|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Oxygen depletion off the Changjiang (Yangtze River)Estuary显示文摘In a survey on the Yellow Sea and the East China Sea on August 20-30 of 1999, we found a hypoxic zone (<2 mg/L) of 13700 km2 with an average thickness of 20m at the bottom of the Changjiang (Yangtze River) Estuary, with an oxygen minimum value of 1 mg/L. The extension of the dissolved oxygen deficiency extended to the 100m isobath in a southeastward direction along the bottom of the continental shelf of the East China Sea. During the last two decades, the minimum dissolved oxygen values in the low oxygen region of the Changjiang Estuary have decreased from 2.85 mg/L to 1 mg/L. In the hypoxic zone, the apparent oxygen utilization (AOU) was 5.8 mg/L and the total oxygen depletion approximately 1.59×106 t. The strong halocline above the hypoxic zone, as a result of affluent water from the Changjiang, Taiwan Warm Current (TWC), and the high concentrations of particle organic carbon (POC) and nitrogen (PON) are the major factors causing the formation of the hypoxic zone. The POC: PON ratios and nutrient concentration distributions in the hypoxic zone suggest that the oxygen deficiency in the bottom water during the summer in the East China Sea off the Changjiang is the result of organic carbon production enhanced by nutrients from the Changjiang and fluvial organic matter input, followed by a shift in regeneration of nutrients in the East China Sea. | LI Daoji (李道季) ZHANG Jing (张经) HUANG Daji (黄大吉) WU Ying (吴莹) LIANG Jun (梁俊) | 2002 | Science China Earth Sciences2002，45，12： | 80 |
| 2 | Ischemia/reperfusion injury and cardioprotective mechanisms:Role of mitochondria and reactive oxygen species显示文摘Reperfusion therapy must be applied as soon as possible to attenuate the ischemic insult of acute myocardial infarction(AMI).However reperfusion is responsible for additional myocardial damage,which likely involves opening of the mitochondrial permeability transition pore(mPTP).In reperfusion injury,mitochondrial damage is a determining factor in causing loss of cardiomyocyte function and viability.Major mechanisms of mitochondrial dysfunction include the long lasting opening of mPTPs and the oxidative stress resulting from formation of reactive oxygen species(ROS).Several signaling cardioprotective pathways are activated by stimuli such as preconditioning and postconditioning,obtained with brief intermittent ischemia or with pharmacological agents.These pathways converge on a common target,the mitochondria,to preserve their function after ischemia/reperfusion.The present review discusses the role of mitochondria in cardioprotection,especially the involvement of adenosine triphosphate-dependent potassium channels,ROS signaling,and the mPTP.Ischemic postconditioning has emerged as a new way to target the mitochondria,and to drastically reduce lethal reperfusion injury.Several clinical studies using ischemic postconditioning during angioplasty now support its protective effects,and an interesting alternative is pharmacological postconditioning.In fact ischemic postconditioning and the mPTP desensitizer,cyclosporine A,have been shown to induce comparable protection in AMI patients. | Maria-Giulia Perrelli Pasquale Pagliaro Claudia Penna | 2011 | World Journal of Cardiology2011，3，6： | 64 |
| 3 | 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 |
| 4 | Temperature variations in the past 6000 years inferred from δ^(18)O of peat cellulose from Hongyuan,China显示文摘Trends of the temperature variations recorded in δ18O in Hongyuan peat cellulose are similar to those recorded in δ18O of Jinchuan peat cellulose and in δ18O of Dunde ice core. Climate events have been identified to be globally homogeneous. Two notable climate transition periods have been detected in the past 6000 years, namely 4000 aBP with climate shifting from cold to warm and 1500 aBP with climate shifting from warm to relatively cold. Power spectrum analysis was performed to investigate the periodical signals in the δ18O time series. Typical periodicities of 1200-1087 a, 752 a, 444 a, 325 a, 213 a, 127-123 a, 88 a, 79 a were discovered, indicating an integrated influence on Hongyuan climate from solar, monsoon and ocean activities. Solar forcing has been addressed to be the main driving forcing of Hongyuan climate. | XU Hai, HONG Yetang, LIN Qinghua, HONG Bing, JIANG Hongbo & ZHU YongxuanInstitute of Geochemistry, Chinese Academy of Sciences, Guiyang 550002, China Graduate School of Chinese Academy of Sciences, Beijing 100039, China | 2002 | Chinese Science Bulletin2002，47，18： | 31 |
| 5 | Oxygen and carbon isotopic characteristics of rainwater,drip water and present speleothems in a cave in Guilin area,and their environmental meanings显示文摘The studies of the oxgen and carbon isotopes of the rainwater in Guilin area, the drip water and the present carbonate deposit in Panlong cave of Guilin show that: (i) as to the general characteristics of the oxygen isotopes of the rainwater within a year and between years, the δ18O values decrease with an increase of air temperature and the rainfall, and the correlation betweenδ18O values and the mean monthly air temperature is much better than that between δ18O values and the rainfall, and the δ18O values of the rainwater during the summer monsoon are much smaller than those during winter monsoon; (ii) δ18O values of the drip water have a quite good correlation with the δ18O values of the rainwater in the same period; (iii) when the conditions are appropriate, δ13C can be used as an environmental proxy, that is, the smaller δ13C of speleothems is, the larger the proportion of C3 plants is and the more plentiful the rainfall is. On the contrary, C4 plants may be prevailing or the environment | 李彬 袁道先 覃嘉铭 林玉石 张美良 | 2000 | Science China Earth Sciences2000，43，3： | 31 |
| 6 | Use of venous-to-arterial carbon dioxide tension difference to guide resuscitation therapy in septic shock显示文摘The mixed venous-to-arterial carbon dioxide(CO_2)tension difference[P(v-a) CO_2]is the difference between carbon dioxide tension(PCO_2) in mixed venous blood(sampled from a pulmonary artery catheter) and the PCO_2 in arterial blood.P(v-a) CO_2 depends on the cardiac output and the global CO_2 production,and on the complex relationship between PCO_2 and CO_2 content.Experimental and clinical studies support the evidence that P(v-a) CO_2 cannot serve as an indicator of tissue hypoxia,and should be regarded as an indicator of the adequacy of venous blood to wash out the total CO_2generated by the peripheral tissues.P(v-a) CO_2 can be replaced by the central venous-to-arterial CO_2 difference(△PCO_2),which is calculated from simultaneous sampling of central venous blood from a central vein catheter and arterial blood and,therefore,more easy to obtain at the bedside.Determining the △PCO_2 during the resuscitation of septic shock patients might be useful when deciding when to continue resuscitation despite a central venous oxygen saturation(SCVO_2) > 70%associated with elevated blood lactate levels.Because high blood lactate levels is not a discriminatory factor in determining the source of that stress,an increased △PCO_2(> 6 mmHg)could be used to identify patients who still remain inadequately resuscitated.Monitoring the △PCO_2 from the beginning of the reanimation of septic shock patients might be a valuable means to evaluate the adequacy of cardiac output in tissue perfusion and,thus,guiding the therapy.In this respect,it can aid to titrate inotropes to adjust oxygen delivery to CO_2 production,or to choose between hemoglobin correction or fluid/inotrope infusion in patients with a too low ScvO_2 related to metabolic demand.The combination of P(v-a) CO_2 or △PCO_2 with oxygen-derived parameters through the calculation of the P(v-a) CO_2 or △PCO_2/arteriovenous oxygen content difference ratio can detect the presence of global anaerobic metabolism. | Jihad Mallat Malcolm Lemyze Laurent Tronchon Beno?t Vallet Didier Thevenin | 2016 | World Journal of Critical Care Medicine2016，5，1： | 25 |
| 7 | 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 |
| 8 | Pathogenesis of pancreatic encephalopathy in severe acute pancreatitis显示文摘BACKGROUND: Pancreatic encephalopathy (PE) is a serious complication of severe acute pancreatitis (SAP). In recent years, more and more PE cases have been reported worldwide, and the onset PE in the early stage was regarded as a poor prognosis sign of SAP, but the pathogenesis of PE in SAP still has not been clarified in the past decade. The purpose of this review is to elucidate the possible pathogenesis of PE in SAP. DATA SOURCES: The English-language literature concern- ing PE in this review came from the Database of MEDLINE (period of 1991-2005), and the keywords of severe acute pancreatitis and pancreatic encephalopathy were used in the searching. RESULTS: Many factors were involved in the pathogenesis of PE in SAP. Pancreatin activation, excessive release of cytokines and oxygen free radicals, microcirculation abnormalities of hemodynamic disturbance, ET-1/NO ratio, hypoxemia, bacterial infection, water and electrolyte imbalance, and vitamin B1 deficiency participated in the development of PE in SAP. CONCLUSIONS: The pathogenesis of PE in SAP has not yet been fully understood. The development of PE in SAP may be a multi-factor process. To find out the possible inducing factor is essential to the clinical management of PE in SAP. | Zhang, Xi-Ping Tian, Hua | 2007 | Hepatobiliary & Pancreatic Diseases International2007，6，2： | 24 |
| 9 | Enhanced recovery program is safe and improves postoperative insulin resistance in gastrectomy显示文摘AIM: To assess the safety of enhanced recovery after surgery(ERAS) program in gastrectomy and influences on nutrition state and insulin-resistance. METHODS: Our ERAS program involved shortening the fasting periods and preoperative carbohydrate loading. Eighty gastrectomy patients were randomly assigned to either the conventional group(CG) or ERAS group(EG). We assessed the clinical characteristics and postoperative outcomes prospectively. The primary endpoint was noninferiority in timely discharge from the hospital within 12 d. Secondary endpoints were the incidence of aspiration at anesthesia induction, incidence of postoperative complications, health related quality of life(HRQOL) using the SF8 Health Survey questionnaire, nutrition state [e.g., albumin, transthyretin(TTR), retinal-binding protein(RBP), and transferrin(Tf)], the homeostasis model assessment-insulin resistance(HOMA-R) index, postoperative urine volume,postoperative weight change, and postoperative oral intake.RESULTS: The ERAS program was noninferior to the conventional program in achieving discharge from the hospital within 12 d(95.0% vs 92.5% respectively; 95%CI:-10.0%-16.0%). There was no significant difference in postoperative morbidity between the two groups. Adverse events such as vomiting and aspiration associated with the induction of general anesthesia were not observed. There were no significant differences with respect to postoperative urine volume, weight change, and oral intake between the two groups. EG patients with preoperative HOMA-R scores above 2.5 experienced significant attenuation of their HOMA-R scores on postoperative day 1 compared to CG patients(P = 0.014). There were no significant differences with respect to rapid turnover proteins(TTR, RBP and Tf) or HRQOL scores using the SF8 method.CONCLUSION: Applying the ERAS program to patients who undergo gastrectomy is safe, and improves insulin resistance with no deterioration in QOL. | Nobuaki Fujikuni Kazuaki Tanabe Noriaki Tokumoto Takahisa Suzuki Minoru Hattori Toshihiro Misumi Hideki Ohdan | 2016 | World Journal of Gastrointestinal Surgery2016，8，5： | 23 |
| 10 | 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 |
| 11 | Combined APACH Ⅱ score and arterial blood lactate clearance rate to predict the prognosis of ARDS patients显示文摘Objective:To explore the easily applicable indicators of practical value to evaluate the prognosis of acute respiratory distress syndrome(ARDS).Methods:Blood and biochemical tests and bloodgas analyses were performed upon entry into the ICUs,12 h,24 h,48 h and 72 h after that in 72 ARDS patients(who were admitted to the ICUs of our hospital from January 2000 to December 2009).Then APACHEⅡscores were achieved by combining relevant physiological parameters and laboratory results.Results:There was a statistical difference between the death group and survival group at different time points upon entering the ICUs in terms of APACHEⅡscore, alveolar-arterial oxygen difference and arterial blood lactate clearance rate.PaO2/FiO2 values were recorded to be statistically different between the death group and survival group 24 h,48 h and 72 h,respectively after entry into the ICUs.In addition,registered linear regression existed between APACHEⅡscore,alveolar-arterial oxygen difference or PaO2/FiO2 value and time. APACHEⅡscore 24 h and 72 h after entering ICUs predicted mortality with an area under the ROC curve(AUC) standing respectively at 0.919 and 0.9SS.Arterial blood lactate clearance rate 12 h, 24 h,48 h and 72 h after entering ICUs predicted mortality with an area under the ROC curve (AUC) at 0.918,0.918,0.909 and 0.991,respectively.Conclusions:APACHEⅡscore applied in combination with arterial blood lactate clearance rate is of clinical significance in assessing the prognosis of ARDS patients. | Wen-Hui Wu Yuan-Yuan Niu Chang-Ran Zhang Long-Bin Xiao Hui-Shao Ye De-Mao Pan Mian Zeng | 2012 | Asian Pacific Journal of Tropical Medicine2012，5，8： | 21 |
| 12 | 高压氧治疗新生儿窒息显示文摘一、高压氧医学概况高压氧(Hyperbarie Oxygen,HBO)医学经历150年漫长而曲折的历史。随着气体物理学的发展,30年来有了长足进步。 | 彭国忱 | 1990 | 中国新生儿科杂志1990，15，1： | 20 |
| 13 | 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 |
| 14 | 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 |
| 15 | 夏秋季珠江口水域COD、DO、营养盐分布特征及其富营养化评价显示文摘在2012年夏季(8月)和秋季(11月)对珠江口海域进行化学需氧量(COD)、溶解氧(DO)和氮磷营养盐调查分析,并研究了其分布特征,采用富营养化指数法和潜在性富营养化法对珠江口水体营养化状况进行了分析和评价.结果显示,珠江口海域COD质量浓度较低,夏季平均值为1.85 mg/L,秋季为1.10 mg/L;DO质量浓度较高,夏季平均值为6.95 mg/L,秋季为7.63 mg/L;无机氮污染严重,平均质量浓度夏季为0.85 mg/L,秋季为0.79mg/L,总体上从北向南递减;无机磷秋季平均质量浓度(0.015 mg/L)显著低于夏季平均质量浓度(0.010 mg/L).富营养化严重海域主要集中在东北部及伶仃洋一带,基本呈自北向南逐级递减趋势.秋季富营养化程度显著高于夏季,珠江口海域基本上属于磷限制潜在性富营养水平. | 蔡阳扬 岑竞仪 欧林坚 吕颂辉 | 2014 | 暨南大学学报(自然科学与医学版)2014，35，3： | 18 |
| 16 | Porphyrin-like Fe-N4 sites with sulfur adjustment on hierarchical porous carbon for different rate-determining steps in oxygen reduction reaction显示文摘We developed a strategy based on coordination polymer to synthesize singleatom site Fe/N and S-codoped hierarchical porous carbon (Fe1/N,S-PC).The as-obtained Fe1/N,S-PC exhibited superior oxygen reduction reaction (ORR) performance with a half-wave potential (Ev2,0.904 V vs.RHE) that was better than that of commercial Pt/C (E1/2,0.86 V vs.RHE),single-atom site Fe/N-doped hierarchical porous carbon (Fe1/N-PC) without S-doped (E1/2,0.85 V vs.RHE),and many other nonprecious metal catalysts in alkaline medium.Moreover,the Fe1/N,S-PC revealed high methanol tolerance and firm stability.The excellent electrocatalytic activity of Fe1/N,S-PC is attributed to the synergistic effects from the atomically dispersed porphyrin-like Fe-N4 active sites,the heteroatom codoping (N and S),and the hierarchical porous structure in the carbon materials.The calculation based on density functional theory further indicates that the catalytic performance of Fe1/N,S-PC is better than that of Fe1/N-PC owing to the sulfur doping that yielded different rate-determining steps. | Konglin Wu Xin Chen Shoujie Liu Yuan Pan Weng-Chon Cheong Wei Zhu Xing Cao Rongan Shen Wenxing Chen Jun LUO Wensheng Yan Lirong Zheng Zheng Chen Dingsheng Wang Qing Peng Chen Chen Yadong Li | 2018 | Nano Research2018，11，12： | 18 |
| 17 | 氧化应激诱导细胞凋亡的机制显示文摘细胞凋亡(apoptosis)是指为维持机体内环境稳定,由基因控制的细胞自主有序的死亡.诱导细胞凋亡的因素很多,既往研究证实,活性氧分子(reactive oxygen species,ros)在细胞凋亡过程中起着举足轻重的作用.ros是外源性氧化剂或细胞内有氧代谢过程中产生的具有很高生物活性的含氧化合物的总称,其中最常见的有超氧化物、过氧化氢、单线态氧和氢氧根阴离子等.正常情况下,机体会产生少量ros,它们发挥着重要的生理作用.然而,在某些因素的影响下,ros会大量产生,导致机体处于一种氧化应激状态,参与疾病的发生和发展.目前,关于ros诱导细胞凋亡的机制存在多种观点,研究较多的是其在凋亡信号转导和调节细胞凋亡相关基因表达中的作用,本文拟结合最近几年的研究进展作一综述. | 刘仪 王凯 王介非 | 2008 | 中华临床感染病杂志2008，1，3： | 17 |
| 18 | Chinese stalagmite paleoclimate researches: A review and perspective显示文摘Stalagmite is one kind of secondary carbonates formed in limestone caves(speleothem). After cave water droplets containing Ca2+and HCO3 drip onto floor, carbonate in the water might become supersaturated due to CO2 degassing under certain conditions, resulting in the formation of stalagmite in a process year after year. Stalagmite is one of important geological archives for paleoclimate research. The advantages include wide spatial distribution, suitable for U-Th and U-Pb dating, enriched in climate proxies, continuity, long time span, comparability and lower sampling cost etc. These factors have propelled stalagmite paleoclimate research to the forefront of global paleoclimatology with an irreplaceable role. The stalagmite paleoclimate study started in the western countries, mainly in Europe and America in 1960 s–1970 s, while the relevant research in China was progressively developed in the 1980 s–1990 s after the Reform and Opening up. Although there was a huge gap between the overall research level in China and western countries, a solid research foundation, as well as a number of talent teams were established during the period. In the 21 st century, starting from the publication of stalagmite records from Hulu Cave in Nanjing in 2001, the stalagmite paleoclimate research in China has ushered in a flourishing development and a real leap on the basis of international cooperation, resulting in significant international impacts. The landmark achievements, including establishment of the world’s longest(640000 years) East Asian monsoon stalagmite record, as well as the longest Indian monsoon(280000 years),South American monsoon(250000 years), North American westerly climate(330000 years), Central Asian westerly climate(135000 years), and northwestern China westerly climate(500000 years), have laid a milestone in the paleoclimate study in these climate domains. Importantly, these stalagmite records have revealed the relationship of Asian monsoon variations with solar insolation climate change in polar regions, and the South American monsoon changes on orbital-suborbital timescales, which have provided new geological observations for the development of orbital-suborbital climate theory;elaborated coupling and differentiation relationships between the Asian monsoon and the westerly climate;reconstructed the history of Asian monsoon changes in the Holocene in detail, and thus the hydrological and climate variances behind Chinese and Indian civilizationcultural evolutions. Furthermore, a large number of high-resolution stalagmite records over the past 2000 years have been reconstructed, which are important for understanding short-term climate variability and magnitude, events, cycles, and thus the future climate projection. The achievements have also involved the improvements of a number of important techniques, such as U-Th dating method, the establishments of various hydroclimatic proxies, as well as the contributions to the reconstruction of the atmosphere14C variation history over the past ~54000 years. On the perspective of the future, the Chinese stalagmite community should continue to develop key techniques, further clarify the hydroclimatic significance of stalagmite proxies, impel the integration of related disciplines, and concentrate on key scientific issues in global climate change and major social demands. | Hai CHENG Haiwei ZHANG Jingyao ZHAO Hanying LI Youfeng NING Gayatri KATHAYAT | 2019 | Science China Earth Sciences2019，62，10： | 17 |
| 19 | 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 |
| 20 | 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 |
您所在的机构暂未开通此部分的功能，请联系管理员