Biomedical subjects

J Cen

Publications and source records attributed to J Cen.

17 recordsLinked to original sources

PubMed2001

[In vitro effect of lovastatin on NB4 promyelocytic leukemia cells].

OBJECTIVE: To explore the effect of lovastatin(LOV) on cell growth, apoptosis and differentiation of NB4 cells and elucidate some of the possible mechanism. METHODS: Cell proliferation and viability were analyzed by MTT assay and trypan blue exclusion assay, cell differentiation by NBT reduction. Cell morphological examination, DNA electrophoresis, flow cytometry, TUNEL in situ hybridization and semi-quantitative RT-PCR were performed to determine cell apoptosis. H,K,N-ras gene expression was investigated by RT-PCR and p21Ras protein expression by flow cytometry. RESULTS: 1. LOV inhibited the proliferation of NB4 cells with a lC50 of 12.59 mumol/L. 2. LOV induced apoptosis of NB4 cells, affected the cell cycle progression and arrested NB4 cells in G1/S phase. Bcl-2 mRNA was down-regulated by LOV in a time-dependent manner. 3. LOV could not induce the differentiation of NB4. 4. LOV did not increase the expression of H,K,N-ras mRNA, but decrease p21Ras protein expression on the cellular membrane. CONCLUSION: LOV can inhibit proliferation, induce apoptosis and interfere with cell cycle progression, but not induce differentiation of NB4. Inhibition of p21Ras protein isoprenylation is considered to be the major mechanism of LOV affecting NB4 cells.

Antineoplastic Agents↗

PubMed2000

Expression of the human multidrug resistance gene mdr1 in leukemic cells and its application in studying P-glycoprotein antagonists.

OBJECTIVE: To investigate the retrovirus-mediated transfer and expression of multidrug resistance gene (mdr1) in hematopoietic cells and to develop a model for studying the possible reversal of the MDR-mediated phenotype. METHODS: A retroviral vector HaMDR expressing the human mdr1 gene was packaged by PA317 cells with a titer of up to 8.5 x 10(5) CFU/ml. K562 leukemia cells were infected with MDR retrovirus, and transfectant K562/MDR cells were generated. The integration and expression of the exogenous mdr1 gene in K562/MDR cells were determined by polymerase chain reaction and flow cytometry. The reversal ability of P-glycoprotein (P-gp) antagonists was analyzed by in vitro drug sensitivity, accumulation and efflux of rhodamine 123 (Rh123) in this model. RESULTS: Transduction with amphotropic MDR retrovirus resulted in integration and expression of the mdr1 gene in the resistant cells, where an aberrant splicing transcript of the mdr1 gene was found. The K562/MDR cells displayed a classic MDR phenotype with a 41-78 fold resistance to vincristine and colchicine in comparison with parental K562 cells. The drug sensitivity of K562/MDR cells to vincristine can be completely restored by cyclosporin A (CsA, 2 mg/L) and Cremophor EL (CRE 132 mg/L), either individually or in combination (P < 0.05). CsA (3 mg/L) can block the efflux pump function of P-gp shown by the significantly increased accumulation and efflux reduction of Rh123 in K562/MDR cells. CONCLUSIONS: Retroviral vector HaMDR allows transfection with high-level expression of the mdr1 gene in human myeloid progenitor cells K562. The transfected K562/MDR provides a simple, sensitive model for developing antagonists of P-gp and studying their mechanism of action.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2000

[Adjustable interatrial communication in management of severe congenital heart disease].

OBJECTIVE: To assess the use of adjustable interatrial communication in patient with severe congenital heart disease undergoing open heart surgery. METHODS: From February 1998 to June 1999, 13 patients with severe and complex congenital heart disease underwent open heart surgery. Seven patients underwent total cavopulmonary connection, five patients repair of Ebstein's anomaly, and one patient right atrial-pulmonary connection. Adjustable interatrial communication was made in all patients. Four patients had the communication closed at the time of operation, 4 patients had the communication opened at the time of operation, and 5 patients had the communication adjusted and closed postoperatively. RESULTS: All patients had a smooth postoperative process. There were no postoperative death and no severe postoperative complications. CONCLUSION: Adjustable interatrial communication for the patients undergoing modified Fontan procedure or correction of Ebstein's anomaly may be advantageous.

Adolescent↗

PubMed2000

[Study on the differentiation and apoptosis of promyelocytic leukemia cells induced by tributyrin].

OBJECTIVE: To investigate the differentiation of NB4 and MR2 cells induced by tributyrin (TB) in combination with different doses of all-trans retinoic acid (ATRA) and to see if TB can induce apoptosis of NB4 and MR2 cells. METHODS: Cell differentiation was analyzed by NBT reduction and CD(11b), CD(14) and CD(33), apoptosis by morphology, DNA electrophoresis, flow cytometry (FCM) and TUNEL in situ hybridization, bcl-2 expression by reverse transcriptase polymerase chain reaction. RESULTS: 0.2 mmol/L TB in combination with different doses of ATRA could potentiate the differentiation of NB4 cells induced by ATRA alone. No MR2 cell could be markedly induced by ATRA alone or in combination with TB. Treated with 1 mmol/L TB for 24 hours NB4 and MR2 cells exhibited a morphological characteristic of apoptosis and typical DNA ladder on gel electrophoresis. FCM analysis showed that TB could interfere with cell cycle in NB4 and MR2 cells, with a similar ratio of sub-G(1) in both cell lines. TUNEL in situ hybridization confirmed these results. Further study showed that TB could gradually down-regulated bcl-2 expression. CONCLUSION: TB exerts synergetic effect on ATRA-induced differentiation and induces apoptosis in promyelocytic leukemic cells.

Apoptosis↗

PubMed1999

[Surgical treatment of ventricular septal defect in infants: report of 230 cases].

OBJECTIVE: To review the experience of surgical treatment of ventricular septal defect (VSD) in infants. METHODS: 230 infants with VSD of less than 3 years old underwent surgical repair from Feb. 1990 to Dec. 1997. Their ages ranged from 3 to 36 months. Their weight was 3.2 to 15.5 kg. The number of patients with perimembranous VSD was 192, and that of subpulmonary VSD 36. Two patients had multiple VSDs. 150 patients (65.2%) had moderate or severe pulmonary hypertension before operation. RESULTS: Thirteen patients died during hospitalization period, with a hospital mortality of 5.65%. The main causes of death were pulmonary hypertensive crisis and arrhythmia. The leading complications were pulmonary infections, arrhythmia and pulmonary hypertensive crisis. CONCLUSIONS: Surgical treatment of VSD in infancy may have a satisfactory outcome, it standardized surgical techniques and the improved perioperative management are used.

Cardiac Surgical Procedures↗

PubMed1998

[Efficient gene transfer mediated by retrovirus vector in leukemic cells].

OBJECTIVE: To establish an efficient and safe gene transfer system mediated by retrovirus for providing an experimental basis of gene therapy in human leukemia. METHODS: The retrovirus vector pLXSN, carrying the NeoR, was transferred into amphotropic packaging cell line GP + envAm12 by liposome method or by transduction. Retrovirus with higher titer was used to infect human leukemic cell lines NB4, U937 and THP-1. The efficiency of gene transduction was tesed on colonies formed by K562 cells after gene transduction. RESULTS: The titer of DOSPER liposome transfected GP + envAm12 pool on NIH3T3 cells was 8.0 x 10(5) CFU/ml while that of producer pool infected with mouse retrovirus was 1.6 x 10(7) CFU/ml. Integration of NeoR into human leukemic cells was confirmed by PCR. By both nested PCR and NeoR rescue assay, no helper virus was found. NeoR gene transfer with the efficiency as high as 93.3 to 100% in K562 cells was verified by semi-nested PCR on the colonies after seven days' culture. CONCLUSION: The efficiency and safety of the gene transfer system may provide an optimal experimental system in gene therapy for human leukemia.

Animals↗

PubMed1994