Effect of biochars pyrolyzed in N2 and CO2, and feedstock on microbial community in metal(loid)s contaminated soils

Little is known about the effects of applying amendments on soil for immobilizing metal(loid)s on the soil microbial community. Alterations in the microbial community were examined after incubation of treated contaminated soils. One soil was contaminated with Pb and As, a second soil with Cd and Zn. Red pepper stalk (RPS) and biochars produced from RPS in either N2 atmosphere (RPSN) or CO2 atmosphere (RPSC) were applied at a rate of 2.5% to the two soils and incubated for 30 days. Bacterial communities of control and treated soils were characterized by sequencing 16S rRNA genes using the Illumina MiSeq sequencing. In both soils, bacterial richness increased in the amended soils, though somewhat differently between the treatments. Evenness values decreased significantly, and the final overall diversities were reduced. The neutralization of pH, reduced available concentrations of Pb or Cd, and supplementation of available carbon and surface area could be possible factors affecting the community changes. Biochar amendments caused the soil bacterial communities to become more similar than those in the not amended soils. The bacterial community structures at the phylum and genus levels showed that amendment addition might restore the normal bacterial community of soils, and cause soil bacterial communities in contaminated soils to normalize and stabilize

The presence of high level soluble herpes virus entry mediator in sera of gastric cancer patients

The development of gastric cancer (GC) is closely related to chronic inflammation caused by Helicobacter pylori infection, and herpes virus entry mediator (HVEM) is a receptor expressed on the surface of leukocytes that mediates potent inflammatory responses in animal models. However, the role of HVEM in human GC has not been studied. Previously, we showed that the interaction of HVEM on human leukocytes with its ligand LIGHT induces intracellular calcium mobilization, which results in inflammatory responses including induction of proinflammatory cytokine production and anti-bacterial activities. In this study, we report that leukocytes from GC patients express lower levels of membrane HVEM (mHVEM) and have lower LIGHT-induced bactericidal activities than those from healthy controls (HC). In contrast, levels of soluble HVEM (sHVEM) in the sera of GC patients were significantly higher than in those of HC. We found that monocyte membrane-bound HVEM is released into the medium when cells are activated by proinflammatory cytokines such as TNF-α and IL-8, which are elevated in the sera of GC patients. mHVEM level dropped in parallel with the release of sHVEM, and release was completely blocked by the metalloprotease inhibitor, GM6001. We also found that the low level of mHVEM on GC patient leukocytes was correlated with low LIGHT-induced bactericidal activities against H. pylori and S. aureus and production of reactive oxygen species. Our results indicate that mHVEM on leukocytes and sHVEM in sera may contribute to the development and/or progression of GC

Effect of Dieckol, a Component of Ecklonia cava, on the Promotion of Hair Growth

This study was conducted to evaluate the effect of Ecklonia cava, a marine alga native to Jeju Island in Korea, on the promotion of hair growth. When vibrissa follicles were cultured in the presence of E. cava enzymatic extract (which contains more than 35% of dieckol) for 21 days, E. cava enzymatic extract increased hair-fiber length. In addition, after topical application of the 0.5% E. cava enzymatic extract onto the back of C57BL/6 mice, anagen progression of the hair-shaft was induced. The treatment with E. cava enzymatic extract resulted in the proliferation of immortalized vibrissa dermal papilla cells (DPC). Especially, dieckol, among the isolated compounds from the E. cava enzymatic extract, showed activity that increased the proliferation of DPC. When NIH3T3 fibroblasts were treated with the E. cava enzymatic extract and the isolated compounds from the E. cava enzymatic extract, the E. cava enzymatic extract increased the proliferation of NIH3T3 fibroblasts, but the isolated compounds such as eckol, dieckol, phloroglucinol and triphlorethol-A did not affect the proliferation of NIH3T3 fibroblasts. On the other hand, the E. cava enzymatic extract and dieckol significantly inhibited 5α-reductase activity. These results suggest that dieckol from E. cava can stimulate hair growth by the proliferation of DPC and/or the inhibition of 5α-reductase activity

Dasatinib Accelerates Valproic Acid-Induced Acute Myeloid Leukemia Cell Death by Regulation of Differentiation Capacity

<div><p>Dasatinib is a compound developed for chronic myeloid leukemia as a multi-targeted kinase inhibitor against wild-type BCR-ABL and SRC family kinases. Valproic acid (VPA) is an anti-epileptic drug that also acts as a class I histone deacetylase inhibitor. The aim of this research was to determine the anti-leukemic effects of dasatinib and VPA in combination and to identify their mechanism of action in acute myeloid leukemia (AML) cells. Dasatinib was found to exert potent synergistic inhibitory effects on VPA-treated AML cells in association with G₁ phase cell cycle arrest and apoptosis induction involving the cleavage of poly (ADP-ribose) polymerase and caspase-3, -7 and -9. Dasatinib/VPA-induced cell death thus occurred via caspase-dependent apoptosis. Moreover, MEK/ERK and p38 MAPK inhibitors efficiently inhibited dasatinib/VPA-induced apoptosis. The combined effect of dasatinib and VPA on the differentiation capacity of AML cells was more powerful than the effect of each drug alone, being sufficiently strong to promote AML cell death through G₁ cell cycle arrest and caspase-dependent apoptosis. MEK/ERK and p38 MAPK were found to control dasatinib/VPA-induced apoptosis as upstream regulators, and co-treatment with dasatinib and VPA to contribute to AML cell death through the regulation of differentiation capacity. Taken together, these results indicate that combined dasatinib and VPA treatment has a potential role in anti-leukemic therapy.</p></div

HVEM signaling in monocytes is mediated by intracellular calcium mobilization

Herpes virus entry mediator (HVEM) is a member of the TNF receptor (TNFR) superfamily and is expressed on many immune cells, including T and B cells, NK cells, monocytes, and nentrophils. Interaction of HVEM with its ligand, LIGHT, costimulates T cells and increases the bactericidal activity of monocytes and neutrophils. The interaction recruits cytoplasmic TNFR-associated factor adaptor proteins to the intracellular domain of HVEM. This leads to NF kappa B activation as a result of I kappa B alpha degradation and/or JNK/AP-1 activation, and ultimately results in the expression of genes required for cell survival, cytokine production, or cell proliferation. In this study, we show that treatment of human monocytes with recombinant human LIGHT (rhLIGHT) induces rapid elevation of intracellular calcium concentration ([Ca2+](i)) in a HVEM-specific manner in parallel with TNF-alpha production, and enhances the bactericidal activities of monocytes. Immunoprecipitation and Western blotting analyses revealed phosphorylation of phospholipase C gamma 1 (PLC-gamma 1) but not PLC gamma 2. rhLIGHT-induced Ca2+ response was completely abolished by silencing PLC gamma 1, or preincubating monocytes with PLC inhibitors, antagonists of the inositol-1,4,5-triphosphate receptor, or [Ca2+](i) chelators. Furthermore, these PLC/Ca2+ inhibitors also blocked rhLIGHT-mediated I kappa B alpha degradation, generation of reactive oxygen species, TNF-a production and the bactericidal activities of monocytes. Our results indicate that Ca(2+)is a downstream mediator of the LIGHT/HVEM interaction in monocytes.close121

Mechanism by which dasatinib potentiates VPA-treated AML cell death.

<p>The combination of dasatinib and VPA on AML cell differentiation capacity is more potent than that of each drug alone. The combination is enough to promote intensive AML cell death through G₁ cell cycle arrest and caspase-dependent apoptosis. In addition, MEK/ERK and p38 MAPK control dasatinib/VPA-evoked apoptosis as upstream regulators. Eventually, the regulation of cell differentiation capacity contributes to AML cell death.</p

Effects of VPA and dasatinib on the cell viability.

<p>These data represent the means ± SEM. Significantly different from control (*) or combination of VPA and D (#); ***, ###: <i>P</i><0.001. *: <i>P</i><0.05. VPA, Valproic acid; D, dasatinib.</p

Dasatinib/VPA-induced apoptosis is via a caspase-dependent pathway and depends on MEK/ERK and p38 MAPK.

<p>Cells were preincubated with caspase-3 inhibitor (10 µM Z-DEVD-FMK), caspase-9 inhibitor (10 µM LEHD-CHO), MEK/ERK inhibitor (5 µM U0126 and 10 µM PD98059), p38 MAPK inhibitor (10 µM SB203580) and JNK inhibitor (10 µM SP600125) for 1 hr prior to treatment with 0.5 mM of VPA and 5 µM of dasatinib for 72 hr. (A, D) Caspase-9 activity; (B, E) caspase-3 activity (C, F); apoptotic cells. These data represent the means ± SEM. Significantly different from the control (*) or combination of VPA and dasatinib (#); ***, ###: <i>P</i><0.001. Cas3i, caspase-3 inhibitor; cas9i, caspase-9 inhibitor; U, U0126; PD, PD98059; SB, SB203580; SP, SP600125.</p