The Implantation and Transmission of Plague Culture by the Five Plague Gods in Shuilu Murals

The Five Plague Gods(五瘟神) in the Shuilu(水陆) murals from the Ming and Qing dynasties exemplify a distinctive manifestation of plague gods image developed under the pedigree of Taoist gods.As a significant system for expelling disasters in Shuilu,the depiction of the Five Plague Gods prominently merges human beings and livestock.This shape form to a large extent,draws on the image of Nuo(傩),a figure reflecting an imagination of the host of plague pathogens.In terms of the numbers of gods,it aligns with the conceptual framework of Wu Xing(五行 the five elements),a foundational principle in traditional Chinese medicine.The internal cultural connection highlights the means of plague prevention and control in China,as well as the external reflection of plague culture.Through multi-dimensional interpretations with the double proof method,this article dissects the formation,core elements,and cultural characteristics of the beliefs in the Five Plague Gods reflected in the Shuilu murals,and transcends mere visual semantics,offering a deeper understanding of these complex cultural symbols.

Pro-resolving lipid mediator reduces amyloid-β42–induced gene expression in human monocyte–derived microglia

Specialized pro-resolving lipid mediators including maresin 1 mediate resolution but the levels of these are reduced in Alzheimer's disease brain, suggesting that they constitute a novel target for the treatment of Alzheimer's disease to prevent/stop inflammation and combat disease pathology. Therefore, it is important to clarify whether they counteract the expression of genes and proteins induced by amyloid-β. With this objective, we analyzed the relevance of human monocyte–derived microglia for in vitro modeling of neuroinflammation and its resolution in the context of Alzheimer's disease and investigated the pro-resolving bioactivity of maresin 1 on amyloid-β42–induced Alzheimer's disease–like inflammation. Analysis of RNA-sequencing data and secreted proteins in supernatants from the monocyte-derived microglia showed that the monocyte-derived microglia resembled Alzheimer's disease–like neuroinflammation in human brain microglia after incubation with amyloid-β42. Maresin 1 restored homeostasis by down-regulating inflammatory pathway related gene expression induced by amyloid-β42 in monocyte-derived microglia, protection of maresin 1 against the effects of amyloid-β42 is mediated by a re-balancing of inflammatory transcriptional networks in which modulation of gene transcription in the nuclear factor-kappa B pathway plays a major part. We pinpointed molecular targets that are associated with both neuroinflammation in Alzheimer's disease and therapeutic targets by maresin 1. In conclusion, monocyte-derived microglia represent a relevant in vitro microglial model for studies on Alzheimer's disease-like inflammation and drug response for individual patients. Maresin 1 ameliorates amyloid-β42–induced changes in several genes of importance in Alzheimer's disease, highlighting its potential as a therapeutic target for Alzheimer's disease.

Jiaohong pills attenuate neuroinflammation and amyloid-βprotein-induced cognitive deficits by modulating the mitogen-activated protein kinase/nuclear factor kappa-B pathway

Background:Jiaohong pills(JHP)consist of Pericarpium Zanthoxyli(PZ)and Radix Rehmanniae,two herbs that have been extensively investigated over many years due to their potential protective effects against cognitive decline and memory impairment.However,the precise mechanisms underlying the beneficial effects remain elusive.Here,research studies were conducted to investigate and validate the therapeutic effects of JHP on Alzheimer's disease.Methods:BV-2 cell inflammation was induced by lipopolysaccharide.AD mice were administered amyloid-β(Aβ).Behavioral experiments were used to evaluate learning and memory ability.The levels of nitric oxide(NO),tumor necrosis factor-alpha(TNF-α),interleukin-1β(IL-1β),and interleukin-10(IL-10)were detected using enzymelinked immunosorbent assay(ELISA).The protein expressions of inducible nitric oxide synthase(iNOS)and the phosphorylation level of mitogen-activated protein kinase(MAPK)and nuclear factor kappa-B(NF-κB)were detected using Western blot.Nissl staining was used to detect neuronal degeneration.Results:The results demonstrated that an alcoholic extract of PZ significantly decreased the levels of NO,IL-1β,TNF-α,and iNOS;increased the expression level of IL-10;and significantly decreased the phosphorylation levels of MAPK and NF-κB.These inhibitory effects were further confirmed in the AD mouse model.Meanwhile,JHP improved learning and memory function in AD mice,reduced neuronal damage,and enriched the Nissl bodies in the hippocampus.Moreover,IL-1βand TNF-αin the cortex were significantly downregulated after JHP administration,whereas IL-10showed increased expression.Conclusions:It was found that JHP reduced neuroinflammatory response in AD mice by targeting the MAPK/NF-κB signaling pathway.

FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression

Alzheimer's disease is characterized by deposition of amyloid-β,which forms extracellular neuritic plaques,and accumulation of hyperphosphorylated tau,which aggregates to form intraneuronal neurofibrillary tangles,in the brain.The NLRP3 inflammasome may play a role in the transition from amyloid-βdeposition to tau phosphorylation and aggregation.Because NLRP3 is primarily found in brain microglia,and tau is predominantly located in neurons,it has been suggested that NLRP3 expressed by microglia indirectly triggers tau phosphorylation by upregulating the expression of pro-inflammatory cytokines.Here,we found that neurons also express NLRP3 in vitro and in vivo,and that neuronal NLRP3 regulates tau phosphorylation.Using biochemical methods,we mapped the minimal NLRP3 promoter and identified FUBP3 as a transcription factor regulating NLRP3 expression in neurons.In primary neurons and the neuroblastoma cell line Neuro2A,FUBP3 is required for endogenous NLRP3 expression and tau phosphorylation only when amyloid-βis present.In the brains of aged wild-type mice and a mouse model of Alzheimer's disease,FUBP3 expression was markedly increased in cortical neurons.Transcriptome analysis suggested that FUBP3 plays a role in neuron-mediated immune responses.We also found that FUBP3 trimmed the 5′end of DNA fragments that it bound,implying that FUBP3 functions in stress-induced responses.These findings suggest that neuronal NLRP3 may be more directly involved in the amyloid-β-to–phospho-tau transition than microglial NLRP3,and that amyloid-βfundamentally alters the regulatory mechanism of NLRP3 expression in neurons.Given that FUBP3 was only expressed at low levels in young wild-type mice and was strongly upregulated in the brains of aged mice and Alzheimer's disease mice,FUBP3 could be a safe therapeutic target for preventing Alzheimer's disease progression.

Enhanced autophagic clearance of amyloid-βvia histone deacetylase 6-mediated V-ATPase assembly and lysosomal acidification protects against Alzheimer's disease in vitro and in vivo

Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal function and rebalancing lysosomal acidification in neurons in the brain may be a new treatment strategy for Alzheimer's disease.Microtubule acetylation/deacetylation plays a central role in lysosomal acidification.Here,we show that inhibiting the classic microtubule deacetylase histone deacetylase 6 with an histone deacetylase 6 shRNA or thehistone deacetylase 6 inhibitor valproic acid promoted lysosomal reacidification by modulating V-ATPase assembly in Alzheimer's disease.Fu rthermore,we found that treatment with valproic acid markedly enhanced autophagy.promoted clearance of amyloid-βaggregates,and ameliorated cognitive deficits in a mouse model of Alzheimer's disease.Our findings demonstrate a previously unknown neuroprotective mechanism in Alzheimer's disease,in which histone deacetylase 6 inhibition by valproic acid increases V-ATPase assembly and lysosomal acidification.

Understanding the prevention and cure of plagues in Daoist medicine

Daoist medicine,a special form of traditional Chinese medicine with distinct Daoist styles,has played an important role in the history of plague control in ancient China.Emerged from the pandemics at the end of the Han Dynasty(146 C.E.-220 C.E.),Daoism,the native Chinese religion,has always had a religious mission to end the spread of plagues;thus,it has actively participated in treating plagues through various techniques of medicine and religion.In the practice of plague treatment for thousands of years,Daoist medicine has developed a special etiology of plague that includes Qi-based theories(Qi is considered to be the force that informs and animates all things in Daoism,thus,plague is also considered to be caused by specific and hazardous Qi.)and worm-based theories,forming a strategy of plague control that includes prevention before an epidemic,active treatment during the epidemic,and recovery after the epidemic;these developed plague prevention methods combine isolation,disinfection,and drug use.Additionally,it is the first to practice a primitive immunoprophylaxis method that uses tissues and secretions of infected persons and animals to infect healthy individuals to gain disease immunity.It has formed a plague treatment method mainly based on drug treatment and ritual treatment,supplemented by acupuncture and physical treatment.It has left behind many effective drugs and prescriptions for plague treatment,some of which have a wide clinical application.Hence,Daoist medicine has made great contributions to plague control in Chinese history.Its strategies,methods,medicines,and prescriptions for plague control still have considerable theoretical and application today,especially in the coronavirus disease 2019(COVID-19)pandemic.

Overexpression of fibroblast growth factor 13 ameliorates amyloid-β-induced neuronal damage

Previous studies have shown that fibroblast growth factor 13 is downregulated in the brain of both Alzheimer’s disease mouse models and patients,and that it plays a vital role in the learning and memory.However,the underlying mechanisms of fibroblast growth factor 13 in Alzheimer’s disease remain unclear.In this study,we established rat models of Alzheimer’s disease by stereotaxic injection of amyloid-β(Aβ_(1-42))-induced into bilateral hippocampus.We also injected lentivirus containing fibroblast growth factor 13 into bilateral hippocampus to overexpress fibroblast growth factor 13.The expression of fibroblast growth factor 13 was downregulated in the brain of the Alzheimer’s disease model rats.After overexpression of fibroblast growth factor 13,learning and memory abilities of the Alzheimer’s disease model rats were remarkably improved.Fibroblast growth factor 13 overexpression increased brain expression levels of oxidative stress-related markers glutathione,superoxide dismutase,phosphatidylinositol-3-kinase,AKT and glycogen synthase kinase 3β,and anti-apoptotic factor BCL.Furthermore,fibroblast growth factor 13 overexpression decreased the number of apoptotic cells,expression of pro-apoptotic factor BAX,cleaved-caspase 3 and amyloid-βexpression,and levels of tau phosphorylation,malondialdehyde,reactive oxygen species and acetylcholinesterase in the brain of Alzheimer’s disease model rats.The changes were reversed by the phosphatidylinositol-3-kinase inhibitor LY294002.These findings suggest that overexpression of fibroblast growth factor 13 improved neuronal damage in a rat model of Alzheimer’s disease through activation of the phosphatidylinositol-3-kinase/AKT/glycogen synthase kinase 3βsignaling pathway.

The relationship among amyloid-βdeposition,sphingomyelin level,and the expression and function of P-glycoprotein in Alzheimer’s disease pathological process

In Alzheimer’s disease,the transporter P-glycoprotein is responsible for the clearance of amyloid-βin the brain.Amyloid-βcorrelates with the sphingomyelin metabolism,and sphingomyelin participates in the regulation of P-glycoprotein.The amyloid cascade hypothesis describes amyloid-βas the central cause of Alzheimer’s disease neuropathology.Better understanding of the change of P-glycoprotein and sphingomyelin along with amyloid-βand their potential association in the pathological process of Alzheimer’s disease is critical.Herein,we found that the expression of P-glycoprotein in APP/PS1 mice tended to increase with age and was significantly higher at 9 and 12 months of age than that in wild-type mice at comparable age.The functionality of P-glycoprotein of APP/PS1 mice did not change with age but was significantly lower than that of wild-type mice at 12 months of age.Decreased sphingomyelin levels,increased ceramide levels,and the increased expression and activity of neutral sphingomyelinase 1 were observed in APP/PS1 mice at 9 and 12 months of age compared with the levels in wild-type mice.Similar results were observed in the Alzheimer’s disease mouse model induced by intracerebroventricular injection of amyloid-β1-42 and human cerebral microvascular endothelial cells treated with amyloid-β1-42.In human cerebral microvascular endothelial cells,neutral sphingomyelinase 1 inhibitor interfered with the changes of sphingomyelin metabolism and P-glycoprotein expression and functionality caused by amyloid-β1-42 treatment.Neutral sphingomyelinase 1 regulated the expression and functionality of P-glycoprotein and the levels of sphingomyelin and ceramide.Together,these findings indicate that neutral sphingomyelinase 1 regulates the expression and function of P-glycoprotein via the sphingomyelin/ceramide pathway.These studies may serve as new pursuits for the development of anti-Alzheimer’s disease drugs.

Mapping the Child’s Grey Interior:Authenticity of Plague Narrative in The Great Plague

The Great Plague:The Diary of Alice Paynton,London 1665-1666 adopts the realistic painting style and direct writing to the painful experience,describes the situation of the Great Plague in London truly from the perspective of children,and breaks people’s cognitive expectation of children’s literature,the construction of children’s Gray inner world is completed behind the true description of the Great Plague in London with the true brushwork,which presents a different world of childlike innocence.Despite the importance of epidemics writing in literature,the child’s diary perspective of them is one of the least developed of Plague Narrative.Only when authenticity and the child’s grey interior are integrated will we reveal a true picture of society as it was.

The Historical and Current Characteristics of“Plague Writing”-Rereading Chi Zijian’s Novel White Snow Crow in the Post Epidemic Era

Chi Zijian’s novel White Snow Crow is about the pestis in Northeast China from the autumn and winter of 1910 to the spring of 1911,focusing on the living conditions of people in Fujiadian,Harbin,under the shadow of the pestis,and thus connects the vicissitudes of Harbin in the development of modern Chinese history.Re-reading this novel in the context of the post-epidemic era not only allows us to immerse ourselves in the specific temporal and spatial fields described in the text with an immersive reading mindset,feel the heavy impact that the disaster has brought to the people of Northeast China,but also provide us with a different perspective to observe the current social reality.In particular,the social problems shown by the novel through the pestis and the description of ordinary people’s life experience under the plague still deserve further discussion.

Cannabidiol-Mediated Sequestration of Alzheimer’s Amyloid-β Peptides in ADDL Oligomers

Cannabidiol (CBD), one of the most studied phytocannabinoids, is non-psychotropic and can induce protective effects on the central nervous system against acute and chronic brain injury. Interestingly, CBD inhibits processes relating to amyloid beta (Aβ)-induced neurotoxicity in mouse models of Alzheimer’s disease, though the detailed molecular mechanism underlying the CBD neurotoxicity modulation is not fully understood. In this study, using atomic force microscopy, we find that CBD promotes the aggregation of Aβ peptides, enhancing the formation of Aβ oligomers, also known as Aβ-derived diffusible ligands (ADDLs). The CBD-mediated sequestration of Aβ monomers in soluble ADDLs could reduce neurotoxicity. This study highlights a possible role of CBD in modulating the formation of ADDL aggregates and provides insight into potentially neuroprotective properties of CBD in Alzheimer’s disease.

敌鼠钠盐和溴敌隆毒饵对康保牧场长爪沙鼠灭效研究

目的 通过现场试验,观察不同药物及毒饵在夏季对长爪沙鼠的灭鼠效果,为鼠疫防控提供参考依据。方法 夏季,在康保牧场分别使用0.05%敌鼠钠盐、0.005%溴敌隆开展现场灭鼠试验,同时设置空白对照组,试验组按洞投药,对照组除不投药外,一切与投药区一致;用堵洞查盗法调查鼠密度,待药物生效后,再用同种方法调查灭后鼠密度,计算校正灭效。长爪沙鼠对不同毒饵的适口性通过计数投饵后1、2、3 d的盗食率、耗饵量和耗饵率来计算。结果 荒地0.05%敌鼠钠盐毒饵对长爪沙鼠的校正灭效为90.07%;人工草场0.05%敌鼠钠盐毒饵、0.005%溴敌隆玉米渣毒饵、0.005%溴敌隆莜麦毒饵对长爪沙鼠的校正灭效分别是86.52%、85.94%、83.87%;2种生境,不同毒饵灭鼠效果均较好;长爪沙鼠对3种不同毒饵适口性存在统计学差异,0.005%溴敌隆莜麦毒饵适口性最好。结论 夏季,抗凝血灭鼠剂敌鼠钠盐和溴敌隆仍对长爪沙鼠有较好的杀灭效果,仍然可以应用毒饵法对长爪沙鼠进行杀灭。灭鼠药物首选第一代抗凝血灭鼠剂敌鼠钠盐,若长爪沙鼠对敌鼠钠盐产生抗性,再选择第二代抗凝血灭鼠剂溴敌隆;莜麦作为诱饵的适口性最优。

一起输入性小鹅瘟疫情的紧急流行病学调查

2023年9月30日,云南省腾冲市某肉鹅养殖场购入的雏鹅发生疫情,表现精神萎靡、食欲不振、腹泻、流鼻涕,并大量死亡。为查明病因,开展了紧急流行病学调查。结果显示:雏鹅累计发病2 567只、死亡2 450只,袭击率为98.7%(2 567/2 600),病死率为95.4%(2 450/2 567)。综合流行病学调查结果、雏鹅临床症状、剖检变化和实验室检测结果,确诊本起疫情为鹅细小病毒感染引起的小鹅瘟。不规范引种、长途运输应激和育雏不当等是引起疫情的主要原因。本起疫情提示,养殖场应规范引种,加强饲养管理,相关部门需加大检疫监管力度,尽可能避免输入性疫情发生。

三江源地区鼠疫耶尔森菌CRISPR基因分型及流行特征研究

目的了解三江源地区鼠疫菌株分布情况,进行规律间隔成簇短回文重复序列(Clustered regularly in-terspaced short palindromic repeats)基因分型研究,为该地区鼠疫疫源地菌株鉴定溯源、科学防控提供理论依据。方法选取三江源地区310株鼠疫菌提取DNA,分别PCR扩增、测序3个CRISPR的位点YPa、YPb和YPc,所测得CRISPR序列与CRISPR Dictionary数据库最新数据进行比对,鉴定CRISPR spacer阵列并对三江源地区鼠疫菌进行基因分型。对310株鼠疫菌结合CRISPR基因型和分离宿主信息进行统计分析。结果310株鼠疫菌共发现26种spacer,分别为YPa15种、YPb8种、YPc3种;310株鼠疫菌被分成16个不同CRISPR基因型,G22型和G22-a1′型分布于整个三江源地区包括称多县、治多县、玉树市、曲麻莱县、囊谦县、杂多县、玛多县、玛沁县、同仁县、泽库县、共和县、同德县、贵德县;G24型分布于泽库县、玛多县、囊谦县、称多县;G26-a1′型主要分布于共和县、兴海县、贵德县、玛多县、称多县、杂多县,16个基因型归类为7个CRISPR类群:Cb4、Cb4′、Ca7、Ca7′、Ca8、Ca35′、Cc3′。结论三江源地区鼠疫菌CRISPR基因型具有多样性,不同疫源地基因型分布特征显著,且不同菌株基因型存在差异。

新型冠状病毒肺炎中西医诊疗概述

检索并整理2022年9月13日(含)以前的各省、直辖市及自治区官方发布的新型冠状病毒肺炎(COVID-19)的中医药诊疗方案及文献,对COVID-19疫情暴发后中西医研究进展情况进行总结分析,为COVID-19下一阶段的中西医诊疗提供借鉴,以期寻找终结COVID-19流行的可能。COVID-19毒株的传播越来越隐匿,患病人群重症感染率明显下降,西医目前没有特效治疗药物,而中医药在防治COVID-19、控制轻症患者转重、重症患者的中西医协同治疗以及康复期治疗方面都能发挥较大优势。

现代抗疫中的温疫学派透法理念与实践论要

明清温疫学派透法治疫之精髓在于“通其郁闭,和其阴阳”,及时祛除阻滞气机之病理因素,郁闭内伏之疫邪方能顺利透达于外。文章回顾性考察近百年来波及范围广、中医介入多的四次抗疫历程,从中探究今人对于温疫学派透法理念的继承与发挥。文章以透法治疫为主线贯穿上述中医抗疫历程,主要从宣透清解、复合透邪以解毒开闭、先期透邪、扶正透邪、全程通络与细化通络等五个方面进行挖掘阐述,对现代疫病防治具有重要的借鉴意义。

当代文学艾滋叙事的隐喻修辞

作为一种疾病,艾滋病在自身之外还附加了众多的隐喻与偏见。当代文学早期艾滋叙事讲述的大多是国外艾滋病患者的故事,显示了一种盲目排外的他者想象。与此同时,艾滋病又被视为一种世纪瘟疫,是对道德犯禁者的天降惩罚。当代文学艾滋叙事文本中存在着大量的军事话语,表现出一种明显的战争修辞特质。艾滋叙事中存在一些话语转义行为,用“爱滋病”“爱之病”或“热病”等指代艾滋病。艾滋叙事在艾滋病的污名建构中发挥了巨大作用,一些话语使用不当容易造成艾滋病的污名化,给艾滋病患者带来严重的精神伤害。

试论厄德里克小说《鸽灾》中的个人主义狂妄

个人主义的狂妄是美国殖民主义霸权的一个重要表征。本文以美国本土裔作家路易斯·厄德里克的小说《鸽灾》为蓝本,从理性的狂妄、实践利益的狂妄和鉴赏的狂妄三个极端个人主义的维度切入,深度透析在资本功利主义的驱使下,殖民者的狂妄偏执对人性的摧残,资本欲望的膨胀对人性扭曲和道德背离的催化,重申了音乐在精神救赎和创伤疗愈方面的重大作用,凸显了作者对原住民被消声了的小写历史的关切,对被删除了的历史记忆的愤懑和对当代美国殖民压迫的再思考。

论阿特伍德《疯癫亚当》三部曲中的瘟疫隐喻

在《疯癫亚当》三部曲中,加拿大作家玛格丽特·阿特伍德创造性地使用了隐喻手法书写瘟疫。作品以《圣经》为叙事原型将瘟疫比喻为洪水,通过绿色宗教“伊甸崖”的创始人亚当一号诠释了人性之恶和遭受天罚的末日想象。瘟疫病毒的载体——“喜福多”药丸在人类的狂欢中变化为蒙着面具的“红死魔”,这种通往所谓极乐天堂的良药实质上是将人类投入地狱的毒药,而极乐的背后又隐藏着社会痼疾给研发者和传播者带来的心灵创伤。瘟疫种子承载了病毒研发者终结人类之恶的幻想,但是这不仅遮掩了灭绝人类的血腥,也质疑了当下科技发展至上的理念,其所开启的后人类世界也充满了诸多不确定性。

清季庚辛鼠疫中的信息疫情与叙事景观

庚辛年间,清政府在东北地区扑灭了鼠疫,然而“信息疫情”的危害动摇了信息安全与国家安全。其原因在于,信息接受者本身的知识局限和认知障碍、信息放送者的情境失察与监管缺位,以及信息生产与传播环节的无序竞争及恶意操作,分别成为清政府治理信息疫情的死穴、短板和软肋。当时各种叙事文本不仅记录了“信息疫情”的形成过程,而且还表现出各自不同的理数与言路。奏折类的历史文本展示了清廷在高纬度的道义战,为避免“口实”与“滋事”而处处“留白”,表现“无能”;报章文学文本记录了民众在低纬度的生死战,他们的呻吟成为疫情的“道白”,展示“无助”;日记类的文学文本展示了官员在中维度的攻坚战,各自为战的防疫经验成为“补白”,显得“无为”。它们并未形成关于疫情对话式的同声合唱,而是自言自语、众声喧哗,最后汇聚成错位式的叙事景观。