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Copyright of Gefaesschirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The molecular progression of endometrial cancer is poorly understood, and both genetic and epigenetic factors play a role. Survivin is a member of the inhibitor of apoptosis (IAP) gene family and contains a canonical CpG island that has been described as epigenetically regulated. As survivin is overexpressed in endometrial tumors, we hypothesized that hypomethylation could explain this expression pattern. Surprisingly, methylation-specific PCR and pyrosequencing showed that survivin was hypermethylated in endometrial tumors and correlated with increased survivin expression. We speculated that methylation could inhibit the binding of p53, a repressor of survivin expression. Our data indicates that demethylation of the survivin promoter by decitabine results in p53-dependent survivin repression and that p53 binding can be inhibited by DNA methylation. We are the first to report survivin de-repression by DNA methylation. We also present microarray data, which suggest that de-repression by methylation is a general mechanism of p53 regulation. Demethylation induced by decitabine is traditionally thought to be active in tumors by allowing the re-expression of tumor suppressor genes. However, our results indicate that an additional important mechanism is to decrease the expression of oncogenes.Oncogene (2009) 28, 2046–2050; doi:10.1038/onc.2009.62; published online 13 April 2009 [ABSTRACT FROM AUTHOR]

Copyright of Gefaesschirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Gefaesschirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Discusses the controversial issues in contemporary diagnosis and management of congenital vascular malformation (CVM). Acceptance of primary lymphedema as CVM; Limitation of traditional arteriography in diagnosis of CVM; Use of venography for the management of venous malformation.

Evolution of contemporary concept for the advanced management of congenital vascular malformation (CVM) took a long and difficult path through decades, in spite of tremendous efforts by many scholars and surgeons throughout the world. The enormous progress particularly for the last decade would not have been possible but for the guidance of the late Professor Stefan Belov of Bulgaria. A few surgeons, mostly of the European camp, led by Belov and his disciples, were able to continue to wage war against the CVM with scaled-down surgery and more logical and broad based approach; containing the complication and morbidity within acceptable as well as affordable range.

Experimental studies demonstrated a severe cardiac load of the CO2 pneumoperitoneum caused by an accelerated after- and a decreased preload. Patients displaying cardiovascular risks are therefore often rejected from laparoscopic surgery. Hence, the pathophysiological changes and the intraoperative risk of the CO2 pneumoperitoneum in high-risk cardiopulmonary patients (NYHA II-III, n = 15) undergoing laparoscopic cholecystectomy are described. The changes in cardiac after- and preload seem to be due to the elevated intraabdominal pressure rather than transperitoneally resorbed CO2 and are reversible by desufflation. In one patient conversion to open operation had to be performed because of a severe drop in cardiac output and right ventricle ejection fraction. Mixed oxygen saturation was predicting intraoperative worsening in this case. The described pathophysiological changes may seem to be well tolerated even in high-risk cardiac patients. Monitoring of hemodynamics should include an arterial catheter line and blood gas analyses. Pharmacologic interventions or pressureless laparoscopic procedures might not be necessary as long as laparoscopic cholecystectomy is performed. [ABSTRACT FROM AUTHOR]

Copyright of Langenbecks Archiv fuer Chirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Langenbecks Archiv fuer Chirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)