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Volume 61, Issue 4
Displaying 1-3 of 3 articles from this issue
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REVIEW
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Kazuo Kishi, Keisuke Okabe, Ruka Shimizu, Yoshiaki Kubota2012 Volume 61 Issue 4 Pages 101-108
Published: December 25, 2012
Released on J-STAGE: December 21, 2012
JOURNAL FREE ACCESSUntil a certain developmental stage, cutaneous wounds in mammalian fetuses heal rapidly without scars with complete regeneration of the skin. In the process of fetal wound healing, inflammatory responses, granulation proliferation, and scar formation that are observed in adults are not seen. Numerous studies have reported the causes of fetal scarless cutaneous regeneration, including reduced expression of TGF-β1 and higher levels of hyaluronan in the extracellular matrix, from the viewpoints of molecular biology and cellular biology, but the mechanisms are not completely understood. Although a variety of substances that inhibit scar formation have been investigated, currently it is almost impossible for adult cutaneous wounds to heal completely without scars. Except for a few animal species, perfect regeneration after wounding can occur only during the gestation period. By strictly comparing the stages before and after the transition from the regeneration of skin to scarring, it will be possible to investigate the mechanisms of cutaneous regeneration.View full abstractDownload PDF (1580K) -
Hidekazu Suzuki, Toshihiro Nishizawa, Hitoshi Tsugawa, Toshifumi Hibi2012 Volume 61 Issue 4 Pages 109-119
Published: December 25, 2012
Released on J-STAGE: December 21, 2012
JOURNAL FREE ACCESSThirty years have passed since Warren and Marshall’s discovery of Helicobacter pylori (H.pylori). Since then, not only peptic ulcer diseases and chronic gastritis but also non-cardia gastric cancers have been recognized as diseases originating from H. pylori infection. Several combination therapies consisting of multiple antibiotics have been developed as first- or second-line regimens to eradicate H. pylori infection. Our extensive experience in the field of anti-H. pylori medicine suggests that clinicians should consider a possible role for unidentified, invisible pathogens to elucidate the pathogenesis and improve the treatment of refractory diseases of unknown etiology.View full abstractDownload PDF (1439K)
ORIGINAL ARTICLE
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Yasunari Takada, Koichi Matsuo2012 Volume 61 Issue 4 Pages 120-127
Published: December 25, 2012
Released on J-STAGE: December 21, 2012
JOURNAL FREE ACCESSGefitinib is an anticancer drug developed to inhibit the tyrosine kinase activity of the epidermal growth factor receptor (EGFR). Two structurally-related EGFR tyrosine kinase inhibitors, gefitinib (Iressa) and erlotinib (Tarceva), are used as oral chemotherapy by patients with non-small-cell lung cancer. Immediately after introduction of gefitinib to clinical practice, interstitial lung disease was identified as a life-threatening adverse effect, although this condition can be well managed. It is still unclear whether gefitinib and other EGFR inhibitors induce similar adverse effects in lung. We previously established mouse models of interstitial lung disease in which gefitinib induces expression of Fosl1 (which encodes the AP-1 transcription factor Fra-1) in the presence of exogenous or endogenous Toll-like receptor ligands, leading to abnormal cytokine and chemokine expression. Here, we compared and monitored the effects of EGFR inhibitors gefitinib, erlotinib and AG1517 (PD153035) on the mRNA expression levels of Fosl1, Tnf and Ccl2. Unexpectedly, gefitinib, but not the other tyrosine kinase inhibitors, elicited the Fosl1 expression profile proposed to be predictive of interstitial lung disease, suggesting that gefitinib-induced interstitial lung disease is an off-target effect not elicited by erlotinib.View full abstractDownload PDF (2106K)
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