# 高校生の頃は、二足歩行は夢のまた夢だと聞いていました
# 再掲ですがこちらの記事の方が正確です
ark F. Meier F. Meier, Mark B. Dyurgerov, Ursula K. Rick, Shad O'Neel, W. Tad Pfeffer, Robert S. Anderson, Suzanne P. Anderson, Andrey F. Glazovsky.
Science, Science Express | DOI: 10.1126/science.1143906
Ice loss to the sea currently accounts for virtually all of sea-level rise not attributable to ocean warming; about 60% of the ice loss is from glaciers and ice caps rather than from the two ice sheets. The contribution of these smaller glaciers has accelerated over the last decade, in part due to dramatic thinning and retreat of marine-terminating glaciers associated with a dynamic instability generally not considered in mass balance/climate modeling. This acceleration of glacier melt may cause 0.1-0.25 m of additional sea-level rise by 2100.# 全体の割合から考えると、小規模な氷河を全てモニターしていく方が重要なようです
Keyue Liu, Shuji Mori, Hideo K. Takahashi, Yasuko Tomono, Hidenori Wake, Toru Kanke, Yasuharu Sato, Norihito Hiraga, Naoto Adachi, Tadashi Yoshino, and Masahiro Nishibori.
FASEB Journal, New Articles | doi: 10.1096/fj.07-8770com
The high mobility group box-1 (HMGB1), originally identified as an architectural nuclear protein, exhibits an inflammatory cytokine-like activity in the extracellular space. Here we show that treatment with neutralizing anti-HMGB1 monoclonal antibody (mAb; 200 µg, twice) remarkably ameliorated brain infarction induced by 2-h occlusion of the middle cerebral artery in rats, even when the mAb was administered after the start of reperfusion. Consistent with the 90% reduction in infarct size, the accompanying neurological deficits in locomotor function were significantly improved. Anti-HMGB1 mAb inhibited the increased permeability of the blood-brain barrier, the activation of microglia, the expression of TNF-α and iNOS, and suppressed the activity of MMP-9, whereas it had little effect on blood flow. Intracerebroventricular injection of HMGB1 increased the severity of infarction. Immunohistochemical study revealed that HMGB1 immunoreactivity in the cell nuclei decreased or disappeared in the affected areas, suggesting the release of HMGB1 into the extracellular space. These results indicate that HMGB1 plays a critical role in the development of brain infarction through the amplification of plural inflammatory responses in the ischemic region and could be an outstandingly suitable target for the treatment. Intravenous injection of neutralizing anti-HMGB1 mAb provides a novel therapeutic strategy for ischemic stroke.# 壊死の分子機序から攻めるとはかしこい
