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Advances in Understanding Aortic Diseases by Geoffrey D. Rubin (auth.), Teruhisa Kazui M.D., Shinichi

By Geoffrey D. Rubin (auth.), Teruhisa Kazui M.D., Shinichi Takamoto M.D. (eds.)

Following the 1st overseas symposium ever held in Asia on Advances in figuring out Aortic illnesses (AUAD), this quantity of lawsuits comprises the papers provided in either the oral and poster classes. The eighth AUAD symposium vastly contributed to the certainty of aortic ailments, particularly in Asia. Aortic ailments, in particular thoracic aortic illnesses, are extra universal in Japan than in Western international locations, which provides extra significance to this compilation that covers contemporary advancements and advances in thoracic aortic surgical procedure and its results. Divided into lectures, panel discussions, symposiums, and poster classes, the e-book comprises, between different issues, advances in imaging and prognosis with 3D-CT, MRS, and US; cutting-edge fix of the thoracic aorta; novel points of aortic root substitute; reconstruction; and prosthetic graft surgical procedure. This priceless number of paintings presents the reader with an elevated wisdom and figuring out of aortic illnesses not just in Japan yet worldwide.

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J Clin Invest 102:1413–20 43. Newman KM, Malon AM, Shin RD (1994) Matrix metalloproteinases in abdominal aortic aneurysms: characterization, purification, and their possible sources. Connect Tissue Res 30:265–276 44. Irizarry E, Newman KM, Gandhi RH, et al (1993) Demonstration of intestinal collagenase in abdominal aortic aneurysm disease. J Surg Res 54:571–574 45. Newman KM, Ogata Y, Malon AM, et al (1994) Identification of matrix metalloproteinases 3 (stromelysin-1) and 9 (gelatinase B) in abdominal aortic aneurysm.

Am J Med Genet 62:417–426 3. Dietz HC, Cutting GR, Pyeritz RE, et al (1991) Marfan syndrome caused by a recurrent de novo missense mutation in the fibrillin gene. Nature 352:337–339 4. Collod-Beroud G, Le Bourdelles S, Ades L, et al (2003) Update of the UMD-FBN1 mutation database and creation of an FBN1 polymorphism database. Hum Mutat. 22:199–208 5. Katzke S, Booms P, Tiecke F, et al (2002) TGGE screening of the entire FBN1 coding sequence in 126 individuals with marfan syndrome and related fibrillinopathies.

Three strains of transgenic mice, each harboring a different type of Fbn1 mutation, displayed several MFS features with variable severity [20–22]. Increased TGFβ activity was observed in at least four organs (lung, mitral valve, aortic and dural tissues), possibly as a result of excess free large latency complex due to inadequate stabilization within the ECM. Administration of an anti-TGFβ neutralizing antibody rescued the lung, mitral valve, and aortic tissue phenotypes in mice [23–25]. Furthermore, aortic aneurysm was prevented by the administration of losartan, an angiotensin II type 1 receptor blocker that alleviates increased TGF-β activity in mouse models [23].

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