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Purpose: The primary purpose of this study is to examine the relationships among a firm's industrial cluster involvement, organizational learning and its ability to successfully adapt to external environment. Methodology: Field survey research method was used and data were collected from 943 high technology companies in US, China, Taiwan and Sweden. Multiple regression analysis as well as mediation test were conducted to analyze the data. Findings: The study finds that being positioned in an industrial cluster enhances a firm's learning and further leads to a firm's desired adaptive outcomes. Research Limitation: Using self-reported data could be a potential limitation of this study. It would be preferable to have other forms of data for a study. Further, cross-cultural comparisons are needed to enhance our understandings in this multicultural setting. Practical Implication: The findings provide business executives as well as policy makers a new way of thinking in respect to how to develop a holistic learning practices as well as improving inter-firm trust in order to appropriately adapt to the fast changing environment. Originality/Value: The major contribution of this study is an initial attempt to provide a comprehensive approach in analyzing a firm's industrial cluster involvement. Further, the study attempts to empirically examine learning and cluster involvement in relation to organizational adaptation. [ABSTRACT FROM AUTHOR]

Objective: To explore the role of Ca 2+ -NFAT signaling pathway in Ph + -ALL drug resistance mediated by bone marrow stromal cells., Methods: The transcription level of NFAT mRNA in Sup-B15 cells and Ph + ALL primary cells was detected by polymerase chain reaction. The expression of P-glycoprotein in Sup-B15 cells was detected by flow cytometry. The change of NFAT protein in Sup-B15 cells was detected by Western blot. AnnexinV/7-AAD was used to label cells. Flow cytometry was used to detect cell apoptosis; Fluo 3-AM dye was used to label cells, and flow cytometry used to detect changes of Ca 2+ concentration in leukemia cells., Results: NFAT expression could be detected in both Sup-B15 and Ph + ALL primary cells; P-glycoprotein could not be detected by flow cytometry; CAS could significantly inhibit NFAT protein expression in clinically applied drug concentrations (2.5, 5 μmol/L); Clinically applied concentration of CAS (2.5, 5 μmol / L) has no significant effect on the apoptosis of Sup-B15 cells, while higher concentration of CAS (10 μmol / L) could induce apoptosis of Sup-B15 cells. Bone marrow stromal cells OP9 could, decrease the sensitivity of Sup-B15 cells and Ph + ALL primary cells to imatinib (IM); After co-culture with bone were marrow stromal cells, the Ca 2+ concentration in Sup-B15 cells was enhanced, the levels of NFAT protein and nullear protein in sup-B15 cells also were enhanced. The addition of CAS in co-culture system could inlibit the Ca 2+ -NFAT signaling pathway, reduce the protective effect of OP9 on Sup-B15 cells.Conclution:The Ca 2+ -NFAT sigualing pathway, contributes to the survival of Ph + ALL cells. Bone marrow stromal cells can mediate the resistance of Ph + ALL cells to IM by activating Ca 2+ -NFAT signaling pathway.

Objective: To investigate the effect of Statins on proliferation and apoptosis in human acute T lymphocytic leukemia (T-ALL) cells and its possible mechanism., Methods: Jurkat and CCRF-CEM cells were cultured in different concentrations of Fluvastatin and Simvastatin for 24 h respectively. Then, the cell growth inhibition level was defected by CCK-8; the DNA replication was analyzed by EdU; the cell apoptosis was analyzed by Annexin V/7-AAD double labeling; the cell cycle changes were analyzed by flow cytometry; the expressions of Cyclin D1, p21, p27, BAX, BCL-2 and p-Akt were determined by Western blot., Results: Fluvastatin and Simvastatin both significantly inhibited the growth of Jurkat and CCRF-CEM cells in a dose-dependent manner. The inhibitory rate of Jurkat and CCRF-CEM cells at 0.2 mmol/L Fluvastatin was 41.14% and 57.08% respectively, while the 0.2 mmol/L Simvastatin could supress 68.42% of Jurkat and 77.10% of CCRF-CEM cells. Half or more than half of cell inhibition were observed in Statins-treated groups with significantly statistical differences, compared with the control groups (P<0.05). After the Jurkat and CCRF-CEM cells were treated with Fluvastation and Simvastation of different concentrations for 24 hours, the proportion of early and later apoptotic cells both increased; moreover, the total apoptotic rate increased significantly(P<0.05) at 0.2 mmol/L and 0.3 mmol/L concentration of Fluvastatin and Simvastatin. The detection of cell cycle showed that both of Jurkat and CCRF-CEM cells were arrested in G 1 phase. Western blot revealed that, in comparison with the control group, the expressions of BAX, p21 and p27 in cells treated with Statins were up-regulated, while Cyclin D1, BCL-2 and p-Akt expressions were down-regulated., Conclusion: Statins can suppress T-ALL cell proliferation and induce cell apoptosis through the inhibition of Akt pathway.

Objective: To investigate the effect of alantolactone on perliferation and apoptosis of multiple myeloma (MM) RPMI-8226 cells, and to explore its possible mechism in vitro and in vivo., Methods: The RPMI-8226 cells were treated with alantolactone (1, 2.5, 5, 7.5 and 10 µmol/L) for 48 h, cell viability was detected by CCK-8 assay and the value of IC50 was calculated; The RPMI-8226 cells were treated with alantolactone (2.5, 5 and 7.5 µmol/L) for 48 h, the apoptotic rate was detected by flow cytmetry with Annexin V/PI staining; the expression level of cleaved caspase-3 and phosphorylation of ERK were measured by Western blot; the nude mice was used to further confirm the proapoptotic effect of alantolactone on MM cells in vivo., Results: The alantolactone inhibited RPMI-8226 cell viability remarkably with a dose-dependent manner; the IC50 value of RPMI-8226 cells at 48 h was 4.32 ± 0.15 µmol/L; the apoptotic rate increased observably with a dose-dependent manner; the levels of cleaved-caspase-3 increased and the phosphorylation of ERK decreased significantly; as compared to control, the volum of tumor was much smaller, the expression levels of Ki67 and p-ERK decreased., Conclusion: The alantolactone can efficiently inhibit the proliferation and induce the apoptosis of multiple myeloma RPMI-8226 cells in vitro and in vivo through inhibiting the activation of ERK signal pathway.

This study was aimed to investigate the effect of MEK inhibitor AZD8330 on proliferation and apoptosis of multiple myeloma IM9 and NCI-H929 cell lines and its possible mechanism. These two cell line cells were exposed to different concentrations of AZD8330 for 48 h. The CCK-8 assay was used to detect cell viability and the IC50 value at 48 h. These above-mentioned IM9 and NCI-H929 cells were treated with 5,10 and 100 nmol/L of AZD8330, then the change of cell cycle was analysed by flow cytometry with PI staining. The Wester blot was used to detect the expression levels of cyclin D and cyclin E, and multiple myeloma cells were treated with 10, 100, 1000 and 2000 nmol/L of AZD8330, the AnnexinV/7-AAD double staining was used to analyse cell apoptosis and the Western blot was used to detect the expression level of caspase-3. The results showed that AZD8330 could significantly inhibit the cell viability of IM9 and NCI-H929 cell lines in a time-and dose-dependent manner, the IC50 value (48 h) of IM9 and NCI-H929 were 19.88 ± 2.7 nmol/L and 29.3 ± 2.03 nmol/L respectively, these two cell lines were arrested on G1 phase of cell cycle, the apoptosis cells increased along with enhancement of AZD8330 concentration, and the expression level of cleaved caspase-3 protein was up-regulated. It is concluded that AZD8330 can efficiently inhibit the proliferation of NCI-H929 and IM9 cell lines, and induce apoptosis, suggesting that the AZD8330 may be a potential chemotherapeutic candidate for multiple myeloma therapy.