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In JoVE (1)
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Articles by Rafael F. Perini in JoVE
Gebrekkige PMS2, ERCC1, Ku86, CcOI in Field Gebreken Tijdens Progressie naar Colon Cancer
Huy Nguyen1, Cristy Loustaunau1, Alexander Facista1, Lois Ramsey1, Nadia Hassounah1, Hilary Taylor1, Robert Krouse2,3, Claire M. Payne1,4, V. Liana Tsikitis3, Steve Goldschmid5, Bhaskar Banerjee5, Rafael F. Perini5, Carol Bernstein1
1Department of Cell Biology and Anatomy, College of Medicine, University of Arizona, Tucson, 2Southern Arizona Veterans Affairs Health Care System, Tucson, AZ, 3Department of Surgery, College of Medicine, University of Arizona, Tucson, 4Biomedical Diagnostics and Research, Tucson, AZ, 5Department of Medicine, College of Medicine, University of Arizona, Tucson
Verminderd / afwezige uitdrukking van PMS2 en / of ERCC1 in hele crypten is een frequent geval binnen 10 cm aan elke kant van colon adenocarcinomen, waarschijnlijk de basis van een gezichtsveld met een hoge veranderlijkheid en de progressie van kanker. Deficiƫntie in Ku86 of CcOI is veel minder frequent in deze veld gebreken.
Other articles by Rafael F. Perini on PubMed
Mucosal Repair and COX-2 Inhibition
Current Pharmaceutical Design. 2003 | Pubmed ID: 14529401
The healing of gastric ulcer is a complicated process that involves the proliferation of epithelial and endothelial cells and the concerted actions of a wide range of growth factors. Prostaglandins play an important role in ulcer healing. Expression of cyclooxygenase-2 (COX-2) is markedly upregulated around the margins of gastric ulcers and its inhibition leads to a delay of ulcer healing. Several of the growth factors that promote ulcer healing may work in part through COX-2-dependent mechanisms. Angiogenesis, which is crucial to ulcer healing, is tightly regulated by growth factors. Treatment with selective COX-2 inhibitors appears to alter the balance of serum levels of growth factors, favoring an inhibition of angiogenesis. Given the importance of COX-2 in regulating ulcer healing, caution should be taken in the use of selective inhibitors of COX-2 by patients at risk of ulcer disease.
Post-sphincterotomy Bleeding After the Introduction of Microprocessor-controlled Electrosurgery: Does the New Technology Make the Difference?
Gastrointestinal Endoscopy. Jan, 2005 | Pubmed ID: 15672056
Bleeding as a complication of endoscopic sphincterotomy is influenced by several factors. The objective of this study was to compare rates of bleeding after sphincterotomy performed with two different electrosurgical current generators (Valleylab SSE2L and ERBE ICC200).
Isolated Right Segmental Hepatic Duct Injury Following Laparoscopic Cholecystectomy
Cardiovascular and Interventional Radiology. Mar-Apr, 2005 | Pubmed ID: 15770390
Laparoscopic cholecystectomy (LC) is the treatment of choice for gallstones. There is an increased incidence of bile duct injuries in LC compared with the open technique. Isolated right segmental hepatic duct injury (IRSHDI) represents a challenge not only for management but also for diagnosis. We present our experience in the management of IRSHDI, with long-term follow-up after treatment by a multidisciplinary approach.
Pathogenesis of Portal Hypertensive Gastropathy: Translating Basic Research into Clinical Practice
Nature Clinical Practice. Gastroenterology & Hepatology. Mar, 2009 | Pubmed ID: 19190600
Portal hypertensive gastropathy (PHG) is often seen in patients with portal hypertension, and can lead to transfusion-dependent anemia as well as acute, life-threatening bleeding episodes. This Review focuses on the mechanisms that underlie the pathogenesis of PHG that provide reasonable grounds for the treatment of this condition, and ultimately enable translation of basic research into clinical practice. Increased portal pressure associated with cirrhosis and liver dysfunction is critical for the development of clinically significant PHG, and leads to impaired gastric mucosal defense mechanisms that render the stomach susceptible to mucosal injury. The use of pharmacological agents such as beta-blockers reduces the frequency of bleeding episodes in PHG. As a last resort, surgical decompression of the portal system, transjugular intrahepatic stent placement and liver transplantation can resolve this condition. Elimination of known risk factors for gastric injury such as alcohol, aspirin and traditional NSAIDs is critical. The role of Helicobacter pylori colonization of the gastric mucosa in PHG is not clear. Careful and critical interpretation of human and experimental data can be helpful to establish a rationale for the medical management of this important condition.
