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| 1 | Pathogenesis of alcoholic liver disease:Role of oxidative metabolism显示文摘Alcohol consumption is a predominant etiological factor in the pathogenesis of chronic liver diseases,resulting in fatty liver,alcoholic hepatitis,fibrosis/cirrhosis,and hepatocellular carcinoma(HCC).Although the pathogenesis of alcoholic liver disease(ALD)involves complex and still unclear biological processes,the oxidative metabolites of ethanol such as acetaldehyde and reactive oxygen species(ROS)play a preeminent role in the clinical and pathological spectrum of ALD.Ethanol oxidative metabolism influences intracellular signaling pathways and deranges the transcriptional control of several genes,leading to fat accumulation,fibrogenesis and activation of innate and adaptive immunity.Acetaldehyde is known to be toxic to the liver and alters lipid homeostasis,decreasing peroxisome proliferator-activated receptors and increasing sterol regulatory element binding protein activity via an AMP-activated protein kinase(AMPK)-dependent mechanism.AMPK activation by ROS modulates autophagy,which has an important role in removing lipid droplets.Acetaldehyde and aldehydes generated from lipid peroxidation induce collagensynthesis by their ability to form protein adducts that activate transforming-growth-factor-β-dependent and independent profibrogenic pathways in activated hepatic stellate cells(HSCs).Furthermore,activation of innate and adaptive immunity in response to ethanol metabolism plays a key role in the development and progression of ALD.Acetaldehyde alters the intestinal barrier and promote lipopolysaccharide(LPS)translocation by disrupting tight and adherent junctions in human colonic mucosa.Acetaldehyde and LPS induce Kupffer cells to release ROS and proinflammatory cytokines and chemokines that contribute to neutrophils infiltration.In addition,alcohol consumption inhibits natural killer cells that are cytotoxic to HSCs and thus have an important antifibrotic function in the liver.Ethanol metabolism may also interfere with cell-mediated adaptive immunity by impairing proteasome function in macrophages and dendritic cells,and consequently alters allogenic antigen presentation.Finally,acetaldehyde and ROS have a role in alcohol-related carcinogenesis because they can form DNA adducts that are prone to mutagenesis,and they interfere with methylation,synthesis and repair of DNA,thereby increasing HCC susceptibility. | Elisabetta Ceni Tommaso Mello Andrea Galli | 2014 | World Journal of Gastroenterology2014，20，47： | 72 |
| 2 | Reactive capillary hemangiomas: a novel dermatologic toxicity following anti-PD-1 treatment with SHR-1210显示文摘Objective: SHR-1210 is a new and promising anti-PD-1 agent for solid tumors. During the phase I study of SHR-1210, we encountered a novel but prevalent immune-related dermatologic toxicity: reactive capillary hemangiomas(RCHs). Thus we tried to summarize the features of RCHs and estimate their relationship with tumor response.Methods: This prospective observational study systematically enrolled 98 patients with advanced solid tumors from April 27th,2016 to June 8th, 2017 in the context of the phase I clinical study of SHR-1210. This report focused on the skin toxicities. Patients underwent entire skin inspection every two weeks while taking medication. The clinical course of RCHs was recorded and their association with tumor response was estimated. The data cut-off date was November 15th, 2017.Results: After a median follow-up of 242(range, 29–567) days, RCHs were observed in 85.7%(84/98) of patients on cutaneous/mucosal surfaces; 84.5%(71/84) of the RCHs were evaluated as grade 1 adverse events. No grade 3 or 4 RCHs were observed. The time of onset of RCHs was dose dependent and shortest in the 400 mg-dose cohort(P < 0.001). Spontaneous and complete regression of RCHs was observed both during and after treatment. The objective response rate of tumors for patients with RCHs was 28.9%(24/83). However, no responders were observed among the patients without RCHs.Conclusions: RCHs were prevalent but manageable during treatment with SHR-1210. It might add to the expanding literature regarding immune-related dermatologic adverse events. | Xuelian Chen Lanying Ma Xi Wang Hongnan Mo Dawei Wu Bo Lan Dong Qu Hongtu Zhang Jing Huang Binghe Xu | 2019 | Cancer Biology & Medicine2019，16，1： | 53 |
| 3 | A review:On path planning strategies for navigation of mobile robot显示文摘This paper presents the rigorous study of mobile robot navigation techniques used so far.The step by step investigations of classical and reactive approaches are made here to understand the development of path planning strategies in various environmental conditions and to identify research gap.The classical approaches such as cell decomposition(CD),roadmap approach(RA),artificial potential field(APF);reactive approaches such as genetic algorithm(GA),fuzzy logic(FL),neural network(NN),firefly algorithm(FA),particle swarm optimization(PSO),ant colony optimization(ACO),bacterial foraging optimization(BFO),artificial bee colony(ABC),cuckoo search(CS),shuffled frog leaping algorithm(SFLA)and other miscellaneous algorithms(OMA)are considered for study.The navigation over static and dynamic condition is analyzed(for single and multiple robot systems)and it has been observed that the reactive approaches are more robust and perform well in all terrain when compared to classical approaches.It is also observed that the reactive approaches are used to improve the performance of the classical approaches as a hybrid algorithm.Hence,reactive approaches are more popular and widely used for path planning of mobile robot.The paper concludes with tabular data and charts comparing the frequency of individual navigational strategies which can be used for specific application in robotics. | B.K. Patle Ganesh Babu L Anish Pandey D.R.K. Parhi A. Jagadeesh | 2019 | Defence Technology(防务技术)2019，15，4： | 60 |
| 4 | 动态监测呼吸道感染患者血清PCT和CRP的临床价值显示文摘 | 卢志勇 单平囡 许德顺 | 2010 | 放射免疫学杂志2010，23，1： | 37 |
| 5 | C-反应蛋白水平与脑梗死病情及预后的量化研究显示文摘目的探讨脑梗死患者血清C-应蛋白(C-reactive protein,CRP)水平与病情严重程度及反预后的量化关系。方法对病程为2周以内的90例脑梗死患者进行入院时和1周后血清C-应蛋白水反平测定。入院时C-应蛋白测定值为CRP11周后检测值为CRP2据入院时C-应蛋白测定值进行反,;根反分组。A组:CRP1≤2.00m g/L,B组:2.00m g/L9.50m g/L。应用美国国立卫生研究院卒中量表(NIH SS)及Barthel指数(BI)记分法,对入院时90例患者(NIH SS1及BI1)和随访的58例患者(NIH SS2及BI2)进行神经功能缺损程度评分。结果入院时血清C-应蛋白水平与发病时反及治疗后3个月随访时的神经功能缺损严重程度呈显著相关(P≤0.001),且这种相关性存在量化关系:CRP1≤2.00m g/L时,N IH SS1中位数为5.00分,BI2中位数为100.00分;2.00m g/L9.50m g/L时,N IH SS1中位数为13.00分,BI2中位数为47.50分。入院时血清C-应蛋白水平与相应的神经功能缺损程度及治疗后3个月恢复期水平反之间差异具有显著意义(P<0.05或P<0.001)。血清CRP2水平与入院时及治疗后3个月时的神经功能缺损程度间差异无显著性意义(P>0.05)。 | 曹红 孙长凯 赵耿毅 汪秋艳 刘新胜 许晶 陶定波 唐树良 黄爱莉 | 2005 | 中国现代神经疾病杂志2005，5，2： | 34 |
| 6 | CRP与心血管疾病显示文摘 | 李建勇 胡大一 | 2005 | 中国心血管病研究2005，3，5： | 29 |
| 7 | 超敏C反应蛋白与动脉粥样硬化的研究进展显示文摘已有研究表明,炎症在动脉粥样硬化(atherosclerosis,AS)及心血管相关疾病的发生和发展过程中都起着重要的作用。而AS是危害人类健康的主要疾病,目前认为其是一种特殊的炎症反应。C-反应蛋白(C—reactive Drotein,CRP)作为一种重要的炎症因子,是机体非特异性炎症反应的敏感标记物之一,它的变化与AS、原发性高血压(EH)、急性冠脉综合征(ACS)和糖尿病等多种疾病密切相关。尤其是超敏C-反应蛋白(hs—CRP)检测技术得到应用,可准确测定低浓度CRP(0.15~10mg/L),hs—CRP作为炎症标志物被认为是未来心血管事件危险最强有力的预测因子之一。 | 潘巍巍 江珊 | 2007 | 中国心血管病研究2007，5，12： | 30 |
| 8 | Alcoholic liver disease:Utility of animal models显示文摘Alcoholic liver disease(ALD) is a major cause of acute and chronic liver injury. Extensive evidence has been accumulated on the pathological process of ALD during the past decades. However, effective treatment options for ALD are very limited due to the lack of suitable in vivo models that recapitulate the full spectrum of ALD. Experimental animal models of ALD, particularly rodents, have been used extensively to mimic human ALD. An ideal animal model should recapitulate all aspects of the ALD process, including significant steatosis, hepatic neutrophil infiltration, and liver injury. A better strategy against ALD depends on clear diagnostic biomarkers, accurate predictor(s) of its progression and new therapeutic approaches to modulate stop or even reverse the disease. Numerous models employing rodent animals have been established in the last decades to investigate the effects of acute and chronic alcohol exposure on the initiation and progression of ALD. Although significant progress has been made in gaining better knowledge on the mechanisms and pathology of ALD, many features of ALD are unknown, and require further investigation, ideally with improved animal models that more effectively mimic human ALD. Although differences in the degree and stages of alcoholic liver injury inevitably exist between animal models and human ALD, the acquisition and translational relevance will be greatly enhanced with the development of new and improved animal models of ALD. | Arantza Lamas-Paz Fengjie Hao Leonard J Nelson Maria Teresa Vázquez Santiago Canals Manuel Gómez del Moral Eduardo Martínez-Naves Yulia A Nevzorova Francisco Javier Cubero | 2018 | World Journal of Gastroenterology2018，24，45： | 26 |
| 9 | Mitophagy links oxidative stress conditions and neurodegenerative diseases显示文摘Mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. Mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases. | Ulfuara Shefa Na Young Jeong In Ok Song Hyung-Joo Chung Dokyoung Kim Junyang Jung Youngbuhm Huh | 2019 | Neural Regeneration Research2019，14，5： | 21 |
| 10 | Dissecting the molecular pathophysiology of drug-induced liver injury显示文摘Drug-induced liver injury(DILI) has become a major topic in the field of Hepatology and Gastroenterology. DILI can be clinically divided into three phenotypes: hepatocytic, cholestatic and mixed. Although the clinical manifestations of DILI are variable and the pathogenesis complicated, recent insights using improved preclinical models, have allowed a better understanding of the mechanisms that trigger liver damage. In this review, we will discuss the pathophysiological mechanisms underlying DILI. The toxicity of the drug eventually induces hepatocellular damage through multiple molecular pathways, including direct hepatic toxicity and innate and adaptive immune responses. Drugs or their metabolites, such as the common analgesic, acetaminophen, can cause direct hepatic toxicity through accumulation of reactive oxygen species and mitochondrial dysfunction. The innate and adaptive immune responses play also a very important role in the occurrence of idiosyncratic DILI. Furthermore, we examine common forms of hepatocyte death and their association with the activation of specific signaling pathways. | Hui Ye Leonard J Nelson Manuel Gómez del Moral Eduardo Martínez-Naves Francisco Javier Cubero | 2018 | World Journal of Gastroenterology2018，24，13： | 19 |
| 11 | Oxidative stress and inflammatory signaling in cerulein pancreatitis显示文摘Oxidative stress is considered to be an important regulator of the pathogenesis of acute pancreatitis.Reactive oxygen species(ROS)regulate the activation of inflammatory cascades,the recruitment of inflammatory cells and tissue damage in acute pancreatitis.A hallmark of the inflammatory response in pancreatitis is the induction of cytokine expression,which is regulated by a number of signaling molecules including oxidant-sensitive transcription factors such as nuclear factor-κB(NF-κB)and activator protein-1(AP-1),signal transducer and activator of transcription 3(STAT3),and mitogen-activated protein kinases(MAPKs).Cross-talk between ROS and pro-inflammatory cytokines is mediated by NF-κB,AP-1,STAT3,and MAPKs;this crosstalk amplifies the inflammatory cascade in acute pancreatitis.Therapeutic studies have shown that antioxidants and natural compounds can have beneficial effects for patients with pancreatitis and can also influence the expression of proinflammatory cytokines in cerulein-induced pancreatitis.Since oxidative stress may activate inflammatory signaling pathways and contribute to thedevelopment of pancreatitis,antioxidant therapy may alleviate the symptoms or prevent the development of pancreatitis.Since chronic administration of high doses of antioxidants may have deleterious effects,dosage levels and duration of antioxidant treatment should be carefully determined. | Ji Hoon Yu Hyeyoung Kim | 2014 | World Journal of Gastroenterology2014，20，46： | 19 |
| 12 | Fluorine-containing oxidizers for metal fuels in energetic formulations显示文摘Fluorine containing oxidizers, primarily polymers, are extensively used in pyrotechnic compositions.Fluorinated oxidizers are less explored for metalized propellants and explosives despite a potential advantage of substantial heat release combined with gaseous combustion products. This review summarizes different types of fluorinated oxidizers used in energetic formulations or of potential interest for such systems, including gases, polymers, and inorganic compounds. Types of energetic formulations employing metals and fluoropolymers are discussed in more detail, including methods used to prepare composites and resulting salient features of the obtained materials. Laboratory experiments characterizing such materials, in particular, electron microscopy and thermal analysis, are discussed, showing characteristic morphologies and reaction sequences observed in different metal-fluorinated oxidizer composites. Striking similarities are noted in reaction sequences for diverse compositions hinting at possible similarities in the respective reaction mechanisms. Experiments probing ignition and combustion of metal-fluorinated oxidizer composites in laboratory conditions are also reviewed, including impact, flash heating and shock ignition. Finally, some practical performance tests for energetic formulations are described following by a brief discussion of the reaction mechanisms expected to govern ignition and combustion in various metal-fluorinated oxidizer composites. The conclusions are combined with recommendation for future research in the area of reactive metal-fluorinated oxidizer composites. | Siva Kumar Valluri Mirko Schoenitz Edward Dreizin | 2019 | Defence Technology(防务技术)2019，15，1： | 17 |
| 13 | C-反应蛋白的测定及临床应用显示文摘 | 税国顺 何代莉 杨晓红 | 2005 | 现代医药卫生2005，21，11： | 17 |
| 14 | Mutual interaction between oxidative stress and endoplasmic reticulum stress in the pathogenesis of diseases specifically focusing on non-alcoholic fatty liver disease显示文摘Reactive oxygen species(ROS) are produced during normal physiologic processes with the consumption of oxygen. While ROS play signaling roles, when they are produced in excess beyond normal antioxidative capacity this can cause pathogenic damage to cells. The majority of such oxidation occurs in polyunsaturated fatty acids and sulfhydryl group in proteins, resulting in lipid peroxidation and protein misfolding, respectively. The accumulation of misfolded proteins in the endoplasmic reticulum(ER) is enhanced under conditions of oxidative stress and results in ER stress, which, together, leads to the malfunction of cellular homeostasis. Multiple types of defensive machinery are activated in unfolded protein response under ER stress to resolve this unfavorable situation. ER stress triggers the malfunction of protein secretion and is associated with a variety of pathogenic conditions including defective insulin secretion from pancreatic β-cells and accelerated lipid droplet formation in hepatocytes. Herein we use nonalcoholic fatty liver disease(NAFLD) as an illustration of such pathological liver conditions that result from ER stress in association with oxidative stress. Protecting the ER by eliminating excessive ROS viathe administration of antioxidants or by enhancing lipidmetabolizing capacity via the activation of peroxisome proliferator-activated receptors represent promising therapeutics for NAFLD. | Junichi Fujii Takujiro Homma Sho Kobayashi Han Geuk Seo | 2018 | World Journal of Biological Chemistry2018，9，1： | 17 |
| 15 | C反应蛋白在疾病诊断和预后评估中的研究进展显示文摘C反应蛋白(C—reactive protein,CRP)因能在钙离子存在时与肺炎球菌C多糖起沉淀反应而得名,它是机体受到微生物入侵或组织损伤等炎症性刺激时由肝脏合成的一种重要的急性期蛋白。CRP在健康人血清中浓度很低,而在细菌感染引发炎症或组织损伤后,其浓度显著增高可达百倍甚至千倍,在炎症进程开始后6-12h就可检测到,因此目前的临床疾病诊断检测中通常将其作为独特的炎症标记物进行检测。 | 刘桂香 | 2012 | 实用医技杂志2012，19，1： | 16 |
| 16 | Ferrostatin-1 protects HT-22 cells from oxidative toxicity显示文摘Ferroptosis is a type of programmed cell death dependent on iron.It is different from other forms of cell death such as apoptosis,classic necrosis and autophagy.Ferroptosis is involved in many neurodegenerative diseases.The role of ferroptosis in glutamate-induced neuronal toxicity is not fully understood.To test its toxicity,glutamate(1.25–20 mM)was applied to HT-22 cells for 12 to 48 hours.The optimal experimental conditions occurred at 12 hours after incubation with 5 mM glutamate.Cells were cultured with 3–12μM ferrostatin-1,an inhibitor of ferroptosis,for 12 hours before exposure to glutamate.The cell viability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Autophagy was determined by monodansylcadaverine staining and apoptosis by caspase 3 activity.Damage to cell structures was observed under light and by transmission electron microscopy.The release of lactate dehydrogenase was detected by the commercial kit.Reactive oxygen species were measured by flow cytometry.Glutathione peroxidase activity,superoxide dismutase activity and malondialdehyde level were detected by the appropriate commercial kit.Prostaglandin peroxidase synthase 2 and glutathione peroxidase 4 gene expression was detected by real-time quantitative polymerase chain reaction.Glutathione peroxidase 4 and nuclear factor erythroid-derived-like 2 protein expression was detected by western blot analysis.Results showed that ferrostatin-1 can significantly counter the effects of glutamate on HT-22 cells,improving the survival rate,reducing the release of lactate dehydrogenase and reducing the damage to mitochondrial ultrastructure.However,it did not affect the caspase-3 expression and monodansylcadaverine-positive staining in glutamate-injured HT-22 cells.Ferrostatin-1 reduced the levels of reactive oxygen species and malondialdehyde and enhanced superoxide dismutase activity.It decreased gene expression of prostaglandin peroxidase synthase 2 and increased gene expression of glutathione peroxidase 4 and protein expressions of glutathione peroxidase 4 and nuclear factor(erythroid-derived)-like 2 in glutamate-injured HT-22 cells.Treatment of cultured cells with the apoptosis inhibitor Z-Val-Ala-Asp(OMe)-fluoromethyl ketone(2–8μM),autophagy inhibitor 3-methyladenine(100–400μM)or necrosis inhibitor necrostatin-1(10–40μM)had no effect on glutamate induced cell damage.However,the iron chelator deferoxamine mesylate salt inhibited glutamate induced cell death.Thus,the results suggested that ferroptosis is caused by glutamate-induced toxicity and that ferrostatin-1 protects HT-22 cells from glutamate-induced oxidative toxicity by inhibiting the oxidative stress. | Jun Chu Chen-Xu Liu Rui Song Qing-Lin Li | 2020 | Neural Regeneration Research2020，15，3： | 16 |
| 17 | Neuroprotection of Cyperus esculentus L. orientin against cerebral ischemia/reperfusion induced brain injury显示文摘Orientin is a flavonoid monomer.In recent years,its importance as a source of pharmacological active substance is growing rapidly due to its properties such as anti-myocardial ischemia,anti-apoptosis,anti-radiation,anti-tumor,and anti-aging.However,the neuroprotective effects of Orientin on stroke injury have not been comprehensively evaluated.The aim of the present study was thus to investigate the neuroprotective capacity and the potential mechanisms of Cyperus esculentus L.orientin(CLO)from Cyperus esculentus L.leaves against ischemia/reperfusion(I/R)injury using standard orientin as control.For in vitro studies,we treated HT22 cells with CoCl2 as an in vitro ischemic injury model.HT22 cells in the control group were treated with CoCl2.For in vivo studies,we used rat models of middle cerebral artery occlusion,and animals that received sham surgery were used as controls.We found that CLO protected CoCl2-induced HT22 cells against ischemia/reperfusion injury by lowering lipid peroxidation and reactive oxygen species formation as well as decreasing protein oxidation.However,CLO did not reduce the release of lactate dehydrogenase nor increase the activity of superoxide dismutase.Results showed that CLO could decrease neurological deficit score,attenuate brain water content,and reduce cerebral infarct volume,leading to neuroprotection during cerebral ischemia-reperfusion injury.Our studies indicate that CLO flavonoids can be taken as a natural antioxidant and bacteriostastic substance in food and pharmaceutical industry.The molecular mechanisms of CLO could be at least partially attributed to the antioxidant properties and subsequently inhibiting activation of casepase-3.All experimental procedures and protocols were approved on May 16,2016 by the Experimental Animal Ethics Committee of Xinjiang Medical University of China(approval No.IACUC20160516-57). | Si-Qun Jing Sai-Sai Wang Rui-Min Zhong Jun-Yan Zhang Jin-Zi Wu Yi-Xian Tu Yan Pu Liang-Jun Yan | 2020 | Neural Regeneration Research2020，15，3： | 16 |
| 18 | Sequential fractionation of reactive phosphorus in the sediment of a shallow eutrophic lake——Donghu Lake, China显示文摘IntroductionSedimentphosphorushasbeenthefocusofanumberofstudiesduetoitsroleintheeutrophicationoflakes.Phosphorusfractionsinse?.. | FU Yong\|qing, ZHOU Yi\|yong\+*, LI Jian\|qiu (Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China) | 2000 | Journal of Environmental Sciences2000，12，1： | 15 |
| 19 | C反应蛋白与胰腺坏死的相关性探讨显示文摘C反应蛋白(C reactive protein,CRP)是一种非特异的急性反应蛋白,在重症急性胰腺炎(severe acute pancreatitis.SAP)时明显增高,并与胰腺坏死的发生有关。根据CRP水平判断胰腺坏死的报道很多,诊断标准不一,但对于检测时间的影响以及判断胰腺坏死程度方面较少涉及。本研究拟结合发病时间因素,对CRP诊断胰腺坏死以及判断坏死程度方面进行全面研究,为临床早期判断胰腺坏死及程度提供理论依据。 | 刘岩 路筝 李兆申 董元航 张文俊 潘雪 | 2006 | 中华消化杂志2006，26，12： | 14 |
| 20 | C反应蛋白与代谢综合征显示文摘 | 张世阳 谈敏 | 2007 | 中国临床保健杂志2007，10，5： | 14 |
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