Diagnostic accuracy of abdominal contrast-enhanced multi-slice spiral CT after oral diluted iodide in a time segment for gastrointestinal fistula in patients with severe acute pancreatitis.

PURPOSE: To evaluate the diagnostic accuracy of abdominal contrast-enhanced multi-slice spiral CT after oral diluted iodide in a time segment (post-ODI ACE-MSCT) for gastrointestinal fistula (GIF) in severe acute pancreatitis (SAP). MATERIALS AND METHODS: Patients with SAP who underwent both post-ODI ACE-MSCT and endoscopy/surgery from 2017 to 2023 were continuously retrospectively involved. Their demographic information and clinical features were recorded prospectively in an in-hospital database. Using endoscopy/surgery results as the reference standard, the sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of post-ODI ACE-MSCT for diagnosing GIF in SAP were calculated by a four-cell table. The consistency of the two diagnostic methods was evaluated by the Kappa test and McNemar's test. RESULTS: Using endoscopy/surgery as the reference standard, a total of 86 cases were divided into the GIF group (N = 52) and the non-GIF group (N = 34). Among the 52 cases of GIF, 88.5% (46/52) cases had a positive result and 11.5% (5/52) cases had a negative result of post-ODI ACE-MSCT for GIF. Among the 34 cases of non-GIF, 2.9% (1/34) case had a positive result and 97.1% (33/34) cases had a negative result of post-ODI ACE-MSCT for GIF. Post-ODI ACE-MSCT had a sensitivity of 88.5% (95% CI 75.9%-95.2%), a specificity of 97.1% (95% CI 82.9%-99.8%), a positive predictive value of 97.9% (95% CI 87.3%-99.9%), a negative predictive value of 84.6% (95% CI 68.8%-93.6%), and an accuracy of 91.9% (83.4%-96.4%). The kappa value was 0.834, and P < 0.001 by McNemar's test. There were no significant differences in diagnostic test characteristics between the two modalities. CONCLUSION: Post-ODI ACE-MSCT can diagnose GIF in SAP in a simple, noninvasive, and accurate way, and can provide earlier imaging evidence for clinical diagnosis and treatment.

Autologous Costal Cartilage Grafting for a Large Osteochondral Lesion of the Femoral Head: A 1-Year Single-Arm Study with 2 Additional Years of Follow-up.

BACKGROUND: There is currently no ideal treatment for osteochondral lesions of the femoral head (OLFH) in young patients. METHODS: We performed a 1-year single-arm study and 2 additional years of follow-up of patients with a large (defined as >3 cm 2 ) OLFH treated with insertion of autologous costal cartilage graft (ACCG) to restore femoral head congruity after lesion debridement. Twenty patients ≤40 years old who had substantial hip pain and/or dysfunction after nonoperative treatment were enrolled at a single center. The primary outcome was the change in Harris hip score (HHS) from baseline to 12 months postoperatively. Secondary outcomes included the EuroQol visual analogue scale (EQ VAS), hip joint space width, subchondral integrity on computed tomography scanning, repair tissue status evaluated with the Magnetic Resonance Observation of Cartilage Repair Tissue (MOCART) score, and evaluation of cartilage biochemistry by delayed gadolinium-enhanced magnetic resonance imaging of cartilage (dGEMRIC) and T2 mapping. RESULTS: All 20 enrolled patients (31.02 ± 7.19 years old, 8 female and 12 male) completed the initial study and the 2 years of additional follow-up. The HHS improved from 61.89 ± 6.47 at baseline to 89.23 ± 2.62 at 12 months and 94.79 ± 2.72 at 36 months. The EQ VAS increased by 17.00 ± 8.77 at 12 months and by 21.70 ± 7.99 at 36 months (p < 0.001 for both). Complete integration of the ACCG with the bone was observed by 12 months in all 20 patients. The median MOCART score was 85 (interquartile range [IQR], 75 to 95) at 12 months and 75 (IQR, 65 to 85) at the last follow-up (range, 24 to 38 months). The ACCG demonstrated magnetic resonance properties very similar to hyaline cartilage; the median ratio between the relaxation times of the ACCG and recipient cartilage was 0.95 (IQR, 0.90 to 0.99) at 12 months and 0.97 (IQR, 0.92 to 1.00) at the last follow-up. CONCLUSIONS: ACCG is a feasible method for improving hip function and quality of life for at least 3 years in young patients who were unsatisfied with nonoperative treatment of an OLFH. Promising long-term outcomes may be possible because of the good integration between the recipient femoral head and the implanted ACCG. LEVEL OF EVIDENCE: Therapeutic Level IV . See Instructions for Authors for a complete description of levels of evidence.

Immunotherapy combined with antiangiogenic agents in patients with advanced malignant pleural mesothelioma: A case report.

BACKGROUND: Malignant pleural mesothelioma has limited therapeutic options and a poor outcome. Antiangiogenic agents might increase the efficacy of immunotherapy as second-line treatment of advanced-stage malignancies. CASE SUMMARY: A patient with stage IIIB pleural mesothelioma received second-line treatment with a combination of pembrolizumab, bevacizumab and chemotherapy following standard chemotherapy under the guidance of second-generation sequencing. He achieved a partial response after four cycles of treatment with progression-free survival of 5 mo. Pembrolizumab was suspended due to grade 2 immunerelated pneumonia, which was resolved by oral glucocorticoids. However, disease progression was observed after immunotherapy rechallenge and anlotinib therapy. The patient had disease progression, multiorgan dysfuntion and died suddenly in October 2019. CONCLUSION: The combination of immune checkpoint inhibitor, anti-angiogenic agents and chemotherapy showed effective response for advanced pleural mesothelioma, but with adverse reactions.

The value of drain fluid amylase as a predictor of postoperative pancreatic fistula after pancreaticogastrostomy.

BACKGROUND: Drain fluid amylase is commonly used as a predictor of pancreatic fistula after pancreaticoduodenectomy (PD). This study aimed to determine the ideal cut-off value of drain fluid amylase on postoperative day 1 (DFA1) for predicting pancreatic fistula after pancreaticogastrostomy (PG). METHODS: Prospective data of 272 consecutive patients undergoing PG between 2010 and 2020 was collected and analysed to determine the postoperative pancreatic fistula (POPF) risk factors. RESULTS: The incidence of POPF was 143 cases (52.6%). The median DFA1 in patients with POPF was significantly higher than that of patients with NO-POPF (5483 versus 311, P < 0.001). DFA1 correlated with POPF in the area under the curve (AUC) of 0.84 (P < 0.001). When DFA1 was 2300 U/L, Youden index was the highest, with a sensitivity of 72.7% and a specificity of 82.9%. Logistic regression analysis showed that DFA1 ≥ 2300 U/L was an independent predictor of POPF (P < 0.001; OR: 12.855; 95% CI: 7.019-23.544). The AUC of DFA1 and clinically relevant postoperative pancreatic fistula (CR-POPF) was 0.674 (P < 0.001). CONCLUSION: DFA1 ≥ 2300 U/L can be used as an independent predictor of POPF after PG. DFA1 ≥ 3000 U/L can predict the occurrence of CR-POPF, when DFA1 ≥ 3000 U/L, the patients should be observed closely active for complications.

Identification of key genes in ruptured atherosclerotic plaques by weighted gene correlation network analysis.

The rupture of atherosclerotic plaques is essential for cardiovascular and cerebrovascular events. Identification of the key genes related to plaque rupture is an important approach to predict the status of plaque and to prevent the clinical events. In the present study, we downloaded two expression profiles related to the rupture of atherosclerotic plaques (GSE41571 and GSE120521) from GEO database. 11 samples in GSE41571 were used to identify the differentially expressed genes (DEGs) and to construct the weighted gene correlation network analysis (WGCNA) by R software. The gene oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment tool in DAVID website, and the Protein-protein interactions in STRING website were used to predict the functions and mechanisms of genes. Furthermore, we mapped the hub genes extracted from WGCNA to DEGs, and constructed a sub-network using Cytoscape 3.7.2. The key genes were identified by the molecular complex detection (MCODE) in Cytoscape. Further validation was conducted using dataset GSE120521 and human carotid endarterectomy (CEA) plaques. Results: In our study, 868 DEGs were identified in GSE41571. Six modules with 236 hub genes were identified through WGCNA analysis. Among these six modules, blue and brown modules were of the highest correlations with ruptured plaques (with a correlation of 0.82 and -0.9 respectively). 72 hub genes were identified from blue and brown modules. These 72 genes were the most likely ones being related to cell adhesion, extracellular matrix organization, cell growth, cell migration, leukocyte migration, PI3K-Akt signaling, focal adhesion, and ECM-receptor interaction. Among the 72 hub genes, 45 were mapped to the DEGs (logFC > 1.0, p-value < 0.05). The sub-network of these 45 hub genes and MCODE analysis indicated 3 clusters (13 genes) as key genes. They were LOXL1, FBLN5, FMOD, ELN, EFEMP1 in cluster 1, RILP, HLA-DRA, HLA-DMB, HLA-DMA in cluster 2, and SFRP4, FZD6, DKK3 in cluster 3. Further expression detection indicated EFEMP1, BGN, ELN, FMOD, DKK3, FBLN5, FZD6, HLA-DRA, HLA-DMB, HLA-DMA, and RILP might have potential diagnostic value.

Long Noncoding RNA LINC00657 Acting as a miR-590-3p Sponge to Facilitate Low Concentration Oxidized Low-Density Lipoprotein-Induced Angiogenesis.

Angiogenesis in atherosclerotic plaque promotes plaque growth, causes plaque hemorrhage, and violates plaque stability. LINC00657 is a long noncoding RNA highly conserved and abundantly expressed in vascular endothelial cells. The present study was designed to investigate the effects and mechanisms of LINC00675 on low concentrations of oxidized low-density lipoprotein (oxLDL)-induced angiogenesis. Cell proliferation, transwell, wound healing, and tube formation assays were conducted to detect the effects of low concentrations of oxLDL on angiogenesis; the results discovered that oxLDL promoted cell proliferation, migration, and tube formation. oxLDL also upregulated LINC00657 expression. Inhibition of LINC00657 by siRNA significantly suppressed oxLDL-induced endothelial cell proliferation, migration, and tube formation. Bioinformatic assay indicated six binding sites in the LINC00657 sequence to miR-590-3p. The upregulation of LINC00657 was related to the downregulation of miR-590-3p in oxLDL-treated endothelial cells; while downregulation of LINC00657 resulted in upregulation of miR-590-3p. The antiangiogenesis effects of si-LINC00657 were partly abrogated by miR-590-3p inhibitor. Further dual-luciferase assay found miR-590-3p inhibited the expression of hypoxia-inducible factor 1α (HIF-1α) by binding to the position of 689-696 in HIF-1α 3'-untranslated region directly. MiR-590-3p also inhibited the oxLDL-induced upregulation of HIF-1α, vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2), and matrix metalloproteinase-9 (MMP-9). These results suggested that in oxLDL-treated endothelial cells, LINC00657 acted as a miR-590-3p sponge to attenuate the suppression of miR-590-3p on HIF-1α, and to promote angiogenesis through VEGF, MMP-2, and MMP-9. The present study provided new insight into the roles of LINC00657 and miR-590-3p in preventing oxLDL-induced angiogenesis and may provide a novel strategy for atherosclerosis treatment.

NF-κB-Regulated miR-99a Modulates Endothelial Cell Inflammation.

Objective. The present study was performed to investigate the effects and mechanisms of miR-99a on LPS-induced endothelial cell inflammation, as well as the regulation of NF-κB on miR-99a production. Methods and Results. ELISA showed that LPS treatment significantly promoted the secretion of inflammatory factors (TNF-α, IL-6, IL-1ß, and MCP-1). LPS treatment also inhibited miR-99a production and promoted mTOR expression and NF-κB nuclear translocation. Overexpression of miR-99a suppressed the LPS-induced TNF-α, IL-6, IL-1ß, and MCP-1 overproduction, mTOR upregulation, and NF-κB nuclear translocation. The PROMO software analysis indicated NF-κB binding site in the -1643 to -1652 region of miR-99a promoter. Dual luciferase reporter analysis, electrophoretic mobility shift assays (EMSA), and chromosome immunoprecipitation (ChIP) assays demonstrated that NF-κB promoted the transcription of miR-99a by binding to the -1643 to -1652 region of miR-99a promoter. Further studies on HUVECs verified the regulatory effects of NF-κB on miR-99a production. Conclusion. MiR-99a inhibited the LPS-induced HUVECs inflammation via inhibition of the mTOR/NF-κB signal. NF-κB promoted miR-99a production by binding to the -1643 to -1652 region of miR-99a promoter. Considering the importance of endothelial inflammation on cardiovascular diseases, such as atherosclerosis, our results may provide a new insight into the pathogenesis and therapy of atherosclerosis.

Effects of miR­590 on oxLDL­induced endothelial cell apoptosis: Roles of p53 and NF­κB.

Oxidized low­density lipoprotein (oxLDL)­induced endothelial cell apoptosis is considered to be important in atherogenesis. MicroRNA (miR)­590 has been reported to inhibit oxLDL­induced endothelial cell apoptosis. However, the mechanism underlying the inhibition of oxLDL­induced endothelial cell apoptosis by miR­590 remains to be elucidated. In the present study, the expression levels of miR­590 were quantified using reverse transcription­quantitative polymerase chain reaction analysis. Cell apoptosis was investigated using Hoechst staining and flow cytometry, and cell viability was measured using an MTS method. The protein expression levels of p53, B cell lymphoma 2 (Bcl­2), Bcl­2­associated X protein (Bax), caspase­3, lectin­like low­density lipoprotein receptor 1 (LOX­1), p38 mitogen­activated protein kinase (MAPK) and nuclear factor (NF)­κB were quantified using western blot analyses. The results of the present study showed that oxLDL treatment inhibited the expression levels of miR­590 in a time­dependent and concentration­dependent manner. The overexpression of miR­590 inhibited oxLDL­induced endothelial cell apoptosis, expression of p53 and Bax, reduction of Bcl­2 and activation of caspase­3. miR­590 also inhibited the oxLDL­induced upregulation of the expression of LOX­1, overproduction of reactive oxygen species (ROS), phosphoryation of p38MAPK and translocation of NF­κB. These findings demonstrated the anti­apoptotic effects of miR­590 in oxLDL­treated endothelial cells, with the mechanisms underlying the effects of miR­590 involved, in part, in the LOX­1­ROS­p38MAPK­NF­κB signaling cascade and the p53­Bcl­2/Bax­caspase­3 signaling pathway. The present study may provide novel insights into the protective properties of miR­590 in preventing atherosclerosis.

Basic transcription factor 3 is involved in gastric cancer development and progression.

AIM: To further analyse cancer involvement of basic transcription factor 3 (BTF3) after detection of its upregulation in gastric tumor samples. METHODS: BTF3 transcription rates in human gastric tumor tissue samples (n = 20) and adjacent normal tissue (n = 18) specimens as well as in the gastric cancer cell lines AGS, SGC-7901, MKN-28, MKN-45 and MGC803 were analyzed via quantitative real-time polymerase chain reaction. The effect of stable BTF3 silencing via infection with a small interfering RNA (siRNA)-BTF3 expressing lentivirus on SGC-7901 cells was measured via Western blotting analysis, proliferation assays, cell cycle and apoptosis profiling by flow cytometry as well as colony forming assays with a Cellomic Assay System. RESULTS: A significant higher expression of BTF3 mRNA was detected in tumors compared to normal gastric tissues (P < 0.01), especially in section tissues from female patients compared to male patients, and all tested gastric cancer cell lines expressed high levels of BTF3. From days 1 to 5, the relative proliferation rates of stable BTF3-siRNA transfected SGC7901 cells were 82%, 70%, 57%, 49% and 44% compared to the control, while the percentage of cells arrested in the G1 phase was significantly decreased (P = 0.000) and the percentages of cells in the S (P = 0.031) and G2/M (P = 0.027) phases were significantly increased. In addition, the colony forming tendency was significantly decreased (P = 0.014) and the apoptosis rate increased from 5.73% to 8.59% (P = 0.014) after BTF3 was silenced in SGC7901 cells. CONCLUSION: BTF3 expression is associated with enhanced cell proliferation, reduced cell cycle regulation and apoptosis and its silencing decreased colony forming and proliferation of gastric cancer cells.

Edaravone, a novel free radical scavenger, prevents steroid-induced osteonecrosis in rabbits.

OBJECTIVE: To investigate the efficacy of edaravone, a novel free radical scavenger, on preventing steroid-induced osteonecrosis (ON) in a rabbit model. METHODS: Thirty-six New Zealand white rabbits were divided into control (C; n = 6), steroid-administered (S; n = 15) and edaravone-administered groups (E; n = 15) after receiving an established protocol of steroid-induced ON. Before and after steroid administration, plasma levels of reduced glutathione (GSH) and lipid peroxidation (LPO) were measured for oxidative stress. Two weeks later bilateral proximal femurs were dissected for micro-CT-based micro-angiography, and the presence or absence of ON and intravascular thrombi were examined histopathologically. Immunohistochemical examination of oxidative injury in bone tissue was conducted using the anti-8-hydoxy-2'-deoxyguanosine and anti-malondialdehyde mAbs. RESULTS: The incidence of ON in the E group (20%) was significantly lower than in the S group (73%). Three to five days after steroid administration, the plasma GSH level was significantly higher and LPO level was significantly lower in the E group than the S group. Compared with the S group, there were significantly more small-sized perfusion vessels and fewer large-sized dilated vessels in the E group. Thrombosis incidence was significantly lower in the E group than the S group. Intraosseous vessels and haematopoietic cells that sustained oxidative injury were significantly fewer in the E group than the S group. CONCLUSION: Edaravone exerted beneficial effects on reducing incidence of steroid-induced ON by suppressing the accumulation of lipid peroxidative products and oxidative DNA damage in endothelial cells and haematopoietic cells.

[Application of serum hepatitis B virus large surface protein determination in lamivudine anti-viral therapy for patients with hepatitis B].

OBJECTIVE: To study the correlation between serum hepatitis B virus large surface protein (HBV-LP) and hepatitis B virus DNA (HBV-DNA) load in hepatitis B patients treated with lamivudine, and the application of serum HBV-LP measurement in evaluation of lamivudine therapeutic effect and end point judgement. METHODS: HBV DNA was detected by fluorescent quantitative PCR (FQ-PCR), serum HBV-LP was detected by enzyme linked immunosorbent assay (ELISA). RESULTS: Both HBV-DNA and HBV-LP decreased in patients responding to lamivudine therapy, and HBV-LP turned negative 3 months later than HBV-DNA. In patients resistant to lamivudine therapy, neither HBV-DNA nor HBV-LP turned negative. In patients whose symptoms relapsed, HBV-LP didn't turn negative, while HBV-DNA was undetectable only transitorily. CONCLUSION: Measuring serum HBV-LP dynamically can be useful in evaluation of lamivudine therapeutic effect.

[Effect of carbon dioxide pneumoperitoneum-laparoscopic surgery on tumor seeding and metastases in endometrial cancer].

OBJECTIVE: To explore the influence of carbon dioxide pneumoperitoneum-laparoscopic surgery on tumor cell seeding and metastases in endometrial cancer. METHODS: Twenty patients with endometrial cancer who underwent laparoscopic surgery and 10 patients with endometrial cancer who underwent laparotomic surgery were enrolled. Each patient was in preoperative clinical StageIand the uterus size in each patient was less than 12 weeks of pregnancy. Carbon dioxide pneumoperitoneum was established and maintained with CO2 insufflation at 4 approximately 6 L/min and intraperitoneal pressure of 13 mmHg with an automatic pneumoperitoneum machine. Cytologic examination of peritoneal fluid(at the beginning and end of the operation), CO2 filtrated gas and the lavage fluid of instruments during the laparoscopic surgery were performed. The protein expressions of E-cadherin,beta-catenin,P-selectin,matrix metalloproteinase-2(MMP-2),vascular endothelial growth factor (VEGF),and CD44v6 in tumor tissues before and after the operation were detected by DAKO Envision. RESULTS: There were no case of positive washing cytology in the peritoneal fluid,CO2 filtrated gas, and the lavage fluid of instruments during the laparoscopic surgery. The expressions of E-cadherin and beta-catenin proteins were obviously abnormal in endometrial cancer. The abnormal expressions of E-cadherin and beta-catenin protein between the pre- and post-operations were not significantly different in both the laparoscopic group and the laparotomic group(P>0.05).The changes of abnormal expressions of E-cadherin and beta-catenin protein were no statistical difference between the two groups(P>0.05). The positive protein expressions of P-selectin,MMP-2,VEGF,and CD44v6 were not significantly different between the pre- and post-operations both in the laparoscopic group and the laparotomic group(P>0.05),and there was also no significant difference between the laparoscopic group and the laparotomic group(P>0.05).The follow-up period in the laparoscopic group was 7 approximately 19 (14.25+/-3.65) months and 7 approximately 19 (13.10+/-4.23) months in the laparotomic group. One patient got infection in the urinary system in the laparoscopic group and one patient had lower extremity venous thrombosis in the laparoscopic group.No recurrence was detected in both groups. CONCLUSION: Laparoscopic surgery for endometrial cancer has no effect on protein expressions of E-cadherin,beta-catenin,P-selectin,MMP-2,VEGF,and CD44v6 in tumor tissues. No evidence has been found that CO2 pneumoperitoneum-laparoscopic surgery may favor endometrial cancer cell seeding and metastases.

[Analysis of operative patterns of 2272 laparoscopic hysterectomies].

OBJECTIVE: To evaluate the clinical efficacy of four different operative patterns of laparoscopic hysterectomy: laparoscopically assisted vaginal hysterectomy (LAVH), laparoscopically introfasial subtotal hysterectomy (LISH), laparoscopically subtotal hysterectomy (LSH) and laparoscopically total hysterectomy (LTH). METHODS: A retrospective analysis on 2272 cases of laparoscopic hysterectomy was carried out, including operating time, blood loss, complication and postoperative recovery. RESULTS: For the two groups which preserved cervix, LISH was performed in 1323 cases. The operating time was (91 +/- 21) min, blood loss (93 +/- 23) ml, complication rate 4.1%. LSH was conducted in 229 cases, with an operating time (70 +/- 18) min, blood loss (69 +/- 17) ml, complication rate 0. The difference between the two groups was significant (all P < 0.01). For the two groups which excised cervix, LAVH was performed in 588 cases, with an operating time (119 +/- 28) min, blood loss (156 +/- 23) ml, complication rate 1.5%; while LTH was carried out in 132 cases, with an operating time (121 +/- 30) min, blood loss (193 +/- 38) ml, complication rate 1.2%. There were no significant differences between the two groups (all P > 0.05). All patients recovered well postoperatively. CONCLUSIONS: The four operative patterns are ideal for hysterectomy. Young patients should be operated with laparoscopic hysterectomy with preservation of cervix, old patients or patients with CIN should be operated with excision of cervix.

[Correlation between local hormones and CD36 transcription level in women with polycystic ovary].

OBJECTIVE: To detect CD(36) expressions in polycystic ovary (PCO), and to explore its correlation with local androgen and insulin at transcription level. METHODS: From August 2002 to February 2003, 12 patients with asymmetric PCO, 15 primary or secondary infertile patients without endocrine disorders and 8 polycystic ovary syndrome (PCOS) with bilateral PCO were recruited. Extraction of follicular fluid and detection of testosterone (T), dehydroepiandrosterone sulfate (DHEAS), insulin (INS) and androstenedione (A(2)) were performed. Relative CD(36) mRNA expression level of human ovarian inner thecal cells was analyzed by auto image analysis system (IAS) after RT-PCR. RESULTS: The level of CD(36) mRNA expression in thecal cells was 0.24 +/- 0.07 in polycystic ovary of PCO group and 0.21 +/- 0.05 in bilateral ovaries of PCOS group, respectively, which were significantly lower than 0.83 +/- 0.13 in normal ovaries (P < 0.01). T and INS levels of follicle fluid in PCO were significantly higher than that in normal ovaries (P < 0.01). T and INS levels of follicle fluid were negatively related to CD(36) mRNA expression of follicular theca interna (r = -0.6810, r = -0.6708, P < 0.01). CONCLUSION: Decrease of scavenger receptor gene CD(36) mRNA may play a role in the pathogenesis of PCO by increasing the level of T and INS in follicular fluid.

[Effects of mifepristone on the proliferation, apoptosis, and cis-platinum (DDP) sensitivity of chemo-resistant human ovarian cancer cells].

BACKGROUND & OBJECTIVE: Mifepristone is an effective progesterone receptor antagonist. It was reported that mifepristone can inhibit the growth of ovarian carcinoma cells either in vitro or in vivo, but the exact mechanism is unknown. The effect of mifepristone on the growth, apoptosis and cis-platinum (DDP)-sensitivity of chemo-resistant ovarian carcinoma cell lines have scarcely been reported. The purpose of this study was to investigate the effect and its mechanism of mifepristone on the proliferation, apoptosis and DDP sensitivity of DDP-resistant human ovarian carcinoma cells, and to give experimental basis for treating refractory ovarian carcinoma with mifepristone. METHODS: DDP-resistant human ovarian carcinoma cell line SK-OV-3 cells were cultured in vitro, and the MTT assay was used to examine the antiproliferative effect of mifepristone with or without DDP on SK-OV-3 cells. The cooperative effects between mifepristone and DDP in inhibiting the growth of SK-OV-3 cells were analyzed. TdT mediated dUTP nick end labeling (TUNEL) and flow cytometry (FCM) were used to examine the effects of mifepristone with or without DDP on the apoptosis and cell cycle of SK-OV-3 cells. RESULTS: Mifepristone produced concentration-dependent antiproliferative effect on SK-OV-3 cells at all experimental concentrations.Enhanced antiproliferative effects were found when SK-OV-3 cells were cultured with mifepristone at 0.625, 1.25, 2.5, 5, 10, and 20 microg/ml combined with 1.25 microg/ml or 2.5 microg/ml DDP (q >1.15). Only additive effects were found when the cells were cultured with mifepristone and 0.625 microg/ml or 5.0 microg/ml DDP (0.85< q< 1.15). Mifepristone induced concentration-dependent apoptosis in SK-OV-3 cells and arrested cells in the G(0)/G(1)-phase of cell cycle. The apoptosis rate were 14.52%, 36.14%, and 53.22%,respectively,when the cells were cultured with mifepristone at 1.25, 2.50, and 5.00 microg/ml. The percentage of G(0)/G(1)-phase cells was increased with the concentration of mifepristone. Synergic effect between mifepristone (at 1.25, 2.5, and 5 microg/ml) and 2.5 microg/ml DDP was found in inducing SK-OV-3 cells apoptosis (q >1.15) and G0/G1-phase stasis. CONCLUSION: Mifepristone can inhibit the growth of chemo-resistant human ovarian carcinoma cells,and enhance its DDP sensitivity. This may be associated with the synergic effect between mifepristone and DDP in inducing apoptosis and G(0)/G(1)-phase stasis.