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| 1 | Beyond the stomach: An updated view of Helicobacter pylori pathogenesis, diagnosis, and treatment显示文摘Helicobacter pylori(H. pylori) is an extremely common, yet underappreciated, pathogen that is able to alter host physiology and subvert the host immune response, allowing it to persist for the life of the host. H. pylori is the primary cause of peptic ulcers and gastric cancer. In the United States, the annual cost associated with peptic ulcer disease is estimated to be $6 billion and gastric cancer kills over 700000 people per year globally. The prevalence of H. pylori infection remains high(> 50%) in much of the world, although the infection rates are dropping in some developed nations. The drop in H. pylori prevalence could be a double-edged sword, reducing the incidence of gastric diseases while increasing the risk of allergies and esophageal diseases. The list of diseases potentially caused by H. pylori continues to grow; however, mechanistic explanations of how H. pylori could contribute to extragastric diseases lag far behind clinical studies. A number of host factors and H. pylori virulence factors act in concert to determine which individuals are at the highest risk of disease. These include bacterial cytotoxins and polymorphisms in host genes responsible for directing the immune response. This review discusses the latest advances in H. pylori pathogenesis, diagnosis, and treatment. Up-todate information on correlations between H. pylori and extragastric diseases is also provided. | Traci L Testerman James Morris | 2014 | World Journal of Gastroenterology2014,20,36: | 47 |
| 2 | Helicobacter pylori arginase mutant colonizes arginase Ⅱ knockout mice显示文摘AIM: To investigate the role of host and bacterial arginases in the colonization of mice by Helicobacter pylori (H.pylori).METHODS: H.pylori produces a very powerful urease that hydrolyzes urea to carbon dioxide and ammonium,which neutralizes acid.Urease is absolutely essential to H.pylori pathogenesis;therefore,the urea substrate must be in ample supply for urease to work efficiently.The urea substrate is most likely provided by arginase activity,which hydrolyzes L-arginine to L-ornithine and urea.Previous work has demonstrated that H.pylori arginase is surprisingly not required for colonization of wild-type mice.Hence,another in vivo source of the critical urea substrate must exist.We hypothesized that the urea source was provided by host arginase Ⅱ,since this enzyme is expressed in the stomach,and H.pylori has previously been shown to induce the expression of murine gastric arginase Ⅱ.To test this hypothesis,wild-type and arginase (rocF) mutant H.pylori strain SS1 were inoculated into arginase Ⅱ knockout mice.RESULTS: Surprisingly,both the wild-type and rocF mutant bacteria still colonized arginase Ⅱ knockout mice.Moreover,feeding arginase Ⅱ knockout mice the host arginase inhibitor S-(2-boronoethyl)L-cysteine (BEC),while inhibiting > 50% of the host arginase Ⅰ?activity in several tissues,did not block the ability of the rocF mutant H.pylori to colonize.In contrast,BEC poorly inhibited H.pylori arginase activity.CONCLUSION: The in vivo source for the essential urea utilized by H.pylori urease is neither bacterial arginase nor host arginase Ⅱ;instead,either residual host arginase Ⅰ?or agmatinase is probably responsible. | Songhee H Kim Melanie L Langford Jean-Luc Boucher Traci L Testerman David J McGee | 2011 | World Journal of Gastroenterology2011,17,28: | 3 |
| 3 | Evaluation of ankle instability using the biodex stability systems显示文摘 | Testerman C Griend RV | | 0,,: | 1 |
| 4 | Adverse outcomes in younger rib fracture patients显示文摘 | | 2006 | South Med J2006,99,: | 1 |
| 5 | Adverse outcomes in younger rib frac-ture patients显示文摘 | Testerman GM | | 0,,04: | 1 |
| 6 | Adverse outcomes in younger rib fracture patients 显示文摘 | Testerman GM | 2006 | South Med J2006,99,4: | 1 |
| 7 | Endoscopic clipping of bleeding ascending colon dieulafoy lesion显示文摘 | Testerman GM Osborne JB Easparam SA | | 0,,: | 1 |
| 8 | Endoscopic clipping of bleeding ascending colon dieulafoy lesion显示文摘 | Testerman GM Osborne JB Easparam SA | | 0,,: | 1 |
| 9 | Cytokine induction in mice by the immunomodulator imiquimod显示文摘 | Reiter MJ Testerman TL Miller RL | 1994 | J Leukocyte Biol1994,55,: | 1 |
| 10 | Adverse outcomes in younger rib fracture patients显示文摘 | Testerman GM | 2006 | South Med J2006,99,4: | 1 |
| 11 | Cytokine induction by the immunomodulators imiquimod and S-27609 显示文摘 | Testerman TL Gerster JF Imbertson LM | 1995 | J Leukoc Biol1995,58,: | 1 |
| 12 | A statistical reservoir-zonation technique显示文摘 | Testerman J D | 1962 | JPT1962,7,2: | 1 |
| 13 | Homocysteine antagonism of nitric oxide-related cytostasis in Salmonella typhimurium显示文摘 | Testerman T Xu Y | 1996 | Science1996,272,: | 1 |
| 14 | A statistical reservoir zonation technique显示文摘 | TESTERMAN J D | 1962 | Journal of Petroleum Technology1962,14,8: | 1 |
| 15 | Cytokine induction in mice by the immunomodulator imiquimod 显示文摘 | Reiter M Testerman T Miller R | 1994 | J Leukoc Biol1994,13,: | 1 |
| 16 | Cytokine induction by immunomodulators and S- 270609 显示文摘 | Testerman T Imberston L Reiter M | 1995 | J Leukoc Biol1995,58,: | 1 |
| 17 | Adverse outcomes in younger rib fracture patients显示文摘 | Testerman GM | 2006 | South Med J2006,99,4: | 1 |
| 18 | Adverse outcomes in younger rib fracture patients显示文摘 | Testerman GM | 2006 | South Med J2006,99,4: | 1 |
| 19 | Adverse outcomes in younger rib fracture patients显示文摘 | Testerman GM | 2006 | South Med J2006,99,4: | 1 |
| 20 | Electrical stimulation as therapy for neurological disorders显示文摘 | TESTERMAN R L RISE M T STYPULKOWSKI P H | 2006 | Engineering in Medicine and Biology Magazine2006,25,5: | 1 |