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| 1 | 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 |
| 2 | Ursodeoxycholic acid improves gastrointestinal motility defects in gallstone patients显示文摘AIM: To simultaneously evaluate the presence of defects in gallbladder and gastric emptying, as well as in intestinal transit in gallstone patients (GS) and the effect of chronic ursodeoxycholic acid (UDCA) administration on these parameters and on serum bile acids and clinical outcome in GS and controls (CTR). METHODS: After a standard liquid test meal, gallbla-dder and gastric emptying (by ultrasound), oroileal transit time (OITT) (by an immunoenzymatic technique) and serum bile acids (by HPLC) were evaluated before and after 3 mo of UDCA (12 mg/kg bw/d) or placebo administration in 10 symptomatic GS and 10 matched healthy CTR. RESULTS: OITT was longer in GS than in CTR (P < 0.0001); UDCA significantly reduced OITT in GS (P < 0.0001), but not in CTR. GS had longer gastric half-emptying time (t1/2) than CTR (P < 0.0044) at baseline; after UDCA, t1/2 significantly decreased (P < 0.006) in GS but not in CTR. Placebo administration had no effect on gastric emptying and intestinal transit in both GS and CTR. CONCLUSION: The gallstone patient has simultaneous multiple impairments of gallbladder and gastric emptying, as well as of intestinal transit. UDCA administration restores these defects in GS, without any effect in CTR. These results confirm the pathogenetic role of gastrointestinal motility in gallstone disease and suggest an additional mechanism of action for UDCA in reducing bile cholesterol supersaturation. | A Colecchia G Mazzella L Sandri F Azzaroli M Magliuolo P Simoni ML Bacchi-Reggiani E Roda D Festi | 2006 | World Journal of Gastroenterology2006，12，33： | 4 |
| 3 | Low-dose Oral Methotrexateand Cyelophosphamide in Metastatic Breast Cancer: Antitumor Activity and Correlation with Vascular Endothelial Growth Factor Levels显示文摘 | Colleoni M Rocca A Sandri M T | 2002 | Ann Oncol2002，13，1： | 1 |
| 4 | Signalling pathways regula- ring muscle mass in ageing skeletal muscle : the role of the IGF1-Akt- mTOR-FoxO pathway 显示文摘 | Sandri M Barberi L Bijlsma A Y | 2013 | Biogerontolagy2013，14，3： | 1 |
| 5 | Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy显示文摘 | Sandri M Sandri C Gilbert A | 2004 | Cell2004，117，3： | 1 |
| 6 | FoxO transcription factors induce the atrophy-related ubiquitin ligase atrogin-I and cause skeletal muscle atrophy 显示文摘 | Sandri M Sandri C Gilbert A | 2004 | Cell2004，117，3： | 1 |
| 7 | Ion-beam machining of millimeter scale optics显示文摘 | Feinberg M R Sandri G | 2000 | Applied Optics2000，39，4： | 1 |
| 8 | Vitamin D at the onset of type 1 diabetes in Italian children显示文摘 | Franchi B Piazza M Sandri M | 2013 | Eur J Pedi- atr2013，，： | 1 |
| 9 | Effects of exercise and ischemia on mobilization and functional activation of blood-derived progenitor cells in patients with ischemic syndromes:results of 3 randomized studies显示文摘 | Sandri M Adams V Gielen S | 2005 | Circulation2005，111，： | 1 |
| 10 | Cellular and molecular mechanisms of muscle atrophy显示文摘 | Bonaldo P Sandri M | 2013 | Dis Model Mech2013，6，1： | 1 |
| 11 | Comparison of hybrid capture 2 High-Risk HPV results in the low positive range with cobas- HPV Testresults from the ATHENA study显示文摘 | Rao A Sandri MT Sideri M | 2013 | Journal of clinical virology:Theofficial publication of the Pan American Society for ClinicalVirology2013，58，1： | 1 |
| 12 | Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy显示文摘 | Sandri M Sandri C Gilbert A | 2004 | Cell2004，117，3： | 1 |
| 13 | Evaluation of association between exercise-induced bronehoconstriction and childhood asth- ma control test questionnaire scores in children 显示文摘 | Chinellato I Piazza M Sandri M | 2012 | Pediatr Pul- mono12012，47，3： | 1 |
| 14 | Mimicking natural bio-mineraliza tion processes:a new tool for osteochondral scaffold development显示文摘 | Tampieri A Sprio S Sandri M | | 0，，10： | 1 |
| 15 | Vitamin D serum levelsand markers of asthma control in Italian children 显示文摘 | Chinellato I Piazza M Sandri M | 2011 | J Pediatr2011，158，43： | 1 |
| 16 | N-terminal pro-B-type natriuretic peptide after high-dose chemotherapy: a marker predictive of cardiac dysfunction? 显示文摘 | Sandri MT Salvatici M Cardinale D | 2005 | Clin Chem2005，51，8： | 1 |
| 17 | Signaling in muscle atrophy and hypertrophy显示文摘 | Sandri M | 2008 | Physiology (Bethesda)2008，23，： | 1 |
| 18 | Apoptosis, DNA damage and ubiquitin expression in normal and mdx muscle fibers after exercise显示文摘 | Sandri M Carraro U Podhorska-Okolov M Rizzi C Arslan P Monti D Franceschi C | 1995 | FEBS Lett1995，373，3： | 1 |
| 19 | Apoptosis and atrophy in rat slow skeletal muscles in chronic heart failure 显示文摘 | Libera LD Zennaro R Sandri M | 1999 | Am J Physiol1999，277，51： | 1 |
| 20 | Foxo transcription factors in-duce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletalmuscle atrophy显示文摘 | Sandri M Sandri C Gilbert A | 2004 | Cell2004，117，3： | 1 |
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