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Shikoku Basin is unique as being located within a trench-ridge-trench triple junction. Here, we report mineral compositions, major, trace-element, and Sr-Nd-Pb isotopic compositions of bulk-rocks from Sites C0012 (>18.9 Ma) and 1173 (13–15 Ma) of the Shikoku Basin. Samples from Sites C0012 and 1173 are tholeiitic in composition and display relative depletion in light rare earth elements (REEs) and enrichment in heavy REEs, generally similar to normal mid-ocean ridge basalts (N-MORB). Specifically, Site C0012 samples display more pronounced positive anomalies in Rb, Ba, K, Pb and Sr, and negative anomalies in Th, U, Nb, and Ta, as well as negative Nb relative to La and Th. Site 1173 basalts have relatively uniform Sr-Nd-Pb isotopic compositions, close to the end member of depleted mantle, while Site C0012 samples show slightly enriched Sr-Nd-Pb isotopic signature, indicating a possible involvement of enriched mantle 1 (EM1) and EM2 sources, which could be attributed to the metasomatism of the fluids released from the dehydrated subduction slab, but with the little involvement of subducted slab-derived sedimentary component. Additionally, the Shikoku Basin record the formation of the back-arc basin was a mantle conversion process from an island arc to a typical MORB. The formation of the Shikoku Basin is different from that of the adjacent Japan Sea and Parece Vela Basin, mainly in terms of the metasomatized subduction-related components, the nature of mantle source, and partial melting processes. [ABSTRACT FROM AUTHOR]

Short-chain chlorinated paraffins (SCCPs) are an emerging class of persistent organic pollutants (POPs) that are widely detected in environmental matrices and human samples. Because of their environmental persistence, long-range transport potential, bioaccumulation potential, and biotoxicity, SCCPs pose a significant threat to human health. In this study, metabolomics technology was applied to reveal the metabolomic interference in human normal hepatic (L02) cells after exposure to low (1 μg/L), moderate (10 μg/L), and high (100 μg/L) doses of SCCPs. Principal component analysis (PCA) and metabolic effect level index (MELI) values showed that all three SCCP doses caused notable metabolic perturbations in L02 cells. A total of 72 metabolites that were annotated by MS/MS and matched with the experimental spectra in the Human Metabolome Database (HMDB) or validated by commercially available standards were selected as differential metabolites (DMs) across all groups. The low-dose exposure group shared 33 and 36 DMs with the moderate- and high-dose exposure groups, respectively. The moderate-dose exposure group shared 46 DMs with the high-dose exposure group. In addition, 33 DMs were shared among the three exposure groups. Among the 72 DMs, 9, 9, and 45 metabolites participated in the amino acid, nucleotide, and lipid metabolism pathways, respectively. The results of pathway enrichment analysis showed that the most relevant metabolic pathways affected by SCCPs were the lipid metabolism, fatty acid β-oxidation, and nucleotide metabolism pathways, and that compared with low-dose exposure, moderate- and high-dose SCCP exposures caused more notable perturbations of these metabolic pathways in L02 cells. Exposure to SCCPs perturbed glycerophospholipid and sphingolipid metabolism. Significant alterations in the levels of phosphatidylcholines, phosphatidylethanolamines, and sphingomyelins indicated SCCP-induced biomembrane damage. SCCPs inhibited fatty acid β-oxidation by decreasing the levels of short- and medium-chain acylcarnitines in L02 cells, indicating that the energy supplied by fatty acid oxidation was reduced in these cells. Furthermore, compared with low- and moderate-dose SCCPs, high-dose SCCPs produced a significantly stronger inhibition of fatty acid β-oxidation. In addition, SCCPs perturbed nucleotide metabolism. The higher hypoxanthine levels observed in L02 cells after SCCP exposures indicate that SCCPs may induce several adverse effects, including hypoxia, reactive oxygen species production, and mutagenesis in L02 cells.

Background: To investigate the expression of insulin-like growth factor-I receptor (IGF-IR) and sushi domaincontaining protein 3 (SUSD3) in breast cancer tissue, and analyze their relationship with clinical parameters and the correlation betweenthe two proteins., Materials and Methods: The expression of IGF-IR and SUSD3 in 100 cases of breast cancer tissues and adjacent normal breast tissues after surgery was detected by immunohistochemical technique MaxVisionTM, and the relationship with clinical pathological features was further analyzed., Results: The positive rate of IGF-IR protein was 86.0% in breast cancer, higher than 3.0% in adjacent normalbreast tissue (P<0.05) .The positive expression rate of SUSD3 protein was 78.0% in breast cancer, higher than 2.0% in adjacent normal breast tissue (P<0.05). The expression of IGF-IR and SUSD3 was related to estrogen receptor and pathological types (P<0.05),but not with age, stage, the expression of HER-2 and Ki-67 (P>0. 05). The expression of IGF-IR and SUSD3 in breast cancer tissue was positively related (r= 0.553, P<0.01)., Conclusions: The expression of IGF-IR and SUSD3 may be correlated to the occurrence and development of breast cancer. The combined detection of IGF-IR, SUSD3 and ER may play an important role in judging prognosis and guiding adjuvant therapy after surgery of breast cancer.

We tested the effect of Astragalus membranaceus (AM) on acute hemorrhagic stroke. Seventy-eight patients were randomly assigned to Group A (3 g of AM three times/day for 14 days); or Group B (3 g of placebo herb). A total of 68 patients (Group A 36, Group B 32) completed the trial. The increase of functional independence measure scale score between baseline and week 4 was 24.53 ± 23.40, and between baseline and week 12 was 34.69 ± 28.89, in the Group A was greater than 11.97 ± 11.48 and 23.94 ± 14.8 in the Group B (both P≦0.05). The increase of Glasgow outcome scale score between baseline and week 12 was 0.75 ± 0.77 in the Group A was greater than 0.41 ± 0.50 in the Group B (P < 0.05). The results are preliminary and need a larger study to assess the efficacy of AM after stroke.