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| 1 | Clinically detected gastroenteropancreatic neuroendocrine tumors are on the rise: Epidemiological changes in Germany显示文摘AIM:To study the epidemiologic changes of gastroenteropancreatic neuroendocrine tumors(GEP-NET)in Germany,we analyzed two time periods 1976-1988 and1998-2006.METHODS:We evaluated epidemiological data of GEP-NET from the former East German National Cancer Registry(DDR Krebsregister,1976-1988)and its successor,the Joint Cancer Registry(GKR,1998-2006),which was founded after German reunification.Due to a particularly substantial database the epidemiological data from the federal states of Mecklenburg-Western Pomerania,Saxony,Brandenburg and Thuringia,covering a population of more than 10.8 million people,were analyzed.Survival probabilities were calculated using life table analysis.In addition,GEP-NET patients were evaluated for one or more second(non-GEP-NET)primary malignancies.RESULTS:A total of 2821 GEP neuroendocrine neoplasms were identified in the two registries.The overall incidence increased significantly between 1976 and2006 from 0.31(per 100.000 inhabitants per year)to2.27 for men and from 0.57 to 2.38 for women.In the later period studied(2004-2006),the small intestine was the most common site.Neuroendocrine(NE)neoplasms of the small intestine showed the largest absolute increase in incidence,while rectal NE neoplasms exhibited the greatest relative increase.Only the incidence of appendiceal NET in women showed little change between 1976 and 2006.Overall survival of patients varied for sex,tumor site and the two periods studied but improved significantly over time.Interestingly,about 20%of the GEP-NET patients developed one or more second malignancies.Their most common location was the gastrointestinal tract.GEP-NET patients without second malignancies fared better than those with one or more of them.CONCLUSION:The number of detected GEP-NET increased about 5-fold in Germany between 1976 and2006.At the same time,their anatomic distribution changed,and the survival of GEP-NET patients improved significantly.Second malignancies are common and influence the overall survival of GEP-NET patients.Thus,GEP-NET warrant our attention as well as intensive research on their tumorigenesis. | Hans Scherübl Brigitte Streller Roland Stabenow Hermann Herbst Michael Hopfner Christoph Schwertner Joachim Steinberg Jan Eick Wanda Ring Krishna Tiwari Soren M Zappe | 2013 | World Journal of Gastroenterology2013，19，47： | 16 |
| 2 | Systematic mechanism-orientated approach to chronic pancreatitis pain显示文摘Pain in chronic pancreatitis(CP) shows similarities with other visceral pain syndromes(i.e.,inflammatory bowel disease and esophagitis),which should thus be managed in a similar fashion.Typical causes of CP pain include increased intrapancreatic pressure,pancreatic inflammation and pancreatic/extrapancreatic complications.Unfortunately,CP pain continues to be a major clinical challenge.It is recognized that ongoing pain may induce altered central pain processing,e.g.,central sensitization or pro-nociceptive pain modulation.When this is present conventional pain treatment targeting the nociceptive focus,e.g.,opioid analgesia or surgical/endoscopic intervention,often fails even if technically successful.If central nervous system pain processing is altered,specific treatment targeting these changes should be instituted(e.g.,gabapentinoids,ketamine or tricyclic antidepressants).Suitable tools are now available to make altered central processing visible,including quantitative sensory testing,electroencephalograpy and(functional) magnetic resonance imaging.These techniques are potentially clinically useful diagnostic tools to analyze central pain processing and thus define optimum management approaches for pain in CP and other visceral pain syndromes.The present review proposes a systematic mechanism-orientated approach to pain management in CP based on a holistic view of the mechanisms involved.Future research should address the circumstances under which central nervous system pain processing changes in CP,and how this is influenced by ongoing nociceptive input and therapies.Thus we hope to predict which patients are at risk for developing chronic pain or not responding to therapy,leading to improved treatment of chronic pain in CP and other visceral pain disorders. | Stefan AW Bouwense Marjan de Vries Luuk TW Schreuder Soren S Olesen Jens B Frokjær Asbjorn M Drewes Harry van Goor Oliver HG Wilder-Smith | 2015 | World Journal of Gastroenterology2015，21，1： | 6 |
| 3 | In silico analysis of regulatory networks underlines the role of miR-10b-5p and its target BDNF in huntington’s disease显示文摘Non-coding RNAs(ncRNAs)play various roles during central nervous system development.MicroRNAs(miRNAs)are a class of ncRNAs that exert their function together with argonaute proteins by post-transcriptional gene silencing of messenger RNAs(mRNAs).Several studies provide evidence for alterations in miRNA expression in patients with neurodegenerative diseases.Among these is huntington‘s disease(HD),a dominantly inherited fatal disorder characterized by deregulation of neuronal-specific mRNAs as well as miRNAs.Recently,next-generation sequencing(NGS)miRNA profiles from human HD and neurologically normal control brain tissues were reported.Five consistently upregulated miRNAs affect the expression of genes involved in neuronal differentiation,neurite outgrowth,cell death and survival.We re-analyzed the NGS data publicly available in array express and detected nineteen additional differentially expressed miRNAs.Subsequently,we connected these miRNAs to genes implicated in HD development and network analysis pointed to miRNA-mediated downregulation of twenty-two genes with roles in the pathogenesis as well as treatment of the disease.In silico prediction and reporter systems prove that levels of BDNF,a central node in the miRNA-mRNA regulatory network,can be post-transcriptionally controlled by upregulated miR-10b-5p and miR-30a-5p.Reduced BDNF expression is associated with neuronal dysfunction and death in HD.Moreover,the 3’UTR of CREB1 harbors a predicted binding site for these two miRNAs.CREB1 is similarly downregulated in HD and overexpression decreased susceptibility to 3-nitropropionic-induced toxicity in a cell model.In contradiction to these observations,it is presumed that miR-10b-5p upregulation in HD exerts a neuroprotective role in response to the mutation in the huntingtin gene.Therefore,the function of miR-10b-5p and especially its effect on BDNF expression in HD requires further academic research. | Soren Müller | 2014 | Translational Neurodegeneration2014，3，1： | 2 |
| 4 | Identification of ex- pressed and conserved human noncoding RNAs 显示文摘 | Morten M Disa T Soren V | 2014 | RNA2014，20，： | 1 |
| 5 | Antifouling technology-past present and future steps towards efficient and environmen- tally friendly antifouling coatings显示文摘 | Diego M Y Soren K Kim D J | 2004 | Prog Org Coat2004，50，： | 1 |
| 6 | Effects of marine microbial biofilms on the biocide release rate from antifouling paints- A model-based analysis显示文摘 | Diego M Y Soren K Claus E | 2006 | Prog Org Coat2006，57，： | 1 |
| 7 | Antifouling technology- past, present and future steps towards efficient and environ- mentally friendly antifouling coatings 显示文摘 | DIEGO M Y SOREN K KIM D J | 2004 | Progress in Organic Coatings2004，，50： | 1 |
| 8 | Fluorinated bio-acceptable polymers via an ATRP macroioitiator approach 显示文摘 | Natanya M L David M Soren H | 2007 | Journal of Polymer Science Part A: Polymer Chemistry2007，45，24： | 1 |
| 9 | Biologic basic for combining drugs and radiation 显示文摘 | George D Soren M Paul M | 2006 | Sere in Radiat Ocology2006，，： | 1 |
| 10 | Effects of different levels of coconut oil supplementation on performance,digestibility,rumen fermentation and carcass traits of Malpura lambs显示文摘 | BHATT R S SOREN N M TRIPATHI M K | 2011 | Anim Feed Sci Technol2011，164，12： | 1 |
| 11 | Biologic basic for combining drugs and radiation 显示文摘 | George D Soren M PaulM | 2006 | Semin Radiat Oeology2006，16，1： | 1 |
| 12 | Sensori-neural hearing loss after radiotherapy for nasopharyngeal carcinoma:individualized risk estimation显示文摘 | Henriette B Honore Soren M | 2002 | Radiotherapy and Oncology2002，65，1： | 1 |
| 13 | Cloning and Expression in Escherichia Coli of the Gene for Extracellular Phospholipase A1fromSerratia Liquefaciens显示文摘 | G Michael O Lars M Soren | 1988 | Journal of Bacteriology1988，170，12： | 1 |
| 14 | The applicalion of CDIO standards in the evaluation of Swedish engineering degree programmers 显示文摘 | M John E Kristina O Soren | 2012 | World Transaction on Engineering and Technology Education2012，5，2： | 1 |
| 15 | Cloning and expression in Escherichia coli of the gene for extracellular phospholipase Al from serratia liquefaciens显示文摘 | Michael G Lars O Soren M | | 0，，12： | 1 |
| 16 | Noninvasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis 显示文摘 | CELERMAJER D S SOREN K E GOOCH V M | 1992 | Lancet1992，340，8828： | 1 |
| 17 | The (r,Q) control of a periodic-review inventory system with continuous demand and lost sales显示文摘 | Soren Glud Johansen Roger M Hill | 2000 | Int J Production Economics2000，，68： | 1 |
| 18 | Sensori-neural hearing loss after radiotherapy for nasopharyngeal carcinoma: individualized risk estimation显示文摘 | Henriette B Honore Soren M | 2002 | Radiotherapy and Oncology2002，65，： | 1 |
| 19 | Biologic basic for combining drugs and radiation显示文摘 | George D Soren M Paul M | 2006 | Semin Radiat Oncol2006，16，1： | 1 |
| 20 | Experiment investigation and modeling of a wet flue gas desulfurization pilot plant显示文摘 | SOREN KILL MICHAEL L M KIM D J | 1998 | Ind Eng Chem Res1998，37，： | 1 |
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