Cost of Illness ; Humans ; Quality-Adjusted Life Years

Adult ; Epilepsy ; chemically induced ; therapy ; Humans ; Male ; Nitrobenzenes ; poisoning ; Occupational Exposure ; Poisoning ; complications ; therapy

This study was aimed to investigate the inhibitory effect of emodin on the proliferation of HEL cells, the inducing apoptosis effect of HEL cells and their mechanisms. The proliferation inhibition was detected by MTT method; the change of morphology was observed by AO/EB stains; the cell cycle and apoptosis was analyzed by flow cytometry; the expressions of Akt, P-Akt, P-GSK3β and HSP70 proteins were determined by Western blot. The results indicated that emodin displayed significant anti-proliferative effect on HEL cells in a dose dependent manner(r = 0.99), with IC(50) value of 4.19 µmol/L; AO/EB stains showed that the morphology of HEL cells obviously changed after emodin treatment for 24 hours, and at 24 and 48 hours the apoptosis rates of HEL cells treated by emodin were (27.35 ± 1.68)% and (58.49 ± 1.55)% respectively. Compared with blank control group, the cell ratio in G(0)/G(1) phase increased while that in S phase decreased (p < 0.01); the expression of Akt protein was not changed (p > 0.05), and that of P-Akt, P-GSK3β and HSP70 proteins were down-regulated (p < 0.05). It is concluded that emodin efficiently inhibits the HEL cell proliferation and induces apoptosis of HEL cells, which may be related to the down-regulation of P-Akt, P-GSK3β and HSP70 proteins expression.
Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Emodin ; pharmacology ; Glycogen Synthase Kinase 3 ; metabolism ; Glycogen Synthase Kinase 3 beta ; HSP70 Heat-Shock Proteins ; metabolism ; Humans ; Leukemia, Erythroblastic, Acute ; metabolism ; pathology ; Proto-Oncogene Proteins c-akt ; metabolism

AIM:To investigate the differentiation-inducing effects of baicalin on HL-60 leukemia cells.METHODS:The effect of baicalin on differential induction in AML cell line HL-60 was evaluated by cellular morphology,clone formation assay,CD11b and CD33 expression and NBT assay.RESULTS:Baicalin inhibited the proliferation of HL-60 cells.It enhanced the expression of CD11b on HL-60 cells,also increased the expression of CD33.HL-60 cells showed differentiation morphology after the drug treatment examined by Wright-Gimesa staining and NBT assay.CONCLUSION:Baicalin possessed differentiation-inducing effects on HL-60 cells.

According to Chinese medicine, the atlantoaxial joint is a composite joint composed of tendons and bones, and the stability of the joint depends on the 'tendon-bone balance' involving tendons, ligaments, atlas and axis. Multiple causes of 'tendon off-position, joint subluxation' will lead to joint 'tendon-bone imbalance', which will evolve into atlantoaxial subluxation (AAS), endangering human health. Chinese therapeutic massage (tuina) is a very effective treatment for AAS in adults, but conventional manipulations are prone to ineffectiveness or accidents due to neglect of the causal relationship of the 'tendon-bone imbalance' and inappropriate manipulations. Compared with conventional manipulations, the rational choice of modified manipulations under the guidance of 'tendon-bone balance' theory is more effective and less risky, and more worthy of clinical promotion. From the 'tendon-bone balance' theory, we considered the shortcomings of conventional manipulations, and introduced several modified manipulations that have their own strengths in 'tendon smoothing' and 'bone setting', in order to provide new ideas for treatment of AAS in adults.

ObjectiveTo examine the relationship between ankle brachial index (ABI) and the extent of coronary stenosis and evaluate the usefulness of ABI to predict the extent of coronary stenosis in old patients.Methods118 patients with coronary angiography were examined by ABI and hemostatic factors evaluation in addition to history collection.ResultsABI was inversely and significantly associated with Gensini score. ABI reduced significantly (P<0.001) in the patients with 3-vessel or left main coronary artery disease (CAD). But there were no significant differences in ABI among the patients with no CAD, 1-vessel or 2-vessel CAD. The corresponding area under the ROC curve was 0.75±0.045, with 95% CI=0.67～0.84 (P<0.001) in ABI in 3-vessel or left main CAD. When ABI≤0.9, it had a relatively high specificity (89.1%) and sensitivity (55.6%) for predicting the presence of 3-vessel disease or left main CAD.ConclusionIn the old patients, ABI is inversely and significantly associated with the extent of coronary stenosis, and ABI≤0.9 has a relatively high specificity and sensitivity for predicting the presence of 3-vessel or left main CAD.

This study was aimed to construct model cell line of NPM1-RNAi in HL-60 cells and its resistant line (HL-60/ADR) so as to provide a experimental basis for investigating the potential role of NPM1 gene in leukemia drug resistance. The shRNA targeting to NPM1 was ligated into linear pGCSIL-GFP vector, and transformed into E.coli DH5α. Positive clone was identified by PCR and DNA sequencing. pHelper 1.0, pHelper 2.0 and pGCSIL-GFP-NPM1-shRNA were cotransformed into 293T cells by lentivirus vector system. NPM1-RNAi-LV was transfected into HL-60 and HL-60/ADR cell lines. The efficiency of NPM-RNAi-LV was detected by using real-time quantitative RT-PCR and Western blot. The results showed that the recombinant eukaryotic expression vector pGCSIL-GFP-NPM1-shRNA was constructed. pGCSIL-GFP-NPM1-shRNA was packed into NPM1-RNAi-LV by lentivirus vector system, and transfected into HL-60 and HL-60/ADR cell lines. At mRNA level, the efficiency of NPM1 mRNA knockdown was more than 90% (p < 0.05). At protein level, obvious down-regulation of NPM protein was noted, indicating that NPM1 gene in HL-60 and HL-60/ADR cell lines was knocked down after transfected with NPM1-RNAi-LV. The resistance of HL-60/ADR cell line to adriamycin decreased to a certain degree after NPM1 gene silencing. It is concluded that the model cell lines of NPM1-RNAi in HL-60 and HL-60/ADR are successfully constructed, which can be used for investigating the potential role of NPM1 gene in drug resistance of leukemia.
Cell Line, Tumor ; Doxorubicin ; pharmacology ; Drug Resistance, Neoplasm ; genetics ; Genetic Vectors ; HL-60 Cells ; Humans ; Lentivirus ; genetics ; Nuclear Proteins ; genetics ; RNA Interference

This study was aimed to compare the expression level of eIF4E in patients with leukemia and normal controls, and to explore its role in leukemogenesis. White blood cells were collected in 76 leukemia patients and 10 healthy volunteers. The mRNA and protein expressions of eIF4E were detected by QT-PCR and Western blot in 39 cases of acute myeloid leukemia (AML), 15 cases of chronic myeloid leukemia (CML), 22 cases of acute lymphocytic leukemia (ALL) and 10 healthy volunteers as normal controls. The results demonstrated that compared with normal controls, the absolute expression levels of eIF4E mRNA increased in patients with AML, ALL and CML in blastic phase (P < 0.05), but had no significant change between groups of CML in chronic and accelerated phase although some increasing in group of CML in accelerated phase. The relative expression level of eIF4E mRNA had no significant change in AML, ALL, CML groups except the two subtypes of leukemia M4 and M5. Furthermore, the protein expression level in group of CML in accelerated phase and blastic phase and all acute leukemia patients including AML and ALL were higher than that in normal controls (P < 0.05). It is concluded that although its mRNA relative expressions had no significant change in most leukemia patients, the absolute expression level of eIF4E mRNA and its protein expression is up-regulated in most leukemia patients, which may play an important role in leukemogenesis, so the eIF4E may be a promising target for leukemia therapy and eIF4E-targeted therapy may be an option especially for the relapse and refractory leukemia.
Adolescent ; Adult ; Aged ; Case-Control Studies ; Eukaryotic Initiation Factor-4E ; genetics ; metabolism ; Female ; Humans ; Leukemia ; genetics ; metabolism ; pathology ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Leukemia, Myeloid, Acute ; Male ; Middle Aged ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; RNA, Messenger ; genetics ; Young Adult

The purpose of this study was to compare the differences of the protein expression profiles between human myeloid leukemia K562 cells and adriamycin-resistant K562/A02 cells, as well as to select novel resistance-related proteins in myeloid leukemia by means of proteomics. The total cellular proteins were separated from K562 and adriamycin-resistant K562/A02 cells by using technique of two dimensional difference in gel electrophoresis (2D-DIGE). Differentially expressed proteins were analyzed by matrix-assisted laser desorption ionization/time of flight-mass spectrometry (MALDI-TOF/MS), and by protein database searching. Moreover, the differentially expressed proteins were verified at protein and mRNA levels by Western blot assay and quantitative real time PCR. The results showed that 8 proteins differentially expressed in adriamycin-resistant K562/A02 cells, among them 2 proteins were identified to be down-regulated and 6 to be up-regulated. These identified proteins involved in the cell energy metabolism, cell proliferation, cell apoptosis, signal transduction, gene transcription and translation respectively. The results assayed by Western blot were similar to those detected by 2D-PAGE. Two up-regulated proteins Stathmin and CrkL were selected for verification in K562 and K562/A02 cells. As a result, the results detected by Western blot were identical with results from 2D-DIGE; real time quantitative PCR assay showed that the changes of CrkL at mRNA level were identical with changes at protein level, but no complete identity of Stathmin changes at mRNA level and protein level was observed. It is concluded that the difference of protein expression profile exists in K562 and K562/A02 cells. Stathmin and CrkL proteins may be involved in the drug resistance and suggest a novel clue for the resistant mechanisms in myeloid leukemia, which is worth further to explore.
Adaptor Proteins, Signal Transducing ; metabolism ; Doxorubicin ; pharmacology ; Drug Resistance, Neoplasm ; Humans ; K562 Cells ; Leukemia ; metabolism ; Nuclear Proteins ; metabolism ; Stathmin ; metabolism

OBJECTIVETo investigate the effects of emodin on apoptosis induction and proliferation inhibition in human apoptosis and on c-myc protein and mRNA expression in human myeloid leukemia cell line HL-60 cells.

METHODSHL-60 cells were exposed to emodin at different dosages. Growth inhibition was detected by MTT assay and colony formation assay, and cell apoptosis by flow cytometry, TUNEL labeling method, DNA fragmentation and MitoCapture apoptosis detection. The expression of c-myc was detected by RT-PCR and Western-blot.

RESULTSEmodin remarkably inhibited the cell proliferation, with an IC(50) value of 20 micromol/L. HL-60 cells apoptosis could be efficiently induced by emodin in a dose dependent manner. The c-myc protein and mRNA expressions on HL-60 cells were decreased after emodin treatment.

CONCLUSIONEmodin could efficiently induce growth inhibition and apoptosis in HL-60 cells. c-myc may be involved in this process.

Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Emodin ; pharmacology ; HL-60 Cells ; drug effects ; Humans ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism ; physiology ; RNA, Messenger ; genetics