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Objective Our preliminary study demonstrates that quercetin can inhibit the proliferation of HL-60 cells. This sudy aimed to find some drugs which could have synergistic effects with quercetin on apoptosis of HL-60 cells. Methods HL-60 cells were cultured with bortezomib at different concentrations (1, 2, 4, 8, 16, and 32μmol/L) alone or combined with quercetin at different concentrations for 48 h. HL-60 cells were cultured with lenalidomide at different concentrations (5, 10, 20, 40, 80, 160, and 320 μmol/L) alone or in combination with quercetin at different concentrations for 48 h. The CCK-8 assay was used to determine the effects on proliferation of HL-60 cells. Results Bortezomib significantly inhibited the proliferation of HL-60 cells (P 0.05). The results of cell viability of HL-60 cells treated by lenalidomide at higher concentrations (160 and 320μmol/L) were lower than those of the control group (P<0.05). IC50 of quercetin after cells treated by quercetin combined with bortezomib was not different from that treated by quercetin alone. Isobolographic analysis revealed the two drugs had no synergistic effect. Conclusions Bortezomib can inhibit the proliferation of HL-60 cells and it has a synergistic effect with quercetin on HL-60 cells. Lenalidomide has a weaker role in inhibition of the proliferation of HL-60 cells, and it has no synergistic effect with quercetin on HL-60 cells.
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Objective To investigate the effect of membrane-bound prostaglandin E2 synthase 1 (mPGES-1) inhibitor MK886 on cell cycle of the human acute myeloid leukemia HL-60/A cells.Methods Flow cytometry,Western blot and ELISA were used to measure the difference of cell cycle,expression of cyclin D1, mPGES-1 among HL-60/A cells,MNC and HL-60 cells.The effect of MK886 on cell cycle,cyclin D1,mPGES-1,PGE2,P-Akt and c-myc of HL-60/A cells were observed.Results Compared with MNC and HL-60 cells,the expression of cyclin D1 and mPGES-1 were higher in HL-60/A cells,the percentage of G0-G1 phase was decreased [MNC (62.63±6.58) ％,HL-60 (38.86±2.25) ％,HL-60/A (30.53±2.15) ％]and S phase increased[MNC (12.18±4.43) ％,HL-60 (47.70±1.88）％,HL-60/A (57.56±1.54) ％](all P＜ 0.05).After treated with MK886,cell cycle was arrested in G0-G1 phase.The expression of mPGES-1,cyclin D1,P-Akt and c-myc and synthesis of PGE2 were decreased.Conclusion MK886 can arrest HL-60/A cell cycles in G0-G1 phase,which possibly through down-regulation of mPGES-1/PGE2,reduction cyclin D1,P-Akt and c-myc expression.
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Objectiye To investigate the effect of selective COX-2 inhibitor, nimesulide, on inhibiting proliferation of the human acute myeloid leukemia HL-60 cells. Methods HL-60 cells were treated with different concentration of nimesulide. HL-60 cell proliferation was examined by CCK-8 method. Flow cytometry, Western blotting and ELISA were used to measure the effect of nimesulide on apoptosis, cell cycle,COX-2, PGE2, bax, bcl-2 and c-myc. Results Nimesulide inhibited HL-60 cells proliferation in a dose and time dependence manner. Nimesulide induced cell apoptosis and arrested cell cycle in G0-G1 phase. The expression of COX-2 protein declined after treated with nimesulide 48 h, the total apoptosis in 100, 200,400 μmol/L nimesulide-treated group and control group were (24.97 ± 6.36) %, (34.22 ± 5.76) %, (44.59 ±6.69) % and (4.11 ± 1.26) %, there were significant differences (P ＜ 0.05). Nimesulide inhibited the synthesis of PGE2, the expressions of bcl-2 and c-myc protein and upregulated the expression of bax protein simultaneity.Conclusion Nimesulide significantly inhibited the proliferation of HL-60 cells and induced cell apoptosis,which may be associated with the downregulation of COX-2 expression, reduction of PGE2 synthesis, arrest of cell cycle and regulation bcl-2, c-myc and bax protein expression.
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Objective To explore the correlation of atheroselerosis progression and the expression of platelet derived endothelial nitric oxide synthase (eNOS) in rabbits. Methods A total of 24 male New Zealand white rabbits were used in this study. Six of the animals were fed with normal food (control group). Eighteen rabbits were fed with cholesterol-rich food (1 g/d) for 12 weeks to establish the atherosclerosis model. Among 18 models, 6 rabbits were executed immediately and their aorta and platelet samples were collected for further analysis (model group), 6 rabbits were orally administered with pravastatin (10 rag/d) for additional 12 weeks (treated group), and the remaining 6 rabbits were left untreated until the end of the study (untreated group). The control, treated and untreated animals were then killed, and the aorta and platelet samples were collected for eNOS expression analysis (RT-PCR). Results The aorta samples in model and untreated group exhibited rough intima and a lot of longitudinal fatty streaks, which indicated that atherosclerosis models were established successfully. While in treated group, the degree of atherosclerosis was decreased. The average percent of thickness of fatty streaks or atheroselerotic plaques relative to the whole thickness of vessel walls was 0. 04±0. 02, 0. 82±0. 16, 0. 33±0. 18,0. 77±0. 14 in control, model, treated and untreated group, respectively. The thickness of fatty streaks or atherosclerotic plaques was significantly increased in the model and untreated groups and decreased in treated group compared with the control group (both P<0. 05). The expressions of platelet derived eNOS/mRNA were 1. 02± 0. 28, 0. 41± 0. 27, 1.00 ± 0. 77, 0. 40±0. 29 in control, model, treated and untreated group, respectively. The expression of eNOS/mRNA was markedly decreased in model group and untreated group compared with the control group, but was increased in treated group compared with untreated and model groups (F=3. 544, P = 0. 024). Conclusions There is a negative correlation between eNOS expression and atherosclerosis development, which suggests that the reversal effect of pravastatin on atheroselerosis progression and plaque formation may relate to the expression of platelet derived eNOS.
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Objective To detect the expression of VEGF in NHL and analyze the relation of the expression levels with malignant aggressiveness,treatment response,and prognosis.Methods The expression of VEGF in lymph nodes taken from 39 NHL patients Wag measured by immunohistochemical-staining method.9 patients with benign lymphadenopathy were acted as control.Results The expression of VEGF in NHL(79.5%)was higher than that in the contrel(44.4%)(P=0.048＜0.05).In NHL,the VEGF level was higher in aggressive lympboma than that in indolent lymphoma(x2=5.284,P=0.044＜0.05).The patients had the higher-level expression as the Ann Arbor stage Wag higher,and the patients who had the higher-level expression of VEGF had higher serum LDH level,lower chemotherapy remission,unfavorable prognosis and lower 3-year survival (P＜0.05).Conclusion The expression of VEGF in NHL was increased.It was correlated with histopathological grade,Ann Arbor stage,chemotherapy response and prognosis.
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<p><b>OBJECTIVE</b>To identify valid measures for preventing outbreaks of severe acute respiratory syndrome (SARS) among protected healthcare workers in isolation units.</p><p><b>METHODS</b>Architectural factors, admitted SARS cases and infection of healthcare workers in different isolation wards between January 30 and March 30, 2003 were analyzed.</p><p><b>RESULTS</b>Four types of isolation wards were analyzed, including the ward where the thirty-first bed was located on the twelfth floor, the laminar flow ward in the Intensive Care Unit where the tenth bed was located on the fifteenth floor, the ward where the twenty-seventh bed was located on the thirteenth floor of the Lingnan Building, and thirty wards on the fourteenth to eighteenth floors of the Zhongshan Building. The ratios (m(2)/m(3)) of the area of the ventilation windows to the volume of the rooms were 0, 0, 1:95 and 1:40, respectively. Numbers of SARS cases in the wards mentioned above were 1, 1, 1 and 96, respectively. Total times of hospitalization were 43, 168, 110 and 1272 hours, respectively. The infection rates of the healthcare workers in the areas mentioned above were 73.2%, 32.1%, 27.5% and 1.7%, respectively. The difference in the infection rates was of statistical significance.</p><p><b>CONCLUSIONS</b>Isolating SARS cases in wards with good ventilation could reduce the viral load of the ward and might be the key to preventing outbreaks of SARS among healthcare workers along with strict personal protection measures in isolation units.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Disease Outbreaks , Facility Design and Construction , Hospital Units , Infectious Disease Transmission, Patient-to-Professional , Patient Isolation , Severe Acute Respiratory Syndrome , VentilationABSTRACT
<p><b>OBJECTIVE</b>To describe a hospital outbreak of severe acute respiratory syndrome (SARS) and summarize its clinical features and therapeutic approaches.</p><p><b>METHODS</b>The outbreak started with a SARS patient from the community, and a total of 96 people (76 women and 20 men, mean age (29.5 +/- 10.3) years, 93.8% of whom were health care workers) who had exposure to this source patient became infected in a short time. Clinical data in this cohort were collected prospectively as they were identified.</p><p><b>RESULTS</b>(1) The incubation period ranged from 1 to 20 (mean: 5.9 +/- 3.5) days. The duration of hospitalization was (17.2 +/- 8.0) days. (2) The initial temperature was (38.3 +/- 0.6) degrees C, while the highest was (39.2 +/- 0.6) degrees C (P < 0.001), with fever duration of (9.0 +/- 4.2) days. (3) Other most common symptoms included fatigue (93.8%), cough (85.4%), mild sputum production (66.7%), chills (55.2%), headache (39.6%), general malaise (35.4%) and myalgia (21.9%). (4) The radiographic changes were predominantly bilateral in the middle or lower lung zones. The number of affected lung fields was 1.2 +/- 0.8 on presentation, which increased to 2.9 +/- 1.4 after admission (P < 0.001). The interval from the beginning of fever to the onset of abnormal chest radiographs was (3.5 +/- 2.3) days, which increased in size, extent, and severity to the maximum (6.7 +/- 3.5) days later. The time before the lung opacities were basically absorbed was (14.9 +/- 7.8) days. (5) Leukopenia was observed in 67.7% of this cohort. The time between the onset of fever and leukopenia was (4.4 +/- 2.3) days, with the lowest white blood cell count of (2.80 +/- 0.72) x 10(9)/L. (6) The lowest arterial oxygen saturation was (94.8 +/- 3.1)% with supplementary oxygen. (7) Antibiotical therapies included tetracyclines (91.0%), aminoglycosides (83.3%), quinolones (79.2%); 18.8% of the patients received a combination of tetracyclines and aminoglycosides, while 11.5% received a combination of tetracyclines and quinolones, and 63.5% received a combination of tetracyclines, aminoglycosides and quinolones. Vancomycin was used in 13.5% of the patients. (8) 68.8% of the patients were treated with methylprednisolones for a mean interval of (4.9 +/- 2.4) days. The initial dose was (67.3 +/- 28.2) mg/d and the maximal dose was (82.4 +/- 30.5) mg/d. (9) Human gamma-globulin, interferon-alpha, antiviral drugs (oral ribavirin or oseltamivir) were used respectively in 68.6%, 46.9% and 92.7% of the patients. (10) Ninety-five patients (99.0%) had a complete clinical recovery, and only 1 patient (1.0%) died.</p><p><b>CONCLUSIONS</b>SARS appears to be quickly infectious and potentially lethal among health care workers, characterized by acute onset and rapid progression, and mostly bilateral lung involvement on chest radiographs. Proper administration of glucocorticosteroids seems to be of some benefits. Antibiotics, human gamma-globulin, interferon-alpha, and antiviral drugs, although empirically, might be useful to shorten the clinical course.</p>
Subject(s)
Adult , Female , Humans , Male , China , Epidemiology , Cross Infection , Diagnosis , Epidemiology , Therapeutics , Disease Outbreaks , Severe Acute Respiratory Syndrome , Diagnosis , Epidemiology , TherapeuticsABSTRACT
<p><b>OBJECTIVE</b>To assess the effects of hormone replacement therapy (HRT) on platelet activation in postmenopausal women compared with premenopausal women.</p><p><b>METHODS</b>The expressions of CD41 and CD62P in fifteen postmenopausal women before and after HRT were detected using flow cytometry (FCM), with fifteen premenopausal women with a mean age of 47 years as controls.</p><p><b>RESULTS</b>The expressions of CD41 and CD62P in postmenopausal women were higher than those in the control group. CD62P(%), CD62P(I) and CD41 were reduced from 36.40 +/- 5.9, 37.75 +/- 5.8, and 470.11 +/- 74.0 to 27.97 +/- 5.6, 26.64 +/- 4.9, and 303.23 +/- 72.8 after six months of HRT (P < 0.05).</p><p><b>CONCLUSIONS</b>Platelet activation in postmenopausal women was higher than in premenopausal women and was reduced significantly after six months of HRT. HRT may have a favorable effect on reduction of platelet activity.</p>