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2005Volume 37Issue 1 Pages
1
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[in Japanese]
2005Volume 37Issue 1 Pages
3
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2005Volume 37Issue 1 Pages
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[in Japanese], [in Japanese]
2005Volume 37Issue 1 Pages
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[in Japanese]
2005Volume 37Issue 1 Pages
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[in Japanese]
2005Volume 37Issue 1 Pages
26-30
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Tatsuhiko Komiya, Nobushigc Tamura, Cenichi Sakaguchi, Shinji Masuyama ...
2005Volume 37Issue 1 Pages
31-35
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[in Japanese]
2005Volume 37Issue 1 Pages
36-37
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Eitaro Umehara, Shintaro Nemoto, Shigeru Kato, Takeshi Nishina, Yutaka ...
2005Volume 37Issue 1 Pages
38-41
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[in Japanese]
2005Volume 37Issue 1 Pages
42-43
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Masafumi Takeda, Hiroya Kawai, Hiroshi Kamiryo, Masatsugu Yamamoto, No ...
2005Volume 37Issue 1 Pages
44-50
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[in Japanese]
2005Volume 37Issue 1 Pages
51-52
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Masayuki Ishikawa, Kazuhito Imanaka, Motonobu Nishimura, Masanori Ogiw ...
2005Volume 37Issue 1 Pages
53-57
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2005Volume 37Issue 1 Pages
59-60
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2005Volume 37Issue 1 Pages
61-62
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Richard A. Walsh
2005Volume 37Issue 1 Pages
63-75
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Congestive heart failure is a major and growing public health problem in all developed countries. Therapy for this clinical syndrome was initially based upon a cardiorenal hemodynamic paradigm. Current therapeutics are based upon neurohormonal inhibition of pathways known to accelerate the progression of cardiac dysfunction and fluid retention. Despite much progress the morbidity and mortality of heart failure using state of the art pharmocotherapy equals or exceeds many solid tumors. New therapies are and will emerge from a genetic, molecular and cellular paradigm of disease. In particular inhibition of aberrantly activated protein kinase signaling pathways promise to be important therapeutic targets in cancer, cardiovascular disease in general and congestive heart failure in particular.
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Toshlhiro Tanaka
2005Volume 37Issue 1 Pages
76-82
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Minoru Horie
2005Volume 37Issue 1 Pages
83-92
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Kinya Otsu
2005Volume 37Issue 1 Pages
93-99
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Yasuhiro Ikeda, Masunori Matsuzaki
2005Volume 37Issue 1 Pages
100-107
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