唐诗疫疾书写的文化内涵

唐代疫疾频发,疫疾流行对唐代社会造成了多方面的严重影响,置身其中的诗者文人也难逃为疫疾所困的境况,在他们的诗歌中描画出疫疾之下的社会情景以及个人身体心理状态。这些疫疾书写的诗歌展示了人们面对疫疾的理性认知、心理状态以及家国情怀,蕴含着丰富的文化内涵。

建安疫疾与文学书写——以曹丕《与吴质书》曹植《说疫气》为中心

建安时期疫疾频繁,史书中有许多记载,后世学者亦有研究。曹丕《与吴质书》和曹植《说疫气》用文学的笔触留下了很深的时代印记,以书信和论说的不同方式,真实记载了疫疾的肆虐,表达了对故友去世的怀念和痛苦,对生命无常的无限感慨以及生命意识的觉醒。疫疾灾害强化了文人的生命意识,突出了人的主体,增强了文人对文学意义和文学功能的认识,表现了面对死亡而引发出以“立言”来建功立业的积极人生态度。

美国科幻小说中的疫疾想象

疫疾想象是美国科幻小说的经典主题。这一文类的作品聚焦于美国乃至全球的卫生危机与医学灾难,展现出美国社会各个阶层对传染病的态度,承载了科幻文学对于美国公共卫生体系和治理体制的深沉忧虑,以及对疫病中人民处境的深切观照。瘟疫主题的美国科幻小说关注助长瘟疫肆虐的政治体制、生命在瘟疫中的脆弱、疫病后社会的创伤与重建,将传染病对人类生存的影响具象化,发挥着重要的警世作用,对当代美国文学文化研究具有重要参考价值。

从《鼠死行》浅议清代不可磨灭的疫疾记忆

疫疾文学在浩如烟海的古今载籍中,构成了一个独特的文学传统,死亡始终是一个沉重的话题,但是疫疾带来的伤痛无法忽视,清代是中国历史上的疫灾多发期,仅乾隆一朝就有多起记载,师道南以精湛而深刻的笔法真实地记录了鼠疫发生时社会的惨状,尤其是《鼠死行》一篇,具有较高价值,表现了作者赤诚的爱国之情。对于疫疾中的悲惨状态进行描述,保留一个民族不可磨灭的集体记忆,这些记忆能使人以史为鉴,敬畏自然,预防灾难。

古代疫疾与文学的“生命意识”——以汉末魏晋时期为例

生命意识是人精神世界的重要组成部分,它体现一个人的生死情怀与精神关怀。汉末魏晋时期疫疾连连爆发,灾难不期而至,在世人的主体意识里对待生死就变得异常敏感,主要表现为:人极度忧患生命,感慨时光去而不返,同时惧怕死亡,唯恐灾祸及身。生命意识也是古代文学的重要话题,具有独特的思想内涵和文化价值,研究古代文学中的生命意识,有助解读古人的生死观,探索其中的文化内涵。

唐代政府对疫疾的应对举措

唐代是中国历史上难得的疫疾低发期,这一方面与当时社会安宁稳定有着直接的关联,但同时也离不开当时政府对疫疾的重视以及行之有效的应对措施。通过对唐代政府的疫疾应对举措的考察,不仅有利于我们了解当时的社会运行机制,也对当今的疫病防治有着借鉴意义。

19世纪末20世纪初民众疾疫迷思——立足于江南地区的文学文本

“鬼神致病”说的疫疾观对 19世纪末 20世纪初民众之于疫疾的理解与应对产生了很大的影响,该时期江南地区的文学文本相关疫疾的记录也体现了这一点。通过细读文本,并结合该时期中国医疗卫生事业的状况,可以发现“鬼神致疫”说之所以会成为该时期一种较为普遍的疫疾理解,离不开实践层面科学知识的失灵与大众自救的本能,以及认知层面医学知识发展的局限和分配的不平均。

天水市秦州区小型猪场疫病防控现状及对策

猪是农村常见的养殖牲畜之一,近年来随着社会的发展和美丽乡村建设的要求,以家庭散养式的养猪模式已经逐渐退出历史舞台,应运而生的是以养殖大户、养殖专业合作社和家庭农场等新型养殖实体为主的养殖模式。本文以天水市秦州区娘娘坝镇小型猪场疫病防控现状为例,针对小型猪场疫病防控中存在的问题,结合实际生产情况,因地制宜地提出相关防控对策,旨在为养猪场的疫病防控工作提供一定参考。

Two-sample Mendelian randomization analysis of causal relationship between eczema and autoimmune diseases

Objective:The causal relationship between eczema and autoimmune diseases has not been previously reported.This study aims to evaluate the causal relationship between eczema and autoimmune diseases.Methods:The two‐sample Mendelian randomization(MR)method was used to assess the causal effect of eczema on autoimmune diseases.Summary data from the Genome-Wide Association Study Catalog(GWAS)were obtained from the Integrative Epidemiology Unit(IEU)database.For eczema and autoimmune diseases,genetic instrument variants(GIVs)were identified according to the significant difference(P<5×10−8).Causal effect estimates were generated using the inverse‐variance weighted(IVW)method.MR Egger,maximum likelihood,MR-PRESSO,and MR-RAPS methods were used for alternative analyses.Sensitivity tests,including heterogeneity,horizontal pleiotropy,and leave-one-out analyses,were performed.Finally,reverse causality was assessed.Results:Genetic susceptibility to eczema was associated with an increased risk of Crohn’s disease(OR=1.444,95%CI 1.199 to 1.738,P<0.001)and ulcerative colitis(OR=1.002,95%CI 1.001 to 1.003,P=0.002).However,no causal relationship was found for the other 6 autoimmune diseases,including systemic lupus erythematosus(SLE)(OR=0.932,P=0.401),bullous pemphigoid(BP)(OR=1.191,P=0.642),vitiligo(OR=1.000,P=0.327),multiple sclerosis(MS)(OR=1.000,P=0.965),ankylosing spondylitis(AS)(OR=1.001,P=0.121),rheumatoid arthritis(RA)(OR=1.000,P=0.460).Additionally,no reverse causal relationship was found between autoimmune diseases and eczema.Conclusion:Eczema is associated with an increased risk of Crohn’s disease and ulcerative colitis.No causal relationship is found between eczema and SLE,MS,AS,RA,BP,or vitiligo.

Immunologic pathogenesis of multiple sclerosis

Multiple sclerosis （MS） is an autoimmune disease. The etiology and pathogenesis of MS remain unclear. At present, there are substantial evidences to support the hypothesis that genetics plays a crucial role. The people who have genetic predisposing genes easily develop immune-mediated disorder, probably in conjunction with environmental factors. The aim of this review is to describe recent observations regarding the immunologic pathogenesis of MS.

Location of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus in Tissues of Natural Cases

[ Objective] The aim of this study was to provide a theoretical basis for the prevention and treatment of highly pathogenic porcine reproductive and respiratory syndrome （HP-PRRS）. [Method] Antigen location and histopathological observation in natural cases infected by highly pathogenic porcine reproductive and respiratory syndrome virus （HP-PRRSV） were analyzed by immunohistochemistry and H. E. staining. [Result] The virus antigen mainly existed in epithelial calls, and also a few in mecrophages, lymphocytes and brain nerve cells. [ Conclusion] The cell and tissue tropism of HP-PRRSV strain in natural cases is different from that of previous strains.

Effect of Echinacea purpurea Polysaccharide on IL-6 m RNA Expression Level in IEC-6 Cell after LPS Injury

[Objective] The aim was to investigate the effect of Echinacea purpurea polysaccharide （EPS） on IL-6 mRNA expression level in IEC-6 cell after lipopolysac- charide （LPS） injury. [Method] Total RNA of IEC-6 cell was extracted with TRIzon reagent and amplified by R-r-PCR. The amplification products were examined by a- garose gel electrophoresis and graphed for analysis. [Result] After stimulation by LPS, the IL-6 mRNA expression level in iEC-6 cell increased. However, EPS could inhibit this effect, and the inhibitory effect was dose-dependent. At the concentration of 50 μg/ml, EPS could partially inhibit the IL-6 mRNA expression in IEC-6 cell after LPS stimulation; in the concentration range of 100-500 μg/ml, the inhibitory effect of EPS on IL-6 mRNA expression in iEC-6 cell increased with the increase of con- centration. When the IEC-6 cell was pre-treated with EPS （50, 100, 200 and 500 μg/ml） for 24 h and then stimulated with LPS （10 μg/ml） for 1 and 4 h, respectively, it was found that the LPS-induced mRNA expression of IL-6 in IEC-6 cell was in- hibited by EPS, and this kind of inhibitory effect was time-dependent. [Conclusion] After small intestinal epithelial cells were stimulated by LPS, the IL-6 mRNA expres- sion level increased. However, EPS could inhibit the LPS-induced mRNA expression of IL-6, thus protecting the intestinal mucosa. In addition, this kind of inhibitory effect showed time and concentration dependence.

IgG4-related sclerosing disease

Based on histological and immunohistochemical exami- nation of various organs of patients with autoimmune pancreatitis （AIP）, a novel clinicopathological entity of IgG4-related sclerosing disease has been proposed. This is a systemic disease that is characterized by extensive IgG4-positive plasma cells and T-lymphocyte infiltration of various organs. Clinical manifestations are apparent in the pancreas, bile duct, gallbladder, salivary gland, retroperitoneum, kidney, lung, and prosrate, in which tissue fibrosis with obliterative phlebitis is pathologically induced. AlP is not simply pancreatitis but, in fact, is a pancreatic disease indicative of IgG4- related sclerosing diseases. This disease includes AlP, sclerosing cholangitis, cholecystitis, sialadenitis, retro-peritoneal fibrosis, tubulointerstitial nephritis, interstitial pneumonia, prostatitis, inflammatory pseudotumor and lymphadenopathy, all IgG4-related. Most IgG4-related sclerosing diseases have been found to be associated with AlP, but also those without pancreatic involvement have been reported. In some cases, only one or two organs are clinically involved, while in others, three or four organs are affected. The disease occurs predominantly in older men and responds well to steroid therapy. Serum IgG4 levels and immunos-taining with anti-IgG4 antibody are useful in making the diagnosis. Since malignant tumors are frequently suspected on initial presentation, IgG4-related sclerosing disease should be considered in the differential diagnosis to avoid unnecessary surgery.

Therapeutic approaches targeting intestinal microflora in inflammatory bowel disease

Inflammatory bowel diseases, ulcerative colitis, and Crohn＇s disease, are chronic intestinal disorders of unknown etiology in which in genetically susceptible individuals, the mucosal immune system shows an aberrant response towards commensal bacteria. The gastrointestinal tract has developed ingenious mechanisms to coexist with its autologous microflora, but rapidly responds to invading pathogens and then returns to homeostasis with its commensal bacteria after the pathogenic infection is cleared. In case of disruption of this tightly-regulated homeostasis, chronic intestinal inflammation may be induced. Previous studies showed that some commensal bacteria are detrimental while others have either no influence or have a protective action. In addition, each host has a genetically determined response to detrimental and protective bacterial species. These suggest that therapeutic manipulation of imbalance of microflora can influence health and disease. This review focuses on new insights into the role of commensal bacteria in gut health and disease, and presents recent findings in innate and adaptive immune interactions. Therapeutic approaches to modulate balance of intestinal microflora and their potential mechanisms of action are also discussed.

Interleukin-12 and Th1 immune response in Crohn’s disease: Pathogenetic relevance and therapeutic inplication

Crohn’s disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of the gastrointestinal tract that share clinical and pathological characteristics. The most accredited hypothesis is that both CD and UC result from a deregulated mucosal immune response to normal constituents of the gut microflora. Evidence, however, indicates that the main pathological processes in these two diseases are distinct. In CD, the tissue- damaging inflammatory reaction is driven by activated type 1 helper T-cell (Th1), whereas a humoral response predominates in UC. Consistently, a marked accumulation of macrophages making interleukin (IL)-12, the major Th1-inducing factor, is seen in CD but not in UC mucosa. Preliminary studies also indicate that administration of a monoclonal antibody blocking the IL-12/p40 subunit can be useful to induce and maintain clinical remission in CD patients. Notably, the recently described IL-23 shares the p40 subunit with IL-12, raising the possibility that the clinical benefit of the anti-IL-12/p40 antibody in CD may also be due to the neutralization of IL-23 activity. This review summarizes the current information on the expression and functional role of IL-12 and IL- 12-associated signaling pathways both in patients with CD and experimental models of colitis, thus emphasizing major differences between IL-12 and IL-23 activity on the development of intestinal inflammation.

Lack of specific association between gastric autoimmunity hallmarks and clinical presentations of atrophic body gastritis

AIM： To investigate the possible relationships between gastric autoimmune phenomena and clinical presentations of this disorder, in consecutive atrophic body gastritis patients. METHODS： A total of 140 atrophic body gastritis patients, diagnosed as consecutive outpatients presenting with macrocytic or iron deficiency anemia, or longstanding dyspepsia underwent gastroscopy with antral and body biopsies, assay of intrinsic factor, parietal cells and Helicobacter pylori （ H pylon） antibodies. Gastritis was assessed according to Sydney System. RESULTS： Parietal cell antibodies were equally distributed in all clinical presentations, whereas the positivity of intrinsic factor antibodies （49/140, 35%） was significantly higher in pernicious anemia patients （49.2%） than in iron deficiency （21.1%） and dyspeptic patients （27.8%）. No specific pattern of autoantibodies was related to the clinical presentations of atrophic body gastritis. A positive correlation was obtained between the body atrophy score and the intrinsic factor antibody levels （r=0.2216, P=0.0085）. Associated autoimmune diseases were present in 25/140 （17.9%） patients, but the prevalence of autoimmune diseases was comparable, irrespective of the clinical presentations. CONCLUSION： The so-called hallmarks of gastric autoimmunity, particularly in intrinsic factor antibody cannot be usefully employed in defining an autoimmune pattern in the clinical presentations of ABG.

Coeliac disease in Dutch patients with Hashimoto’s thyroiditis and vice versa

AIM: To define the association between Hashimoto’s thyroiditis and coeliac disease in Dutch patients. METHODS: A total of 104 consecutive patients with Hashimoto’s thyroiditis underwent coeliac serological tests (antigliadins, transglutaminase and endomysium antibodies) and HLA-DQ typing. Small intestinal biopsy was performed when any of coeliac serological tests was positive. On the other hand, 184 patients with coeliac disease were subjected to thyroid biochemical (thyroid stimulating hormone and free thyroxine) and thyroid serological tests (thyroglobulin and thyroid peroxidase antibodies). RESULTS: Of 104 patients with Hashimoto’s thyroiditis, sixteen (15%) were positive for coeliac serology and five patients with documented villous atrophy were diagnosed with coeliac disease (4.8%; 95% CI 0.7-8.9). HLA-DQ2 (and/or -DQ8) was present in all the five and 53 patients with Hashimoto’s thyroiditis (50%; 95% CI 43-62). Of 184 patients with coeliac disease, 39 (21%) were positive for thyroid serology. Based on thyroid biochemistry, the 39 patients were subclassified into euthyroidism in ten (5%; 95% CI 2-9), subclinicalhypothyroidism in seven (3.8%; 95% CI 1.8-7.6), and overt hypothyroidism (Hashimoto’s thyroiditis) in 22 (12%; 95% CI 8-16). Moreover, four patients with coeliac disease had Graves’ disease (2%; 95% CI 0.8-5) and one patient had post-partum thyroiditis. CONCLUSION: The data from a Dutch population confirm the association between Hashimoto’s thyroiditis and coeliac disease. Screening patients with Hashimoto’s thyroiditis for coeliac disease and vice versa is recom- mended.

New insights into the pathophysiology of achalasia and implications for future treatment

Idiopathic achalasia is an archetype esophageal motor disorder, causing significant impairment of eating ability and reducing quality of life. The pathophysiological underpinnings of this condition are loss of esophageal peristalsis and insufficient relaxation of the lower esophageal sphincter(LES). The clinical manifestations include dysphagia for both solids and liquids, regurgitation of esophageal contents, retrosternal chest pain, cough, aspiration, weight loss and heartburn. Even though idiopathic achalasia was first described more than 300 years ago, researchers are only now beginning to unravel its complex etiology and molecular pathology. The most recent findings indicate an autoimmune component, as suggested by the presence of circulating anti-myenteric plexus autoantibodies, and a genetic predisposition, as suggested by observed correlations with other well-defined genetic syndromes such as Allgrove syndrome and multiple endocrine neoplasia type 2 B syndrome. Viral agents(herpes, varicella zoster) have also been proposed as causative and promoting factors. Unfortunately, the therapeutic approaches available today do not resolve the causes of the disease, and only target the consequential changes to the involved tissues, such as destruction of the LES, rather than restoring or modifying the underlying pathology. New therapies should aim to stop the disease at early stages, thereby preventing the consequential changes from developing and inhibiting permanent damage. This review focuses on the known characteristics of idiopathic achalasia that will help promote understanding its pathogenesis and improve therapeutic management to positively impact the patient's quality of life.

Fenofibrate for patients with asymptomatic primary biliary cirrhosis

AIM:Primary biliary cirrhosis (PBC) is a chronic, cholestatic disease of autoimmune etiology,the histology of which shows a destruction of the intrahepatic bile duct and portal inflammation. Ursodeoxycholic acid (UDCA) is now used as a first-line drug for asymptomatic PBC (aPBC) because it is reported that UDCA decreases mortality and prolongs the time of liver transplantation.However, only 20-30% of patients respond fully to UDCA.Recently,lipoprotein-lowering agents have been found to be effective for PBC.The aim of this study was to examine the safety and efficacy of fenofibrate, a member of the fibrate class of hypolipidemic and anti-inflammatory agent via peroxysome proliferatory-activated receptor α,in patients with aPBC.METHODS:Fenofibrate was administered for twelve weeks in nine patients with aPBC who failed to respond to UDCA.UDCA was used along with fenofibrate during the study.The data from aPBC patients were analyzed to assess the biochemical effect of fenofibrate during the study.RESULTS: The serum levels of alkaline phosphatase (ALP)(285±114.8IU/L) and immunoglobulin M (IgM) (255.8±85.9mg/dl) significantly decreased to 186.9±76.2IU/L and 192.9±67.5mg/dL respectively, after fenofibrate treatment in patients with aPBC (P<0.05). Moreover,the titer of antimitochondrial antibody (AMA) also decreased in 4 of 9 patients with aPBC. No adverse reactions were observed in any patients.CONCLUSION:Fenofibrate appears to be significantly effective in treating patients with aPBC who respond incompletely to UDCA alone.Although the mechanism of fenofibrate on aPBC has not yet been fully clarified,combination therapy using fenofibrate and UDCA might be related to the anti-immunological effects, such as the suppression of AMA production as well as its antiinflammatory effect.

What caused the increase of autoimmune and allergic diseases:A decreased or an increased exposure to luminal microbial components?

The dramatic increase of allergic and autoimmune diseases such as asthma, atopic dermatitis （eczema）, allergic rhinitis, inflammatory bowel disease （IBD, including both Crohn＇s disease and ulcerative colitis）, multiple sclerosis, and insulin-dependent diabetes mellitus （type Ⅰ diabetes） in the developed countries in the last century is a big puzle. ＂Hygiene Hypothesis＂ was proposed more than two decades ago and it suggested that the increase in these allergic and autoimmune diseases is caused by the aberrant development and response of the immune system due to a reduced exposure to microorganisms along with the improved hygiene. Interestingly, recent studies revealed that these allergic and autoimmune diseases are closely related to the microbes in the gut. For instance, even asthma, an allergic reaction of the lung to inhaled antigens, is closely related to a reduced exposure to foodborne and orofaecal microbes, rather than the amount of allergens in the air or the exposure to airborne microbes. It is known that bacteria in the gut could be 10 times in number of the eukaryotic cells of the body. Therefore, it would be not too surprising that microbes in the gut may have a great impact on these autoimmune and allergic diseases.