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| 1 | Cirrhotic portal hypertension: From pathophysiology to novel therapeutics显示文摘Portal hypertension and bleeding from gastroesophageal varices is the major cause of morbidity and mortality in patients with cirrhosis. Portal hypertension is initiated by increased intrahepatic vascular resistance and a hyperdynamic circulatory state. The latter is characterized by a high cardiac output, increased total blood volume and splanchnic vasodilatation, resulting in increased mesenteric blood flow. Pharmacological manipulation of cirrhotic portal hypertension targets both the splanchnic and hepatic vascular beds. Drugs such as angiotensin converting enzyme inhibitors and angiotensin Ⅱ type receptor 1 blockers, which target the components of the classical renin angiotensin system(RAS), are expected to reduce intrahepatic vascular tone by reducing extracellular matrix deposition and vasoactivity of contractile cells and thereby improve portal hypertension. However, these drugs have been shown to produce significant offtarget effects such as systemic hypotension and renal failure. Therefore, the current pharmacological mainstay in clinical practice to prevent variceal bleeding and improving patient survival by reducing portal pressure is non-selective-blockers(NSBBs). These NSBBs work by reducing cardiac output and splanchnic vasodilatation but most patients do not achieve an optimal therapeutic response and a significant proportion of patients are unable to tolerate these drugs.Although statins, used alone or in combination with NSBBs, have been shown to improve portal pressure and overall mortality in cirrhotic patients, further randomized clinical trials are warranted involving larger patient populations with clear clinical end points. On the other hand, recent findings from studies that have investigated the potential use of the blockers of the components of the alternate RAS provided compelling evidence that could lead to the development of drugs targeting the splanchnic vascular bed to inhibit splanchnic vasodilatation in portal hypertension. This review outlines the mechanisms related to the pathogenesis of portal hypertension and attempts to provide an update on currently available therapeutic approaches in the management of portal hypertension with special emphasis on how the alternate RAS could be manipulated in our search for development of safe, specific and effective novel therapies to treat portal hypertension in cirrhosis. | Lakmie S Gunarathne Harinda Rajapaksha Nicholas Shackel Peter W Angus Chandana B Herath | 2020 | World Journal of Gastroenterology2020，26，40： | 24 |
| 2 | Sharing Clinical Trial Data: A Proposal from the International Committee of Medical Journal Editors显示文摘The International Committee of Medical Journal Editors (ICMJE) believes that there is an ethical obligation to responsibly share data generated by interventional clinical trials because participants have put themselves at risk.In a growing consensus,many funders around the world-foundations,government agencies,and industry-now mandate data sharing.Here,we outline ICMJE's proposed requirements to help meet this obligation.We encourage feedback on the proposed requirements.Anyone can provide feedback at www.icmje.org by April 18,2016. | Darren B Taichman Joyce Backus Christopher Baethge Howard Bauchner Peter W de Leeuw Jeffrey M Drazen John Fletcher Frank Frizelle Irish Groves Abraham Haileamlak Astrid James Christine Laine Larry Peiperl Anja Pinborg Peush Sahni Si-Nan Wu | 2016 | Chinese Medical Journal2016，，2： | 20 |
| 3 | Diagnostic and prognostic potential of tissue and circulating long non-coding RNAs in colorectal tumors显示文摘Long non-coding RNAs(lncRNAs)are members of the non-protein coding RNA family longer than 200 nucleotides.They participate in the regulation of gene and protein expression influencing apoptosis,cell proliferation and immune responses,thereby playing a critical role in the development and progression of various cancers,including colorectal cancer(CRC).As CRC is one of the most frequently diagnosed malignancies worldwide with high mortality,its screening and early detection are crucial,so the identification of disease-specific biomarkers is necessary.LncRNAs are promising candidates as they are involved in carcinogenesis,and certain lncRNAs(e.g.,CCAT1,CRNDE,CRCAL1-4)show altered expression in adenomas,making them potential early diagnostic markers.In addition to being useful as tissue-specific markers,analysis of circulating lncRNAs(e.g.,CCAT1,CCAT2,BLACAT1,CRNDE,NEAT1,UCA1)in peripheral blood offers the possibility to establish minimally invasive,liquid biopsy-based diagnostic tests.This review article aims to describe the origin,structure,and functions of lncRNAs and to discuss their contribution to CRC development.Moreover,our purpose is to summarise lncRNAs showing altered expression levels during tumor formation in both colon tissue and plasma/serum samples and to demonstrate their clinical implications as diagnostic or prognostic biomarkers for CRC. | Orsolya Galamb Barbara K Barták Alexandra Kalmár Zsófia B Nagy Krisztina A Szigeti Zsolt Tulassay Peter Igaz Béla Molnár | 2019 | World Journal of Gastroenterology2019，25，34： | 18 |
| 4 | Probiotic effects on intestinal fermentation patterns in patients with irritable bowel syndrome显示文摘AIM: To determine whether Lactobacillus casei strain Shirota (Yakult ) can alter small intestinal bacterial overgrowth (SIBO), as tested by the lactulose breath test, and whether this is associated with changes in symptoms in irritable bowel syndrome (IBS). METHODS: 18 patients with IBS (Rome Ⅱ criteria), who showed an early rise in breath hydrogen with lactulose (ERBHAL), consumed 65 mL of Yakult daily for 6 wk. Lactulose breath test was repeated at the end of the treatment period. Symptoms were recorded daily using a 10 cm visual analogue scale. RESULTS: 14 patients completed the study, 9 (64%) had reversal of ERBHAL, with the median time of f irst rise in breath hydrogen increasing from 45 to 75 min (P = 0.03). There was no signifi cant improvement in the symptom score with probiotic therapy, except for wind (P=0.04). Patients commencing with at least moderate symptoms and who no longer had ERBHAL at the end of treatment, showed improvement in the overall symptoms scores [median fi nal score 5.3 (IQR3.9-5.9), 55% reduction; n=6] to a greater extent than those who had had persisting ERBHAL [final score 6.9 (5.0-7.0), 12% reduction; n = 5; P = 0.18]. CONCLUSION: Yakult is effective in altering fermentation patterns in the small bowel, consistent with reducing SIBO. The loss of ERBHAL was associated with reduced symptoms. The true interpretation of these fi ndings awaits a randomised, controlled trial. | Jacqueline S Barrett Kim EK Canale Richard B Gearry Peter M Irving Peter R Gibson | 2008 | World Journal of Gastroenterology2008，14，32： | 16 |
| 5 | Percutaneous left atrial appendage closure:Technical aspects and prevention of periprocedural complications with the watchman device显示文摘Transcatheter closure of the left atrial appendage has been developed as an alternative to chronic oral anticoagulation for stroke prevention in patients with atrial fibrillation, and as a primary therapy for patients with contraindications to chronic oral anticoagulation. The promise of this new intervention compared with warfarin has been supported by several, small studies and two pivotal randomized trial with the Watchman Device. The results regarding risk reduction for stroke have been favourable although acute complications were not infrequent. Procedural complications, which are mainly related to transseptal puncture and device implantation, include air embolism, pericardial effusions/tamponade and device embolization. Knowledge of nature, management and prevention of complications should minimize the risk of complications and allow transcatheter left atrial appendage closure to emerge as a therapeutic option for patients with atrial fibrillation at risk for cardioembolic stroke. | Sven M bius-Winkler Nicolas Majunke Marcus Sandri Norman Mangner Axel Linke Gregg W Stone Ingo D hnert Gerhard Schuler Peter B Sick | 2015 | World Journal of Cardiology2015，7，2： | 14 |
| 6 | Identification of CD13,CD107a,and CD164 as novel basophil-activation markers and dissection of two response patterns in time kinetics of IgE-de-pendent upregulation显示文摘Using two-colour flow cytometry >200 antibodies submitted to the 8th International Workshop of Human Leukocyte Differentiation Antigens (HLDA8) have been analyzed for their reactivity with resting and activated CD203c+ basophils. Four antibodies either non-reactive or weakly reactive with resting basophils exhibited an increased reactivity with basophils activated by anti-IgE-mediated cross-linking of the high affinity IgE receptor (FcεRI). These include antibod- ies against CD164 (WS-80160, clone N6B6 and WS-80162, clone 67D2), as well as two reagents with previously unknown specificities that were identified as CD13 (WS-80274, clone A8) and CD107a (WS-80280, clone E63-880). The activation patterns followed either the “CD203c-like” or “CD63-like” activation profile. The CD203c profile is characterized by a rapid and significant upregulation (of CD13, CD164, and CD203c), reaching maximum levels after 5- 15 min of stimulation. The phosphoinositide-3-kinase (PI3K)-specific inhibitor wortmannin inhibited the upregulation of these markers whereas 12-O-tetradecanoyl-phorbol-13-acetate (TPA) induced a rapid and FcεRI-independent upregulation within 1-2 min. In the CD63 profile, maximum upregulation (of CD63 and CD107a) was detected only after 20-40 min, and upregulation by TPA reached maximum levels after 60 min. In summary, our data identify CD13, CD107a, and CD164 as novel basophil-activation antigens. Based on time kinetics of upregulation, we hypothesize that molecules of the “CD203c group” and the “CD63 group” are linked to two different mechanisms of basophil activation. | Florian HENNERSDORF Stefan FLORIAN Andreas JAKOB Katharina BAUMGRTNER Karoline SONNECK Alfred NORDHEIM Tilo BIEDERMANN Peter VALENT Hans-Jrg BüHRING | 2005 | Cell Research2005，15，5： | 9 |
| 7 | Therapeutic potential of targeting the renin angiotensin system in portal hypertension显示文摘Portal hypertension is responsible for the bulk of the morbidity and mortality in patients with cirrhosis.Drug therapy to reduce portal pressure involves targeting two vascular beds.The first approach is to reduce intra hepatic vascular tone induced by the activity of powerful vasocontrictors such as angiotensin Ⅱ,endothelin-1 and the sympathetic system and mediated via contraction of perisinusoidal myofibroblasts and pervascular smooth muscle cells.The second approach is to reduce mesenteric and portal blood flow.Non-selective b-blockers are widely used and have been shown to prolong patient survival and reduce oesophageal variceal bleeding in advanced cirrhosis.However many patients are unable to tolerate these drugs and they are ineffective in a significant proportion of patients.Unfortunately there are no other drug therapies that have proven efficacy in the treatment of portal hypertension and prevention of variceal bleeding.This review briefly outlines current therapeutic approaches to themanagement of portal hypertension,and the evidence supporting the role of the renin angiotensin system(RAS) and the use of RAS blockers in this condition.It will also outline recent advances in RAS research that could lead to the development of new treatments focusing in particular on the recently discovered 'alternate axis' of the RAS. | Chandana B Herath Josephine A Grace Peter W Angus | 2013 | World Journal of Gastrointestinal Pathophysiology2013，4，1： | 9 |
| 8 | Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease显示文摘AIM To determine if manipulation of dietary advanced glycation end product(AGE), intake affects nonalcoholic fatty liver disease(NAFLD) progression and whether these effects are mediated via RAGE. METHODS Male C57Bl6 mice were fed a high fat, high fructose, high cholesterol(HFHC) diet for 33 wk and compared with animals on normal chow. A third group were given a HFHC diet that was high in AGEs. Another group was given a HFHC diet that was marinated in vinegar to prevent the formation of AGEs. In a second experiment, RAGE KO animals were fed a HFHC diet or a high AGE HFHC diet and compared with wildtype controls. Hepatic biochemistry, histology, picrosirius red morphometry and hepatic mR NA were determined. RESULTS Long-term consumption of the HFHC diet generated significant steatohepatitis and fibrosis after 33 wk. In this model, hepatic 4-hydroxynonenal content(a marker of chronic oxidative stress), hepatocyte ballooning, picrosirius red staining, α-smooth muscle actin and collagen type 1A gene expression were all significantly increased. Increasing the AGE content of the HFHC diet by baking further increased these markers of liver damage, but this was abrogated by pre-marination in acetic acid. In response to the HFHC diet, RAGE-/-animals developed NASH of similar severity to RAGE+/+ animals but were protected from the additional harmful effects of the high AGE containing diet. Studies in isolated Kupffer cells showed that AGEs increase cell proliferation and oxidative stress, providing a likely mechanism through which these compounds contribute to liver injury. CONCLUSION In the HFHC model of NAFLD, manipulation of dietary AGEs modulates liver injury, inflammation, and liver fibrosis via a RAGE dependent pathway. This suggests that pharmacological and dietary strategies targeting the AGE/RAGE pathway could slow the progression of NAFLD. | Christopher Leung Chandana B Herath Zhiyuan Jia Sof Andrikopoulos Bronwyn E Brown Michael J Davies Leni R Rivera John B Furness Josephine M Forbes Peter W Angus | 2016 | World Journal of Gastroenterology2016，22，35： | 7 |
| 9 | Association between calcium sensing receptor gene polymorphisms and chronic pancreatitis in a US population:Role of serine protease inhibitor Kazal 1type and alcohol显示文摘AIM: To test the hypothesis that calcium sensing receptor (CASR) polymorphisms are associated with chronic pancreatitis (CP), and to determine whether serine protease inhibitor Kazal 1type (SPINK1) N34S oralcohol are necessary co-factors in its etiology. METHODS: Initially, 115 subjects with pancreatitis and 66 controls were evaluated, of whom 57 patients and 21 controls were predetermined to carry the high-risk SPINK1 N34S polymorphism. We sequenced CASR gene exons 2, 3, 4, 5 and 7, areas containing the majority of reported polymorphisms and novel mutations. Based on the initial results, we added 223 patients and 239 controls to analyze three common nonsynonymous single nucleotide polymorphisms (SNPs) in exon 7 (A986S, R990G, and Q1011E). RESULTS: The CASR exon 7 R990G polymorphism was signifi cantly associated with CP (OR, 2.01; 95% CI, 1.12-3.59; P = 0.015). The association between CASR R990G and CP was stronger in subjects who reported moderate or heavy alcohol consumption (OR, 3.12; 95% CI, 1.14-9.13; P = 0.018). There was no association between the various CASR genotypes and SPINK1 N34S in pancreatitis. None of the novel CASR polymorphisms reported from Germany and India was detected. CONCLUSION: Our United States-based study confirmed an association of CASR and CP and for the first time demonstrated that CASR R990G is a signifi cant risk factor for CP. We also conclude that the risk of CP with CASR R990G is increased in subjects with moderate to heavy alcohol consumption. | Venkata Muddana Janette Lamb Julia B Greer Beth Elinoff Robert H Hawes Peter B Cotton Michelle A Anderson Randall E Brand Adam Slivka David C Whitcomb | 2008 | World Journal of Gastroenterology2008，14，28： | 7 |
| 10 | Standard forward-viewing colonoscopy versus full-spectrum endoscopy: an international, multicentre, randomised, tandem colonoscopy trial显示文摘 | Ian M Gralnek Peter D Siersema Zamir Halpern Ori Segol Alaa Melhem Alain Suissa Erwin Santo Alan Sloyer Jay Fenster Leon M G Moons Vincent K Dik Ralph B D’Agostino Douglas K Rex | 2014 | Lancet Oncology2014，，3： | 6 |
| 11 | Management of Hyperglycemia in Type 2 Diabetes: A Patient-Centered Approach: Position Statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD)显示文摘 | Inzucchi Silvio E Bergenstal Richard M Buse John B Diamant Michaela Ferrannini Ele Nauck Michael Peters Anne L Tsapas Apostolos Wender Richard Matthews David R | 2012 | EN2012，，3： | 6 |
| 12 | Intermittent energy restriction in type 2 diabetes: A short discussion of medication management显示文摘AIM To discuss type 2 diabetes mellitus(T2DM) medication changes required during the popular 5:2 intermittent energy restriction(IER) diet. METHODS A search was conducted in MEDLINE, EMBASE, AMED, CINAHL and Cochrane library for original research articles investigating the use of very low calorie diets(VLCD) in people with T2 DM. The search terms used included 'VLCD' or 'very low energy diet' or 'very low energy restriction' or 'IER' or 'intermittent fasting' or 'calorie restriction' or 'diabetes mellitus type 2' and 'type 2 diabetes'. Reference lists of selected articles were also screened for relevant publications. Only research articles written in English, which also included an explanation of medication changes were included. A recent pilot trial using the 5:2 IER method, conducted by our research group, will also be summarized.RESULTS A total of 8 studies were found that investigated the use of VLCD in T2 DM and discussed medication management. Overall these studies indicate that the use of a VLCD for people with T2 DM usually require the cessation of medication to prevent hypoglycemia. Therefore, the 5:2 IER method will also require medication changes, but as seen in our pilot trial, may not require total cessation of medication, rather a cessation on the 2 IER days only. CONCLUSION Guidelines outlined here can be used in the initial stages of a 2-d IER diet, but extensive blood glucose monitoring is still required to make the necessary individual reductions to medications in response to weight loss. | Sharayah Carter Peter M Clifton Jennifer B Keogh | 2016 | World Journal of Diabetes2016，7，20： | 6 |
| 13 | Cyclin A2:At the crossroads of cell cycle and cell invasion显示文摘Cyclin A2 is an essential regulator of the cell division cycle through the activation of kinases that participate to the regulation of S phase as well as the mitotic entry. However,whereas its degradation by the proteasome in mid mitosis was thought to be essential for mitosis to proceed,recent observations show that a small fraction of cyclin A2 persists beyond metaphase and is degraded by autophagy. Its implication in the control of cytoskeletal dynamics and cell movement has unveiled its role in the modulation of Rho A activity. Since this GTPase is involved in both cell rounding early in mitosis and later,in the formation of the cleavage furrow,this suggests that cyclin A2 is a novel actor in cytokinesis. Taken together,these data point to this cyclin as a potential mediator of cell-niche interactions whose dysregulation could be taken as a hallmark of metastasis. | Abdelhalim Loukil Caroline T Cheung Nawal Bendris Bénédicte Lemmers Marion Peter Jean Marie Blanchard | 2015 | World Journal of Biological Chemistry2015，6，4： | 6 |
| 14 | Burden of Clostridium difficile infection between 2010 and 2013:Trends and outcomes from an academic center in Eastern Europe显示文摘AIM:To analyze the incidence and possible risk factors in hospitalized patients treated with Clostridium difficile infection(CDI).METHODS:A total of 11751 patients were admitted to our clinic between 1 January 2010 and 1 May2013.Two hundred and forty-seven inpatients were prospectively diagnosed with CDI.For the risk analysis a 1:3 matching was used.Data of 732 patients matched for age,sex,and inpatient care period and unit were compared to those of the CDI population.Inpatient records were collected from an electronic hospital database and comprehensively reviewed.RESULTS:Incidence of CDI was 21.0/1000 admissions(2.1%of all-cause hospitalizations and 4.45%of total inpatient days).The incidence of severe CDI was 12.6%(2.63/1000 of all-cause hospitalizations).Distribution of CDI cases was different according to the unit type,with highest incidence rates in hematology,gastroenterology and nephrology units(32.9,25 and24.6/1000 admissions,respectively) and lowest rates in 1.4%(33/2312) in endocrinology and general internal medicine(14.2 and 16.9/1000 admissions)units.Recurrence of CDI was 11.3%within 12 wk after discharge.Duration of hospital stay was longer in patients with CDI compared to controls(17.6 ± 10.8d vs 12.4 ± 7.71 d).CDI accounted for 6.3%of allinpatient deaths,and 30-d mortality rate was 21.9%(54/247 cases).Risk factors for CDI were antibiotic therapy[including third-generation cephalosporins or fluoroquinolones,odds ratio(OR) = 4.559;P < 0.001],use of proton pump inhibitors(OR = 2.082,P< 0.001),previous hospitaiization within 12 mo(OR = 3.167,P < 0.001),previous CDI(OR = 15.32;P < 0.001),while presence of diabetes mellitus was associated with a decreased risk for CDI(OR = 0.484;P< 0.001).Treatment of recurrent cases was significantly different from primary infections with more frequent use of vancomycin alone or in combination(P < 0.001),and antibiotic therapy duration was longer(P < 0.02).Severity,mortality and outcome of primary infections and relapsing cases did not significantly differ.CONCLUSION:CDI was accounted for significant burden with longer hospitaiization and adverse outcomes.Antibiotic,PPI therapy and previous hospitaiization or CDI were risk factors for CDI. | Zsuzsanna Kurti Barbara D Lovasz Michael D Mandel Zoltan Csima Petra A Golovics Bence D Csako Anna Mohas Lorant Gnczi Krisztina B Gecse Lajos S Kiss Miklos Szathmari Peter L Lakatos | 2015 | World Journal of Gastroenterology2015，21，21： | 6 |
| 15 | 温度限制串联相关神经网络及其在细菌辨识中的应用显示文摘蛋白质在微生物研究中可用作生物标记物, 故在生物技术中其表征工作很重要. 各种质谱技术已被用于细菌的表征[1~3]. 1994年, Cain等[4]首先报道了将色谱和基体辅助激光解离/电离飞行时间质谱(MALDI-TOF-MS)用于细菌的辨识. Holland等[5]采用高质量离子MALDI-TOF-MS对细菌全细胞进行辨识. 最近, Lay[6]对该技术的细菌辨识做了综述. MALDI-TOF-MS是目前对细菌全细胞分析的最佳手段. | 张卓勇 Aaron Urbas Peter de B Harrington Kent J.Voorhees Jon Rees | 2002 | 高等学校化学学报2002，23，4： | 4 |
| 16 | Ruptured angiosarcoma of the liver treated by emergency catheter-directed embolization显示文摘血管肉瘤是有差的预后的肝的一个稀罕的主要的恶意的瘤。这里,我们与被紧急情况对待的一个破裂的肝的血管肉瘤报导一个病人的一个案例指导导管的 embolization,由左边的偏身出汗列在后面。 | Christine Leowardi Yura Hormann UIf Hinz Moritz N Wente Peter Hallscheidt Christa Flechtenmacher Markus W Büchler Helmut Friess Matthias HM Schwarzbach | 2006 | World Journal of Gastroenterology2006，12，5： | 4 |
| 17 | A systematic review and meta-analysis of laparoscopic versus open distal pancreatectomy for benign and malignant lesions of the pancreas: It’s time to randomize显示文摘 | Arianeb Mehrabi Mohammadreza Hafezi Jalal Arvin Majid Esmaeilzadeh Camelia Garoussi Golnaz Emami Julia K?ssler-Ebs Beat Peter Müller-Stich Markus W. Büchler Thilo Hackert Markus K. Diener | 2014 | Surgery2014，，： | 4 |
| 18 | Participation of CD45,NKR-P1A and ANK61 antigen in rat hepatic NK cell(pit cell)-mediated target cell cytotoxicity显示文摘AIM Several triggering receptors have beendescribed to be involved in natural killer(NK)cell-mediated target cytotoxicity.In these studies,NKcells derived from blood or spleen were used.Pitcells are liver-specific NK cells that possess ahigher level of natural cytotoxicity and a differentmorphology when compared to blood NK cells.The aim of this study was to characterize the roleof the NK-triggering molecules NKR-P1A,ANK61antigen,and CD45 in pit cell-mediated killing oftarget cells.METHODS 51Cr-release and DNA fragmentationwere used to quantify target cell lysis andapoptosis,respectively.RESULTS Flow cytometric analysis showed thatpit cells expressed CD45,NKR-P1A,and ANK61antigen.Treatment of pit cells with monoclonalantibody(mAb)to CD45(ANK74)not onlyinhibited CC531s or YAC-1 target lysis but alsoapoptosis induced by pit cells.The mAbs to NKR-P1A(3.2.3)and ANK61 antigen(ANK61)had no effect on pit cell-mediated CC531s or YAC-1 targetcytolysis or apoptosis,while they did increase theFcγ receptor positive(FcγR+)P815 cytolysis andapoptosis.This enhanced cytotoxicity could beinhibited by 3,4-dichloroisocoumarin,an inhibitorof granzymes.CONCLUSION These results indicate that CD45participates in pit cell-mediated CC531s and YAC-1target cytolysis and apoptosis.NKR-P1A andANK61 antigen on pit cells function as activationstructures against FcγR+ P815 cells,which wasmediated by the perforin/granzyme pathway. | David Vermiilen Bülent Ahishali Vasilis Triantis Karin Vanderkerken Peter J. K.Kuppen Eddie Wisse | 2000 | World Journal of Gastroenterology2000，6，4： | 4 |
| 19 | Biological therapy in inflammatory bowel diseases:Access in Central and Eastern Europe显示文摘Biological drugs opened up new horizons in the management of inflammatory bowel diseases(IBD).This study focuses on access to biological therapy in IBD patients across 9 selected Central and Eastern European(CEE)countries,namely Bulgaria,the Czech Republic,Estonia,Hungary,Latvia,Lithuania,Poland,Romania and Slovakia.Literature data on the epidemiology and disease burden of IBD in CEE countries was systematically reviewed.Moreover,we provide an estimation on prevalence of IBD as well as biological treatment rates.In all countries with the exception of Romania,lower biological treatment rates were observed in ulcerative colitis(UC)compared to Crohn’s disease despite the higher prevalence of UC.Great heterogeneity(up to 96-fold)was found in access to biologicals across the CEE countries.Poland,Bulgaria,Romania and the Baltic States are lagging behind Hungary,Slovakia and the Czech Republic in their access to biologicals.Variations of reimbursement policy may be one of the factors explaining the differences to a certain extent in Bulgaria,Latvia,Lithuania,and Poland,but association with other possible determinants(differences in prevalence and incidence,price of biologicals,total expenditure on health,geographical access,and cost-effectiveness results)was not proven.We assume,nevertheless,that healthdeterioration linked to IBD might be valued differently against other systemic inflammatory conditions in distinct countries and which may contribute to the immense diversity in the utilization of biological drugs for IBD.In conclusion,access to biologicals varies widely among CEE countries and this difference cannot be explained by epidemiological factors,drug prices or total health expenditure.Changes in reimbursement policy could contribute to better access to biologicals in some countries. | Fanni Rencz Márta Péntek Martin Bortlik Edyta Zagorowicz Tibor Hlavaty Andrzej Sliwczyński Mihai M Diculescu Limas Kupcinskas Krisztina B Gecse László Gulácsi Peter L Lakatos | 2015 | World Journal of Gastroenterology2015，21，6： | 4 |
| 20 | Ischemia/Reperfusion Injury in Liver Surgery and Transplantation: Pathophysiology显示文摘 | Kilian Weigand Sylvia Brost Niels Steinebrunner Markus Büchler Peter Schemmer Martina Müller John J. Lemasters | 2012 | HPB Surgery2012，，： | 4 |
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