While interesting and unprecedented material characteristics of two dimensionality (2-D) layered nanomaterials are emerging, their reliable synthetic methodologies are not well developed. In this study we demonstrate general applicability of synthetic protocols to a wide range of colloidal 2-D layered transition-metal chalcogenide (TMC) nanocrystals. As distinctly different from other nanocrystals, we discovered that 2-D layered TMC nanocrystals are unstable in the presence of reactive radicals from elemental chalcogen during the crystal formation. We first introduce the synthesis of titanium sulfide and selenide where well-defined single crystallinity and lateral size controllability are verified, and then such synthetic protocols are extended to all of group IV and V transition-metal sulfide (TiS(2), ZrS(2), HfS(2), VS(2), NbS(2), and TaS(2)) and selenide (TiSe(2), ZrSe(3), HfSe(3), VSe(2), NbSe(2), and TaSe(2)) nanocrystals. The use of appropriate chalcogen source is found to be critical for the successful synthesis of 2-D layered TMC nanocrystals. CS(2) is an efficient chalcogen precursor for metal sulfide nanocrystals, whereas elemental Se is appropriate for metal selenide nanocrystals. We briefly discuss the effects of reactive radical characteristics of elemental S and Se on the formation of 2-D layered TMC nanocrystals.
A solution-phase synthetic protocol to form two-dimensional (2D) single-layer transition-metal chalcogenides (TMCs) has long been sought; however, such efforts have been plagued with the spontaneous formation of multilayer sheets. In this study, we discovered a solution-phase synthetic protocol, called "diluted chalcogen continuous influx (DCCI)", where controlling the chalcogen source influx (e.g., H2S) during its reaction with the transition-metal halide precursor is the critical parameter for the formation of single-layer sheets as examined for the cases of group IV TMCs. The continuous influx of dilute H2S throughout the entire growth period is necessary for large sheet formation through the exclusive a- and b-axial growth processes. By contrast, the burst influx of highly concentrated H2S in the early stages of the growth process forms multilayer TMC nanodiscs. Our DCCI protocol is a new synthetic concept for single-layer TMCs and, in principle, can be operative for wide range of TMC nanosheets.
Karyotypic abnormalities in cultured embryonic stem cells (ESCs), especially near-diploid aneuploidy, are potential obstacles to ESC use in regenerative medicine. Events causing chromosomal abnormalities in ESCs may be related to events in tumor cells causing chromosomal instability (CIN) in human disease. However, the underlying mechanisms are unknown. Using multiparametric permeabilized-cell flow cytometric analysis, we found that the mitotic-spindle checkpoint, which helps maintain chromosomal integrity during all cell divisions, functions in human and mouse ESCs, but does not initiate apoptosis as it does in somatic cells. This allows an unusual tolerance to polyploidy resulting from failed mitosis, which is common in rapidly proliferating cell populations and which is reduced to near-diploid aneuploidy, which is also common in human neoplastic disease. Checkpoint activation in ESC-derived early-differentiated cells results in robust apoptosis without polyploidy/aneuploidy similar to that in IntroductionAn important task facing living organisms from birth to death is maintenance of the genome and its transfer to offspring. Elaborate mechanisms have developed to detect, repair, and prevent transfer of genome damage. 1,2 Mechanisms such as DNA repair or apoptotic culling of damaged cells have been evolutionarily conserved from the simplest multicellular organisms. Genome maintenance is especially important in cells of developing mammalian embryos deriving from a single zygotic cell and in adult stem cells, such as hematopoietic stem cells. A particularly vulnerable time in the life of eutherian mammals is the time from fertilization through cleavage and blastocyst formation, prior to uterine implantation, where developing embryos must survive almost independent from maternal nurturing. A highly specialized program of cellular regulation operates during this time, especially in pluripotent embryonic stem cells (ESCs) derived from the blastocyst that give rise to all adult somatic tissues. [3][4][5][6][7][8][9][10][11] ESCs from several mammalian species, including humans, isolated and cultured in vitro as immortalized cell lines, 12,13 provide the potential for therapeutic use in humans. Understanding these specialized embryonic strategies of genome maintenance is necessary to ensure their safe and effective use and may also reveal clues for studies of potentially similar behavior in adult stem cells.Immortalized mouse (m) and human (h) ESCs are subject to genetic and epigenetic instability, primarily chromosomal aberrations such as loss of heterozygosity, uniparental disomy, and aneuploidy. [14][15][16][17][18][19][20][21] This increases the risk of tumorigenic potential and other complications if hESCs are to be used therapeutically. Such behavior is likely related to their specialized strategies for genome maintenance, such as truncated cell cycles with very short or absent gap phases and differences in certain cell-cycle checkpoints compared with somatic cells. 2-5 A problem with analyzing protein biochemi...
Fucoidan is a sulfated polysaccharide found in edible brown algae, such as Undaria pinnatifida, Fucus vesiculosus and Ecklonia cava. Fucoidan usually contains a large proportion of L-fucose and sulfate. Fucoidan has been reported to show various biological activities such as anti-tumor, [1][2][3][4] anti-coagulant, 5,6) anti-viral, 7) and anti-inflammatory. 8) Furthermore, its anti-tumor activity may be due to the inhibition of tumor angiogenesis in Ehrlich ascites carcinoma 1) and lung carcinoma, 9) as well as the direct induction of apoptosis in U9373) and HS-sultan cells. 4) Several marine algal polysaccharides, fucoidan in particular, have been found to induce apoptosis in cancer cells. [10][11][12] Nevertheless, there is no report on the effect of fucoidan in colon cancer, one of the most malignant neoplasias and a frequently occurring tumor in the world.Recently, it has been demonstrated that the phosphorylation/de-phosphorylation states of some regulatory proteins are crucial events along the pathways controlling cell growth and apoptosis. A well-established apoptotic signaling cascade is regulated by mitogen activated protein (MAP) kinases.13) The MAPK pathway consists of a three-tiered kinase core where MAP3K activates an MAP2K which in turn activates an MAPK (ERK, JNK; c-Jun N-terminal kinase, and p38), resulting in the activation of nuclear factor-kB (NF-kB) and cell survival.14,15) Akt signaling is another important transduction pathway that plays a critical role in controlling the balance between cell survival and apoptosis. 16) In this study, we investigated the effect of fucoidan on the induction of apoptosis in HCT-15 cells, human colon adenocarcinoma cells. Because MAPK and PI3K/Akt pathways are involved in cellular proliferation, differentiation, and apoptosis, [17][18][19][20] the phosphorylation and activities of two MAPKs, ERK and p38 MAPK as well as Akt were investigated. Understanding of the underlying mechanism of the induction of apoptosis by fucoidan will benefit the development of chemopreventive and/or chemotherapeutics for colon cancer. MATERIALS AND METHODS Fucoidan and Diallyl DisulfideFucoidan (from Fucus vesiculosus) and diallyl disulfide (DADS) were purchased from Sigma (St. Louis, MO, U.S.A.). The fucoidan was dissolved in phosphate-buffered saline (PBS; Sigma, St. Louis, MO, U.S.A.) to 50 mg/ml and the DADS was dissolved in dimethylsulfoxide (DMSO; Sigma, St. Louis, MO, U.S.A.) to 50 mM at Ϫ20°C until further use.Cell Culture The HCT-15 human colon cancer cells were purchased from the Korea Cell Line Bank (KCLB) and cultured in RPMI1640 (Gibco BRL, Grand Island, NY, U.S.A.) medium supplemented with 10% fetal bovine serum (FBS) (Gibco BRL, Grand Island, NY, U.S.A.) at 37°C in a 5% CO 2 atmosphere. The exponentially growing cells were used throughout the experiments.MTT Assay The 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) (Sigma, Saint Louis, MO, U.S.A.) assay was performed as previously described. 21) In brief, HCT-15 cells were cultured in a 96-well pla...
Fucoidan, a sulfated polysaccharide, has a variety of biological activities, such as anti-cancer, anti-angiogenic and anti-inflammatory. However, the mechanisms of action of fucoidan as an anti-cancer agent have not been fully elucidated. The present study examined the anti-cancer effect of fucoidan obtained from Undaria pinnatifida in PC-3 cells, human prostate cancer cells. Fucoidan induced the apoptosis of PC-3 cells by activating both intrinsic and extrinsic pathways. The induction of apoptosis was accompanied by the activation of extracellular signal-regulated kinase mitogen-activated protein kinase (ERK1/2 MAPK) and the inactivation of p38 MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt. In addition, fucoidan also induced the up-regulation of p21Cip1/Waf and down-regulation of E2F-1 cell-cycle-related proteins. Furthermore, in the Wnt/β-catenin pathway, fucoidan activated GSK-3β that resulted in the decrease of β-catenin level, followed by the decrease of c-myc and cyclin D1 expressions, target genes of β-catenin in PC-3 cells. These results suggested that fucoidan treatment could induce intrinsic and extrinsic apoptosis pathways via the activation of ERK1/2 MAPK, the inactivation of p38 MAPK and PI3K/Akt signaling pathway, and the down-regulation of Wnt/β-catenin signaling pathway in PC-3 prostate cancer cells. These data support that fucoidan might have potential for the treatment of prostate cancer.
Matrix metalloproteinase (MMP)-1 promotes ultraviolet (UV)-triggered long-term detrimental effects such as cancer formation and premature skin aging. Although histone modifications may play a crucial role in the transcriptional regulation of MMP-1, the relationship between UV-induced histone modification and MMP-1 expression is not completely understood. Here, we identify regulators of histone acetylation that may link UV-mediated DNA damage and MMP-1 induction by UV in cultured human dermal fibroblasts (HDFs) in vitro. UV irradiation of HDFs induced MMP-1 expression and increased the level of phosphorylation of H2AX (γ-H2AX), p53 and the acetylation of histone H3 (acetyl-H3). Total histone deacetylase (HDAC) enzymatic activity was decreased by UV irradiation, while histone acetyltransferase (HAT) activity was increased. Suppression of p300 histone acetyltransferase (p300HAT) activity by the p300HAT inhibitor anacardic acid (AA) or by down-regulation of p300 by siRNA prevented UV-induced MMP-1 expression and inhibited UV-enhanced γ-H2AX, p53 level, and acetyl-H3. Using chromatin immunoprecipitation assays, we observed that γ-H2AX, p53, acetyl-H3, p300 and c-Jun were consistently recruited by UV to a distinct region (−2067/−1768) adjacent to the p300 binding site (−1858/−1845) in the MMP-1 promoter. In addition, these recruitments of γ-H2AX, p53, acetyl-H3, p300 and c-Jun to the p300-2 site were significantly abrogated by post-treatment with AA. Furthermore, overexpression of p300 increased the basal and UV-induced MMP-1 promoter activity. Our results suggest that p300HAT plays a critical role in the transcriptional regulation of MMP-1 by UV.
Non-Hodgkin's lymphomas of the orbit and ocular adnexa (OOA), the majority of which are extranodal marginal zone B-cell lymphomas of mucosa-associated lymphoid tissue-type (MALT lymphomas), are a rare disorder. The aim of this study was to evaluate the clinical features and treatment outcomes and complications in patients with MALT lymphoma of OOA. Thirty-seven patients with a histologically verified diagnosis of MALT lymphoma of OOA were included in this retrospective, observational case study. There were 22 (59%) men and 15 (41%) women, with a median age of 44 years (range, 21-80 years). The most common presenting complaint was a slowly growing orbital mass. The stages were IA(E) in 74%, IA(EE) (bilateral involvement) in 18%, IIIA(E) in 6%, and IVA(E) in 3%. None of the patients had an elevated value of LHD or beta(2)-microglobulin. Surgical resection alone was attempted as the sole treatment in two patients, but tumor recurred 19 and 24 months after surgery. Radiotherapy, with a median tumor dose of 3,060 cGy, was administered in 29 patients; all of the patients achieved complete remission, and none of them had severe later complications. Combination chemotherapy alone was employed in three patients with stage IIIA(E) or IVA(E). With a median follow-up duration of 21 months, the 3-year overall survival (OS) rate and event-free survival (EFS) rate were 97% and 86%, respectively. Subgroup analysis of the patients with localized disease, who received radiotherapy as an initial treatment modality, revealed that 3-year OS rate and EFS rate were 100% and 93%, respectively. All disease recurrences were documented histologically as MALT lymphoma. In conclusion complete staging evaluation is needed to select an adequate treatment modality. Radiotherapy alone can produce excellent local control and survival in patients with localized MALT lymphoma of OOA. Systemic chemotherapy should be considered in patients with advanced stages or systemic manifestation.
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