意涵与保护:美国言论自由的考察与分析——从煽动性诽谤谈起

煽动性诽谤是英美法历史上的一项普通法罪名,其核心和实质是禁止人们对政府及其官员进行批评。煽动性诽谤尽管被认为钳制着美国"宪法第一修正案的中心意义",但其在美国的废止经历了一个漫长的过程。如果仅局限于个人权利,即使人们对言论自由的认识经历了由个人权益到公共权益的变化,依然无法达到废除煽动性诽谤之目的。故美国直至1964年纽约时报案明确了言论自由的政治权力属性后,煽动性诽谤方被彻底废止。煽动性诽谤的废止及美国言论自由的转向是美国民主由共和民主向多元民主转型的必然结果。美国言论自由的历史告诉我们,言论自由得到有效保障是以其政治自由属性为基础的。

群体性事件中煽动性言论及谣言应对研究

群体性事件中通常伴随有煽动性言论及谣言,煽动性言论及谣言常以口头、有形介质、短信、网络等形式出现。煽动性言论的目的是小事闹大;谣言的目的主要有发泄不满、唯恐不乱、盲目从众和表现心切等。煽动性言论及谣言的危害大致有掩盖事实真相、促使事态升级和矛盾激化、转变矛盾性质、导致政府公信力下降等。应从加强政府应对能力、提升公安预防应对能力、引导规范媒体行为、建立健全公众参与机制等方面着手。

论对煽动性案件的处理

本文就煽动性案件的处理，从法律角度阐述了其处理依据，并提出了在实际工作中对煽动性案件处理的基本方法。

网络煽动性研究

互联网的开放性和受众的广泛性、交互性为信息传播在速度、广度、便捷性方面提供了优势,但在此过程中煽动性信息的传播也必然给社会带了许多不安定因素。本文主要结合传播学、社会学、心理学、法学的相关知识,对传统媒介在煽动性信息传播上的特点,将二者进行了比较研究。

当前煽动性案件侦查中的几个问题

煽动性案件大大下降，但侦查工作形势依然严峻，必须正视物证查定、人头查找、情况见底、群众配合以及技术、队伍等方面存在的困难。在煽动性案件侦查工作的具体操作中，要认真解决好案情分析和排查中存在的诸多问题。不重视案情分析，分析表面化、主观化，抓不住特殊性，知识水平不高以及盲从等，是案件分析中存在的问题。排查工作则存在仓促上阵、方法不当途径少、抓不住关键线索、不实不深不细、缺乏耐心和韧劲以及基层基础工作薄弱等问题。

当前煽动性案件侦查中存在问题的对策

侦查煽动性案件，应把案情分析摆到极其重要的位置，多途径多视角将案件中一切可利用的信息发掘出来，抓住特殊信息和关键特征，积极求取多方意见，慎重斟酌，调整思路，在侦查中逐步深化与完善对案件的认识。排查工作应精心设计，严密部署，快稳兼顾，注重实效，慎选重点，狠抓关键线索，强调精兵作战，保证实、深、细，并依靠群众，讲究方法。

日本黄色新闻潮与报业煽动机制

明治中后期,日本报界以《万朝报》和《二六新报》为代表展开了与美国黄色新闻潮相似的历史时期。报纸通过耸人听闻的犯罪报道和揭黑运动吸引了大批底层民众的眼球,增加了销量。报纸通过黄色新闻对底层民众影响日趋增加,逐渐积累了强大的社会动员力量,直至1905年在"日比谷公园烧打事件"中展现出了惊人的煽动性。不同于美国社会对黄色新闻的抵制和反思,这种煽动性此后一直存在于日本报纸的基因内,在侵华战争和太平洋战争中发挥着作用。这是黄色新闻潮在日本新闻界的异化。

网络谣言的宪法规制

谣言是信息不确定时所产生的一种社会现象,政府需要规制的是那些可能对公民权利和公共利益产生危害后果的谣言,即诽谤性言论和煽动性言论。谣言虽然是一种低价值言论,但为了防止在遏制谣言的同时也扼杀有益言论,政府需要在中国宪法所规定的言论自由、监督权、公共利益之间进行衡量。

英国早期出版专制和清教徒的抗争

研究新闻出版自由的历史,英国是最丰富、最完整的案例。到19世纪,随着君主立宪制度在英国的稳固,民主法治和言论出版自由得到确立,以至于英国已被马克思夫人燕妮赞誉为出版自由的"圣地"。但是历史拒绝遗忘。曾几何时,英国的专制统治者曾经设计出那么多有效的钳制言论和出版自由的花招和机制。经过包括清教徒在内的无数仁人志士的几百年努力,这些出版自由的拦路虎历经多年被逐一搬移。本文所探究的就是这种早期抗争中的一段出版专制和反专制的斗争史。

美国公共诽谤法的发展和言论自由的扩张

本文以美国大众传播中的公共诽谤问题为主要研究对象,考察美国的公共诽谤法在不同历史阶段的发展状况,以及它们所代表的社会价值、政治制度和法律理念,重点考察现代司法系统如何在民主宪政的理念下协调公共官员(公众人物)的名誉权和新闻媒介的言论自由权之间的冲突。

红土上的精魂——抗战时期的东南诗坛

抗战时期,以浙、闽、赣为中心的东南地区,聚集着一批来自于全国各地的新老诗人和在战火中诞生的本土青年诗人,他们建立诗歌团体,创作诗歌作品,掀起了声势颇大的战时东南诗歌运动。文章对活跃于这一时空的诗人和他们的诗歌活动作一较为具体的描述。

MicroRNAs in inflammatory bowel disease-pathogenesis,diagnostics and therapeutics

The pathogenesis of inflammatory bowel disease (IBD) is complex and largely unknown. Until recently, research has focused on the study of protein regulators in inflammation to reveal the cellular and molecular networks in the pathogenesis of IBD. However, in the last few years, new and promising insights have been generated from studies describing an association between an altered expression of a specific class of non-coding RNAs, called microRNAs (miRs or miRNAs) and IBD. The short (approximately 22 nucleotides), endogenous, single-stranded RNAs are evolutionary conserved inanimals and plants, and regulate specific target mRNAs at the post-transcriptional level. MiRNAs are involved in several biological processes, including development, cell differentiation, proliferation and apoptosis. Furthermore, it is estimated that miRNAs may be responsible for regulating the expression of nearly one-third of the genes in the human genome. Thus, miRNA deregulation often results in an impaired cellular function, and a disturbance of downstream gene regulation and signaling cascades, suggesting their implication in disease etiology. Despite the identification of more than 1900 mature human miRNAs, very little is known about their biological functions and functional targets. Recent studies have identified dysregulated miRNAs in tissue samples of IBD patients and have demonstrated similar differences in circulating miRNAs in the serum of IBD patients. Thus, there is great promise that miRNAs will aid in the early diagnosis of IBD, and in the development of personalized therapies. Here, we provide a short review of the current state-of-the-art of miRNAs in IBD pathogenesis, diagnostics and therapeutics.

Distinct gut microbiota profiles in patients with primary sclerosing cholangitis and ulcerative colitis

To characterize the gut bacterial microbiota of patients with primary sclerosing cholangitis (PSC) and ulcerative colitis (UC). METHODSStool samples were collected and relevant clinical data obtained from 106 study participants, 43 PSC patients with (n = 32) or without (n = 11) concomitant inflammatory bowel disease, 32 UC patients, and 31 healthy controls. The V3 and V4 regions of the 16S ribosomal RNA gene were sequenced on Illumina MiSeq platform to cover low taxonomic levels. Data were further processed in QIIME employing MaAsLin and LEfSe tools for analysis of the output data. RESULTSMicrobial profiles in both PSC and UC were characterized by low bacterial diversity and significant change in global microbial composition. Rothia, Enterococcus, Streptococcus, Veillonella, and three other genera were markedly overrepresented in PSC regardless of concomitant inflammatory bowel disease (IBD). Rothia, Veillonella and Streptococcus were tracked to the species level to identify Rothia mucilaginosa, Streptococcus infantus, S. alactolyticus, and S. equi along with Veillonella parvula and V. dispar. PSC was further characterized by decreased abundance of Adlercreutzia equolifaciens and Prevotella copri. Decrease in genus Phascolarctobacterium was linked to presence of colonic inflammation regardless of IBD phenotype. Akkermansia muciniphila, Butyricicoccus pullicaecorum and Clostridium colinum were decreased in UC along with genus Roseburia. Low levels of serum albumin were significantly correlated with enrichment of order Actinomycetales. CONCLUSIONPSC is associated with specific gut microbes independently of concomitant IBD and several bacterial taxa clearly distinguish IBD phenotypes (PSC-IBD and UC).

Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury

Macrophage inflammatory protein(MIP)-2 is one of the CXC chemokines and is also known as chemokine CXC ligand(CXCL2). MIP-2 affects neutrophil recruitment and activation through the p38 mitogen-activatedprotein-kinase-dependent signaling pathway, by binding to its specific receptors, CXCR1 and CXCR2. MIP-2 is produced by a variety of cell types, such as macrophages, monocytes, epithelial cells, and hepatocytes, in response to infection or injury. In liver injury, activated Kupffer cells are known as the major source of MIP-2. MIP-2-recruited and activated neutrophils can accelerate liver inflammation by releasing various inflammatory mediators. Here, we give a brief introduction to the basic molecular and cellular sources of MIP-2, and focus on its physiological and pathological functions in acute liver injury induced by concanavalin A, lipopolysaccharides, irradiation, ischemia/reperfusion, alcohol, and hypoxia, and hepatectomy-induced liver regeneration and tumor colorectal metastasis. Further understanding of the regulatory mechanisms of MIP-2 secretion and activation may be helpful to develop MIP-2-targeted therapeutic strategies to prevent liver inflammation.

Management of inflammatory bowel disease with Clostridium difficile infection

To address the management of Clostridium difficile (C. difficile) infection (CDI) in the setting of suspected inflammatory bowel disease (IBD)-flare. METHODSA systematic search of the Ovid MEDLINE and EMBASE databases by independent reviewers identified 70 articles including a total of 932141 IBD patients or IBD-related hospitalizations. RESULTSIn those with IBD, CDI is associated with increased morbidity, including subsequent escalation in IBD medical therapy, urgent colectomy and increased hospitalization, as well as excess mortality. Vancomycin-containing regimens are effective first-line therapies for CDI in IBD inpatients. No prospective data exists with regards to the safety or efficacy of initiating or maintaining corticosteroid, immunomodulator, or biologic therapy to treat IBD in the setting of CDI. Corticosteroid use is a risk factor for the development of CDI, while immunomodulators and biologics are not. CONCLUSIONStrong recommendations regarding when to initiate IBD specific therapy in those with CDI are precluded by a lack of evidence. However, based on expert opinion and observational data, initiation or resumption of immunosuppressive therapy after 48-72 h of targeted antibiotic treatment for CDI may be considered.

Role of non-steroidal anti-inflammatory drugs on intestinal permeability and nonalcoholic fatty liver disease

The use of non-steroidal anti-inflammatory drugs(NSAIDs) is widespread worldwide thanks to their analgesic, anti-inflammatory and antipyretic effects. However, even more attention is placed upon the recurrence of digestive system complications in the course of their use. Recent data suggests that the complications of the lower gastro-intestinal tract may be as frequent and severe as those of the upper tract. NSAIDs enteropathy is due to enterohepatic recycling of the drugs resulting in a prolonged and repeated exposure of the intestinal mucosa to the compound and its metabolites. Thus leading to so-called topical effects, which, in turn, lead to an impairment of the intestinal barrier. This process determines bacterial translocation and toxic substances of intestinal origin in the portal circulation, leading to an endotoxaemia. This condition could determine a liver inflammatory response and might promote the development of nonalcoholic steatohepatitis, mostly in patients with risk factors such as obesity, metabolic syndrome and a high fat diet, which may induce a small intestinal bacterial overgrowth and dysbiosis. This alteration of gut microbiota may contribute to nonalcoholic fatty liver disease and its related disorders in two ways: firstly causing a malfunction of the tight junctions that play a critical role in the increase of intestinal permeability, and then secondly leading to the development of insulin resistance, body weight gain, lipogenesis, fibrogenesis and hepatic oxidative stress.

Systematic review and meta-analysis of colon cleansing preparations in patients with inflammatory bowel disease

AIM To performed a systematic review and meta-analysis to determine any possible differences in terms of effectiveness, safety and tolerability between existing colon-cleansing products in patients with inflammatory bowel disease.METHODS Systematic searches were performed( January 1980-September 2016) using MEDLINE, EMBASE, Scopus, CENTRAL and ISI Web of knowledge for randomized trials assessing preparations with or without adjuvants, given in split and non-split dosing, and in high(> 3 L) or low-volume(2 L or less) regimens. Bowel cleansing quality was the primary outcome. Secondary outcomes included patient willingness-torepeat the procedure and side effects/complications.RESULTS Out of 439 citations, 4 trials fulfilled our inclusion criteria(n = 449 patients). One trial assessed the impact of adding simethicone to polyethylene glycol(PEG) 4 L with no effect on bowel cleansing quality, but a better tolerance. Another trial compared senna to castor oil, again without any differences in term of bowel cleansing. Two trials compared the efficacy of PEG high-volume vs PEG low-volume associated to an adjuvant in split-dose regimens: PEG low-dose efficacy was not different to PEG high-dose; OR = 0.84(0.37-1.92). A higher proportion of patients were willing to repeat low-volume preparations vs high-volume; OR = 5.11(1.31-20.0). CONCLUSION In inflammatory bowel disease population, PEG lowvolume regimen seems not inferior to PEG high-volume to clean the colon, and yields improved willingness-torepeat. Further additional research is urgently required to compare contemporary products in this population.

Pseudopolyps in inflammatory bowel diseases: Have we learned enough?

Pseudopolyps are a well described entity in the literature and even though the exact pathogenesis of their formation is not completely understood, they are considered non-neoplastic lesions originating from the mucosa after repeated periods of inflammation and ulceration associated with excessive healing processes. Their occurrence is less common in Crohn's disease than in ulcerative colitis, and their overall prevalence ranges from 4% to 74%; moreover, they are found more often in colon but have been detected in other parts of the gastrointestinal tract as well. When their size exceeds the arbitrary point of 1.5 cm, they are classified as giant pseudopolyps. Clinical evaluation should differentiate the pseudopolyps from other polypoid lesions, such as the dysplasiaassociated mass or lesion, but this situation represents an ongoing clinical challenge. Pseudopolyps can provoke complications such as bleeding or obstruction, and their management includes medical therapy, endoscopy and surgery; however, no consensus exists about the optimal treatment approach. Patients with pseudopolyps are considered at intermediate risk for colorectal cancer and regular endoscopic monitoring is recommended. Through a review of the literature, we provide here a proposed classification of the characteristics of pseudopolyps.

Circulating miR-125a but not miR-125b is decreased in active disease status and negatively correlates with disease severity as well as inflammatory cytokines in patients with Crohn's disease

AIM To determine the association of circulating mi R-125 a/b expression with the risk and disease severity of Crohn's disease(CD), and with inflammatory cytokines.METHODS Plasma samples were collected from patients with active CD(A-CD), or CD in remission(R-CD) and from healthy controls(HCs). The levels of the inflammatory cytokines interleukin-17(IL-17), tumour necrosis factor-α(TNF-α), and interferon-γ(IFN-γ) were measured by enzyme-linked immunosorbent assay. The expression of mi R-125 a/b was assessed by quantitative polymerase chain reaction(q PCR).RESULTS Twenty-nine A-CD patients, 37 R-CD patients, and 37 HCs were included in the study. Plasma mi R-125 a expression was decreased in A-CD patients comparedwith that in R-CD patients(P < 0.001) and HCs(P < 0.001). mi R-125 a expression levels enabled the differentiation of A-CD from R-CD patients [area under curve(AUC) = 0.854] and from HCs(AUC = 0.780), whereas mi R-125 b expression did not. mi R-125 a was negatively correlated with C-reaction protein(CRP)(P = 0.017), erythrocyte sedimentation rate(ESR)(P = 0.026), Crohn's disease activity index(CDAI)(P = 0.003), IL-17(P = 0.015), and TNF-α(P = 0.004) in A-CD patients. Furthermore, mi R-125 a was negatively associated with CRP(P = 0.038) and CDAI(P = 0.021) in R-CD patients. Regarding mi R-125 b, no association with CRP, CDAI, IL-17, TNF-α, or IFN-γ was found in A-CD or in R-CD patients. mi R-125 a levels gradually increased in A-CD patients who achieved clinical remission(P = 0.009) after 3-mo treatment, whereas they remained unchanged among patients who failed to achieve remission. No changes in mi R-125 b expression were detected in remission or non-remission patients after treatment. CONCLUSION Circulating mi R-125 a but not mi R-125 b is decreased in patients with active disease status and negatively correlates with disease severity and inflammatory cytokines in patients with CD.

Systemic interleukin-9 in inflammatory bowel disease: Association with mucosal healing in ulcerative colitis

To evaluate circulating IL9 in inflammatory bowel disease and disease-associated anemia/cachexia and assess its potential as a mucosal healing marker.METHODSSerum IL9 as well as other cytokines (IL1β, IL6, IL13, IFNγ, TNFα, and VEGF-A) were determined in 293 individuals: 97 patients with Crohn’s disease (CD) and 74 with ulcerative colitis (UC) and in 122 apparently healthy controls. The clinical activity of CD and UC was expressed in terms of the Crohn’s Disease Activity Index (CDAI) and the Mayo Scoring System (MDAI), respectively, and the severity of bowel inflammation in UC patients was assessed using Mayo endoscopic score. Cytokine concentrations were measured by a flow cytometry-based method using Luminex xMAP® technology. High-sensitive C-reactive protein concentrations (hsCRP) were determined in CD and UC patients using the enhanced immunoturbidimetric method.RESULTSSystemic IL9 was significantly lower in healthy individuals [9 pg/mL (95%CI: 8.2-10)] than in patients with inflammatory bowel disease (IBD): both inactive [14.3 pg/mL (11.9-19.9)] and active [27.6 pg/mL (24.5-32), P < 0.0001]. Cytokine concentrations were significantly higher in active CD [27.4 pg/mL (23.4-32.2)] and in active UC [32.7 pg/mL (27-38.9)] compared to inactive diseases [15.9 pg/mL (10.8-23.4) in CD and 19.4 pg/mL (13.9-27.1) in UC, P = 0.001]. IL9 correlated weakly with CDAI (ρ = 0.32, P = 0.003) and MDAI (ρ = 0.35, P = 0.002) and strongly with endoscopic inflammation in UC (ρ = 0.74, P < 0.0001). As a negative marker of mucosal healing (MH), IL9 had an accuracy superior to hsCRP and IL6 [97% (P < 0.0001), 67% (P = 0.071), and 55% (P = 0.525), respectively]. IL9 was significantly higher in cachectic IBD patients [30.25 pg/mL (24.4-37.5) vs 21.88 pg/mL (18-26.5), P = 0.026] and negatively correlated with hemoglobin concentrations (ρ = -0.27, P < 0.001). Multiple regression showed IL1β and IL13 to be the independent predictors of circulating IL9 in healthy individuals, IFNγ or IL6 in active and inactive UC, respectively, and IL13 and VEGF-A in both active and inactive CD.CONCLUSIONThe systemic IL9 level is higher in IBD and corresponds with endoscopic inflammation, suggesting its possible application as a negative marker of mucosal healing in UC.