Impact of Tunnel Excavation Muck dumped along the canyon on Streamwater Chemistry

岩石中に硫化鉄鉱物を含む岩盤にトンネルを掘削し, 残土を周辺の渓谷に埋め立てると, 硫化鉱物が酸素を含んだ降水や地下水と接触し, 酸化・分解することにより硫酸酸性浸出水が発生し, 生物の斃死や有害金属類の流出などにより周辺環境に悪影響を及ぼす可能性がある。掘削残土の中に酸性化を緩衝する能力を有する鉱物が含まれる場合は, 中和作用により浸出水のpHの低下が抑制されるため, 浸出水のpHは, 硫化鉱物の酸化により生ずる硫酸量と, 緩衝鉱物の分解に消費される硫酸量の兼ね合いによって決まると考えられる。本研究では, トンネル掘削残土の埋め立てによる渓流水の溶存物質濃度の長期的な変化を明らかにするために, トンネル掘削残土の埋め立て区間の直上流, 直下流で, 埋め立て前から後まで23年間, 渓流水質をモニタリングし, その結果に基づき検討した。その結果, 1993～94年に埋め立てが終了した後16年が経過しても, 埋め立てによる渓流水質への影響は続いていた。埋め立て区間の下流ではSO4(2-), Ca(2+), アルカリ度が有意に高い状態が続いているが, 渓流水のpHの低下はみられず, Ca(2+)を主とするカチオンが, S含有鉱物の分解によって生じた硫酸を中和し, pHを中性に保ったと考えられる。埋め立てがCa(2+)以外のカチオン濃度を増加させた期間は3～5年間にとどまり, SiO2には埋め立ての影響がなかった。影響の継続期間については, ワサビ沢では31年, トウバク沢では17年から20年と試算された。To show the long-term changes in streamwater quality after dumping tunnel excavation muck along the canyon, streamwater chemistry monitoring was undertaken at points upstream and downstream from the site where rock muck had been dumped in Wasabi and Toubaku Creek over 23 years. The concentrations of SO4(2-) below the dumping site were significantly increased which is consistent with the results found in the previous study that some of the rock muck contained Greigite. The pH of streamwater below the dumping site was, however, not significantly different from that above the dumping site, suggesting that SO4(2-) was neutralized by some cations such as Ca(2+) which was also significantly increased below the dumping site. Although the difference of mean annual SO4(2-) concentration between the points upstream and downstream of the dumping site became smaller, the difference was still significant for 17 years after dumping. It takes about 31 years in the Wasabi creek and from 17 to 20 years in the Toubaku Creek for the SO4(2-) concentration of streamwater downstream of the rock muck to be returned to the level found upstream

Type II NKT Cells Stimulate Diet-Induced Obesity by Mediating Adipose Tissue Inflammation, Steatohepatitis and Insulin Resistance

The progression of obesity is accompanied by a chronic inflammatory process that involves both innate and acquired immunity. Natural killer T (NKT) cells recognize lipid antigens and are also distributed in adipose tissue. To examine the involvement of NKT cells in the development of obesity, C57BL/6 mice (wild type; WT), and two NKT-cell-deficient strains, Jα18−/− mice that lack the type I subset and CD1d−/− mice that lack both the type I and II subsets, were fed a high fat diet (HFD). CD1d−/− mice gained the least body weight with the least weight in perigonadal and brown adipose tissue as well as in the liver, compared to WT or Jα18−/− mice fed an HFD. Histologically, CD1d−/− mice had significantly smaller adipocytes and developed significantly milder hepatosteatosis than WT or Jα18−/− mice. The number of NK1.1+TCRβ+ cells in adipose tissue increased when WT mice were fed an HFD and were mostly invariant Vα14Jα18-negative. CD11b+ macrophages (Mφ) were another major subset of cells in adipose tissue infiltrates, and they were divided into F4/80high and F4/80low cells. The F4/80low-Mφ subset in adipose tissue was increased in CD1d−/− mice, and this population likely played an anti-inflammatory role. Glucose intolerance and insulin resistance in CD1d−/− mice were not aggravated as in WT or Jα18−/− mice fed an HFD, likely due to a lower grade of inflammation and adiposity. Collectively, our findings provide evidence that type II NKT cells initiate inflammation in the liver and adipose tissue and exacerbate the course of obesity that leads to insulin resistance

Natural Killer T Cells Are Involved in Adipose Tissues Inflammation and Glucose Intolerance in Diet-Induced Obese Mice

Objective: Macrophage as well as lymphocyte infiltration in adipose tissue may contribute to the pathogenesis of obesity-mediated metabolic disorders. Natural killer T (NKT) cells, which integrate proinflammatory cytokines, have been demonstrated in the atherosclerotic lesions and also in visceral adipose tissue. We thus determined whether NKT cells are involved in glucose intolerance and adipose tissue inflammation in diet-induced obese mice. Methods and Results: To determine whether NKT cells are involved in the development of glucose intolerance, male β2 microglobulin knockout mice lacking NKT cells (KO) and C57BL/6J (WT) mice were fed with a high fat diet (HFD) for 13 weeks. Body weight and visceral obesity were comparable between WT and KO mice. However, macrophage infiltration was reduced in adipose tissue and glucose intolerance was significantly ameliorated in KO mice. To further confirm that NKT cells are involved in these abnormalities, α-galactosylceramide (αGC, 0.1μg/g body weight), which specifically activates NKT cells, were administered after 13 weeks of HFD feeding. αGC significantly exacerbated glucose intolerance and also macrophage infiltration as well as cytokine gene expression in adipose tissue. Conclusions: NKT cells play a crucial role in the development of adipose tissue inflammation and glucose intolerance in diet-induced obesity

Radiocaesium accumulation capacity of epiphytic lichens and adjacent barks collected at the perimeter boundary site of the Fukushima Dai-ichi Nuclear Power Station.

We investigated the radiocaesium content of nine epiphytic foliose lichens species and the adjacent barks of Zelkova serrata (Ulmaceae, "Japanese elm") and Cerasus sp. (Rosaceae, "Cherry tree") at the boundary of the Fukushima Dai-ichi Nuclear Power Station six years after the accident in 2011. Caesium-137 activities per unit area (the 137Cs-inventory) were determined to compare radiocaesium retentions of lichens (65 specimens) and barks (44 specimens) under the same growth conditions. The 137Cs-inventory of lichens collected from Zelkova serrata and Cerasus sp. were respectively 7.9- and 3.8-times greater than the adjacent barks. Furthermore, we examined the radiocaesium distribution within these samples using autoradiography and on the surfaces with an electron probe micro analyzer (EPMA). Autoradiographic results showed strong local spotting and heterogeneous distributions of radioactivity in both the lichen and bark samples, although the intensities were lower in the barks. The electron microscopy analysis demonstrated that particulates with similar sizes and compositions were distributed on the surfaces of the samples. We therefore concluded that the lichens and barks could capture fine particles, including radiocaesium particles. In addition, radioactivity was distributed more towards the inwards of the lichen samples than the peripheries. This suggests that lichen can retain 137Cs that is chemically immobilised in particulates intracellularly, unlike bark