cross-talk

串扰
  • 文章类型: Journal Article
    背景:骨骼肌处理约80%的胰岛素刺激的葡萄糖摄取,并成为发生胰岛素抵抗(IR)的主要器官。许多研究已经证实巨噬细胞和骨骼肌之间的相互作用调节了骨骼肌的炎症和再生。然而,尽管经过了几十年的研究,高糖(HG)环境下骨骼肌中巨噬细胞的浸润和极化是否会导致IR的发展尚待阐明。C2C12成肌细胞是研究生肌调节及其对刺激的反应的完善和优良的模型。有必要进一步探索巨噬细胞在成肌细胞IR中的作用及其浸润和极化的动力学。
    目的:为了评估HG下成肌细胞和巨噬细胞之间的相互作用,及其对骨骼肌炎症和IR的影响。
    方法:我们通过苏木精和伊红染色和免疫组织化学染色检测了IR小鼠骨骼肌浸润的巨噬细胞的极化状态。然后,我们开发了一种体外共培养系统来研究HG环境下成肌细胞和巨噬细胞之间的相互作用。通过形态学观察探讨成肌细胞对巨噬细胞的影响,CCK-8测定,流式细胞仪,和酶联免疫吸附测定。通过形态学观察检测巨噬细胞对肌生成和胰岛素敏感性的介导,CCK-8测定,免疫荧光,和2-NBDG测定。
    结果:F4/80以及F4/80和CD86的共同定位增加,IR组肌纤维大小减小(P<0.01,g=6.26)。与Mc组相比,F4/80+CD86+CD206-细胞,肿瘤坏死因子-α(TNFα),白细胞介素-1β(IL-1β)和IL-6降低,McM组IL-10升高(P<0.01,g>0.8)。在McM+HG组中,F4/80+CD86+CD206-细胞,单核细胞趋化蛋白1,TNFα,IL-1β和IL-6升高,与Mc+HG组和McM组比拟,F4/80+CD206+CD86-细胞和IL-10降低(P<0.01,g>0.8)。按M组计算,肌管面积,MMc组肌管数量和E-MHC增加(P<0.01,g>0.8)。在MMc+HG组中,肌管面积,肌管编号,E-MHC,与M+HG组和MMc组比拟,GLUT4和葡萄糖摄取降低(P<0.01,g>0.8)。
    结论:成肌细胞和巨噬细胞在HG环境下的相互作用导致炎症和IR,这支持巨噬细胞可以作为骨骼肌萎缩和IR的有希望的治疗靶标。
    BACKGROUND: Skeletal muscle handles about 80% of insulin-stimulated glucose uptake and become the major organ occurring insulin resistance (IR). Many studies have confirmed the interactions between macrophages and skeletal muscle regulated the inflammation and regeneration of skeletal muscle. However, despite of the decades of research, whether macrophages infiltration and polarization in skeletal muscle under high glucose (HG) milieus results in the development of IR is yet to be elucidated. C2C12 myoblasts are well-established and excellent model to study myogenic regulation and its responses to stimulation. Further exploration of macrophages\' role in myoblasts IR and the dynamics of their infiltration and polarization is warranted.
    OBJECTIVE: To evaluate interactions between myoblasts and macrophages under HG, and its effects on inflammation and IR in skeletal muscle.
    METHODS: We detected the polarization status of macrophages infiltrated to skeletal muscles of IR mice by hematoxylin and eosin and immunohistochemical staining. Then, we developed an in vitro co-culture system to study the interactions between myoblasts and macrophages under HG milieus. The effects of myoblasts on macrophages were explored through morphological observation, CCK-8 assay, Flow Cytometry, and enzyme-linked immunosorbent assay. The mediation of macrophages to myogenesis and insulin sensitivity were detected by morphological observation, CCK-8 assay, Immunofluorescence, and 2-NBDG assay.
    RESULTS: The F4/80 and co-localization of F4/80 and CD86 increased, and the myofiber size decreased in IR group (P < 0.01, g = 6.26). Compared to Mc group, F4/80+CD86+CD206- cells, tumor necrosis factor-α (TNFα), inerleukin-1β (IL-1β) and IL-6 decreased, and IL-10 increased in McM group (P < 0.01, g > 0.8). In McM + HG group, F4/80+CD86+CD206- cells, monocyte chemoattractant protein 1, TNFα, IL-1β and IL-6 were increased, and F4/80+CD206+CD86- cells and IL-10 were decreased compared with Mc + HG group and McM group (P < 0.01, g > 0.8). Compered to M group, myotube area, myotube number and E-MHC were increased in MMc group (P < 0.01, g > 0.8). In MMc + HG group, myotube area, myotube number, E-MHC, GLUT4 and glucose uptake were decreased compared with M + HG group and MMc group (P < 0.01, g > 0.8).
    CONCLUSIONS: Interactions between myoblasts and macrophages under HG milieus results in inflammation and IR, which support that the macrophage may serve as a promising therapeutic target for skeletal muscle atrophy and IR.
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  • 文章类型: Journal Article
    志贺洛类假单胞菌,革兰氏阴性杆菌,是肠杆菌科的唯一成员,能够产生极性和外侧鞭毛并引起人类胃肠道和肠外疾病。志贺氏菌的鞭毛转录层次目前未知。在这项研究中,我们确认了FlaK,FlaM,Flia,FliAL是志贺氏菌中负责极性和侧向鞭毛调节的四种调节剂。为了确定志贺氏菌的鞭毛转录层次,WT和ΔflaK的转录组,ΔflaM,ΔFIA,在这项研究中,进行了ΔfliAL的比较。定量实时聚合酶链反应(qRT-PCR)和发光筛选试验用于验证RNA-seq结果,电泳迁移率变化分析(EMSA)结果表明,FlaK可以直接与fliK的启动子结合,FLIE,flha,chey,虽然FlaM蛋白可以直接与flgO的启动子结合,flgT,和flgA。同时,我们还观察到VI型分泌系统(T6SS)和II型分泌系统2(T2SS-2)基因在转录组谱中下调,杀伤试验显示对ΔflaK的杀伤能力较低,ΔflaM,ΔFIA,和ΔFLAL与WT相比,表明鞭毛等级系统和细菌分泌系统之间存在串扰。入侵试验还表明,ΔflaK,ΔflaM,ΔFIA,和ΔfliAL在感染Caco-2细胞方面不如WT有效。此外,我们还发现鞭毛调节因子的缺失导致志贺氏菌的一些生理代谢基因的差异表达。总的来说,这项研究旨在揭示控制志贺氏菌鞭毛基因表达的转录层次,以及运动性之间的串扰,毒力,以及生理和代谢活动,为将来研究志贺洛芝在自然环境中的协调生存和感染宿主的机制奠定基础。
    Plesiomonas shigelloides, a Gram-negative bacillus, is the only member of the Enterobacteriaceae family able to produce polar and lateral flagella and cause gastrointestinal and extraintestinal illnesses in humans. The flagellar transcriptional hierarchy of P. shigelloides is currently unknown. In this study, we identified FlaK, FlaM, FliA, and FliAL as the four regulators responsible for polar and lateral flagellar regulation in P. shigelloides. To determine the flagellar transcription hierarchy of P. shigelloides, the transcriptomes of the WT and ΔflaK, ΔflaM, ΔfliA, and ΔfliAL were carried out for comparison in this study. Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and luminescence screening assays were used to validate the RNA-seq results, and the Electrophoretic Mobility Shift Assay (EMSA) results revealed that FlaK can directly bind to the promoters of fliK, fliE, flhA, and cheY, while the FlaM protein can bind directly to the promoters of flgO, flgT, and flgA. Meanwhile, we also observed type VI secretion system (T6SS) and type II secretion system 2 (T2SS-2) genes downregulated in the transcriptome profiles, and the killing assay revealed lower killing abilities for ΔflaK, ΔflaM, ΔfliA, and ΔfliAL compared to the WT, indicating that there was a cross-talk between the flagellar hierarchy system and bacterial secretion system. Invasion assays also showed that ΔflaK, ΔflaM, ΔfliA, and ΔfliAL were less effective in infecting Caco-2 cells than the WT. Additionally, we also found that the loss of flagellar regulators causes the differential expression of some of the physiological metabolic genes of P. shigelloides. Overall, this study aims to reveal the transcriptional hierarchy that controls flagellar gene expression in P. shigelloides, as well as the cross-talk between motility, virulence, and physiological and metabolic activity, laying the groundwork for future research into P. shigelloides\' coordinated survival in the natural environment and the mechanisms that infect the host.
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  • 文章类型: Journal Article
    脱氧雪腐镰刀菌烯醇(DON)是由镰刀菌产生的一种霉菌毒素,姜黄素(CUR)是姜黄中发现的天然多酚化合物。然而,CUR与DON联合治疗探讨CUR对DON的缓解作用及其联合作用机制尚不明确。因此,在这项研究中,我们建立了四个治疗组(CON,CUR,DON和CUR+DON)研究其在猪肠上皮细胞(IPEC-J2)中的作用机制。此外,通过体外实验评估了CUR干扰DON诱导的细胞毒性因子的串扰和缓解潜力。结果表明,CUR可以有效抑制DON暴露的激活的TNF-α/NF-κB通路,减弱DON诱导的细胞凋亡,并通过PERK/CHOP通路缓解DON诱导的内质网应激和氧化应激,在mRNA和蛋白质水平上都得到了验证。总之,这些有希望的发现可能有助于将来将CUR用作新型饲料添加剂,以保护牲畜免受DON的有害影响。
    Deoxynivalenol (DON) is a mycotoxin produced by Fusarium graminearum, and curcumin (CUR) is a natural polyphenolic compound found in turmeric. However, the combined treatment of CUR and DON to explore the mitigating effect of CUR on DON and their combined mechanism of action is not clear. Therefore, in this study, we established four treatment groups (CON, CUR, DON and CUR + DON) to investigate their mechanism in the porcine intestinal epithelial cells (IPEC-J2). In addition, the cross-talk and alleviating potential of CUR interfering with DON-induced cytotoxic factors were evaluated by in vitro experiments; the results showed that CUR could effectively inhibit DON-exposed activated TNF-α/NF-κB pathway, attenuate DON-induced apoptosis, and alleviate DON-induced endoplasmic reticulum stress and oxidative stress through PERK/CHOP pathways, which were verified at both mRNA and protein levels. In conclusion, these promising findings may contribute to the future use of CUR as a novel feed additive to protect livestock from the harmful effects of DON.
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  • 文章类型: Journal Article
    PM2.5与血管内皮损伤密切相关,已成为人类健康的主要威胁。我们先前的研究表明,暴露于PM2.5会导致支气管上皮中miR-421的释放增加。然而,miR-421在PM2.5诱导的内皮损伤中的作用尚不清楚.
    我们利用小鼠体内亚急性PM2.5暴露模型和体外急性损伤细胞模型来模拟PM2.5相关的内皮损伤。我们还使用了定量实时聚合酶链反应,westernblot,酶联免疫吸附测定,和免疫组化研究miR-421在PM2.5诱导的内皮损伤中的作用。
    我们的研究结果表明,抑制miR-421可以减轻PM2.5诱导的内皮损伤和高血压。机械上,miR-421抑制人脐静脉内皮细胞血管紧张素转换酶2(ACE2)的表达,上调下游分子诱导型一氧化氮合酶(iNOS)的表达,从而加剧PM2.5诱导的内皮损伤。
    我们的结果表明,PM2.5暴露通过miR-421/ACE2/iNOS信号通路促进支气管上皮细胞和内皮细胞之间的串扰,介导内皮损伤和高血压。抑制MiR-421可能为PM2.5诱导的血管内皮损伤的防治提供新的策略。
    UNASSIGNED: PM2.5 is closely linked to vascular endothelial injury and has emerged as a major threat to human health. Our previous research indicated that exposure to PM2.5 induced an increased release of miR-421 from the bronchial epithelium. However, the role of miR-421 in PM2.5-induced endothelial injury remains elusive.
    UNASSIGNED: We utilized a subacute PM2.5-exposure model in mice in vivo and an acute injury cell model in vitro to simulate PM2.5-associated endothelial injury. We also used quantitative real-time polymerase chain reaction, western blot, enzyme-linked immunosorbent assay, and immunohistochemistry to investigate the role of miR-421 in PM2.5-induced endothelial injury.
    UNASSIGNED: Our findings reveal that inhibition of miR-421 attenuated PM2.5-induced endothelial injury and hypertension. Mechanistically, miR-421 inhibited the expression of angiotensin-converting enzyme 2 (ACE2) in human umbilical vein endothelial cells and upregulated the expression of the downstream molecule inducible nitric oxide synthase (iNOS), thereby exacerbating PM2.5-induced endothelial injury.
    UNASSIGNED: Our results indicate that PM2.5 exposure facilitates crosstalk between bronchial epithelial and endothelial cells via miR-421/ACE2/iNOS signaling pathway, mediating endothelial damage and hypertension. MiR-421 inhibition may offer a new strategy for the prevention and treatment of PM2.5-induced vascular endothelial injury.
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  • 文章类型: Journal Article
    尽管先进的临床治疗,癌症患者的死亡率很高。最近的研究将癌症的发展与炎症联系起来。炎症反应的出现加剧了许多癌症,和非编码RNA在炎症中起重要作用。非编码RNA包括microRNA,环状RNA,长链非编码RNA,等。由microRNAs组成的非编码RNA调控网络,环状RNA和长链非编码RNA参与多基因表达的调控过程。它们可以作用于各种信号通路,如wnt/β-catenin,核因子κB,磷脂酰肌醇3激酶/AKT,丝裂原活化蛋白激酶,等等。这些信号通路可以在一定程度上控制炎症反应的发生,如调节炎性细胞因子的表达(如白细胞介素-6,干扰素,肿瘤坏死因子-α,等等),使它们上调或下调。因此,研究非编码RNA在炎症中的作用对癌症的未来有重要意义.
    Despite advanced clinical treatment, the mortality rate of cancer patients is high. Recent studies have linked the development of cancer to inflammation. Many cancers are exacerbated by the emergence of inflammatory responses, and non-coding RNAs play an important role in inflammation. Non-coding RNAs include microRNAs, circular RNAs, long-chain noncoding RNAs, etc. The non-coding RNA regulatory network composed of microRNAs, circular RNAs and long-chain non-coding RNAs is involved in the regulatory process of multiple gene expression. They can act on various signaling pathways, such as wnt/β-catenin, nuclear factorkappa B, phosphatidylinositol 3 kinase/ AKT, mitogen-activated protein kinase, and so on. These signaling pathways can control the occurrence of inflammatory response to some extent, such as regulating the expression of inflammatory cytokines (such as interleukin-6, interferongamma, tumor necrosis factor-α, and so on), making them upregulated or down-regulated. Therefore, it is important to study the role of non-coding RNAs in inflammation to contribute to the future of cancer.
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  • 文章类型: Journal Article
    免疫球蛋白A肾病(IgAN)与炎症性肠病(IBD)之间复杂相关的潜在机制尚不清楚。本研究旨在确定最佳的串扰基因,潜在的途径,以及IBD和IgAN之间相互免疫浸润的微环境,以阐明IBD和IgAN患者之间的联系。IgAN和IBD数据集从基因表达综合(GEO)获得。三种算法,CIBERSORTx,ssGSEA,和xcell,用于评估两种疾病之间浸润微环境的相似性。在IBD数据集中实施加权基因共表达网络分析(WGCNA)以鉴定主要的免疫浸润模块,和Boruta算法,RFE算法,和LASSO回归用于过滤串扰基因。接下来,应用多个机器学习模型来确认最佳串扰基因。最后,相关发现通过IBD小鼠的组织学和免疫组织化学分析得到验证.免疫浸润剖析显示IBD和IgAN样品在多数免疫细胞中没有显著差别。这三种算法确定了10个诊断基因,MAPK3,NFKB1,FDX1,EPHX2,SYNPO,KDF1,METTL7A,Rida,HSDL2和RIPK2;FDX1和NFKB1在IBD小鼠的肾脏中增强。京都基因百科全书和基因组分析显示了两种疾病之间的15条相互通路,脂质代谢在串扰中起着至关重要的作用。我们的发现为IgAN和IBD的共同免疫机制提供了见解。这些共同的途径,诊断串扰基因,细胞介导的异常免疫可能为进一步的实验研究提供信息。
    The mechanisms underlying the complex correlation between immunoglobulin A nephropathy (IgAN) and inflammatory bowel disease (IBD) remain unclear. This study aimed to identify the optimal cross-talk genes, potential pathways, and mutual immune-infiltrating microenvironments between IBD and IgAN to elucidate the linkage between patients with IBD and IgAN. The IgAN and IBD datasets were obtained from the Gene Expression Omnibus (GEO). Three algorithms, CIBERSORTx, ssGSEA, and xCell, were used to evaluate the similarities in the infiltrating microenvironment between the two diseases. Weighted gene co-expression network analysis (WGCNA) was implemented in the IBD dataset to identify the major immune infiltration modules, and the Boruta algorithm, RFE algorithm, and LASSO regression were applied to filter the cross-talk genes. Next, multiple machine learning models were applied to confirm the optimal cross-talk genes. Finally, the relevant findings were validated using histology and immunohistochemistry analysis of IBD mice. Immune infiltration analysis showed no significant differences between IBD and IgAN samples in most immune cells. The three algorithms identified 10 diagnostic genes, MAPK3, NFKB1, FDX1, EPHX2, SYNPO, KDF1, METTL7A, RIDA, HSDL2, and RIPK2; FDX1 and NFKB1 were enhanced in the kidney of IBD mice. Kyoto Encyclopedia of Genes and Genomes analysis showed 15 mutual pathways between the two diseases, with lipid metabolism playing a vital role in the cross-talk. Our findings offer insights into the shared immune mechanisms of IgAN and IBD. These common pathways, diagnostic cross-talk genes, and cell-mediated abnormal immunity may inform further experimental studies.
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  • 文章类型: Journal Article
    目标:幽门螺杆菌(H.幽门螺杆菌)是胃癌(GC)发展的重要危险因素,世界上最致命的恶性肿瘤之一.然而,幽门螺杆菌诱导胃癌发生的机制尚不清楚.这里,我们研究了IL-6在胃癌发生和巨噬细胞-上皮细胞相互作用中的功能。
    方法:我们分析了公开可用的数据集,以研究GC组织中IL-6的表达和M2巨噬细胞的浸润,并在IL-6的背景下确定细胞间的通讯。人胃上皮和巨噬细胞系(GES-1和THP-1衍生的巨噬细胞,分别)用于单培养和共培养实验,以研究响应幽门螺杆菌或IL-6刺激的IL-6表达的自分泌和旁分泌诱导。
    结果:我们发现IL-6在GC中高度表达并调节存活。M2巨噬细胞浸润在GC中占主导地位,并驱动IL-6介导的与胃上皮细胞的通讯。体外,IL-6在GES-1和THP-1衍生的巨噬细胞中触发其自身的表达。此外,这些细胞系能够以自分泌的方式上调彼此的IL-6水平,通过幽门螺杆菌刺激增强。
    结论:这项研究表明,肿瘤微环境中的IL-6对于细胞间通讯至关重要。我们显示幽门螺杆菌增强了巨噬细胞和胃上皮细胞之间的IL-6驱动的自分泌和旁分泌正反馈回路,这可能有助于胃癌的发生。
    Helicobacter pylori (H. pylori) is a significant risk factor for development of gastric cancer (GC), one of the deadliest malignancies in the world. However, the mechanism by which H. pylori induces gastric oncogenesis remains unclear. Here, we investigated the function of IL-6 in gastric oncogenesis and macrophage-epithelial cell interactions.
    We analyzed publicly available datasets to investigate the expression of IL-6 and infiltration of M2 macrophages in GC tissues, and determine the inter-cellular communication in the context of IL-6. Human gastric epithelial and macrophage cell lines (GES-1 and THP-1-derived macrophages, respectively) were used in mono- and co-culture experiments to investigate autocrine-and paracrine induction of IL-6 expression in response to H. pylori or IL-6 stimulation.
    We found that IL-6 is highly expressed in GC and modulates survival. M2 macrophage infiltration is predominant in GC and drives an IL-6 mediated communication with gastric epithelium cells. In vitro, IL-6 triggers its own expression in GES-1 and THP-1-derived macrophages cells. In addition, these cell lines are able to upregulate each other\'s IL-6 levels in an autocrine fashion, which is enhanced by H. pylori stimulation.
    This study indicates that IL-6 in the tumor microenvironment is essential for intercellular communication. We show that H. pylori enhances an IL-6-driven autocrine and paracrine positive feedback loop between macrophages and gastric epithelial cells, which may contribute to gastric carcinogenesis.
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  • 文章类型: Journal Article
    丁酸钠(SB),牲畜必需的营养添加剂,它在反刍动物中增强微生物群发育的潜力引起了人们的极大兴趣。这项研究的目的是评估SB对瘤胃和肠道微生物群的影响,当添加到接近45天龄的断奶前奶牛的牛奶中时。我们在小牛奶中施用了四个水平的SB:0克/天(对照),4.4g/d(低),8.8g/d(中等),17.6g/d(高)。经过六周的试验,每组10次重复,收集瘤胃液和粪便样品进行16SrRNA测序,专门针对V3-V4区域来分析微生物群。结果表明瘤胃微生物群增加,特别是在社区丰富方面,低水平的SB补充,但中等和高水平补充的益处最小。增加SB补充水平对肠道微生物群产生负面影响,影响群落丰富度和一些潜在有益的细菌属。然而,低SB补充可以积极调节瘤胃和肠道微生物群之间的交流。总的来说,这项研究表明,向接近年龄的乳牛饲喂添加低水平SB的牛奶,以促进瘤胃微生物群的发育。
    Sodium butyrate (SB), an essential nutritional additive for livestock, has drawn notable interest for its potential for enhancing microbiota development in ruminant animals. This study aimed to assess SB\'s effects on ruminal and intestinal microbiota when added to milk for preweaning dairy calves nearing 45 days old. We administered SB in the calves\' milk at four levels: 0 g/d (control), 4.4 g/d (low), 8.8 g/d (medium), and 17.6 g/d (high). After a six-week trial with ten replicates per group, ruminal fluid and fecal samples were collected for 16S rRNA sequencing, specifically targeting the V3-V4 regions to analyze microbiota. The results indicated an enhancement in ruminal microbiota, particularly in community richness, with low-level SB supplementation but minimal benefits from medium and high levels of supplementation. Increasing the level of SB supplementation had a negative impact on intestinal microbiota, affecting community richness and some potentially beneficial bacterial genera. However, low SB supplementation could positively adjust the communication between ruminal and intestinal microbiota. Overall, this study suggests feeding milk supplemented with a low level of SB to suckling calves close to an older age to promote ruminal microbiota development.
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  • 文章类型: Review
    昆虫是自然界中最成功的动物之一,在许多生态系统中,昆虫病原真菌在昆虫种群的自然表生控制中起着重要作用。昆虫和昆虫病原真菌之间的相互作用已经持续了数亿年。针对真菌感染的昆虫先天免疫应答的许多组分在整个门内都是保守的。此外,行为反应,其中包括回避,梳理,和/或体温的调制,已被认为是对抗真菌病原体的重要机制。为了研究这些基本生物过程之间可能的串扰和中介机制,最近的研究已经整合和/或探索免疫和行为反应。目前的信息表明,在真菌感染的离散阶段,几种昆虫的行为和免疫反应同时改变,暗示了两个系统之间的重要联系。这篇综述综合了我们对影响行为和先天免疫抗真菌反应之间串扰的生理和分子方面的理解的最新进展。包括化学感知和嗅觉途径。
    Insects are one of the most successful animals in nature, and entomopathogenic fungi play a significant role in the natural epizootic control of insect populations in many ecosystems. The interaction between insects and entomopathogenic fungi has continuously coevolved over hundreds of millions of years. Many components of the insect innate immune responses against fungal infection are conserved across phyla. Additionally, behavioral responses, which include avoidance, grooming, and/or modulation of body temperature, have been recognized as important mechanisms for opposing fungal pathogens. In an effort to investigate possible cross-talk and mediating mechanisms between these fundamental biological processes, recent studies have integrated and/or explored immune and behavioral responses. Current information indicates that during discrete stages of fungal infection, several insect behavioral and immune responses are altered simultaneously, suggesting important connections between the two systems. This review synthesizes recent advances in our understanding of the physiological and molecular aspects influencing cross-talk between behavioral and innate immune antifungal reactions, including chemical perception and olfactory pathways.
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  • 文章类型: Journal Article
    我们优化并制造了一种采用4芯多芯光纤(MCF)的超抗弯曲4芯单工电缆(SXC),适用于O波段的短距离密集空分复用(DSDM)光传输。传输损耗的特点,首先阐明了布线后相邻核心之间的宏观弯曲和串扰(XT)。通过引入梯形指数和优化布线过程,由于在4芯SXC上施加了6mm的弯曲半径的10个环路和0.37dB/10圈的宏观弯曲损耗,因此增加的XT的最大值为1.17dB/km,分别,已实现。P然后,在1.2km长的4核SXC上,使用100GBASE-LR4收发器提出了具有低误码率(BER)的光传输。4芯SXC的优异的抗弯曲性可以为基于DSDM的短距离光学互连(OI)上的空间压力降低和访问密度增加铺平道路。
    We optimized and fabricated an ultra-bend-resistant 4-core simplex cable (SXC) employing 4-core multicore fiber (MCF) suitable for short-reach dense spatial division multiplexing (DSDM) optical transmission in the O-band. The characteristics of transmission loss, macro-bending and cross-talk (XT) between adjacent cores after cabling were firstly clarified. By introducing the trapezoid index and optimizing the cabling process, the maximum values of added XT of 1.17 dB/km due to 10 loops with a bending radius of 6 mm imposed over the 4-core SXC and a macro-bending loss of 0.37 dB/10 turns were, respectively, achieved.P Then, the optical transmission with low bit error rate (BER) was presented using a 100GBASE-LR4 transceiver over the 1.2 km long 4-core SXC. The excellent bending resistance of the 4-core SXC may pave the way for a reduction in space pressure and increase in access density on short-reach optical interconnect (OI) based on DSDM.
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