チキュウ オンダンカ カイギロン ト カンキョウ ジョウホウ

化石燃料から排出される二酸化炭素が地球温暖化を引き起こしていることはすでに通説として定着している。確かに大局的に見れば温暖化に向かっており、少なくてもその一因が人為的二酸化炭素の排出にあることは確かであろうし、将来に備える予防的見地から対策を考えることは合理的である。しかし一方では人為的温暖化という通説を疑問視する見方も多く存在しており、その中には合理的な意見も少なくない。本稿ではこれらの懐疑的意見を5つに大別して整理することを試みた。懐疑論の中で最も中心的な意見は、温暖化に寄与している大きな要因は人為的なものではなく、太陽活動の変動などの自然現象にあるとするものである。残念なことに、これらの懐疑論の存在は世間からは事実上無視されている。なぜ無視される状態が生じているのか。その原因として二つ挙げることができる。一つは、温暖化がすでに科学の世界を離れて政治的課題になってしまっており、科学的な正当性を議論するよりは政治的判断が優先していることである。もう一つは、何事に関しても「悪いニュース」に偏りがちなマスメディアの報道姿勢である。人間活動がすべての原因であることを大前提として、「大変だ」という環境情報を一方的に報道する傾向にあり、結果的に一般大衆がそれ以外の要因の寄与について考える機会を奪っている。The idea that recent global warming is attributed to elevated levels of greenhouse gas CO_2 due to human activity seems to have become a consensus in the general public. However, there are also many controversial opinions against this consensus though at least some of them seem to have a reasonable base. In this paper the skepticism on the consensus is classified into five groups, in which the idea that global warming is primarily caused, not by anthropogenic emission of C0_2, but by natural processes such as variation in solar radiation is a typical opinion. These skeptical opinions, however, are mostly ignored by the world. Why does this occur? There are two possible reasons. Firstly, nature of this theme has changed from a scientific one at the beginning into a political one. Secondly, the posture of the mass-media on environmental information tends to report only \u27bad news\u27, which produces a general public opinion where any factors for global warming other than anthropogenic CO_2 are completely ignored

An Essential Role of Cytosolic Phospholipase A2α in Prostaglandin E2–mediated Bone Resorption Associated with Inflammation

Prostaglandin E (PGE)2 produced by osteoblasts acts as a potent stimulator of bone resorption. Inflammatory bone loss is accompanied by osteoclast formation induced by bone-resorbing cytokines, but the mechanism of PGE2 production and bone resorption in vivo is not fully understood. Using cytosolic phospholipase A2α (cPLA2α)-null mice, we examined the role of cPLA2α in PGE2 synthesis and bone resorption. In bone marrow cultures, interleukin (IL)-1 markedly stimulated PGE2 production and osteoclast formation in wild-type mice, but not in cPLA2α-null mice. Osteoblastic bone marrow stromal cells induced the expression of cyclooxygenase (COX)-2 and membrane-bound PGE2 synthase (mPGES) in response to IL-1 and lipopolysaccharide (LPS) to produce PGE2. Osteoblastic stromal cells collected from cPLA2α-null mice also induced the expression of COX-2 and mPGES by IL-1 and LPS, but could not produce PGE2 due to the lack of arachidonic acid release. LPS administration to wild-type mice reduced femoral bone mineral density by increased bone resorption. In cPLA2α-null mice, however, LPS-induced bone loss could not be observed at all. Here, we show that cPLA2α plays a key role in PGE production by osteoblasts and in osteoclastic bone resorption, and suggest a new approach to inflammatory bone disease by inhibiting cPLA2α

A subset of ocular adnexal marginal zone lymphomas may arise in association with IgG4-related disease

We previously suggested a relationship between ocular immunoglobulin (Ig)G4-related disease (IgG4-RD) and marginal zone lymphomas (MZLs). However, the cytokine background associated with these disorders and whether it differs between ocular adnexal MZLs with (IgG4-associated MZL) and without (IgG4-negative MZL) numerous IgG4+ plasma cells are unknown. In this study, we identified the mRNA expression pattern of Th2 and regulatory T-cell (Treg) cytokines in IgG4-RD and in IgG4-associated MZL and IgG4-negative MZL using real-time polymerase chain reaction analysis. Ocular IgG4-RD and IgG4-associated MZL exhibited significantly higher expression ratios of interleukin (IL)-4/β-actin, IL-10/β-actin, IL-13/β-actin, transforming growth factor (TGF) β1/β-actin, and FOXP3/β-actin than did IgG4-negative MZL (p < 0.05). This finding further supports our prior observations that a significant subset of ocular MZLs arises in the setting of IgG4-RD. Furthermore, the presence of a different inflammatory background in IgG4-negative MZLs suggests that IgG4-associated MZLs may have a different pathogenesis