The dataset for the stages of concerns of public-school teachers towards the use of e-learning platform: Malaysian context.

This dataset contains demographic information of 355 respondents and a validated 32-items Stages of Concerns Questionnaire (SoCQ). The SoCQ questionnaire was developed based on the Concerns-Based Adoption Model (CBAM) which measures seven stages of concerns as the variables. They are and .

[Emodin Induces Apoptosis of K562/Adr Cells Probably through Akt-Caspase 3 Signal Pathway].

Objective: To investigate the apoptosis-inducing effects of emodin on multidrug resistant leukemia cell line K562/Adr, and to explore the role of Akt-Caspase 3 signal pathway in apoptosis of K562/Adr cells treated with emodin.

Methods: K562/Adr cells were exposed to emodin of different doses. The ability of emodin to induce apoptosis of K562/Adr cells was detected by Annexin V/PI double labeled flow cytometry and DNA ploidy analysis, the expressions of procaspase-3, PARP, Akt, p-Akt protein were determined by Western blot.

Interleukin 8/KC enhances G-CSF induced hematopoietic stem/progenitor cell mobilization in Fancg deficient mice.

Background: Fanconi anemia (FA) is a heterogeneous genetic disorder characterized by a progressive bone marrow aplasia, chromosomal instability, and acquisition of malignancies. Successful hematopoietic cell transplantation (HCT) for FA patients is challenging due to hypersensitivity to DNA alkylating agents and irradiation of FA patients. Early mobilization of autologous stem cells from the bone marrow has been thought to be ideal prior to the onset of bone marrow failure, which often occurs during childhood.

Normal hematopoiesis and neurofibromin-deficient myeloproliferative disease require Erk.

Neurofibromatosis type 1 (NF1) predisposes individuals to the development of juvenile myelomonocytic leukemia (JMML), a fatal myeloproliferative disease (MPD). In genetically engineered murine models, nullizygosity of Nf1, a tumor suppressor gene that encodes a Ras-GTPase-activating protein, results in hyperactivity of Raf/Mek/Erk in hematopoietic stem and progenitor cells (HSPCs). Activated Erk1/2 phosphorylate kinases and transcription factors with myriad mitogenic roles in diverse cell types.

[Effect of emodin on proliferation inhibition and apoptosis induction in leukemic K562 cells].

The study was aimed to investigate the effects of emodin on proliferation inhibition and apoptosis induction in human chronic myeloid leukemia cell line K562 cells, and to explore the role of P210 protein and activation of caspase 3 in these processes. K562 cells were exposed to emodin at different doses. The proliferation inhibition was detected by MTT assay and colony formation test.

[Emodin induces leukemic HL-60 cells apoptosis probably by inhibiting Akt signal pathway].

This study is to investigate the effect of emodin on inducing human myeloid leukemia cell line HL-60 apoptosis and the role of Akt signal pathway in the apoptosis. HL-60 cells were exposed to various dosages of emodin. MTT assay was used to detect HL-60 cell proliferation.

[Inhibitory effects of emodin on drug-resistant HL-60/ADR cell proliferation and its induction of apoptosis].

The study was aimed to investigate the effects of emodin on the proliferation and apoptosis of adriamycin-resistant HL-60/ADR cells, and to explore the underlying mechanism. The cell viability and colony formation were detected by MTT assay and colony formation assay respectively. Apoptotic cells were tested by means of cell cycle analysis, mitochondrial transmembrane potential levels, caspase-3 activity detection, Annexin V FITC/PI staining and TUNEL labeling.