Suppression of arsenic leaching from excavated soil and the contribution of soluble and insoluble components in steel slag on arsenic immobilization.

A huge amount of soil is excavated by tunnel and road construction projects in urban, coastal, and mountainous regions. These projects enable the effective use of underground spaces, and generally, the excavated soil is expected to be reused after treatment, which is required due to the potential release of geogenic arsenic from the soil. The present study investigated the level of water-soluble arsenic and arsenic phases in excavated soil in order to identify how arsenic is immobilized by soluble calcium and insoluble components in steel slag. The soluble calcium was found to suppress the level of water-soluble arsenic as well as arsenic in fraction 1 (nonspecifically bound) identified by sequential extraction from the soil but increased the level of fraction 2: specifically bound arsenic. The insoluble component did not suppress the level of water-soluble arsenic, but decreased and increased the arsenic levels in fractions 2 and 3 (amorphous iron/aluminum oxide bound), respectively. A column percolation test demonstrated that the arsenic that was inhibited from leaching by the addition of steel slag was the fractions 1 and 2 arsenic. The amounts of arsenic released in the serial batch leaching test were comparable with levels leached regardless of the addition of steel slag. These results indicate that both soluble calcium and insoluble components of steel slag have different roles in suppressing arsenic leaching from excavated soil. Based on these results, it is suggested that steel slag could be utilized to suppress arsenic release, thus enabling the reuse of excavated soil.

Loss of H3K27 trimethylation is frequent in IDH1-R132H but not in non-canonical IDH1/2 mutated and 1p/19q codeleted oligodendroglioma: a Japanese cohort study.

Oligodendrogliomas are defined by mutation in isocitrate dehydrogenase (NADP(+)) (IDH)1/2 genes and chromosome 1p/19q codeletion. World Health Organisation diagnosis endorses testing for 1p/19q codeletion to distinguish IDH mutant (Mut) oligodendrogliomas from astrocytomas because these gliomas require different treatments and they have different outcomes. Several methods have been used to identify 1p/19q status; however, these techniques are not routinely available and require substantial infrastructure investment. Two recent studies reported reduced immunostaining for trimethylation at lysine 27 on histone H3 (H3K27me3) in IDH Mut 1p/19q codeleted oligodendroglioma. However, the specificity of H3K27me3 immunostaining in this setting is controversial. Therefore, we developed an easy-to-implement immunohistochemical surrogate for IDH Mut glioma subclassification and evaluated a validated adult glioma cohort. We screened 145 adult glioma cases, consisting of 45 IDH Mut and 1p/19q codeleted oligodendrogliomas, 30 IDH Mut astrocytomas, 16 IDH wild-type (Wt) astrocytomas, and 54 IDH Wt glioblastomas (GBMs). We compared immunostaining with DNA sequencing and fluorescent in situ hybridization analysis and assessed differences in H3K27me3 staining between oligodendroglial and astrocytic lineages and between IDH1-R132H and non-canonical (non-R132H) IDH1/2 Mut oligodendroglioma. A loss of H3K27me3 was observed in 36/40 (90%) of IDH1-R132H Mut oligodendroglioma. In contrast, loss of H3K27me3 was never seen in IDH1-R132L or IDH2-mutated 1p/19q codeleted oligodendrogliomas. IDH Mut astrocytoma, IDH Wt astrocytoma and GBM showed preserved nuclear staining in 87%, 94%, and 91% of cases, respectively. A high recursive partitioning model predicted probability score (0.9835) indicated that the loss of H3K27me3 is frequent to IDH1-R132H Mut oligodendroglioma. Our results demonstrate H3K27me3 immunohistochemical evaluation to be a cost-effective and reliable method for defining 1p/19q codeletion along with IDH1-R132H and ATRX immunostaining, even in the absence of 1p/19q testing.

Suppression of arsenic release from alkaline excavated rock by calcium dissolved from steel slag.

Massive quantities of alkaline rocks are excavated from urban coastal and mountain areas to make underground spaces available for infrastructure projects; however, such excavated rock often releases arsenic. In the present study, arsenic release from the excavated rocks with steel slag was investigated using dialysis and batch leaching tests to understand where arsenic is immobilized and which components in the steel slag suppress arsenic release from the excavated rock. Dialysis test indicated that the addition of steel slag at 10 wt% could suppress arsenic release at a level greater than 66%. The total arsenic content in the steel slag did not increase as compared with that before the test. Sequential extraction analysis indicated that the arsenic released during the dialysis test is mainly derived from arsenic fraction 1 (nonspecifically bound) due to the higher amount of this arsenic fraction in the excavated rock with the steel slag. Moreover, the steel slag extract could suppress arsenic release from the excavated rock and remove the arsenic from aqueous solution. The pH dependence test further indicated that the arsenic immobilized by the steel slag extract was stable under alkaline pH conditions. The levels of arsenic release decreased with increasing calcium release from the steel slag regardless of the type of excavated rock with an alkaline pH and were particularly seen at calcium released > 500 mg kg-1. These results indicate that the arsenic immobilization could be occurred not on the surface of steel slag, but on the excavated rock, and the calcium dissolved from the steel slag regulates the behavior of arsenic release from the surface of excavated rock. The findings of the present study suggest that the steel slag could be utilized to enable the reuse of excavated sedimentary and metamorphic rock of alkaline pH for the control of arsenic release.

Pro-inflammatory cytokinemia is frequently found in Down syndrome patients with hematological disorders.

Down syndrome (DS) patients are frequently complicated with infections, autoimmune phenomena and hematological disorders, including transient abnormal myelopoiesis (TAM) in infancy and acute megakaryoblastic leukaemia (AMKL) in later life. In this study, serum levels of cytokines from 23 TAM and 15 AMKL patients were examined using the highly sensitive microsphere fluorescence system. Statistical differences between DS neonates with or without TAM were found in IL-1beta [median 7.0 pg/ml (0.34-271.6) verses 0.05 pg/ml (0.0-2.4), p=0.034], TNF-alpha [8.11 pg/ml (0.1-253.0) verses 0.41 pg/ml (0.1-1.5), p=0.041], and IFN-gamma [20.0 pg/ml (0.14-406.3) verses 1.5 pg/ml (0.14-5.79), p=0.036]. Moreover, abnormal inflammatory cytokinemia was also found in myelodysplastic syndrome (MDS) and AMKL with DS. These abnormal cytokinemia may have a role in the pathophysiology of TAM, MDS and AMKL in DS, especially in liver fibrosis or myelofibrosis.