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| 1 | The Case for Stabilizing China's Exchange Rate:Setting the Stage for Fiscal Expansion显示文摘中国的金融的谜从二来源产生。首先,它的大节省(贸易) 因为是一个不成熟的债权人不能在它的自己的货币借,在货币的剩余结果错配。相反,外国货币宣称(大部分美元) 在国内金融机构以内积聚。第二,经济学家,美国、中国,错误地把剩余归因于低估的 RMB。安无 USA,结果每从 2005 年 7 月的年是对对 6% 的美元或更多的 RMB 的渐渐、可预言的欣赏到 2008 年 7 月。和在美国利率的秋天自从 mid-2007,在外汇的这 oneway 赌注出售不仅吸引的热钱流入而且禁止的私人资本从资助中国的巨大的贸易剩余的流出。因此,人们中国的银行不得不重重地干涉向上阻止 RMB ratcheting,那么变得这个国家正式交换保留的唯一的国际金融中间人爆炸。因为货币失配,漂浮 RMB 既不可行也不合乎需要,并且更高的 RMB 不减少中国的贸易剩余。相反,为贸易剩余的钱的控制和正常私人部门的金融要求回来到在 1995 和 2004 之间存在的类似于那的可信地固定的名字的 RMB/USD 率。然而,为任何最新重设的 RMB/USD 评价作为一个钱的锚可信,猛击得到 RMB 起来的外国中国必须结束。然后,阶段将被设置让财政扩大刺激经济并且减少它的贸易剩余。 | Ronald McKinnon Gunther Schnabl | 2009 | China & World Economy2009，17，1： | 23 |
| 2 | Gut microbiome,liver immunology,and liver diseases显示文摘The gut microbiota is a complex and plastic consortium of microorganisms that are intricately connected with human physiology.The liver is a central immunological organ that is particularly enriched in innate immune cells and constantly exposed to circulating nutrients and endotoxins derived from the gut microbiota.The delicate interaction between the gut and liver prevents accidental immune activation against otherwise harmless antigens.Work on the interplay between the gut microbiota and liver has assisted in understanding the pathophysiology of various liver diseases.Of immense importance is the step from high-throughput sequencing(correlation)to mechanistic studies(causality)and therapeutic intervention.Here,we review the gut microbiota,liver immunology,and the interaction between the gut and liver.In addition,the impairment in the gut-liver axis found in various liver diseases is reviewed here,with an emphasis on alcohol-associated liver disease(ALD),nonalcoholic fatty liver disease(NAFLD),and autoimmune liver disease(AILD).On the basis of growing evidence from these preclinical studies,we propose that the gut-liver axis paves the way for targeted therapeutic modalities for liver diseases. | Rui Wang Ruqi Tang Bo Li Xiong Ma Bernd Schnabl Herbert Tilg | 2021 | Cellular & Molecular Immunology2021，18，1： | 23 |
| 3 | Necrotizing enterocolitis: A multifactorial disease with no cure显示文摘Necrotizing enterocolitis is an inflammatory bowel disease of neonates with significant morbidity and mortality in preterm infants. Due to the multifactorial nature o the disease and limitations in disease models, early diagnosis remains challenging and the pathogenesis elusive. Although preterm birth, hypoxic-ischemic events formula feeding, and abnormal bacteria colonization are established risk factors, the role of genetics and vasoactive/inflammatory mediators is unclear Consequently, treatments do not target the specific underlying disease processes and are symptomatic and surgically invasive. Breast-feeding is the most effective preventative measure. Recent advances in the prevention of necrotizing enterocolitis have focused on bioactive nutrients and trophic factors in human milk. Developmen of new disease models including the aspect of prematurity that consistently predisposes neonates to the disease with multiple risk factors will improve our understanding of the pathogenesis and lead to discovery of innovative therapeutics. | Kareena L Schnabl John E Van Aerde Alan BR Thomson Michael T Clandinin | 2008 | World Journal of Gastroenterology2008，14，14： | 19 |
| 4 | China's Exchange Rate and Financial Repression:The Conflicted Emergence of the RMB as an International Currency显示文摘Instability in the world dollar standard,as most recently manifested in the US Federal Reserve's near-zero interest rate policy,has caused consternation in emerging markets with naturally higher interest rates.China has been provoked into speeding RMB 'internationalization ';that is,openingup domestic financial markets to reduce its dependence on the US dollar for invoicing trade and making international payments.However,despite rapid percentage growth in offshore financial markets in RMB,the Chinese authorities are essentially trapped into maintaining exchange controls(reinforced by financial repression in domestic interest rates) to avoid an avalanche of foreign capital inflows that would threaten inflation and asset price bubbles by driving nominal interest rates on RMB assets down further.Because a floating(appreciating) exchange rate could attract even more hot money inflows,the People's Bank of China should focus on keeping the yuan/dollar rate stable so as to encourage naturally high wage increases to help balance China 's international competitiveness.However,further internationalization of the RMB,as with the proposed Shanghai pilot free trade zone,is best deferred until world interest rates rise to more normal levels. | Ronald McKinnon Gunther Schnabl | 2014 | China & World Economy2014，22，3： | 17 |
| 5 | Gut microbiota,fatty liver disease,and hepatocellular carcinoma显示文摘Intestinal bacteria contribute to the pathogenesis of non-alcoholic fatty liver disease(NAFLD).Recently developed microbial profiling techniques are beginning to shed light on the nature of the changes in the gut microbiota that accompany NAFLD and non-alcoholic steatohepatitis(NASH).In this review,we summarize the role of gut microbiota in the development of NAFLD,NASH,and hepatocellular carcinoma(HCC).We highlight the mechanisms by which gut microbiota contribute to NAFLD/NASH,including through alterations in gut epithelial permeability,choline metabolism,endogenous alcohol production,release of inflammatory cytokines,regulation of hepatic Toll-like receptor(TLR),and bile acid metabolism.In addition,we analyze possible mechanisms for enhanced hepatic carcinogenesis,including alterations in bile acid metabolism,release of inflammatory cytokines,and expression of TLR-4.Finally,we describe therapeutic approaches for NAFLD/NASH and preventive strategies for HCC involving modulation of the intestinal microbiota or affected host pathways.Although recent studies have provided useful information,large-scale prospective studies are required to better characterize the intestinal microbiota and metabolome,in order to demonstrate a causative role for changes in the gut microbiota in the etiology of NAFLD/NASH,to identify new therapeutic strategies for NAFLD/NASH,and to develop more effective methods of preventing HCC. | Huikuan Chu Brandon Williams Bernd Schnabl | 2018 | Liver Research2018，2，1： | 16 |
| 6 | 在与含酒精的肝疾病联系的肠的 microbiome 的细菌的 translocation 和变化显示文摘 Alcoholic liver disease progresses through several stages of tissue damage, from simple steatosis to alcoholic hepatitis, fibrosis, or cirrhosis. Alcohol also affects the intestine, increases intestinal permeability and changes the bacterial microflora. Liver disease severity correlates with levels of systemic bacterial products in patients, and experimental alcoholic liver disease is dependent on gut derived bacterial products in mice. Supporting evidence for the importance of bacterial translocation comes from animal studies demonstrating that intestinal decontamination is associated with decreased liver fibrogenesis. In addition, mice with a gene mutation or deletion encoding receptors for either bacterial products or signaling molecules downstream from these receptors, are resistant to alcohol-induced liver disease. Despite this strong association, the exact molecular mechanism of bacterial translocation and of how changes in the intestinal microbiome contribute to liver disease progression remains largely unknown. In this review we will summarize evidence for bacterial translocation and enteric microbial changes in response to alcoholic liver injury and chronic alcoholic liver disease. We will further describe consequences of intestinal dysbiosis on host biology. We finally discuss how therapeutic interventions may modify the gastrointestinal microflora and prevent or reduce alcoholic liver disease progression. | Arthur W Yan Bernd Schnabl | 2012 | World Journal of Hepatology2012，4，4： | 11 |
| 7 | Initiation of Setaria as a model plant显示文摘Model organisms such as Arabidopsis(Arabidopsis thaliana)and rice(Oryza sativa)have proven essential for efficient scientific discovery and development of new methods.With the diversity of plant lineages,some important processes such as C4 photosynthesis are not found in either Arabidopsis or rice,so new model species are needed.Due to their small diploid genomes,short life cycles,self-pollination,small adult statures and prolific seed production,domesticated foxtail millet(Setaria italica)and its wild ancestor,green foxtail(S.viridis),have recently been proposed as novel model species for functional genomics of the Panicoideae,especially for study of C4 photosynthesis.This review outlines the development of these species as model organisms,and discusses current challenges and future potential of a Setaria model. | Xianmin DIAO James SCHNABLE Jeffrey LBENNETZEN Jiayang LI | 2014 | Frontiers of Agricultural Science and Engineering2014，1，1： | 7 |
| 8 | Interactions Between the Intestinal Microbiome and Liver Diseases显示文摘 | Bernd Schnabl David A. Brenner | 2014 | Gastroenterology2014，，： | 7 |
| 9 | China’s financial conundrum and global imbalances显示文摘China’s financial conundrum arises from two sources: (1) its large trade (saving) surplus results in a currency mismatch because it is an immature creditor that cannot lend in its own currency. Instead foreign currency claims (largely dollars) build up within domestic financial institutions. And (2) economists – both American and Chinese – mistakenly attribute the surpluses to an undervalued renminbi. To placate the United States, the result is a gradual appreciation of the renminbi against the dollar of 6% or more per year. This predictable appreciation since 2004, and the fall in US interest rates since mid 2007, not only attracts hot money inflows but inhibits private capital outflows from financing China’s huge trade surplus. This one-way bet in the foreign exchange markets can no longer be offset by relatively low interest rates in China compared to the United States, as had been the case in 2005-06. Thus, the People’s Bank of China (PBOC) now must intervene heavily to prevent the renminbi from ratcheting upwards – and so becomes the country’s sole international financial intermediary. Despite massive efforts by the PBOC to sterilize the monetary consequences of the reserve buildup, inflation in China is increasing, with excess liquidity that spills over into the world economy. China has been transformed from a deflationary force on American and European price levels into an inflationary one. Because of the currency mismatch, floating the RMB is neither feasible nor desirable – and a higher RMB would not reduce China’s trade surplus. Instead, monetary control and normal private-sector finance for the trade surplus require a return to a credibly fixed nominal yuan/dollar rate similar to that which existed between 1995 and 2004. But for any newly reset yuan/dollar rate to be credible as a monetary anchor, foreign 'China bashing' to get the RMB up must end. Currency stabilization would allow the PBOC to regain monetary control and quash inflation. Only then can the Chinese government take decisive steps to reduce the trade (saving) surplus by tax cuts, increased social expenditures, and higher dividend payouts. But as long as the economy remains overheated, the government hesitates to take these trade-surplus-reduction measures because of their near-term inflationary consequences. | Ronald Mckinnon Gunther Schnabl | 2009 | China Economist2009，4，4： | 7 |
| 10 | Functional Divergence between Subgenomes anc Gene Pairs after Whole Genome Duplications显示文摘 | Zhikai Liang James C. Schnable | 2018 | Molecular Plant2018，11，3： | 4 |
| 11 | Toll-Like Receptor 9 Promotes Steatohepatitis by Induction of Interleukin-1β in Mice显示文摘 | Kouichi Miura Yuzo Kodama Sayaka Inokuchi Bernd Schnabl Tomonori Aoyama Hirohide Ohnishi Jerrold M. Olefsky David A. Brenner Ekihiro Seki | 2010 | Gastroenterology2010，，1： | 3 |
| 12 | Exchange Rate Regime, Financial Market Bubbles and Long-term Growth in China: Lessons from Japan显示文摘 | Gunther Schnabl | 2017 | China & World Economy2017，25，1： | 3 |
| 13 | Different effects of a CD14 gene polymorphism on disease outcome in patients with alcoholic liver disease and chronic hepatitis C infection显示文摘AIM: Clinical and experimental data suggest that gut-derived endotoxins are an important pathogenic factors for progression of chronic liver disease. Recently, a C-T (-159)polymorphism in the promoter region of the CD14 gene was detected and found to confer increased CD14 expression and to be associated with advanced alcoholic liver damage. Here, we investigated this polymorphism in patients with less advanced alcoholic liver disease (ALD)and chronic hepatitis C virus (HCV) infection.METHODS: CD14 genotyping was performed by PCR-RFLP analysis in (a) 121 HCV patients, (b) 62 patients with alcohol-associated cirrhosis (Alc-Ci), (c) 118 individuals with heavy alcohol abuse without evidence of advanced liver damage (Alc-w/o Ci), and (d) 247 healthy controls.Furthermore, serum levels of soluble CD14 (sCD14) and transaminases were determined.RESULTS: The TT genotype was significantly more frequent in Alc-Ci compared to Alc-w/o Ci or controls (40.3% vs 23.7% or 24.0%, respectively). In Alc-w/o Ci,serum levels of transaminases did not differ significantly between patients with different CD14 genotypes. In HCV patients, TT-homozygotes had significantly higher sCD14 levels and sCD14 serum levels were significantly higher in patients with advanced fibrosis or cirrhosis. However,no association was found between CD14 genotypes and histological staging or grading.CONCLUSION: Considering serum transaminases as surrogate markers for alcoholic liver damage, the CD14 polymorphism seems to exhibit different effects during the course of ALD. Differences in genotype distribution between cirrhotic HCV patients and alcoholics and the known functional impact of this polymorphism on CD14 expression levels further indicate differences in the pathophysiological role of CD14 and CD14-mediated lipopolysaccharides signal transduction with regard to the stage as well as the type of the underlying liver disease. | C Meiler M Mühlbauer M Johann A Hartmann B Schnabl N Wodarz G Schmitz J Schlmerich C Hellerbrand | 2005 | World Journal of Gastroenterology2005，11，38： | 3 |
| 14 | Increased catabolism and decreased unsaturation of ganglioside in patients with inflammatory bowel disease显示文摘AIM: To investigate whether accelerated catabolism of ganglioside and decreased ganglioside content contribute to the etiology of pro-inflammatory intestinal disease. METHODS: Intestinal mucosa from terminal ileum or colon was obtained from patients with ulcerative colitis or inflammatory Crohn's disease(n = 11) undergoing bowel resection and compared to control samples of normal intestine from patients with benign colon polyps(n = 6) and colorectal cancer(n = 12) in this observational case-control study. Gangliosides and phospholipids of intestinal mucosa were characterized by class and ceramide or fatty acid composition using liquid chromatography triple-quad mass spectrometry. Content and composition of ganglioside classes GM1, GM3, GD3, GD1 a, GT1 and GT3 were compared among subject groups. Content and composition of phospholipid classes phosphatidylcholine(PC) and phosphatidylethanolamine were compared among subject groups. Unsaturation index of individual ganglioside and phospholipid classes was computed and compared among subject groups. Ganglioside catabolism enzymes beta-hexosaminidase A(HEXA) and sialidase-3(NEU3) were measured in intestinal mucosa using western blot and compared among subject groups. RESULTS: Relative GM3 ganglioside content was 2-fold higher(P < 0.05) in intestine from patients with inflammatory bowel disease(IBD) compared to control intestine. The quantity of GM3 and ratio of GM3/GD3 was also higher in IBD intestine than control tissue(P < 0.05). Control intestine exhibited 3-fold higher(P < 0.01) relative GD1 a ganglioside content than IBD intestine. GD3 and GD1 a species of ganglioside containing three unsaturated bonds were present in control intestine, but were not detected in IBD intestine. The relative content of PC containing more than two unsaturated bonds was 30% lower in IBD intestine than control intestine(P < 0.05). The relative content of HEXA in IBD intestine was increased 1.7-fold(P < 0.05) and NEU3 was increased 8.3-fold(P < 0.01) compared to normal intestine. Intestinal mucosa in IBD is characterized by increased GM3 content, decreased GD1 a, and a reduction in polyunsaturated fatty acid constituents in GD3, GD1 a and PC.CONCLUSION: This study suggests a new paradigm by proposing that IBD occurs as a consequence of increased metabolism of specific gangliosides. | John J Miklavcic Glen K Shoemaker Vera C Mazurak M Tom Clandinin Tasha DL Hart Kareena L Schnabl Gordon M Lees Bodil MK Larsen Oliver F Bathe Alan BR Thomson M Tom Clandinin | 2015 | World Journal of Gastroenterology2015，21，35： | 3 |
| 15 | Histone Lysine Methyltransferase SDG8 Is Involved in Brassinosteroid-Regulated Gene Expression in Arabidopsis thaliana显示文摘植物类固醇荷尔蒙, brassinosteroids (BR ) ,在植物生长,开发,和对 environmentalstresses 的回答起重要作用。BR 通过对血浆膜和另外的发信号的部件局部性的受体发信号调整抄写因素的 BES1/BZR1family,它调制几千基因的表示。BES1/BZR1 和他们的 interactingproteins 怎么工作调整基因的大数字,完全没被理解。这里,我们报导那 histone lysinemethyltransferase SDG8,在 histone 含有 3 离氨酸 36 di- 和 trimethylation (H3K36me2 和 me3 ) ,涉及 BR-regulatedgene 表示。BES1 与 SDG8 交往,直接或间接地通过 IWS1,抄写延伸因素 involvedin 调整 BR 的基因表示。猛烈变异的 sdg8 与损害 BR 回答显示减少的生长显型。全球基因表示研究表明了那, whileBR 在野类型的植物调整大约 5000 基因,荷尔蒙在 sdg8 比 700 基因调整少数变异。另外,多于调整 BR 的基因的一半,差别在 sdg8 异种被影响。一个染色质 Immunoprecipitation (薄片) 实验证明 H3K36me3 在 sdg8 异种在调整 BR 的基因被减少。把结果基于这些,我们建议 SDG8 在调停起一个必要作用调整 BR 的基因表示。Ourresults 因此揭示 histone 修正由支配基因 expression.Key 词的神经质的规定的主要机制: | Xiaolei Wang Jiani Chen Zhouli Xie Sanzhen Liu Trevor Nolan Huaxun Ye Mingcai Zhang Hongqing Guo Patrick S. Schnable Zhaohu Li Yanhai Yin | 2014 | Molecular Plant2014，7，8： | 3 |
| 16 | Toll-Like Receptor 2–Mediated Intestinal Injury and Enteric Tumor Necrosis Factor Receptor I Contribute to Liver Fibrosis in Mice显示文摘 | Phillipp Hartmann Michael Haimerl Magdalena Mazagova David A. Brenner Bernd Schnabl | 2012 | Gastroenterology2012，，5： | 2 |
| 17 | Floret-specific differences in gene expression and support for the hypothesis that tapetal degeneration of Zea mays L. occurs via programmed cell death显示文摘The maize (Zea mays) spikelet consists of two florets, each of which contains three developmentally synchronized anthers. Morpho-logically, the anthers in the upper and lower florets proceed through apparently similar developmental programs. To test for global differences in gene expression and to identify genes that are coordinately regulated during maize anther development, RNA samples isolated from upper and lower floret anthers at six developmental stages were hybridized to cDNA microarrays. Approximately 9% of the tested genes exhibited statistically significant differences in expression between anthers in the upper and lower florets. This finding indicates that several basic biological processes are differentially regulated between upper and lower floret anthers, including metabolism, protein synthesis and signal transduction. Genes that are coordinately regulated across anther development were identified via cluster analysis. Analysis of these results identified stagespecific, early in development, late in development and biphasic expression profiles. Quantita-tive RT-PCR analysis revealed that four genes whose homologs in other plant species are involved in programmed cell death are upregulated just prior to the time the tapetum begins to visibly degenerate (i.e., the mid-microspore stage). This finding supports the hypothesis that developmentally normal tapetal degeneration occurs via programmed cell death. | David S. Skibbe Xiujuan Wang Lisa A. Borsuk Daniel A. Ashlock Dan Nettleton Patrick S. Schnable | 2008 | Journal of Genetics and Genomics2008，35，10： | 2 |
| 18 | Early clinical worsening in patients with TIA or minor stroke: The Austrian Stroke Unit Registry显示文摘 | J Ferrari M Knoflach S Kiechl J Willeit S Schnabl L Seyfang W Lang | 2010 | Neurology2010，，2： | 2 |
| 19 | Role of innate immunity and the microbiota in liver fibrosis: crosstalk between the liver and gut 显示文摘 | Seki E Schnabl B | 2012 | J Physiol2012，590，3： | 1 |
| 20 | Gangliosides protect bowel in an infant model of necrotizing enterocolitis by suppressing proinflammatory signals 显示文摘 | Schnabl KL Larsen B Van Aerde JE | 2009 | J Pediatr Gas- troenterol Nutr2009，49，4： | 1 |
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