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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 | Lrp1 in osteoblasts controls osteoclast activity and protects against osteoporosis by limiting PDGF–RANKL signaling显示文摘Skeletal health relies on architectural integrity and sufficient bone mass, which are maintained through a tightly regulated equilibrium of bone resorption by osteoclasts and bone formation by osteoblasts. Genetic studies have linked the gene coding for low-density lipoprotein receptor-related protein1(Lrp1) to bone traits but whether these associations are based on a causal molecular relationship is unknown. Here, we show that Lrp1 in osteoblasts is a novel regulator of osteoclast activity and bone mass.Mice lacking Lrp1 specifically in the osteoblast lineage displayed normal osteoblast function but severe osteoporosis due to highly increased osteoclast numbers and bone resorption. Osteoblast Lrp1 limited receptor activator of NF-κB ligand(RANKL) expression in vivo and in vitro through attenuation of platelet-derived growth factor(PDGF-BB) signaling. In co-culture, Lrp1-deficient osteoblasts stimulated osteoclastogenesis in a PDGFRβ-dependent manner and in vivo treatment with the PDGFR tyrosine kinase inhibitor imatinib mesylate limited RANKL production and led to complete remission of the osteoporotic phenotype. These results identify osteoblast Lrp1 as a key regulator of osteoblast-to-osteoclast communication and bone mass through a PDGF–RANKL signaling axis in osteoblasts and open perspectives to further explore the potential of PDGF signaling inhibitors in counteracting bone loss as well as to evaluate the importance of functional LRP1 gene variants in the control of bone mass in humans. | Alexander Bartelt Friederike Behler-Janbeck F.Timo Beil Till Koehne Brigitte Müller Tobias Schmidt Markus Heine Laura Ochs Tayfun Yilmaz Martin Dietrich Jan P.Tuckermann Michael Amling Joachim Herz Thorsten Schinke Joerg Heeren Andreas Niemeier | 2018 | Bone Research2018，6，1： | 5 |
| 3 | Impact of hyperglycemia on autoimmune pancreatitis and regulatory T-cells显示文摘AIM To evaluate the influence of hyperglycemia on the progression of autoimmune pancreatitis.METHODS We induced hyperglycemia by repetitive intraperitoneal(ip) injection of 50 mg/kg streptozotocin in MRL/Mp J mice, which develop autoimmune pancreatitis due to a genetic predisposition. We compared the extent of inflammation(histological score, CD3^+ lymphocytes, CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells) in the pancreas of hyperglycemic and normoglycemic mice. We also analyzed the number of leukocytes, lymphocytes, granulocytes and monocytes in the blood. In addition, we determined the percentage of CD3^+ lymphocytes, CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells, Foxp3^+ CD25^+ T-helper and Foxp3^+T-helper cells in the spleen by flow cytometry.RESULTS Treatment with streptozotocin caused a strong induction of hyperglycemia and a reduction in body weight(P < 0.001). Severe hyperglycemia did not, however, lead to an aggravation, but rather to a slight attenuation of autoimmune pancreatitis. In the pancreas, both the histological score of the pancreas as well as the number of CD3+ lymphocytes(P < 0.053) were decreased by hyperglycemia. No major changes in the percentage of CD8^+ T-cells, CD4^+ T-cells, Foxp3^+ T-helper cells were observed between hyperglycemic and normoglycemic mice. Hyperglycemia increased the numbers of leukocytes(P < 0.001), lymphocytes(P = 0.016), granulocytes and monocytes(P = 0.001) in the blood. Hyperglycemia also moderately reduced the percentage of CD3^+ lymphocytes(P = 0.057), significantly increased the percentage of Foxp3^+ T-helper cells(P = 0.018) and Foxp3^+ CD25^+ T-helper cells(P = 0.021) and reduced the percentage of Foxp3^+T-helper cells(P = 0.034) in the spleen. CONCLUSION Hyperglycemia does not aggravate but moderately attenuates autoimmune pancreatitis, possibly by increasing the percentage of regulatory T-cells in the spleen. | Franz-Tassilo Müller-Graff Brit Fitzner Robert Jaster Brigitte Vollmar Dietmar Zechner | 2018 | World Journal of Gastroenterology2018，24，28： | 3 |
| 4 | Relationship between the severity of hepatitis C virus-related liver disease and the presence of Helicobacter species in the liver: A prospective study显示文摘AIM: To determine the presence of Helicobacter species DNA in the liver of chronic hepatitis C (CHC) patients with and without cirrhosis as compared to controls, and to identify the bacterial species involved. METHODS: Seventy-nine consecutive patients (HBV and HIV negative) with a liver sample obtained after liver biopsy or hepatic resection were studied: 41 with CHC without cirrhosis, 12 with CHC and cirrhosis, and 26 controls (HCV negative). Polymerase chain reactions (PCRs) targeting Helicobacter 16S rDNA and species- specific were performed on DNA extracted from the liver. A gastric infection with H pylori was determined by serology and confirmed by 13C-urea breath test. RESULTS: Overall, Helicobacter 16S rDNA was found in 16 patients (20.2%). Although positive cases tended to be higher in CHC patients with cirrhosis (41.6%) than in those without cirrhosis (17.0%) or in controls (15.4%), the difference was not statistically significant (P =0.08). H pylori-like DNA was identified in 12 cases and H. pullorum DNA in 2, while 2 cases remained unidenti- fied. Gastric infection with H pylori was found in only 2 of these patients. CONCLUSION: Our results do not confirm the associ- ation of Helicobacter species DNA in the liver of CHC patients with advanced liver disease. The lack of correlation between positive H pylori serology and the presence of H pylori-like DNA in the liver may indicate the presence of a variant of this species. | Laurent Castéra Anne Pedeboscq Marcia Rocha Brigitte Le Bail Corinne Asencio Victor de Lédinghen Pierre-Henri Bernard Christophe Laurent Marie-Edith Lafon Maylis Capdepont Patrice Couzigou Paulette Bioulac-Sage Charles Balabaud FrancisMégraud Armelle Ménard | 2006 | World Journal of Gastroenterology2006，12，45： | 3 |
| 5 | Histone Methyltransferase Activity of a Drosophila Polycomb Group Repressor Complex显示文摘 | Jürg Müller Craig M. Hart Nicole J. Francis Marcus L. Vargas Aditya Sengupta Brigitte Wild Ellen L. Miller Michael B. O’Connor Robert E. Kingston Jeffrey A. Simon | 2002 | Cell2002，，2： | 1 |
| 6 | Primary Gastric B-Cell Lymphoma: Results of a Prospective Multicenter Study显示文摘 | Wolfgang Fischbach* Brigitte Dragosics? Maria-Elisabeth Kolve-Goebeler§ Christian Ohmann∥ Axel Greiner? Qin Yang∥ Stephan B?hm? Patrick Verreet∥ Olaf Horstmann# Martin Busch** Eckhart Dühmke** Hans-Konrad Müller-Hermelink? Klaus Wilms§ | 2000 | Gastroenterology2000，，5： | 1 |
| 7 | Stress in recombinant protein producing yeasts 显示文摘 | Diethard M Brigitte G Hubertus H | 2004 | Journal of Biotechnology2004，113，13： | 1 |
| 8 | 查看详情显示文摘 | Olayide S L Lechner M D Brigitte H T | | 0，，05： | 1 |
| 9 | Dual and beneficial roles of macrophages during skeletal muscle regeneration显示文摘 | Chazaud B Brigitte M Yacoub-Youssef H | | 0，，01： | 1 |
| 10 | Factors influencing transformation frequency of tomato (Lycopersicon esculentum)显示文摘 | Jeroen S C Brigitte D Leo S M | 1993 | Plant cell rep1993，12，： | 1 |
| 11 | Comparison of the LCx human immunodeficiency virus (HIV) RNA quantitative, RealTime HIV, and COBAS AmpliPrep-COBAS Taq- Man assays for quantitation of HIV type 1 RNA in plasma显示文摘 | Vincent F Brigitte M Marie-Noelle D | 2006 | J Clin Microhiol2006，44，8： | 1 |
| 12 | Muscle resident macrophages control the immune cell reaction in a mouse model of notexin- induced myoinjury 显示文摘 | Brigitte M Schihe C Plonquet A | 2010 | Arthritis Rheum2010，62，1： | 1 |
| 13 | Significance of hepatic arterial responsiveness for adequate tissue oxygenation upon portal vein occlusion in cirrhotic livers显示文摘 | Isabella Mücke Sven Richter Michael D. Menger Brigitte Vollmar | 2000 | International Journal of Colorectal Disease (-)2000，，5： | 1 |
| 14 | A Shape Optimization Method Based on Complex Expressions of 2-Dimensinal Magnetic Fields显示文摘 | MASASHI K BRIGITTE M | 1997 | IEEE Trains on Magnetics1997，33，2： | 1 |
| 15 | Impact of lactic acid bacteria on oxidative DNA damage in human derived colon cells显示文摘 | VERENA J K BRIGITTE M REINHARD S | 2008 | Food and Chemical Toxicology2008，46，： | 1 |
| 16 | CD44s and CD44v6 expression in head and neck epithelia显示文摘 | Brigitte M Olivier G | 2008 | PLoS ONE2008，3，10： | 1 |
| 17 | Dual and beneficial roles of macrophages during skeletal muscle regeneration 显示文摘 | Chazaud B Brigitte M Yacoub-Youssef H | 2009 | Exerc Sport Sci Rev2009，37，1： | 1 |
| 18 | Cortisol dysregulation in school teachers in relation to burnout, vital exhaustion, and effort-reward-imbalance显示文摘 | Silja B Tobias W Brigitte M | 2008 | Biological Psychology2008，78，： | 1 |
| 19 | Endocrine therapy Plus zoledronic acid in premenopausal breast cancer 显示文摘 | Michael G Brigitte M Walter S | 2009 | N Engl J Med2009，360，7： | 1 |
| 20 | Risk Factors and Causes of Death in MEN1 Disease. A GTE (Groupe d’Etude des Tumeurs Endocrines) Cohort Study Among 758 Patients显示文摘 | Pierre Goudet Arnaud Murat Christine Binquet Christine Cardot-Bauters Annie Costa Philippe Ruszniewski Patricia Niccoli Fabrice Ménégaux Georges Chabrier Fran?oise Borson-Chazot Antoine Tabarin Philippe Bouchard Brigitte Delemer Alfred Beckers Claire Boni | 2010 | World Journal of Surgery2010，，2： | 1 |
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