) plus MET TKIs are a potential therapy for non-classical EGFR mutant lung cancers with MET amplification acquired resistance. Herein, we report for the first time the effectiveness of novel combination treatment regimens for patients with EGFR G719X/S768I/L861Q. Until the last follow-up assessment, two patients demonstrated improved survival after they switched to afatinib combined with savolitinib (PFS: 10 months) and furmonertinib combined with crizotinib (PFS: 6 months), respectively, that did not observed increased incidence and severity of adverse events. According to the findings of this study and literature review, various responses were observed from the combined therapy in NSCLC patients who harbored uncommon EGFR mutations and MET amplification. Furthermore, Next generation sequencing (NGS) leads to the discovery of uncommon of EGFR and reveals the co-mutations in NSCLC.

Epstein-Barr virus envelope glycoprotein 110 inhibits NF-κB activation by interacting with NF-κB subunit p65.

Epstein-Barr virus (EBV) is a member of the lymphotropic virus family and is highly correlated with some human malignant tumors. It has been reported that envelope glycoprotein 110 (gp110) plays an essential role in viral fusion, DNA replication, and nucleocapsid assembly of EBV. However, it has not been established whether gp110 is involved in regulating the host's innate immunity. In this study, we found that gp110 inhibits tumor necrosis factor α-mediated NF- κB promoter activity and the downstream production of NF- κB-regulated cytokines under physiological conditions. Using dual-luciferase reporter assays, we showed that gp110 might impede the NF-κB promoter activation downstream of NF-κB transactivational subunit p65. Subsequently, we used coimmunoprecipitation assays to demonstrate that gp110 interacts with p65 during EBV lytic infection, and that the C-terminal cytoplasmic region of gp110 is the key interaction domain with p65. Furthermore, we determined that gp110 can bind to the N-terminal Rel homologous and C-terminal domains of p65. Alternatively, gp110 might not disturb the association of p65 with nontransactivational subunit p50, but we showed it restrains activational phosphorylation (at Ser536) and nuclear translocation of p65, which we also found to be executed by the C-terminal cytoplasmic region of gp110. Altogether, these data suggest that the surface protein gp110 may be a vital component for EBV to antagonize the host's innate immune response, which is also helpful for revealing the infectivity and pathogenesis of EBV.

The effects of long-term hexabromocyclododecanes contamination on microbial communities in the microcosms.

The adaptation of microbial community to the long-term contamination of hexabromocyclododecanes (HBCDs) has not been well studied. Our previous study found that the HBCDs contamination in the microcosms constructed of sediments from two different mangrove forests in 8 months resulted in serious acidification (pH2-3). This study reanalyzed previous sequencing data and compared them with data after 20 months to investigate the adaptive properties of microbial communities in the stress of HBCDs and acidification. It hypothesized that the reassembly was based on the fitness of taxa. The results indicated that eukaryotes and fungi might have better adaptive capacity to these deteriorated habitats. Eukaryotic taxa Eufallia and Syncystis, and fungal taxa Wickerhamomyces were only detected after 20 months of contamination. Moreover, eukaryotic taxa Caloneis and Nitzschia, and fungal taxa Talaromyces were dominant in most of microbial communities (14.467-95.941%). The functional compositions were sediment-dependent and more divergent than community reassemblies. Network and co-occurrence analysis suggested that acidophiles such as Acidisoma and Acidiphilium were gaining more positive relations in the long-term stress. The acidophilic taxa and genes involved in resistance to the acidification and toxicity of HBCDs were enriched, for example, bacteria Acidisoma and Acidiphilium, archaea Thermogymnomonas, and eukaryotes Nitzschia, and genes kdpC, odc1, polA, gst, and sod-2. These genes involved in oxidative stress response, energy metabolism, DNA damage repair, potassium transportation, and decarboxylation. It suggested that the microbial communities might cope with the stress from HBCDs and acidification via multiple pathways. The present research shed light on the evolution of microbial communities under the long-term stress of HBCDs contamination and acidification.