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Objective To investigate the effects of xanthotoxin from Apiaceae medicinal plants on cell proliferation and apoptosis, and explore its mechanism of action against human gastric carcinoma SGC-7901 cells in vitro. Methods SGC-7901, HepG-2, MCF-7, and A549 cells were treated with different concentrations of xanthotoxin (10, 20, 60, 80, 100, 120, 140, and 160 µg/mL) for 48 h, and the cell viability (IC50) was determined by MTT assay; Xanthotoxin-induced apoptosis in cells was observed by using Hoechst 33258 Staining Kit and Annexin V-FITC Apoptosis Detection Kit; Flow cytometry was used to detect apoptosis related proteins of Fas/FasL, Bid, and DR5/TRAIL proteins in human gastric carcinoma SGC-7901 cells after being treated by xanthotoxin; The influence of xanthotoxin on Caspase-8 protein expression in the cells was determined by Flouormetric Assay Kit. Results Xanthotoxin obviously inhibited SGC-7901, HepG-2, MCF-7, and A549 cells proliferation, and its inhibition was in a concentration-dependent manner; flow cytometry results showed that in a certain concentration range, xanthotoxin can increase the expression levels of Fas/FasL and DR5/TRAIL proteins in a concentration-dependence manner. The content of Bid protein in cells was increased, and it showed concentration-dependence. Conclusion Xanthotoxin may induce SGC-7901 cells apoptosis in a certain concentration range through the Fas/FasL protein mediated death receptor pathway, or by DR5/TRAIL mediated death receptor pathway, and increase the expression level of death receptor protein, activation Caspase-8, activating downstream effect factor, inducing cell apoptosis, or activate Caspase-8 cutting activate protein Bid, and then enter the mitochondrial pathway, induction of apoptosis.

ABSTRACT The above-ground (shoot) system of trees can affect slope stability through effects of infiltration facilitation, surcharge and wind loading. The amount of stem flow that infiltrates into soils is determined by diameter at root collar (DRC) of trees. Tree weight (surcharge) is a function of their heights (H) and diameters at breast height (DBH). Wind loading is related to crown area (CA) of trees. To save efforts for measuring all of these traits, we aimed to build regression models which allow researchers to estimate the other three traits with DBH. The study site was located in the Lienhuachih Forest Dynamics Plot, central Taiwan. DBH, DRC, CA and H of 20-30 individuals for the 18 most dominant tree species were measures. Trees which have been snapped off were excluded. Results showed that the regression models between DRC and DBH were linear. The models of CA against DBH and H against DBH was best built with allometric models, indicating that CA and H stop to increase with DBH once DBH reach to a certain size. In terms of model performance, the models of DRC against DBH was best (r2= 0.48- 0.97), followed by those of H against DBH (r2= 0.32- 0.89). The relatively poor performance of CA against DBH models (r2= 0.15- 0.93), especially for light-demanding tree species, indicated the need of incorporating light environment (i.e. crown illumination index) into regression analysis. Key word：allomeric model, broad-leaved forest, diameters at breast height, landslide, Lienhuachih

ABSTRACT Slope stability of forested areas is often determined by tree root strength. After landslides, the early successional species emerged first, followed by the late successional species. This study aimed to examine whether tree root strength varies as tree species change along with the succession sequence. The study site is in the Lienhuachi Experimental Forest in central Taiwan, where multiple landslides happened in 2008. Three dominant early (Mallotus paniculatus, Sapium discolor, and Schefflera octophylla) and three late successional species (Cryptocarya chinensis, Engelhardtia roxburghiana, and Randia cochinchinensis) were sampled to conduct the single-root-pull-out tests in the field. Root strength which varies with root diameters was estimated with the Root Bundle Model with the root-failure Weibull survival function (RBMw). Results showed that the overall root strength of the early successional tree species were higher than that of late successional species only when root diameter was lower than 5.44 mm. However, among the six species, the root strength of Sapium discolor, an early successional species, was highest and the species with the lowest root strength was a late successional species (Engelhardtia roxburghiana). To precisely estimate tree effects on slope stability, our results highlighted the need to collect root strength data specifically for each species, even though it will be a daunting task for areas rich in tree diversity.Keyword: landslide, Root Bundle Model, vegetation succession

The polarity of ameloblasts and odontoblasts is crucial for their differentiation and function. Polarity-related molecules play an important role in this process. This review summarizes the process of polarity formation of ameloblasts and odontoblasts and their related regulators.成釉细胞和成牙本质细胞极性的形成，对二者的分化及功能至关重要，而极性相关分子在这一过程中发挥着不容忽视的作用。本文就成釉细胞和成牙本质细胞的极性形成过程及其相关调控分子的作用作一综述。.

The bone morphogenetic protein (BMP) family is an important factor in the regulation of cell ular life activities and in the development of almost all tissues. BMP-mediated signaling plays an important role in tooth root development, which is a part of tooth development. Epithelial and mesenchymal interactions are involved in tooth root development, but the BMP signaling pathway has a different effect on tooth root development in epithelial and mesenchymal. This review summarizes the advances of BMP signaling in tooth root development.骨形态发生蛋白（BMP）家族是调节细胞生命活动的重要因子，几乎参与了所有组织的发育。BMP介导的信号通路在牙发育过程中发挥十分重要的作用，而牙根发育是牙发育的一部分，是上皮和间充质相互作用的复杂过程。上皮和牙胚间充质中的BMP信号通路在牙根发育中的作用也有所不同，本文综述了BMP信号通路在牙根发育中作用的研究进展。.

Objective To investigate the proliferation capabilities, immunophenotype changes, level of secreted cytokines and activities against lymphoma cells under the condition that cytokine-induced killer (CIK) cells co-cultured with dendritic cells (DC) in vitro.

The purpose of this study was to analyze the effects of bufalin on the gene expression of K562 cells and on the expression of BMI‑1 pathway constituents in K562 cell apoptosis. K562 cells were treated with bufalin, and the inhibition rate and apoptosis were detected by an MTT assay, flow cytometry and a microarray assay. BMI‑1, p16INK4a and p14ARF were examined by quantitative polymerase chain reaction (qPCR). Bufalin induced significant changes in the gene expression of the K562 cells; 4296 genes were differentially expressed, 2185 were upregulated and 2111 were downregulated. The most upregulated genes were associated with transcription regulation, while the most downregulated genes were associated with the non-coding RNA metabolic processes and DNA repair. qPCR analysis demonstrated that BMI‑1 was overexpressed in the K562 cells. Bufalin is able to downregulate BMI‑1 expression levels in K562 cells prematurely and cause an increase in the expression levels of p16INK4a and p14ARF. Moreover, bufalin downregulated BCR/ABL expression levels in a time‑dependent manner, and the expression of BCR/ABL was not associated with the upregulation or downregulation of BMI‑1 expression. Bufalin may induce K562 cell apoptosis by downregulating BMI‑1 expression levels and accordingly upregulating the expression levels of p16INK4a and p14ARF. Bufalin may also induce K562 cell apoptosis via downregulating BCR/ABL expression levels, and this pathway may be independent of the BMI‑1 pathway.

This study was aimed to investigate the effect of cord blood dendritic cells (DCs) on the in vitro proliferation capability, immunophenotype changes, level of secreted cytokines and activity against leukemia cells of the homologous cytokine-induced killer (CIK) cells. DCs and CIK cells were induced from cord blood mononuclear cells. They were co-cultured at the ratio of 1:5, and CIK cells from cord blood or DC-CIK cells from peripheral blood were cultured as controls. Immunophenotypic changes were analyzed by flow cytometry, increased number of cells were counted by trypan-blue staining, the killing activity to leukemia cells was assayed by MTT, the levels of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and interleukin-12 (IL-12) in the cultured supernatant were detected by ELISA. The results showed that the proliferation capability of cord blood DC-CIK cells was significantly higher than that of cord blood CIK cells and peripheral blood DC-CIK cells (p0.05 and p0.05). Under the same condition, the rate of double positive cells with CD3(+)CD8(+) and CD3(+)CD56(+) in CIK cells was significantly enhanced by co-culture with cord blood DCs (p0.05). The level of IL-12, IFN-γ, and TNF-α in cultured supernatants of cord blood DC-CIK cells increased noticeably on day 3 as compared with CIK cells cultured alone (p0.01, p0.05, p0.05). Within the effector-target ratio range between 2.5:1 to 20:1, the activity of cord blood DC-CIK cells against all subtypes of acute leukemia cells was much higher than that of CIK cells (p0.05), and there was no significant difference among all subtypes of acute leukemia cells, which was the same with the killing effect of peripheral blood DC-CIK cells against leukemia cells. It is concluded that the proliferation capability and anti-leukemia effect of the homologous CIK cells can be enhanced by cord blood DCs. The proliferation capability of cord blood DC-CIK cells is stronger than that of peripheral blood DC-CIK cells, but there is no significant differences of cytotoxicity between DCs and CIK cells. As the cord blood is easily gained and does not easily cause a serious graft rejection, the DC-CIK cells should be clinically applied more extensively as novel immune therapy.

This study was aimed to investigate the effect of dendritic cells (DC) on the proliferation capability, immunophenotype changes, level of secreted cytokines and activity against leukemia of cytokine-induced killer (CIK) cells in vitro. DCs and CIK cells were induced from peripheral blood mononuclear cells of healthy volunteers. They were co-cultured meanwhile CIK cells were cultured alone as controls. Increased number of cells were counted by trypan-blue staining; the killing activity was detected by MTT assay; immunophenotype changes were analyzed by flow cytometry; the IL-12 and INF-gamma levels of the cultured supernatants were detected by ELISA kits. The results showed that the proliferation capability of DC-CIK cells was significantly higher than that of CIK cells (p0.05). Under the same condition, the ratio of double positive cells such as CD3(+) CD8(+), CD3(+) CD56(+) in CIK cells was significantly enhanced by co-cultured with DC cells (p0.05). The levels of IL-12 and INF-gamma in cultured supernatants of DC-CIK cells increased noticeably on day 3 as compared with CIK cells cultured alone (p0.01, p0.05). Within the effector-target ratio range between 5:1 to 40:1, the activity of DC-CIK cells against leukemia cells were much higher than that of CIK cells (p0.05), and this effect showed a positive correlation with the effector-target ratio. It is concluded that the proliferation capability of DC-CIK cells, the level of their secreted cytokines and their activity against leukemia cells are significantly higher than those of CIK cells. This research may suggest an approach for clinical immunotherapy against leukemia with DC-CIK cells.

The study was aimed to investigate the influence of interferon alpha (IFN-alpha) on the expressions of Fas and Fas ligand (FasL) in dendritic cells (DCs) from patients with chronic myeloid leukemia (CML). In addition to adding stem cell factor (SCF), granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor alpha (TNF-alpha) and interleukin 4 (IL-4), the IFN-alpha was added to the serum-free medium for DCs. After culturing for 10 - 14 days, cell phenotype and percentage of Ph(1) chromosome were detected by different methods. The expression of Fas or FasL on CML-DCs and cell cycle of DCs labeled with propidium iodine (PI) were measured by flow cytometry. The concentration of sFas in supernatants was analyzed by enzyme-linked immunosorbent assay (ELISA). The results indicated that the expression of co-stimulatory molecules were improved significantly while the percentages of Ph(1) positive cells decreased. The level of Fas on cells was up-regulated and the concentration of sFas decreased. However, the expression of FasL was negative. The ratio of apoptosis rose gradually while the concentration of IFN-alpha increased. It is concluded that IFN-alpha can accelerate the apoptosis of Ph(1) positive cells through Fas/FasL pathway, so the number of Ph(1) negative cells increases relatively.

To study the influence of IFN-alpha on function of CML-DC cultured in vitro and expression of chemokine and its chemokine receptor, bone marrow mononuclear cells from 13 CML patients were cultured in the fetal calf serum culture system supplemented with rhSCF, rhFlt-3L for expansion system, and adding rhGM-CSF, rhTNF-alpha, rhIL-4, with or without rhIFN-alpha to induce DCs. After incubation for two weeks, the phenotypes of CML-DC were analyzed by direct immunofluorescence and flow cytometry. The concentration of MIP-3beta expressed by CML-DC in the supernatant were analyzed by ELISA. The proliferative ability of T cells from healthy volunteers stimulated by CML-DCs were measured by MTT assay. The results showed that expression of CD86, CD83, CD40, MHC-I class molecules, CCR7, the concentration of MIP-3beta expressed by CML-DC, and the proliferative ability of T cells stimulated by CML-DCs in IFN-alpha group were all significantly higher than that in control group (P0.01). It is concluded that the immunophenotype of CML-DCs can be partially changed by IFN-alpha to accelerate the maturation of CML-DCs, enhance the capacity of CML-DCs, and stimulate allogeneic T lymphocyte proliferation.