疫情背景下“童享责信”德育课程构建——以武汉市江岸区为例

武汉抗"疫"是学生宝贵的人生经历。如何利用疫情对学生开展生动有效的德育教学,是基础教育必须思考的课题。"接好责信这一棒"是契合武汉抗疫实际构建的德育课程,紧扣"责任"和"诚信"元素,实现了"童享"与"责信"德育的有机统一,具有丰富的启示意义。

公安机关涉疫舆情引导及其与公众知信行的关系研究

探究公众对新型冠状病毒肺炎(COVID-19)的认知、态度和防护行为(简称知信行),为进一步公安机关舆情引导与管控提供参考。方法:2020年5月25日-6月11日,通过网络形式,共回收问卷553份,有效问卷率89.51%。结果:(1)公众在对COVID-19的认知、防护行为分别在年龄、性别上差异显著(p<0.05),且认知和态度与防护行为之间存在显著相关(p<0.05)。(2)在抗击疫情的过程中,60.8%的公众认为公安机关对舆情的管控适当,10.5%的公众认为公安机关对正面舆情缺乏正确的引导、对负面舆情缺乏管控。结论:(1)公众对COVID-19的认知态度越积极,越有利于采取良好的防护行为。(2)公众的知信行受相关疫情消息的影响,公安机关应进一步加强对涉疫舆情的正面引导与管控。

知信行模式下抗疫精神融入隔离技术的教学设计与实践

探讨基于知信行模式将抗疫精神融入隔离技术的教学效果,为增强教学效果、促进学生对护理专业的认同、提升学生的职业素养提供参考和建议。

“信疫”(Infodemic)的根源、规律及治理对策——新技术背景下国际信息传播秩序的失控与重建

面对智能时代第一场全球性疫情,人类除了要战胜病毒"瘟疫",还需要战胜"信疫"(Infodemic)"。信疫"问题的本质是新技术背景下社会信息传播的无序和失控,是民众、媒体、国家与国际社会整体对新形势不适应的集中、剧烈的爆发。其根源是随着互联网的发展,形成了大众传播、网络传播、自传播和智能传播等多种传播机制交错叠加的融合传播的复杂格局。以全民性社交媒体为基础的自下而上的大集市模式已经成为当今社会信息传播的主导性力量,要能够消除和有效治理"信疫",需要具备对当今传播格局和趋势准确认知的基本知识体系,以及对新的传播特性和规律的把握。在四种传播机制相互博弈的背景下,我们一方面需要有效抑制"信疫",另一方面要形成及时有效应对的反应机制,以及扬长避短的对冲机制,建立新的信息传播秩序。

UBE2C as an Immune-Related Biomarker for Breast Cancer:A Study Based on Multiple Databases

Objective To screen the target genes that are associated with survival of breast cancer(BRCA) and explore their prognostic values and immune correlations with BRCA using multiple databases..Methods The microarray expression datasets of BRCA were downloaded from the Gene Expresssion Omnibus database(GEO) and analyzed to obtain differentially expressed genes(DEGs). Hub genes were obtained by constructing and visualizing the protein-protein interaction network of DEGs. The key gene was determined using R language, STRING, and Cytoscape, and the differential expression of the key gene was verified using external datasets The Cancer Genome Atlas(TCGA) and quantitative real-time PCR(q RT-PCR) for BRCA tissues of 37 patients. The prognostic value and immunological correlation of UBE2C in BRCA were explored using R language, TIMER, and Gene Set Enrichment Analysis(GSEA).Results Of 10 hub genes seleceed from 302 DEGS, UBE2C was identified as the gene associated with BRCA survival. The expression of UBE2C was differentially upregulated in BRCA, as verified by TCGA and q RT-PCR. Prognostic analysis revealed that UBE2C served as an independent prognostic factor. High expression of UBE2C was associated with decreased immune infiltration levels of B cells, CD4+ T cells, CD8+ T cells, macrophages, and myeloid dendritic cells in BRCA tissue. The expression of UBE2C in BRCA showed a significant correlation with immune checkpoints genes PDCD1, CD274, and CTLA4 expressions. There was a positive correlation between the expression of UBE2C and the tumor mutational burden and microsatellite instability. GSEA demonstrated that UBE2C expression significantly enriched 786 immune-related gene sets.Conclusions UBE2C expression in BRCA tissues is closely related to the BRCA immune microenvironment and showes predictive values on the survivals and prognosis of BRCA patients and the effecacy of immunotherapy. UBE2C may be an potential immune-related prognostic biomarker for BRCA.

Prognositic value of anoikis and tumor immune microenvironment-related gene in the treatment of osteosarcoma

Objective:Osteosarcoma is a highly aggressive primary malignant bone tumor commonly seen in children and adolescents,with a poor prognosis.Anchorage-dependent cell death(anoikis)has been proven to be indispensable in tumor metastasis,regulating the migration and adhesion of tumor cells at the primary site.However,as a type of programmed cell death,anoikis is rarely studied in osteosarcoma,especially in the tumor immune microenvironment.This study aims to clarify prognostic value of anoikis and tumor immune microenvironment-related gene in the treatment of osteosarcoma.Methods:Anoikis-related genes(ANRGs)were obtained from GeneCards.Clinical information and ANRGs expression profiles of osteosarcoma patients were sourced from the therapeutically applicable research to generate effective therapies and Gene Expression Omnibus(GEO)databases.ANRGs highly associated with tumor immune microenvironment were identified by the estimate package and the weighted gene coexpression network analysis(WGCNA)algorithm.Machine learning algorithms were performed to construct long-term survival predictive strategy,each sample was divided into high-risk and low-risk subgroups,which was further verified in the GEO cohort.Finally,based on single-cell RNA-seq from the GEO database,analysis was done on the function of signature genes in the osteosarcoma tumor microenvironment.Results:A total of 51 hub ANRGs closely associated with the tumor microenvironment were identified,from which 3 genes(MERTK,BNIP3,S100A8)were selected to construct the prognostic model.Significant differences in immune cell activation and immune-related signaling pathways were observed between the high-risk and low-risk groups based on tumor microenvironment analysis(all P<0.05).Additionally,characteristic genes within the osteosarcoma microenvironment were identified in regulation of intercellular crosstalk through the GAS6-MERTK signaling pathway.Conclusion:The prognostic model based on ANRGs and tumor microenvironment demonstrate good predictive power and provide more personalized treatment options for patients with osteosarcoma.

BIO-INSPIRED SELF-ADAPTIVE MANUFACTURING SYSTEM CONTROL ARCHITECTURE

Future manufacturing systems need to cope with frequent changes and disturbances, therefore their control architectures require constant adaptability, agility, stability, self-organization, intelligence, and robustness. Bio-inspired manufacturing system can well satisfy these requirements. For this purpose, by referencing the biological organization structure and the mechanism, a bio-inspired manufacturing cell is presented from a novel view, and then a bio-inspired self-adaptive manufacturing model is established based on the ultra-short feedback mechanism of the neuro-endocrine system. A hio-inspired self-adaptive manufacturing system coordinated model is also established based on the neuro-endocrine-immunity system （NEIS）. Finally, an example based on pheromone communication mechanism indicates that the robustness of the whole manufacturing system is improved by bio-inspired technologies.

《2021年美国图书馆行业现状特别报告:COVID-19》解读与启示

2021年4月5日,美国图书馆协会(ALA)发布的《2021年美国图书馆行业现状特别报告:COVID-19》,反映了美国图书馆在前所未有的环境下所展现的应变能力、决心和创新理念。文章围绕《2021版报告》中的图书馆开放概况、图书借阅情况、远程学习、图书馆活动、立法与筹资、打击虚假信息等六个方面的核心内容做了重点分析,并结合国内图书馆实践,提出完善图书馆应急服务体系、加强医药类特藏资源建设、提升馆员“嵌入式”决策咨询服务水平、多管齐下防治“信疫”危害等建议。

新国标：我的眼里只有你

2006年的新年，笔者收到一个兽药企业老板的短信：兽药2006年的祈祷——禽流感不再没完没了．口蹄疫不再炒作报道；GMP不再盲目达标．新国标能让大家叫好。读后不仅会心一笑．因为这正是兽药行业历经磨难的2005的写照。但仔细琢磨笔者发现．朋友用了三个“不再”来忘却过去的无奈，用了一个“好”来代表对新年的祝福和期待。是啊！2006年我们最大的担忧也是最大的期待就是地标升国标，因为新标准的出台将直接影响兽药行业的走向和企业核心产品竞争力。

Inflammatory bowel disease requires the interplay between innate and adaptive immune signals

Inflammatory bowl disease （IBD） is a type 1 T helper cell （Th1）-mediated autoimmune disease. Various studies have revealed that environmental pathogens also play a significant role in the initiation and progression of this disease. Interestingly, the pathogenesis of IBD has been shown to be related to nitric oxide （NO） released from innate immune cells. Although NO is known to be highly toxic to the gut epithelia, there is very little information about the regulation of NO production, One major question in the etiology of IBD is how Thl cells and pathogens interact in the induction of IBD. In present study, we focused on the regulation of NO. We show that macrophages require both interferon-γ, （IFN-γ）-mediated and TLR4-mediated signals for the production of NO, which causes inflammation in the intestine and subsequently IBD. Thus, IBD is the result of concerted actions of innate immune signals, such as the binding of LPS to TLR-4, and adaptive immune signals, such as IFN-γ produced by Thl cells.

Late SV40 factor:A key mediator of Notch signaling in human hepatocarcinogenesis

AIM:To investigate the relationship between late SV40 factor(LSF)and Notch signaling in the development and progress of hepatocellular carcinoma(HCC).METHODS:Liver cancer tissue specimens from 25 patients were analyzed for Notch-1 and LSF expression by immunohistochemistry.The correlation between expression and the biological effects of Notch-1 and LSF were analyzed using genetic and pharmacological strategies in HCC cell lines and human normal cell lines,including hepatic stellate cells(HSC)and human embryonic kidney epithelial cells(HEK).RESULTS:Immunohistochemistry showed that both Notch-1 and LSF were significantly upregulated in HCC samples(76%,19/25,P<0.0001 and 84%,21/25,P<0.0001,respectively)compared with non-cancer samples.Activation of Notch-1 by exogenous transfection of Notch1 intracellular domain increased LSF expression in HSC and HEK cells to levels similar to those seen in HepG2 cells.Furthermore,blocking Notch-1 activation with aγ-secretase inhibitor,DAPT,downregulated LSF expression in HepG2 cells.Additionally,a biological behavior assay showed that forced overexpression of LSF promoted HepG2 cell proliferation and invasion.CONCLUSION:LSF is a key mediator of the Notch signaling pathway,suggesting that it might be a novel therapeutic target for the treatment of HCC.

SPARCL1, Shp2, MSH2, E-cadherin, p53, ADCY-2 and MAPK are prognosis-related in colorectal cancer

AIM: To investigate the expression of markers that are correlated with the prognosis of colorectal cancer (CRC) patients. METHODS: One hundred and fifty-six CRC patientswere followed up for more than 3 years after radical surgery. Immunohistochemical (IHC) analysis was performed to detect the expression of 14 pathway-related markers (p53, APC, p21ras, E-cadherin, endothelin-B receptor, Shp2, ADCY-2, SPARCL1, neuroligin1, hsp27, mmp-9, MAPK, MSH2 and rho) in specimens from these patients. Bioinformatics analysis involving a Support Vector Machine (SVM) was used to determine the best prognostic model from combinations of these markers. RESULTS: Seven markers (SPARCL1, Shp2, MSH2, E-cadherin, p53, ADCY-2 and MAPK) were significantly related to the prognosis and clinical pathological features of the CRC patients (P < 0.05). Prognostic models were established through SVM from combinations of these 7 markers and proved able to differentiate patients with dissimilar survival, especially in stage Ⅱ/Ⅲ patients. According to the best prognostic model, the p53/SPARCL1 model, patients having high p53 and low SPARCL1 expression had about 50% lower 3-year survival than others (P < 0.001). CONCLUSION: SPARCL1, Shp2, MSH2, E-cadherin, p53, ADCY-2 and MAPK are potential prognostic markers in CRC. A p53/SPARCL1 bioinformatics model may be used as a supplement to tumor-nodes-metastasis staging.

Changes of the cytokine profile in inflammatory bowel diseases

Cytokines are indispensable signals of the mucosaassociated immune system for maintaining normal gut homeostasis.An imbalance of their profile in favour of inflammation initiation may lead to disease states,such as that is observed in inflammatory bowel diseases(IBD).Although Crohn's disease(CD) is often described as a prototype of T-helper 1-type diseases,and ulcerative colitis(UC) is traditionally viewed as a T-helper 2-mediated condition,the classic paradigm,which categorises cytokines into pro-and anti-inflammatory groups,has recently been changed.The inflammation regulatory pathways may not be mutually exclusive as individual cytokines can have diverse and even opposing functions in various clinical and immunological settings.None the less there are many common immunological responses in IBD that are mediated by cytokines.Although they regulate and influence the development,course and recurrence of the inflammatory process,the concrete pathogenic role of these small signaling molecules is sometimes not unambiguous in the subtypes of the disease.Our aim is to review the current information about pro-and anti-inflammatory effects of traditionally studied and recently discovered cytokines in the pathogenesis of UC and CD.The better understanding of their production and functional activity may lead to the development of new therapeutic modalities.

Structural basis of immunosuppression by the therapeutic antibody daclizumab

Interleukin-2 （IL）-2 signaling plays a pivotal role in the activation of immune responses, and drugs that block this pathway have been shown to be effective for the immunosuppression in patients with organ transplantation to alleviate/eliminate allograft rejection. The first humanized monoclonal antibody （mAb） daclizumab falls into this category and shows high specificity and affinity against a key component of the IL-2 receptor complex, namely IL-2Ra. To reveal the molecular mechanism of the inhibition of the IL-2 signaling pathway by dacllzumab, we determined the crystal structures of the daclizumab Fab in free form and in complex with the IL-2Ra ectodomain at 2.6 and 2.8 A resolution, respectively. The daclizumab Fab adopts a similar conformation in the presence or absence of the IL- 2Ra ectodomain. The antigen-binding site of daclizumab is mainly composed of live complementarity determining regions （CDRs） that form a large positively charged surface depression and two flanking patches that are generally hydrophobic. The conformational epitope consists of several discontinuous segments of the IL-2Ru ectodomain, a large portion of which overlaps with the regions that interact with IL-2, suggesting that the binding of daclizumab to IL-2Ra would prevent the IL-2 binding to IL-2Ra and the subsequent formation of the IL-2fIL-2Ra[~/c complex, and therefore block the IL-2 signaling pathway. These results also have implications for the design and development of improved mAb drugs targeting IL-2Ra.

Inhibition of the activating signals in NK92 cells by recombinant GST-sHLAG1α chain

The soluble HLA-G1 (sHLA-G1) isoform was found to be secreted by trophoblast cells at the matemo-fetal interface, which suggests that it may act as an immunomodulator during pregnancy. In this paper, we reported that GST-sHLA-G1α chain could bind to its receptor ILT-2 on NK92 cells and then the latter recruited Src homology 2 domaincontaining tyrosine phosphatase-1 (SHP-1), which consequently dephosphorylated some important protein tyrosine kinases and blocked the activation of downstream molecules such as MEK and ERK so that the cytotoxicity of natural killer (NK) cells was inhibited. These results indicated that GST-sHLA-G1α chain might be exploited in new immunotherapy strategies aiming at inducing immunotolerance during allograft, xenograft and autoimmune situations. In addition, we found that modification of O-linked β-N-acetylglucosamine (O-GlcNAc) was involved in NK cells' activating and inhibitory signals. This may provide a novel molecular target for inducing immunotolerance but needs further study.

Down-regulation of HIV-1 Infection by Inhibition of the MAPK Signaling Pathway

The human immunodeficiency virus type 1 （HIV-1） can interact with and exploit the host cellular machinery to replicate and propagate itself. Numerous studies have shown that the Mitogen-activated protein kinase （MAPK） signal pathway can positively regulate the replication of HIV-1, but exactly how each MAPK pathway affects HIV-1 infection and replication is not understood. In this study, we used the Extracellular signal-regulated kinase （ERK） pathway inhibitor, PD98059, the Jun N-terminal kinase （JNK） pathway inhibitor, SP600125, and the p38 pathway inhibitor, SB203580, to investigate the roles of these pathways in HIV-1 replication. We found that application of PD98059 results in a strong VSV-G pseudotyped HIV-1NL4-3 luciferase reporter virus and HIV-1NL4-3 virus inhibition activity. In addition, SB203580 and SP600125 also elicited marked VSV-G pseudotyped HIV-INL4-3 luciferase reporter virus inhibition activity but no HIV-1NL4-3 virus inhibition activity. We also found that SB203580 and SP600125 can enhance the HIV-1 inhibition activity of PD98059 when cells were treated with all three MAPK pathway inhibitors in combination. Finally, we show that HIV-1 virus inhibition activity of the MAPK pathway inhibitors was the result of the negative regulation of HIV-1 LTR promoter activity.

MUC5AC/β-catenin expression and KRAS gene alteration in laterally spreading colorectal tumors

AIM： To clarify differences in mucin phenotype, prolif- erative activity and oncogenetic alteration among sub- types of colorectal laterally spreading tumor （LST）. METHODS： LSTs, defined as superficial elevated lesions greater than 10 mm in diameter with a low vertical axis, were macroscopically classified into two subtypes： （1） a granular type （Gr-LST） composed of superficially spread- ing aggregates of nodules forming a fiat-based lesion with a granulonodular and uneven surface; and （2） a non-granular type （NGr-LST） with a flat smooth surface and an absence of granulonodular formation. A total of 69 LSTs, comprising 36 Gr-LSTs and 33 NGr-LSTs, were immunohistochemically stained with MUC2, MUC5AC, MUC6, CD10 （markers of gastrointestinal cell lineage）, p53, 13-catenin and Ki-67 antibodies, and examined for alteration in exon 1 of v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog （KRAS） and exon 15 of v-raf murine sarcoma viral oncogene homologue B1 （BRAF） by poly- merase chain reaction followed by direct sequencing. RESULTS： Histologically, 15 Gr-LST samples were ad- enomas with low-grade dysplasia （LGD）, 12 were high- grade dysplasia （HGD） and 9 were adenocarcinomas invading the submucosa （INV）, while 12 NGr-LSTs demonstrated LGD, 14 HGD and 7 INV. In the proximal colon, MUC5AC expression was significantly higher in the Gr-type than the NGr-type. MUC6 was expressed only in NGr-LST. MUC2 or CD10 did not differ. P53 ex- pression demonstrated a significant stepwise increment in progression through LGD-HGD-INV with both types of LST. Nuclear β-catenin expression was significantly higher in the NGr-type. Ki-67 expression was signifi- cantly higher in the Gr-type in the lower one third zone of the tumor. In proximal, but not distal colon tumors, the incidence of KRAS provided mutation was signifi- cantly higher in the Gr-type harboring a specific muta- tional pattern （G12V）. BRAF mutations （V600E） were detected only in two Gr-LSTs. CONCLUSION： The two subtypes of LST, especially in the proximal colon, have differing phenotypes of gastrointestinal cell lineage, proliferation and activa- tion of Wnt/β-catenin or RAS/RAF/extracellular signal- regulated kinase signaling.

IMMUNE RBF NETWORK AND ITS APPLICATION IN THE MODULATION-STYLE RECOGNITION OF RADAR SIGNALS

Based on Immune Programming(IP), a novel Radial Basis Function (RBF) networkdesigning method is proposed. Through extracting the preliminary knowledge about the widthof the basis function as the vaccine to form the immune operator, the algorithm reduces thesearching space of canonical algorithm and improves the convergence speed. The application ofthe RBF network trained with the algorithm in the modulation-style recognition of radar signalsdemonstrates that the network has a fast convergence speed with good performances.

AN IMMUNITY-BASED SECURITY ARCHITECTURE FOR MOBILE AD HOC NETWORKS

This paper focuses on investigating immunological principles in designing a multi-agent security architecture for intrusion detection and response in mobile ad hoc networks. In this approach, the immunity-based agents monitor the situation in the network. These agents can take appropriate actions according to the underlying security policies. Specifically, their activities are coordinated in a hierarchical fashion while sensing, communicating, decision and generating responses. Such an agent can learn and adapt to its environment dynamically and can detect both known and unknown intrusions. The proposed intrusion detection architecture is designed to be flexible, extendible, and adaptable that can perform real-time monitoring. This paper provides the conceptual view and a general framework of the proposed system. In the end, the architecture is illustrated by an example to show it can prevent the attack efficiently.

Relationship of VEGF/VEGFR with immune and cancer cells:staggering or forward?

Vascular endothelial growth factor(VEGF) is primarily known as a proangiogenic factor and is one of the most important growth and survival factors affecting the vascular endothelium. However, recent studies have shown that VEGF also plays a vital role in the immune environment. In addition to the traditional growth factor role of VEGF and VEGF receptors(VEGFRs), they have a complicated relationship with various immune cells. VEGF also reportedly inhibits the differentiation and function of immune cells during hematopoiesis. Dendritic cells(DCs), macrophages, and lymphocytes further express certain types of VEGF receptors.VEGF can be secreted as well by tumor cells through the autocrine pathway and can stimulate the function of cancer stemness.This review will provide a paradigm shift in our understanding of the role of VEGF/VEGFR signaling in the immune and cancer environment.