Gas chromatography-mass spectrometry analysis of principal lipid-soluble components of Pinellia ternate fermented with Bacillus subtilis, Aspergillus niger and Meyerozyma guillermondii

Purpose: To study the differences in lipid-soluble compounds from naturally-fermented Rhizoma Pinelliae fermentata (BXQ) samples, and fermentation products of BXQ using pure cultures of Bacillus subtilis, Aspergillus niger, and Meyerozyma guillermondii. Methods: First, unfermented BXQ (CTFJ-Q), traditional, naturally-fermented BXQ (CTFJ-H), and fermentation products of BXQ using pure cultures of Bacillus subtilis (XJFJ), Aspergillus niger (MJFJ), and Meyerozyma guillermondii (JMJFJ) were obtained. Their lipid-soluble components were then analyzed using gas chromatography-mass spectrometry (GC-MS) technology and principal component analysis (PCA). Results: GC-MS results showed that there were 26, 24, 27, 31 and 32 types of chemical components in CTFJ-Q, CTFJ-H, XJFJ, MJFJ and JMJFJ, respectively. Furthermore, PCA revealed that samples obtained using fermentation with pure cultures of the three microorganisms had unique chemical components. Conclusion: These results suggest that the microorganisms used for fermentation greatly influence the lipid-soluble components of BXQ. This finding is considered beneficial for the optimization of BXQ fermentation process

Microbial Electricity Generation Enhances Decabromodiphenyl Ether (BDE-209) Degradation

We thank Hao Yu and Ye Deng at the University of Oklahoma for assistance with GeoChip hybridization and data pre-processing. We also thank Professor Bixian Mai and Dr. Leheng Yu in Guangzhou Institute of Geochemistry, CAS, for their helps in PBDE congener analyses.Conceived and designed the experiments: MYX JG GPS. Performed the experiments: YGY MYX. Analyzed the data: MYX YGY. Contributed reagents/materials/analysis tools: ZLH JZZ. Wrote the paper: MYX YGY ZLH.Due to environmental persistence and biotoxicity of polybrominated diphenyl ethers (PBDEs), it is urgent to develop potential technologies to remediate PBDEs. Introducing electrodes for microbial electricity generation to stimulate the anaerobic degradation of organic pollutants is highly promising for bioremediation. However, it is still not clear whether the degradation of PBDEs could be promoted by this strategy. In this study, we hypothesized that the degradation of PBDEs (e.g., BDE-209) would be enhanced under microbial electricity generation condition. The functional compositions and structures of microbial communities in closed-circuit microbial fuel cell (c-MFC) and open-circuit microbial fuel cell (o-MFC) systems for BDE-209 degradation were detected by a comprehensive functional gene array, GeoChip 4.0, and linked with PBDE degradations. The results indicated that distinctly different microbial community structures were formed between c-MFCs and o-MFCs, and that lower concentrations of BDE-209 and the resulting lower brominated PBDE products were detected in c-MFCs after 70-day performance. The diversity and abundance of a variety of functional genes in c-MFCs were significantly higher than those in o-MFCs. Most genes involved in chlorinated solvent reductive dechlorination, hydroxylation, methoxylation and aromatic hydrocarbon degradation were highly enriched in c-MFCs and significantly positively correlated with the removal of PBDEs. Various other microbial functional genes for carbon, nitrogen, phosphorus and sulfur cycling, as well as energy transformation process, were also significantly increased in c-MFCs. Together, these results suggest that PBDE degradation could be enhanced by introducing the electrodes for microbial electricity generation and by specifically stimulating microbial functional genes.Yeshttp://www.plosone.org/static/editorial#pee

Interference in Autophagosome Fusion by Rare Earth Nanoparticles Disrupts Autophagic Flux and Regulation of an Interleukin-1β Producing Inflammasome

Engineered nanomaterials (ENMs) including multiwall carbon nanotubes (MWCNTs) and rare earth oxide (REO) nanoparticles, which are capable of activating the NLRP3 inflammasome and inducing IL-1β production, have the potential to cause chronic lung toxicity. Although it is known that lysosome damage is an upstream trigger in initiating this pro-inflammatory response, the same organelle is also an important homeostatic regulator of activated NLRP3 inflammasome complexes, which are engulfed by autophagosomes and then destroyed in lysosomes after fusion. Although a number of ENMs have been shown to induce autophagy, no definitive research has been done on the homeostatic regulation of the NLRP3 inflammasome during autophagic flux. We used a myeloid cell line (THP-1) and bone marrow derived macrophages (BMDM) to compare the role of autophagy in regulating inflammasome activation and IL-1β production by MWCNTs and REO nanoparticles. THP-1 cells express a constitutively active autophagy pathway and are also known to mimic NLRP3 activation in pulmonary macrophages. We demonstrate that, while activated NLRP3 complexes could be effectively removed by autophagosome fusion in cells exposed to MWCNTs, REO nanoparticles interfered in autophagosome fusion with lysosomes. This leads to the accumulation of the REO-activated inflammasomes, resulting in robust and sustained IL-1β production. The mechanism of REO nanoparticle interference in autophagic flux was clarified by showing that they disrupt lysosomal phosphoprotein function and interfere in the acidification that is necessary for lysosome fusion with autophagosomes. Binding of LaPO4 to the REO nanoparticle surfaces leads to urchin-shaped nanoparticles collecting in the lysosomes. All considered, these data demonstrate that in contradistinction to autophagy induction by some ENMs, specific materials such as REOs interfere in autophagic flux, thereby disrupting homeostatic regulation of activated NLRP3 complexes

Loss of Smad7 Promotes Inflammation in Rheumatoid Arthritis

Objective: Smad7 is an inhibitory Smad and plays a protective role in many inflammatory diseases. However, the roles of Smad7 in rheumatoid arthritis (RA) remain unexplored, which were investigated in this study.Methods: The activation of TGF-β/Smad signaling was examined in synovial tissues of patients with RA. The functional roles and mechanisms of Smad7 in RA were determined in a mouse model of collagen-induced arthritis (CIA) in Smad7 wild-type (WT) and knockout (KO) CD-1 mice, a strain resistant to autoimmune arthritis induction.Results: TGF-β/Smad3 signaling was markedly activated in synovial tissues of patients with RA, which was associated with the loss of Smad7, and enhanced Th17 and Th1 immune response. The potential roles of Smad7 in RA were further investigated in a mouse model of CIA in Smad7 WT/KO CD-1 mice. As expected, Smad7-WT CD-1 mice did not develop CIA. Surprisingly, CD-1 mice with Smad7 deficiency developed severe arthritis including severe joint swelling, synovial hyperplasia, cartilage damage, massive infiltration of CD3+ T cells and F4/80+ macrophages, and upregulation of proinflammatory cytokines IL-1β, TNFα, and MCP-1. Further studies revealed that enhanced arthritis in Smad7 KO CD-1 mice was associated with increased Th1, Th2 and, importantly, Th17 over the Treg immune response with overactive TGF-β/Smad3 and proinflammatory IL-6 signaling in the joint tissues.Conclusions: Smad7 deficiency increases the susceptibility to autoimmune arthritis in CD-1 mice. Enhanced TGF-β/Smad3-IL-6 signaling and Th17 immune response may be a mechanism through which disrupted Smad7 causes autoimmune arthritis in CD-1 mice

A hub gene signature as a therapeutic target and biomarker for sepsis and geriatric sepsis-induced ARDS concomitant with COVID-19 infection

BackgroundCOVID-19 and sepsis represent formidable public health challenges, characterized by incompletely elucidated molecular mechanisms. Elucidating the interplay between COVID-19 and sepsis, particularly in geriatric patients suffering from sepsis-induced acute respiratory distress syndrome (ARDS), is of paramount importance for identifying potential therapeutic interventions to mitigate hospitalization and mortality risks.MethodsWe employed bioinformatics and systems biology approaches to identify hub genes, shared pathways, molecular biomarkers, and candidate therapeutics for managing sepsis and sepsis-induced ARDS in the context of COVID-19 infection, as well as co-existing or sequentially occurring infections. We corroborated these hub genes utilizing murine sepsis-ARDS models and blood samples derived from geriatric patients afflicted by sepsis-induced ARDS.ResultsOur investigation revealed 189 differentially expressed genes (DEGs) shared among COVID-19 and sepsis datasets. We constructed a protein-protein interaction network, unearthing pivotal hub genes and modules. Notably, nine hub genes displayed significant alterations and correlations with critical inflammatory mediators of pulmonary injury in murine septic lungs. Simultaneously, 12 displayed significant changes and correlations with a neutrophil-recruiting chemokine in geriatric patients with sepsis-induced ARDS. Of these, six hub genes (CD247, CD2, CD40LG, KLRB1, LCN2, RETN) showed significant alterations across COVID-19, sepsis, and geriatric sepsis-induced ARDS. Our single-cell RNA sequencing analysis of hub genes across diverse immune cell types furnished insights into disease pathogenesis. Functional analysis underscored the interconnection between sepsis/sepsis-ARDS and COVID-19, enabling us to pinpoint potential therapeutic targets, transcription factor-gene interactions, DEG-microRNA co-regulatory networks, and prospective drug and chemical compound interactions involving hub genes.ConclusionOur investigation offers potential therapeutic targets/biomarkers, sheds light on the immune response in geriatric patients with sepsis-induced ARDS, emphasizes the association between sepsis/sepsis-ARDS and COVID-19, and proposes prospective alternative pathways for targeted therapeutic interventions

イブンカ コミュニケーション ニオケル ダイガクセイ ノ ジコ カイジ ニカンスル ヒカク ケンキュウ : ニッチュウカン ダイガクセイ ノ ヒカク オ チュウシン ニ

日中韓3ヵ国の大学生の自文化における自己開示の傾向には開示行動、開示意向、開示方法について多くの共通点がみられるが、開示動機については相違点がみられる。その傾向の日中韓比較においては各々の特徴も見出される。これらの相違や特徴を背景とした異文化コミュニケーションにおける自己開示に際して、戸惑い、誤解、文化差などが経験される。各々の自己開示は、言語的制約を内包しつつ、文化的社会的制約を常に負う。また、文化的な相互依存と文化的な相互対峙が地球規模で急速に進んでいるグローバリゼーションの状況に人間は直面している。それゆえに、文化的社会的制約を負いつつも他者を他者性として自覚し、対話的な自己開示を遂行していく人間としての在り方が絶えず問題になる。自己開示を通して人間の人間性を問題にし続けること、多文化社会に生きる人間としての在り方を絶えず志向することが大学教育において要請される

Yersinia pestis Interacts With SIGNR1 (CD209b) for Promoting Host Dissemination and Infection

Yersinia pestis, a Gram-negative bacterium and the etiologic agent of plague, has evolved from Yersinia pseudotuberculosis, a cause of a mild enteric disease. However, the molecular and biological mechanisms of how Y pseudotuberculosis evolved to such a remarkably virulent pathogen, Y pestis, are not clear. The ability to initiate a rapid bacterial dissemination is a characteristic hallmark of Y pestis infection. A distinguishing characteristic between the two Yersinia species is that Y pseudotuberculosis strains possess an O-antigen of lipopolysaccharide (LPS) while Y pestis has lost the O-antigen during evolution and therefore exposes its core LPS. In this study, we showed that Y pestis utilizes its core LPS to interact with SIGNR1 (CD209b), a C-type lectin receptor on antigen presenting cells (APCs), leading to bacterial dissemination to lymph nodes, spleen and liver, and the initiation of a systemic infection. We therefore propose that the loss of O-antigen represents a critical step in the evolution of Y pseudotuberculosis into Y pestis in terms of hijacking APCs, promoting bacterial dissemination and causing the plague.Peer reviewe

Bar-Coded Pyrosequencing Reveals the Responses of PBDE-Degrading Microbial Communities to Electron Donor Amendments

Polybrominated diphenyl ethers (PBDEs) can be reductively degraded by microorganisms under anaerobic conditions. However, little is known about the effect of electron donors on microbial communities involved in PBDEs degradation. Here we employed 454 Titanium pyrosequencing to examine the phylogenetic diversity, composition, structure and dynamics of microbial communities from microcosms under the conditions of different electron donor amendments. The community structures in each of the five alternate electron donor enrichments were significantly shifted in comparison with those of the control microcosm. Commonly existing OTUs between the treatment and control consortia increased from 5 to 17 and more than 50% of OTUs increased around 13.7 to 186 times at least in one of the microcosms after 90-days enrichment. Although the microbial communities at different taxonomic levels were significantly changed by different environmental variable groups in redundancy analysis, significant correlations were observed between the microbial communities and PBDE congener profiles. The lesser-brominated PBDE congeners, tri-BDE congener (BDE-32) and hexa-BDE, were identified as the key factors shaping the microbial community structures at OTU level. Some rare populations, including the known dechlorinating bacterium, Dehalobacter, showed significant positive-correlation with the amounts of PBDE congeners in the consortia. The same results were also observed on some unclassified bacteria. These results suggest that PBDEs-degrading microbial communities can be successfully enriched, and their structures and compositions can be manipulated through adjusting the environmental parameters